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Eric GUAGUERE Pascal PRELAUD
A PRACTICAL GUIDE T O
Feline Dermatology Preface by D. W. SCOTT Translation by M . CRAIG
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To Janine, Anne, Adeline, Flore,
To Francoise, Hadrien, Clara, Leo
We love you.
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In memory of Charles Leblois, Clinical director of the National Veterinary School, Alfort, who in the 1920s, was the first to propose a diagnostic approach in animal dermatology, that was based on history taking, clinical examination, differential diagnosis and performing suitable diagnostic tests.
"Diagnosis is an art I pursue with passion Treatment is a chore"
Area of initial presentation of notoedric mange: base of the anterior concha1 cartilage. It is from here that samples should be taken.
Distribution m a s of notoedric mange
Distribution areas of notoedric mange
Documents pour servir d l'~d@cationd'une Dermatologie Animale. ~ d i t i o n Vigot, s 1926
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To Didier Noel Carlotti, Pierre Fourrier. to whom French and European dermatology owes its dynamism and international recognition
To Zeineb Alhaidari, Blaise Hubert, Dominique H&ripret, Thierry Olivry, old friends and companions in veterinary dermatology
To Jean-Pierre Magnol, for teaching us our first steps in dermatohistopathology
To Peter Ihrke, Danny Scott, Ton Willemse, Stephen White, for instilling in us a thorough approach, both clinical and scientific
To all the members of the Groupe d ~ t u d en e Dermatologie des Animaux de Compagnie (GEDAC), for keeping us motivated
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Our thanks go particularly to :
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Merial, who has enabled this ambitious project to take place
- Doctors Alhaidari, Atlee, Bensignor, Bourdeau, Bourdoiseau, Burton, Carlotti, Cozette, Declercq, Degorce, Dehasse, Delabre, Delisle, Denerolle, Devauchelle, Dryden, Ferrer, Fondati, Fontaine, Fritz, Gaultier, Groux, Habran, Hkripret, Hubert, Hugnet, Ihrke, Laubis, Leclercq, Legrand, Lopez, Magnol, Mason, Mege, Mialot, Mueller, (G) Muller, (G.H.) Muller, Noli, Olivry, Paghs, Poirson, Power, Prost, Rivierre, Rzeznik, Saenz de Santa Maria, Scott, Smal, Thomas, Verde, Vroom, White, Wilkinson, Willemse, for contributing their outstanding photographs.
- Doctor Mark Craig for his outstanding translation skills
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Doctors Emmanuel Bensignor, William Bordeau and Cathy Curtis for checking the manuscript. %.
- Professor Gilles Bourdoiseau for his generous encouragement and advice.
- Gabrielle McGarvey, Mary Craig, Aiden Foster, Sarah Heath and Maggie Fisher for assisting in the translation of certain chapters.
- Blackwell Science, PMCAC, Le Recueil de Mkdecine Vktkrinaire, Harcourt Publishers, Saunders for permission to reprint certain illustrations.
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acalGuide to k h DamatoIogy
I Preface I have to share a little something with you.., When my friends, Eric Guagdre and Pascal Prflaud, contacted me and told me that this great work on feline dermatology was being developed... and that they wanted me to write the preface ... I chuckled to myself. You know that you are getting old when folks start asking you topresent overviews and historical perspectives, and to write prefaces ! Eric also told me that I was considered to be the "father " offeline dermatology.Now ... I must say... I never considered myselfto be father of anything but Travis (my son) and Tracy (my daughter). However, as Ipondered the invitation and the acclamation, it certainly gave me a warm,fuzzy (or is thatfurry ?/feeling inside. It is certainly true that dermatology has been my professional life, and that feline dermatology, in particular, has always been my "professional hobby", my little " subspecialty ". But I suppose it was my "fatherly " monograph' and the three addendumsZ4 that followed that publicised and validated my " felinophilic " nature. I want to acknowledge the inspirational writings of three of my predecessors in thefeline dermatology arena :Kenneth P. Baker, Jean Holzworth, and Joan 0.Joshua. Feline dermatology began to " boom " in 1980, with over 3,000 publications being devoted to the subject over the course of the subsequent decade. " Feline endocrine alopecia " evolved from a common to a vanishing cause of bilaterally symetric hypotrichosis, and hypersensitivity (allergy) disorders (atopy, food hypersensitivity, flea-bite hypersensitivity) took its place. The " eosinophilic granuloma complex " vacated the veil of idiopathy and became increasingly recognised as a manifestation of hypersensitivity disorders. " Idiopathic milliary dermatitis " became an endangered species, vanishing before the onslaught of numerous spec$c diseases. " Psychogenic alopecia " retreated to the realm of the rarely diagnosed when we realised that most cats were perfectly sane, they just itched ! In this new millennium, the possibilities are enormous, with more folks interested in, working in, and contributing to the field of feline dermatology than ever before. The knowledge and discoveries in this area can only continue to skyrocket. Continued specialisation in veterinary medicine... look at all the practices andpractitioners now exclusively devoted to cats... will demand increasing expertise and sophistication, be it in the clinic, in the research laboratory, or in the continuing education arena. In this practical guide to feline dermatology, a host of international experts and " stars " have been assembled. You will find, tucked in between the covers of this guide, the absolute most current and useful information in feline dermatology... all thoughtfully, lovingly, and analytically packaged for you. This guide has been expressly designed to be practical, concise, and user-friendly. Use it frequently and use it in good health (yours and that of your feline patients !). Feline dermatology is the best !
Danny W. Scott, DVM, Dip. ACVD Ithaca, New York March 1999 REFERENCES 1 Scott, D.W. J. Amer Anim. Hosp. Assn. 16,331-459 (1980). 2 Scott, D.W. J. Amer. Anim. Hosp. Assn. 23,255-274 (1987). 3 Scott, D.W. J. Amer Anim. Hosp. Assn. 26,515-537 (1990). 4 Norman, P.S. Currenr Opinion in Immunology 5,968-973 (1993).
A Practical Guide to Feline Dermatology
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Blaise HUBERT Clinique VCtCrinaire Foch 38, avenue du MarCchal Foch 34500 BCziers - France
PIN Didier Cabinet de Dermatologie VCt6rinaire HCliopolis B3 -Avenue de Magudas 33700 Bordeaux-MCrignac - France
Chapter :24
Chapter :2
Ken MASON Albert Animal Hospital 333 1 Pacific Highway Springwood 4127 -Australia
Pascal PRELAUD 2, me Gay Lussac 44300 Nantes - France Chapters :1 0 , 1 1 , 2 3 , 2 4 , 2 6
Chapter :12
Catherine MEGE Clinique V6t6rinaire des Grands Cms 60, avenue du 14 juilllet 21300 Chenove - France
Maite VERDE Servicio Dermatologia - Facultad de Veterinaria C/Miguel Servet, 177 Zaragosa - Espana Chapter :25
Chapter :17
Karen A. MORIELLO Department of Medical Sciences School of Veterinaxy Medicine University of Wisconsin-Madison 2015 Linden Drive West Madison-Wisconsin - W 53706 - USA
Margreet VROOM Veterinaire Specialisten Oisterwijk Boxtelsebaan 6 5061 VD - Oisterwijk - The Netherlands Chapter :9
Ralf S. MUELLER Department of Clinical Sciences Colorado State University VTH Fort Collins - CO 80523 - USA
Ton WILLEMSE Utrecht University Faculty of Veterinary Medicine Department of Clinical Sciences of Companion Animals Yalelaan 8 3584 CM - Utrecht - The Netherlands
Chapter :6
Chapter :13
Chapter :4
Chiara NOLI Via Sismondi 62, 20133 - Milano - Italy Chapter :1
Translator Mark CRAIG Re-Fur-All Referrals 3 1 Porchester Rd Newbury, Berks RG14 7QH England
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SUMMARY OP CONTENTS
1
IStructure and functions of skin and coat Chiara Noli
The skin and cutaneous adnexae make up the most important anatomical and physiological barrier between the external environment and the internal organism. Knowledge of the anatomy and histology of the various cutaneous structures, some of which are specific to cats, allows better understanding of all the functions of the skin in the cat (e.g. mechanical protection against water and light, thermoregulation, biochemical homoeostasis, metabolic regulation, immunoregulation, sensory perception and social functions). Genetic determination of coat type and colour, and specific aspects of felime skin and its ecosystem are discussed in detail.
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Diagnostic approach Didier Noel Carlotfi - Didier Pin
The diagnostic approach in feline dermatology must be methodical and include the various steps of a conventional medical consultation as well as additional ones relevant to felime dermatology. Information gleaned from the history and clinical examination, both general and dermatological, allow the practitioner to construct a differential diagnosis. Appropriate diagnostic tests are then chosen to narrow down this list and produce a definitive diagnosis.
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Ectoparasitic skin diseases Eric Guaguere
Skin diseases caused by mites and insects are of prime importance in feline dermatology and enter into the differential diagnosis of many diierent conditions. Although some are often suspected, others are less so because the signs associated with them are non-specific. Some ectoparasitic conditions may be the source of human infestations, unrecognised by either the vet or the dermatologist. This chapter deals with notoedric mange, sarcoptic mange, otodectic mange, cheyletiellosis, trombiculiasis, dernodicosis, pediculosis and flea infestation. Methods of flea control, both mechanical and chemical, are described.
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Dermatophytosis Karen A. Moriello - Douglas J. DeBoer
Dermatophytosis is a superficial fungal infection of the skin. Microsporum canis, the most common cause of feline dermatophytosis, is not p m of the normal fungal flora of cats and its isolation warrants special attention. As dermatophytosis is an important zoonosis, it is very important for veterinary surgeons to be familiar with the condition. Dermatophytosis is transmitted by direct contact involving an infected cat or indirectly via a contaminated environment. Clinical signs are very pleomorphic and dermatophytosis should be considered in the differential diagnosis of all feline skin conditions. Fungal culture is still considered the gold standard for diagnosing feline'dermatophytosis as it allows genus and species identification of the causal organism. Although the disease will resolve spontaneously, treatment is required to speed up resolution, limit the risk of spread to other animals and man, and prevent contamination of the environment. Svstemic antifungal treatment is the treatment of choice. Cliooing oromotes faster healmg and is recommended for long-haired cats and cats with severe infections. Topical therapy limits transmission and the spread of spores in the environment. It needs to be continued until fungal cultures are negative on two or three successive occasions in all animals examined. A contaminated environment is often an important reservoir of spores. Environmental decontamination requires repeated cleaning to eliminate organic debris and frequent application of an antifungal disimfectant. Vaccination is not currently an effective means of preventing dermatophytosis.
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5 ~
e mycoses e ~
Lluis Ferrer - Alessandra Fondati
Deep mycoses are rare in the cat and may affect only the skin (subcutaneous mycoses) or internal organs and the skin (systemic mycoses). They are caused by saprophytic fungi that normally live in the soil, vegetation and decomposing organic matter. Most are considered opportunistic pathogens. Dermatological signs are characterised by nodules, fistulae and ulcers on the ventrum, distal limbs and/or the face. In systemic mycoses, various systemic signs (respiratory, neurological, ocular, bony) are observed. Diagnosis is based on cytology or histopathology to demonstrate fungi in affected tissues. Fungal culture is necessary to identify the causal organism. Immunological techniques can sometimes be used in the diagnosis of systemic mycoses. Treatment of deep mycoses is difficult and definitive cure is rarely possible.
dermatoses 1 6 R.Bacterial Mueller Bacterial dermatoses, also called pyodermas, are rare in the cat despite being so common in the dog. The main reasons for this are perhaps the small number of bacteria on the skin and coat of the cat and also the importance of grooming in this species. Bacterial skin infections are usually secondary to trauma, bites or scratches and resolve easiiy with suitable antimicrobial treatment. However, some specific bacterial infections, possibly secondary to a systemic illness (e.g. retrovirus infection), can be difficult both to diagnose and to treat.
dermatoses 1 7 E.Viral Guaguere Vial dermatoses are a developing field in felime dermatology. They are underdiagnosed because of difficulties in identifying the causal virus, but new investigative procedures (e.g. electron microscopy, immunohistochemistry and molecular biology) now enable these new dermatoses to be characterised. An understanding of them is imoortant as thev enter into the differential diagnosis of many different conditions. Some of these conditions also represent a major zoonotic risk for man. Poxvirus infection, feline infectious peritonitis, papillomavirus infection, retrovirus infections and herpesvirus infection are considered in this chapter.
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8 The cat flea: applied biology M . Dryden
The cat flea Ctenocephalides felis felis is the cause of recurrent infestations in cats, dogs and their environment. Flea control can be difficult without a good understanding of how the flea interacts with its hosts and environment. This chapter deals with the biology, ecology and epidemiology of the cat flea. Practical, effective methods of flea control are presented.
9 Flea allergy dermatitis Margreet W. Vroom
Flea allergy dermatitis (FAD) is the most common pruritic dermatosis in the cat. A diagnosis of FAD cannot be e l i i a t e d by the absence of fleas or flea faeces because allergic cats can remove fleas from their coat by grooming. FAD should be suspected when self-induced, principally dorsolumbar, alopecia, miliary dermatitis or, more rarely, eosiiophiiic plaques or limear granulomas are present. Allergy testing has little diagnostic value. Treatment initially involves rigorous flea control for the affected cat, in-contact animals and the environment. When antipruritic treatment is necessary, the use of corticosteroids produces immediate improvement. Immunotherapy is, currently, of no benefit.
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10 Atopic dermatitis Pascal Prdlaud - Sophie Gilbert
Atopy is the cause of many pruritic dermatoses (e.g. miliary dermatitis, eosinophilic plaques, selfinduced alopecia and cemicofacial pruritus). Lesions can sometimes even resemble those seen in human and canine atopic dermatitis. Diagnosis of atopy is complicated by the unreliability of intradermal testing, poor specificity of serological tests, many normal cats having comparable serum allergen-specific IgE levels, and relatively non-specific clinical signs. Treatment is usually based on avoidance of the allergens involved (e.g. using elimination diets and flea control), antiinflammatory medication, either steroidal or non-steroidal, and as a last resort specific immunotherapy, although the efficacy of this is difficult to assess.
Ill Food intolerance E. Guagu2re
Food intolerance should be considered a possible cause of non-seasonal pmritus in the cat, especially for self-induced lesions of the face and neck, and when lesions are accompanied by gastrointestinalproblems. Diagnosis is based on response to an elimination diet fed over at least 10 weeks. The diet must contain novel sources of protein and should only be formulated after looking very carefully at the cat's previous diet. Either a commercial or home-prepared diet may be given, depending on what suits the animal and its owners. Challenging the cat with its previous diet is the only way to conf~rmthe diagnosis and to select foods for inclusion in the maintenance diet.
12 Eosinophilic granuloma complex K . Mason - G . Burton The eosinophilic granuloma complex is a group of diverse clinical entities. Typical forms (indolent ulcer, eosinophilic plaque and eosinophilic granuloma) and atypical forms (mosquito bite hypersensitivityand familial forms) are described. These entities are, in fact, reaction patterns with many diierent causes. A thorough diagnostic approach is, therefore, required to investigate allergic and infectious causes. For refractory or prolonged cases, an inverse allergy work-up can be implemented. This consists of eliminating all the possible causes, associated with symptomatic treatment, then challenging the cat with one thing at a time, once lesions are under control. Therapy should, primarily, be based on treating the cause. Symptomatic therapy is often required and involves mainly corticosteroids, antibiotics and cyclosporin.
1 1 3 Auto-immune dermatoses Auto-immune dermatoses are rare. They are characterised immunologically by the deposition of auto-antibodies at various levels of the epidermis (pemphigus) and basement membrane (bullous pemphigoid), or immune complexes within the basement membrane (lupus erythematosus). Knowledge of these diseases is important as they enter into the differential diagnosis of many diierent conditions. The pemphigus complex consists of several forms: pemphigus vulgaris (PV), pemphigus foliaceus (PF) and pemphigus erythematosus (PE). Bullous pemphigoid (BP) has just recently been identified in the cat. Discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE) are encountered only exceptionally. Diagnosis is based on the history, clinical examination, and histopathology. For SLE, other procedures such as haematology and antinuclear antibody tesimg, must be canied out. The prognosis for auto-immune disorders is variable; relatively good for PF, PE and DLE, guarded for PV, BP and SLE. Treatment involves mainly oral corticosteroids at immunosuppressive doses and possibly certain alkylating agents (chlorambucyl) and gold salts (aurothioglucose).
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14 ~ermatolo~ical manifestations of systemic diseases D. Hkripizt
Dermatological manifestations of systemic diseases are starting to be documented in the cat, although their pathogenesis is not always understood. They are very diverse, clinically, and relate to various systemic illnesses. Their diagnosis is important as these skin lesions enter into the differential diagnosis of many different conditions and may appear before the underlying illness. Unlike in the dog, endocrinopathies very rarely cause skin lesions in the cat. Spontaneous and iatrogenic Cushing's syndrome are very rare, spontaneous hypothyroidism is exceptionally rare, hyperthyroidism produces a few non-specific changes in the skin, and dermatological signs associated with sex hormone imbalances are now hotly disputed. However, the cat has a whole range of systemic disease-associated dermatological lesions, of its own.
15 Skin tumours Fran~oiseDelisle - Pahick Devauchelle Tumours of the skin and its adnexae are some of the most diverse and common tumours seen in the cat. Such a large variety is possible because the skin is made up of lots of different components, each of which can potentially form a tumour. We, therefore, see epithelial tumours which involve the malpighian layer, the adnexal sebaceous or sweat glands and hair follicles, tumours of the melanogenesis system, mesenchymal tumours developing in the dermis or subcutaneous connective tissue, tumours derived from lymphoid tissue and finally, nerve and vascular tumours. The majority of skin tumours in the cat are primary. Tumours secondary to, for example, a pulmonary adenocarcinoma (which is usually asymptomatic) or a mammary adenocarcinoma are much less frequent.
1 1 6 Genodermatoses Eric Guagusre - Zeineb Alhaidari -Jacques Fontaine
Genodermatoses are rare, although they constitute a developing field in feline dermatology. In recent vears. investieative orocedures such as electron microscopv and immunohistochemis@y have lei to the identification of new genodermatoses. It is imp;&t to be familiar with these conditions as they enter into the differential diagnosis of many different dermatoses. Genodermatoses affect the epidermis and its adnexae, the melanogenesis system, the dermoepidermal junction and the dermis. In this chapter, the following conditions are reviewed: hereditary greasy seborrhoea of the Persian, congenital hypotrichosis, follicular dysplasia, hair dysplasia, pili torti, genetic abnormalities of melanin pigmentation, hereditary cutaneous asthenia, and urticaria pigmentosa of the Sphinx.
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17 Skin conditions associated with behavioural disorders Catherine Mege
Sldn conditions associated with behavioural disorders are probably rare hut remain underdiagnosed in the cat. They are characterised by self-induced lesions (e.g. alopecia, nail chewing and various mutilations). Advances in the study of animal behaviour have enabled these conditions to be placed in the context of behavioural disorders (e.g. anxiety, depression and dysthymia). Thanks to a better understanding of the behaviour of the domestic cat and the availability of new psychotropic drugs, pheromones and behavioural therapies, specific diagnosis and effective treatment are now possible.
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1 1 8 ~ i a ~ n o s tapproach ic to pruritic dermatoses 2.Alhaidari
The diagnostic approach to fel'me pruritic dermatoses must be methodical and should include certain fundamental diagnostic steps: a detailed history, thorough clinical examination, and carefully chosen diagnostic tests, selected according to the differential diagnosis. An initial range of tests (e.g. skin scrapings, tape strips, mycological investigations and skin smears) should be performed routmely, given the incidence of ectoparasitic infestation and dermatophytosis in the cat. Differential allergy diagnosis is based on avoidance measures (e.g. flea control and restricted diet) as allergy tesimg remains unreliable in this species. Skin biopsies are indicated when the history and clinical examination suggest a dermatosis that requires histological diagnosis.
1 1 9 Diagnostic approach to alopecia 2.Alhaidari
The diagnostic approach to alopecia must be methodical, and should involve certain fundamental steps: a detailed history, thorough clinical examination, and carefully chosen diagnostic tests, selected according to the differential diagnosis. An initial range of tests (e.g. skin scrapings, tape strips, and mycological investigations) should he performed routinely, given the incidence of ectoparasitic infestation and dermatophytosis in the cat. Differential allergy diagnosis is based on avoidance measures (e.g. flea control and restricted diet) as allergy testing remains unreliable in this species. Skin biopsies are indicated when the history and clinical examination suggest a dermatosis that requires histological diagnosis.
1 2 0 Diagnostic approach to crusting dermatoses E. Bensignor
Crusting dermatoses are a common reason for consultation in feline dermatology. Crusts can be defined as a mixture of blood. serum. exudate. andlor us which has dried on the surface of the skin and to which scale and hairs have become stuck. t o make a specific diagnosis and institute effective treatment requires a good knowledge of the clinical aspects and causes of crusting dermatoses. The diagnostic approach rests on the history, clinical examination and appropriate diagnostic tests. It is important to distinguish 1) crusts secondary to excoriation, for which the diagnostic approach is the same as that of the pruritic dermatoses, 2) large, spontaneouslyappearing crusts associated with erosions and their dried-up exudate, and 3) punctate crusts seen in miliary dermatitis, a cutaneous reaction pattern usually associated with ectoparasitic infestation or flea allergy dermatitis, and occasionally with dermatophytosis, bacterial folliculitis or atopic dermatitis.
21 Diagnostic approach to erosive and ulcerative dermatoses E. Bensignor
In the cat, erosive and ulcerative dermatoses are a common reason for consultation, probably because of the thinness of the epidermis. Erosions and ulcers K&ed to self-excoriation should be distinguished from those which appear spontaneously. They are usually secondary lesions with little diagnostic significance. The diagnostic approach should involve taking the history, conducting a thorough clinical examination (general and dermatological), and performing appropriate diagnostic tests, especially cytology and skin biopsies.
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1 2 2 ' ~ i a ~ n o s tapproach ic to otitis externa E. Bensignor
Long thought of as a local phenomenon, otitis externa should be reclassified in a broader dermatological context, as it is usually one local manifestation of an underlying dermatosis. The diagnostic approach should be rigorous, including a history, thorough clinical examination (general and dermatological), and simple, appropriate diagnostic tests, especially auroscopic examination, direct microscopical examination of cerumen, cytology and bacteriology. Occasionally, radiography, CT scanning of the tympanic bullae, paracentesis and biopsies are indicated.
1 2 3 Diagnostic approach to facial dermatoses Pascal Prilaud - Eric Guag3re
Facial dermatoses are a very important and diverse group of diseases. In some cases, the face is affected directly whereas in others, facial involvement is a consequence of systemic disease. One reason why the face is frequently involved is that it is a very exposed part of the body, not easy to groom, and with sparse hair cover offering scant protection. Mucocutaneous junctions (e.g. lips, nose and eyelids) are predisposed to infectious, parasitic and immune-mediated dermatoses. W e is such a plethora of potential causes of facial dermatoses that a very rigorous and methodical diagnostic approach is essential. The history and clinical examination (general and dermatological) are used to formulate a differential diagnosis, which can be narrowed down by performing weU-chosen diagnostic tests. The main facial dermatoses (excluding those of the external ear) are dermatophytosis, allergic dermatoses, superficial pemphigus conditions and squamous cell carcinoma.
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Diagnostic approach to feline pododermatoses Eric GlcaguPre - Pascal Prdlaud - Blaise Hubert
Pododepnatoses are a very important and diverse group of diseases. In some cases, feet are affected directly whereas in others, pedal involvement is a consequence of systemic disease. Although pododermatoses are a less frequent reason for consultation than in the dog, the foot can be targeted directly in various specific conditions: bacterial paronychia, plasma cell pododermatitis and cutaneous metastasis of a pulmonary adenocarcinoma. Pedal involvement may also be part of a more generalised dermatological condition. There is such a plethora of potential causes of pododermatoses that a very rigorous and methodical diagnostic approach is essential. The history and clinical examination (general and dermatological) are used to formulate a differential diagnosis, which can be narrowed down by performing weU-chosen diagnostic tests. Used alongside routine diagnostic tests (e.g. Wood's lamp examination, direct examination of hairs and scale, skin scrapings, fungal culture and cytology), the skin biopsy is often the key to diagnosis.
1 2 5 Zoonotic dermatoses Maire Verde
The term 'zoonotic dermatoses' refers to those zoonoses in which the causal agent causes sldn lesions. The most important feline zoonotic dermatoses are dermatophytosis, flea infestations involving possible transmission of cat scratch disease and the plague - cheyletiellosis and notoedric mange. Other zoonotic dermatoses are less common: sporotrichosis, blastomycosis, histoplasmosis, otodectic mange, tuberculosis and poxvirus infection. A detailed knowledge of these diseases in man is essential for clinicians involved in feline dermatology.
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1 2 6 Therapeutic tables Pascal Prdlaud - Eric Guaguere This chapter lists the principal medications used in feline dermatology. Dose, route of administration, indications and whether a product licence exists are outlined for each drug.
1 2 7 General index 1 2 8 Index of illustrations
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Foreword The cat has long been neglected, even ignored, by veterinary medicine,for reasons that are partly cultural andpartly economic. It was only with the development of companion anlmal medicine, in the 1960s, that the cat was seen as an animal species worthy of veterlnary interest. Back in 1964, E.J. Catcott's Felme Medicine and Surgery, thefirst veterinary text book devoted exclusively to the cat, was already predicting the huge increase in impiXZce of the cat as a companion animal. Yet,for a long time, the cat was treated merely as ifit were a small dog. Furthermore, thefact that cats tolerate high doses of corticosteroids so well meant that there was little incentive to research and develop alternative therapies in this species. The 1980s saw the birth of a more spec@ feline medicine, triggeredprobably by the discovery of the retroviruses and diseases that were unique to the cat. Pharmaceutical companies began to show a growing interest in researching new treatments for cats. At the same time, academic bodies like the American Association of Feline Practitioners and the European Society of Feline Medicine and journals - such as Feline Practice, and more recently Journal of Feline Medicine and Surgery - dedicated entirely to the cat, appeared on the scene. Today,feline dermatology is a thriving discipline in its own right, no longer confined to a few paragraphs at the end of a chapter in a small animal dermatology book or severalpages in afeline general medicine text. To our knowledge, the first atlas dedicated entirely to feline dermatology was G.H. Muller's Feline Skin Lesions, in 1974, which contained 35pages on the principal dermatoses. Then came the celebrated monographs by D.W. Scott which appeared in 1980, 1987 and 1990 in the Journal of American Animal Hospital Association. These were to provide the real foundation of modern feline dermatology. In 1981, J.M. Keep, in Australia, produced a series of three dermatology books, each on a different species, one of which was the cat. Finally, in 1995, Veterinary Clinics of North America (Small Animal Practice) asked Gail Kunkle to produce a special Feline Dermatology issue, still seen today as a milestone. We have deliberately excludedfrom our list all the dermatology text books which include chapters on feline dermatology. Our aim, here, has been to provide a guide which is both instructive and easy to read, but without any claim to being an encyclopaedia. We have tried toproduce a book that will allow each vet to develop his or her own expertise infehne dermatology. Such an ambitious project could come to fruitlon only within the framework of internatlonal collaboration between expertsfrom various backgrounds. Veterinary dermatology belng a large family that embraces enthusiasts everywhere, irrespective of nationality or university status, it was easy for us, as scient$c editors, to assemble a team of authorsfrom all corners of the globe. We have been overwhelmed by the enthusiasm shown by the twenty-six authors recruitedfrom eight different countries. We would like to thank them for the excellence of their contributions, as well as for their kindness, encouragement andfriendship. A Practical Guide to Feline Dermatology is divided into two main sections. The first is a detailed study of the main topics in feline dermatology, presenting the most up-to-date information alongside high quality colour plates. The second section, which outlines diagnostic approaches to all the pr~ncipaldermatoses, isreadily accessible to the vet in practice, struggling to make the correct diagnosis.
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We would like to extend our very sincere thanks to one of our mentors, Professor D.W. Scott for doing us the honour of writing the preface. He can be assured of our deepest respect and admiration for his outstanding contribution to feline dermatology, which he refers to as his own 'professional hobby'. Lastly, A Practical Guide to Feline Dermatology would not have been possible without the interest and enthusiasm of Merial, under the direction of Doctors Daniel Gouffd and Ronan Gillard who have had the foresight to see that, in the 21st century, the cat will be the animal species with the greatestpotential for medical development. We hope that this book will instill in you, as it has in us, a new passion for feline dermatology and dispel forever the notion that it is about nothing more than reaching for the bottle of long-acting corticosteroid!
2 September, 1999 Restaurant le Pamphlet, Paris.
Eric GuaguPre Docteur Vdtdrinaire CertGed in Veterinary Dermatology Diplomate of the European College of Veterinary Dermatology
Pascal Prdlaud Docteur Vdtdrinaire Cert$ed in Veterinary Dermatology Diplomate of the European College of Veterinary Dermatology
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1 Structure and functions of skin and coat The skin and its adnexae make up the most important organ of the body and form an essential anatomical and physiological harrier between the external environment and the internal organism. Knowledge of the anatomy and histology of the various cutaneous structures, some of which are specitic to cats, allows better understanding of all the functions of the skin in the cat. The skin also acts as a mirror which reflects the health and comct functioning of the organism.
Structure of the skin and its adnexae The skin of cats is thinner than that of dogs, 0.4 to 2 mm thick on average. It is thicker on the dorsal regions and proximal limbs, and thinner on the ventrum and distal limbs '.
Epidermis The epidermis is a squamous keratinised epithelium made up of 3 to 5 cellular layers (excluding the horny layer), 25 pm thick ' (Diagram 1 : 1) (Fig. 1 : 1). In the non-hairy areas (nasal planurn, footpads), it is thicker (up to 900 p)and lined by a more developed horny layer (Fig. 1 : 2). The thickness of the horny layer is between 3 and 20 p in the hairy areas and between 15 and 35 pm on the footpads '. The epidermis does not contain any blood vessels, its nutrients being provided by diffusion fmm the dermal hlocd supply. Keratinocytes make up the majority (85-90%) of the epidermal cells. Other epidermal cells, such as Langerhans' cells (3-8%), melanocytes (2-5%) and Merkel cells, appear as clear cells under the light microscope. Lymphocytes and occasionally mast cells can also be found ' (Fig. 1 : 3).
Keratinocytes undergo keratinisation or comification, a differentiation and maturation process which progressively transforms the small, round, basal layer cells into large, flat, anuclear, polyhedral corneocytes (Diagram 1 : 1). The corneocytes are shed by desquamation. The replacement rate of keratinocytes has not yet been determined in cats. In dogs (Beagles), it takes 22 days for a basal cell to reach the horny layer '.
Diagram 1 : 1 : Schematic diagmm of the epidermis Horny layer
Granular layel
Spinous (Malpighian) layer
Basal layer Basement membrane
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Melanocytes are dendritic cells which synthesise melanin pigments in specific structures called melanosomes, situated in the epidermal basal layer or in the hair follicle matrix. They generally appear as clear cells, without specific colouration, under the light microscope. In black or grey cats, these melanocytes are easily recognisahle due to their intracytoplasmic black p u l e s . The melanocytes, via their dendrites, are in contact with several keratinocytes to which they transfer their pigment granules. There are up to 25 keratinocytes per melanocyte in the epidermis. Langerhans' cells are antigen-presenting cells which phagocytose antigens at the skin surface, and migrate into the drainmg lymph node where they present the captured antigen to T lymphocytes. They are responsible for triggering specific immune reactions. Langerhans' cells contain specific intracytoplasmic organelles, shaped like rackets, called Birbeck p u l e s 4. Their immunophenotypes are CDlat, M H C P and C D ~ +In. cats, the density of Langerhans' cells in the skin is higher on the p m a e and middle of the back, and lower on the abdomen I. Merkel cells are mechanoreceptor cells situated in the basal layer, in contact with nerve fibres.
Basement membrane The keratinocytes of the basal layer sit on the basement membrane which separates the epidermis from the dermis. They are attached to it by hemidesmosomes and other adhesion molecules. The basement membrane acts as mechanical supporl for the epidermis and regulates metabolic transfer between the dermis and epidermis. It is around 40 nm thick. It can be seen under the light microscope usimg special stains such as Periodic Acid-Schiff (PAS). Ultrastructural studies have enabled three zones to be disimguished: the lamina lucida, in contact with cells of the basal layer, the lamina densa and the sublamina densa which permits adhesion to dermal collagen.
Dermis The dermis is a rich network of fibres, intercellular ground substance, blood and lymphatic vessels, nerves, muscles and cells.
Collagenfibres produced by fibroblasts are made up of 90% collagen, a filamentous protein with great tensile strength. Elastinfibres make up around 4% of dermal fibres and form a network in the dermis beneath the pilosebaceous units. Reticulinfibres are very h e fibres which form a loose network around collagen fibres and other dermal structures. Dermal ground substance is made up of proteoglycans, glycoproteins and large quantities of water. It appears as an amorphous gel, produced by fibroblasts, and has an important barrier function with regard to micro-organisms and large molecules passing between the epidermis and subcutaneous tissue. Three interconnected vascularplen'are found in the dermis. The uppermost sub-epidermal plexus brings nutrients to the epidermis and hair follicle infundibula. The middle plexus, situated at the level of the sebaceous glands, provides a blood supply to the glands, muscles and follicular isthmus. The deep plexus below the hair follicles, supplies the dermal papilla, apocrine glands and the two other plexi. Arteriovenous shunts, situated mainly in the distal limbs, are associated with thermoregulation. Lymph vessels in the deep dermis enable drainage of cutaneous fluids and maintain homeostasis. Nervefibres follow the blood capillaries and are organised in three plexi. Free nerve endings reach the epidermis or form more complex structures such as Pacinian corpuscles.. Dermal cells are numerous. Fibroblasts responsible for collagen synthesis and production of dermal ground substance also produce enzymes, notably a collagenase and a gelatinase, capable of catabolising ground substance and fibres. The fibroblasts are therefore responsible for maintaining the dynamic homeostasis of the dermis. They also play an important role in inflammation and healing. The numerous mast cells in cat skin are situated mainly in the perivascular region and synthesise a range of enzymes (chymase, tryptase) (Fig. 1 : 3). Other cells found in the dermis include macrophages, lymphocytes, neutrophils, eosinophils and plasma cells.
www.vet4arab.co.cc 1 : Strucw and functions of sldn and coat
Figure I :I : Normal cot epidermis: note thinness of the epidermis (HE,x 402)
Figure 1 :2: Normalfoofpadepidermis: note thickness of the horny layer (HE,x l w
Figure I :3 :Intraepidermal mast cells, (+)
Figure 1 :4 : I n ~ u l w ofn a normal hairfoNicle (HE,x 460)
(Tolu~dlneblue, x 100)
Pigave 1 :5 :Hairfoll~clebulb in nnagenphose(HE,x400)
Fkure I : 6 : Tr~ctwgmmof central pnmmy, lateral primnry and secondary h r s (x 100)
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Subcutaneous connective tissue Subcutaneous tissue is composed of a layer of connective tissue, rich in adipose cells. It has many roles, the most important of which are storage of lipids and fat-soluble substances, thermal insulation and protection from physical trauma.
Hair follicles Hair follicles are epidermal invagimations into the dermis, which synthesise and provide support for the hair. Hair follicles are divided into three regions (Diagram 1 :2): the infundibulum (Fig. 1 :4), the isthmus and the bulb (Fig. 1 : 5).
In the adult cat, each follicle has its own bulb and isthmus but several follicles share the same infundibulum. These are called compound hair follicles. Ten to twenty hairs are present per infundibulum. The density of the coat is around 250 hairs/cmi. The coat is denser on the abdomen than on the back. Newly-born kittens up to the age of 3-4 months have simple hair follicles. Types of hair Hair follicles generally contain one central primary hair, up to five lateral primary hairs and up to twenty secondaq hairs. The clusters of follicles on the back have larger primary hairs and fewer secondaq hairs than those on the abdomen.
Central primary hairs (40 to 80 p in diameter) have a large medulla and thin cortex ' (Fig. 1 : 6). They are rigid, cover the whole skin surface, provide protection against the rain and are responsible for coat colour. The primary hair follicles are the largest and longest in the follicular cluster, extending into the deep dermis. They are associated with sebaceous glands, apocrine sweat glands and an m c t o r pili muscle. Lateralprimary hairs (25 to 40 pm in diameter) are moderately supple '. They have a different orientation to the undercoat, therefore providing better thermal insulation. They are characterised by a sub-apical bulge at the base of the hair. Secondary hairs (10 to 20 pm in diameter) are fine and supple with a relatively thin medulla and a thick cortex (Fig, 1 : 6). They form the undercoat responsible for maintaining temperature. Secondary follicles can sometimes have a single sebaceous gland, but never apocrine sweat glands nor m c t o r muscles.
Hair shrcture The hair consists of a colunm of comified, vety adherent, stratified cells, arranged in a cuticle, a cortex and a medulla (Diagram 1 : 2).
The cuticle is made up of a single layer of cuboidal epithelial cells which dierentiate into anuclear, flat and adherent comeocytes. These comeocytes line and protect the hair, like tiles on a roof, and are orientated towards the isthmus. The cuticle cells are oriented in the opposite direction to those of the inner follicular root sheath and are therefore overlapping. This protects the hair follicle and ensures support for the hair during its growth phase in the deep p a s of the hair follicle. In cats, the cuticle cells are thin and arranged in a very smooth flattened manner, which is why cat hair feels softer to the touch than dog hair. The cortex consists of elongated comified cells arranged parallel to the axis of the hair. In primary hairs, the cortex makes up a sixth of the diameter of the hair 3. Secondaq hairs have a relatively thicker cortex than the primary hairs which have a much larger medulla. The medulla is the internal part of the hair. It is produced by the hair matrix and generally contains air, glycogen vacuoles or pigments. The medullary cells of cats are flatter than those of dogs and arranged at a 90" angle to the axis of the hair 9. Structure of the hair follicle The base of the hair follicle is made up of a bulb matrix, a dermal papilla and a hair bulb. Above the bulb are the inner and outer epithelial root sheaths which are surrounded and supported by a layer of dense connective tissue (Diagram 1 : 2). The bulb matrix is formed from small, round, basophilic epithelial cells which divide actively at the centre to create the hair, and at the outside to create the inner root sheath. Melanocytes ate responsible for pigmentation by transfer of melanosomes to the cells of the hair's cortex and medulla. The bulb matrix is nourished by the dermal papilla, made up of connective tissue rich in blood vessels and nemes within a mucopolysaccharide matrix.
www.vet4arab.co.cc 1:Smcture and functlons of skin and coat
F w e I :7 :Xar fdllirle In anugen p b e (HE,&Oil]
P i g m 1 :8 :Holrfollicie inmagenirelogenphme (HE,x 400)
F i g m I :9 : Sebaewur $ I d s ( H E , 4WJ
Fipre 1 :11 :Pac~nrancorpuscle (PAS, x IW)
Figure I :12 :Whrsker note the blood slnur a m m i the h l r (HE,x 100)
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Diagram 1:2 : Schematic diagram of a hair follicle Hair
Cuticle Medulla
Isthmus
Inner root sheath Outer root sheath Apocrine sweat gland
\
Dermal papilla
At the base of the follicle above the bulb matrix, the hair is surrounded by two concentric sheaths. The outer root sheath represents an invagimation of the superficial epidermis into the dermis. In the deeper part of the isthmus and in the bulbal zone, the outer root sheath is not cornifid. In the isthmus and upper bulbal zone, the cells of the outer root sheath appear larger and clearer due to high levels of glycogen. In the deeper parts of the bulb, they appear small and basophilic, like the mahix cells. The inner root sheath swounds and supports the hair, from the matrix where it is produced, up to the isthmus where it is destroyed.
Follicular cycle Hair growth consists of diierent phases: a growth (anagen) phase (Fig. 1 : 7), an intermediate (catagen) phase (Fig. 1.8) and a resting (telogen) phase. Duration of the anagen phase depends on breed and region of skin. Long-haired cats have a longer anagen phase than short-haired cats. Dorsal hair has a longer anagen phase than nasal hair. Hairs grow from 0.04 to 1 mm each day and long hairs grow faster than short hairs.
The genetics of different coat types Hair length is influenced by various genes, a dominant, L "short hair" gene (average 4.5 cm) and a recessive, I "long hair" gene (up to 13 cm). Other lengths (very long as in the Persian, mid-length as in the Norwegian or the Maine Coon) are produced by polygenes or modifier genes. Genes of the series "I", "h" and " W engender important modifications to the texture and structure of hairs. The "I" series is seen in "Rex" cats which do not have central primary hairs, and whose lateral primary and secondary hairs and whiskers are abnormal. There are different types of Rex cats (Cornish, Devon, Oregon, Dutch and Sekirk) depending on recessive or dominant mutations of this gene. The "h" series is expressed in the Sphinx, (no relation to the Rex), which has no primary hairs. However, secondary hairs are present on the extremities (nose, pinnae, limbs, tail). The dominant "Wh" gene is responsible for the development of very curly hair. In this case, the three types of hair are entwined.
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Genetics of hairpigmentation The colour of the skin and coat depends on the quantity, type and location of melanin pigments in the skin. There are two types of melanin, eumelanin @lack/brown)and phaeomelanin (red/yellow). The large number of colours seen in the various breeds of cats depends on the prevalence, combination and distribution of these two types of melanin in the skin. White colouration occurs through an absence of pigmentation resulting from lack of melanisation of melanocytes. This is called albinism when complete ( i s is very light blue or red). The most important gene involved in feline hair pigmentation is the dominantA "agouti" gene responsible for the o r i g ' i , wild, banded pigmentation of primary hairs. Cats carrying this gene have dark-tipped hairs with one or more bands of colour. Those which express the recessive a, "non-agouti" gene, have uniformly pigmented hair. Wid cats also carry the T "tabby" gene, responsible for dark markings on a lighter, generally yellow or grey, base. There are different variants of the "tabby" gene which produce variable distribution of stripes or spots on the body. Colours seen in domestic cats are divided into phaeomelanic colours (orange / g'mger (red) and cream (diluted red)) and eumelanic colom (black, grey (generally called blue, diluted black), chocolate (chestnut), lilac (diluted brown), cinnamon (light chestnut) and fawn (diluted cinnamon). As the genes responsible for hair colour are situated on the X chromosome, cats with concurrent red and black/brown colours are generally females which can carry the two red and black/brown genes on each of the two X chromosomes. Colour dilution is caused by the recessive d gene. In colour-dilute breeds, l i e the C h W u x , hairs contain irregularly distributed melanosomes grouped in melanin clusters in the melanocytes and hair cortex. A foUicular dysplasia of colour-dilute cats has been described in the Cornish Rex. Silver coats are coded by the I "colour inhibitionn gene. Colour is lost in the proximal hair which grows out white. There are different types of silver coat, depending on the extent of hair depigmentation. The recessive variants of one pdcular gene, the C gene, are responsible for "colour point" coats, typical of the Siamese. Tnis gene codes for an enzyme whose activity is temperature-dependent. This causes excessive colouration in colder regions such as the extremities. The ca gene is responsible for blue eye albinism, the c gene for red eye albinism. White spots are due to the expression of a different gene, the S "white spotting" gene, whereas generalised white colouration of the coat is encoded by the dominant W gene. This latter gene is often associated with deafness because it causes degeneration df the cochlea and atrophy of the organ of Corti.
3utaneous glands Sebaceous glands Sebaceous glands are simple alveolar holocrine glands, associated with hair follicles in groups of two or thee (Fig. 1 : 9). Their excretorv ducts open into the follicular isthmus. Sebum is the product of sebaceous gland cell destruction in the Addle of the gland. It combines with sweat, produied by the apocrine glands, to form a lipid emulsion (the surface hydrolipid film) which protects the skin surface. The sebaceous glands are large and numerous in the skin around the lips and on the chin, and play a role in territorial marking when the cat rubs its face against objects and human beings. The perianal glands and supracaudal organ are modified sebaceous glands which are larger than the other glands. As development is hornonally dependant, they may be particularly large in entire male cats. Excessive accumulation of glandular secretion in this region is known as stud tail. Sweat glands Apocrine sweat glands are present over the whole surface of hairy skin and their ducts open above the sebaceous gland ducts into the follicular isthmus. Apocrine glands are simple tubular glands with a straight duct and a convolutedsecretory part surrounded by myoepithelial cells (Fig. 1 : 10).Tney produce an aqueous secretion which forms an emulsion with sebum at the skin surface (the surface hydrolipid film). Eccrine sweat glands have the same structure as apocrine sweat glands but are only found in non-hairy areas of skin l i e footpads. Their ducts open directly at the skin surface. These sweat glands are situated close to blood vessels and are controlled by blood adrenaline and noradrenaline. Hence, frightened cats sweat excessively from their footpads.
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~.4hctical GuidetoFehe Dermatology
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Modified sweat glands make up the mammary glands, ceruminal glands and the glands of the anal sacs There are no sweat glands on the nasal planum '.
Functions of the skin and coat The skin and coat have many important functions including protection from the external environment, thermoregulation and maintenance of biochemical homeostasis. They also have metabolic, sensory, immunological and social functions.
Mechanical protection The coat is the first barrier to mechanical trauma. It is often thick because of an undercoat covering the whole skin surface. Dermal collagen fibres impart a high tensile strength and prevent skin tearing.
Protection against water Thanks to this thick coat and the surface hydrolipid film,water does not readily reach the skin surface. The orientation of primary hairs ensures that water droplets are quickly shed. Constant grooming keeps primary hairs clean and ensures optimal protection from water. Certain breeds, such as the Norwegian Forest, exhibit a very hydrophobic coat. This characteristic is often tested by show judges who let several drops of water fall on the hairs to see if the drops slide off the coat without wetting the animal. If water does reach the skin surface, it cannot pass through it because intercellular spaces in the horny layer contain lipids impermeable to water and water-soluble substances.
Protection from light The coat is an excellent barrier to visible light and ultra-violet (UV) rays. In the areas where the coat is sparse or absent, pigments (mainly melanins), keratin, proteins and blood absorb the UV rays and prevent certain skin lesions. Nevertheless, in white or light-coated cats with little pigment, solar keratotic lesions and epidermal carcinomas can appear in sparsely-haired areas such as the pinnae, nose, eyelids and the a m behind the ears, following prolonged or frequent exposure to the sun.
Thermoregnlation Temperature regulation is also an important function of the coat and skin. The thick coat and the layer of subcutaneous connective tissue, rich in adipose cells, protect the cat when the temperature is cold. An insulating air cushion exists between the hairs. The size of the air cushion can be increased or decreased by the action of arrector muscles. The undercoat is shed in the spring and re-grows in the autumn in breeds which experience large seasonal temperature variations. This is_particularlytrue in the k k i s h Van breed, origimating in central Anatolia, where the temperature variation between summer and winter can be as much as 50°C. The highly developed dermal vascular system plays an important role in thermoregulation. Vasodilatation produces heat loss and vasoconstriction causes closure of arteriovenous shunts, which prevents excessiveheat loss from the circulation. The cutaneous vascular system stores large quantities of blood and peripheral vasoddatation or vasoconstriction can also have an effect on central blood pressure. Cats have a particular way of reducing their body temperature as, unlike in humans, sweat glands are not involved in thermoregulation. Cats constantly wet their coats by licking. This produces a cooling effect as saliva evaporates from the skin surface.
Biochemical homeostasis Many substances are stored in the dermis and subcutaneous comective tissue. Large quantities of water and electrolytes are associated with proteoglycans and other molecules in the ground substance, while lipids and fat-soluble molecules are stored in subcutaneous adipose tissue.
Metabolic and immunological functions For a long One, the skin was considered to be an organ with only a passive protective role, not one that involved the individual's general metabolism or immunological defence mechanisms, with the exception of vitamin D synthesis. Various metabolic pathways prodicing systemic effects (for example, effect of androgens and oestrogens on smell) have recently been demonstrated in the skin. In addition, an
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immunological system has been identified, capable of specitic reactions against micro-organisms, parasites or foreign antigens present on skin.
Sensory functions Various different sensations such as pain, pruritus, heat, cold, pressure and touch are felt at the cutaneous level. Free nerve endimgs in the epidermis are responsible for sensations of pruritus, pain, heat and cold. Specialised structures, l i e Pacinian corpuscles (Fig. 1 : 1l), tylohich pads, whiskers " (Fig. 1 : 12), hair follicles, type C mechanoreceptors and Merkel cells all have mechanoreceptor functions 12.
Social functions The colour of wild cats l i e the Lynx, enables the animal to hide easily in woods and forests (mimicry). Domesticated breeds have lost this characteristic, perhaps with the exception of black cats used in the Middle Ages, to chase mice and rats from the holds of ships. Specialised glands, like the hepatoid circumanal glands, the anal sacs, the supracaudal organ and the sebaceous glands of the lips and chin, produce pheromones. Pheromones are used in territorial marking, facilitate recognition between individuals and influence sexual attraction. Various fractions (F3, F4) have been isolated recently. Cats in dangerous situations raise the hairs on their back and tail and present themselves sideways-on to their adversary in order to appear larger.
Cutaneous microbi9logy -- and barrier functions Horny layer
' The compact horny layer represents the f h t physical banier to infections and parasitic infestations. In normal conditions, water, water-soluble molecules and micro-organisms cannot cross it. Constant shedding of the most supeficial cells reduces excessive bacterial colonisation which could otherwise predispose to infection.
Dermis If a micro-organism or parasite enters the dennis, it must pass through a very dense network of collagen fibres and intercellular ground substance molecules, before fmdiig itself in contact with a very active immune system.
Hydrolipid surface film The sebum and sweat form an emulsion on the skin surface which acts both as a physical banier, preventing the passage of water and water-soluble substances, and a chemical banier, made possible by the presence of certain substances involved in skin defence mechanisms. These include Ransferrin which l i i t s bacterial proliferation, and free fatty acids such as linoleic acid, produced from surface higlycerides by bacterial lipases, which prevent skin colonisation by pathogenic micro-organisms. Other lipids such as glycosphingolipids arising from the decomposition of the horny layer might play an even greater antibacterial role. Specific factors, such as complement and immunoglobulins, can attach themselves to the skin surface and prevent microbial adherence and proliferation. Skin pH in cats varies between 5.73 and 6.01, with the exception of the nose and footpads (areas of eccrine secretion) where it is less acidic, between 6.81 and 7.97". A low pH has bacteriostatic and bactericidal effects.
Resident microbial flora The resident surface flora, which occupies micro-ecological niches, prevents colonisation by pathogenic micro-organisms by producing antibiotics, enzymes or other toxic substances. They utilise available nutrients. Resident bacteria on cat skin include Micrococcus spp., coagulase-negative staphylococci (especially Staphylococcus simulans), a-haemolytic streptococci and Acinetobacter spp. 12. It is possible to isolate more bacteria from cats in close contact with humans than froiii cats living in catteries, which suggests that humans may be involved in transmitting bacteria to cats ". Transient bacteria, isolated from cat skin, include R-haemolyhc streptococci, Escherischia coli, Proteus mirabilis, Pseudomonas spp., Alcaligenes spp., Bacillus spp., and staphylococci 12. These hacteria can occasionally become pathogenic if conditions are favourable for multiplication. Yeasts of the genus Malassezia are commensal micro-organisms found on the skin of cats, especially in
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humid regions such as ears, penanal and inguinal regions Id. Malassezia pachydermatis, Malassezia sympodialis and Malassezia globosa have been isolated from cat skin 14. Van'ous saprophytic fungi can be isolated from the skin and coat of normal cats. These include Alternaria spp., Aspergillus spp., Cladosporium spp., Mucor spp., Penicillium spp. and Rhodotorula spp. ",''. Microsporum canis isolated from normal cats must always be considered a pathogen 16.
REFERENCES
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1. Strickland, J. H. & Lois Calhoun, M. Amer J Vet. Res. 24, 1018-1029 (1963). 2. Scott, D. W Vet.Dermatol. 1,6569 (1990). 3. Baker, B. B. Amer. J. Vet. Res. 3,93 (1973). 4. TsagaraIds, C., Marchd, T., Magnol, J. P., Fournel, C., Dezutter-Dambuyant, C. & Schmitt, D. Research in Virology 145,245-249 (1994). 5. Saint-Andr6 Marchal, I., Dezutter-Dambuyant. C. & Mutin, I. P. and others Br. J. Dermarol. 136,961-965 (1997). 6. Badleston, D. L., Roosje, P. & Goldschmidt, M. H. J. Vet. Allergy Clin. Immunol. 5,54-58 (1997). 7. Blazej, A. Galatik, A. Galatik, I. Krul, Z. & Mladek, M. Atlas of Microscopic Structures of Fur Skins (Elsevier, Amsterdam, 1989). 8. Lochte, m.Atlas der Menschlichen und TierischenHaare (Paul Schps Verlag, Leipzig, 1938). 9. Creed, R. E S. Vet.Rec. 70, 171-175 (1958). 10. Kumamoto, K., Takei, M., Kinoshita, M., Ebara, S. & Matsuura, T. J. Anat. 182,23-28 (1993). 11. Ikeda, M. & Okada, S. Okajimas Folia Anaromia Japanensis 67,365-369 (1990). 12. Scott, D. W Miller Jr, W. H. & Griffin, C. E. Muller & Kirk's Small Animal Dermatology,5th edih'on (Saunders, W.B., Philadelphia, 1995). 13. Meyer, W. & Neurand, K. Arch. Dermatol. Res. 283.16-18 (1991). 14. Bond, R., Howell, S.A.,Haywood, P. I. & Lloyd, D. H. Vet. Rec. 141,200-201 (1997). 15. Moriello, K. A. & DeBoer, D. J. Amer J. Vet. Res. 52,602-606 (1991). 16. Moriello, K. A,, Kunkle, G. A. & DeBoer, D. J. Vet. Dermatol. 5,57-62 (1994).
AKNOWLEDGEMENTS Diagrams 1 : 1 and 1 : 2 have been reprinted with kind permission fmm Peters S.: "Haut und Haarkleid kim Hund", Ferdinand EnkeVerlag, 1997,Pages 4 and 21.
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D. N. Carlotti - D. Pin
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Diagnostic approach The diagnostic approach in feline dermatology must be methodical and include the various steps of a conventional medical consultation as well as additional ones relevant t o feline dermatology. Information gleaned from the history and clinical examination, both general and dermatological, allow the practitioner to construct a differential diagnosis. Appropriate diagnostic tests are then chosen to narrow down this list and produce a definitive diagnosis 14.
History The history is an essential part of the diagnostic approach, and 10-15 mlnutes should be allocated to taking the htstory before examming the ammal. Sometimes, the history alone will suggest the diagnosis. The best method is to use a printed sheet which details most of the questions to ask the owner. This ensures that nothing is forgotten. It also allows the time scale of events to be appreciated, enables the climlcian to gain some time, and demonstrates to the owner that interest 1s being taken in the case 14.
Signalment Breed :Breed predispositions should be known but are less important than in the dog 35-" (Table 2 : 1). However, be careful, knowing the breed alone is not enough to make a diagnosis! Sex :Entire male cats are often aggressive. They are prone to subcutaneous abscesses arising from bites and scratches, certain specific bacteria infections (e.g. nocardiosis and actinomycosis), and indirectly to opportunistic dermatoses associated with retroviral infection. Age :Some dermatoses are more common in certain age groups. For example, parasitic dermatoses (e.g. otitis caused by Otodectes cynotis, cheyletiellosis, demodicosis) and dermatophytosis are more common in kittens. Genodermatoses (e.g. junctional and dystrophic epidermolysis bullosa, follicular dysplasias and cutaneous asthenia) are more likely to be seen in the young cat (aged under a year). Allergic dermatoses tend to appear between 6 months and 3 years. Cats of 10 years and over are more susceptible to auto-immune dermatoses, tumours or systemic diseases with dermatological manifestations. It should be appreciated that age of onset of clinical signs is not always the same as age at diagnosis. Age at diagnosis of an allergic dermatitis varies from 1to 10 years!
Colour : White cats, or cats with white ears, are prone to solar dermatitis and squamous cell carcinoma, whereas gimger cats are prone to lentigo simplex. Persian cats with a mutation for the beige gene are predisposed to Chediak-Higashi Syndrome. Weight :Weigh'mg the cat helps determine if the patient is in the correct weight range. It also allows correct dosing of medications and accurate interpretation of water intake over 24 hours (e.g, if hyperadrenocorticism is suspected).
Diet:Knowledge of the diet is essential in order to institute an appropriate elimmation diet. Origin :Some colonies or pet stores may be known for their poor hygiene and incidence of contagious dermatoses (e.g. dermatophytosis, Otodectes otitis, cheyletiellosis, etc ...). Stray cats should be examined meticulously and checked thoroughly for retroviruses. Some dematoses have been reported to affect cats of the same line: urticaria pigmentosa in the Sphinx, dystrophic epidermolyis bullosa in the Persian, eosinophilic granuloma complex in a lime of Specific Pathogen Free cats 13.
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A h r i c a l Gude to F h e Dermatology
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Persian
Exotic Short Hair Siamese
Abysinnian
Havana Sphinx Birman Burmese
Devon Rex Himalayan
Dematophytosis Cheyletiellosis Histoplasmosis Lupus erythematosus Idiopathic facial dermatitis ' Facial interhigo Hereditary greasy seborrhoea Congenital hypotrichosis Chediak-Higashi syndrome ' Dystrophic epidemolysis bullosa ' Hereditary greasy seborrhoea6 Demodicosis Self-induced alopecia of behavioural origin Food intolerance? Sporotrichosis Cryptococcosis Lupus erythematosus Vitiligo ' Junctional epidetmolysls bullosa Periocular leucohichia Histiocytic mastocytoma Self-induced alopecia of behavioural origin Blastomycosis Cryptococcosis Follicular dysplasia Blastomycosis Urticaria pigmentosa Alopecia universalis Congenital hyponichosis 'I Demodicosis Self-induced alopecia of behavioural origin Congenital hypotrichosis Urticaria pigmentosa " Lupus erythematosus Ehlers-Danlos syndrome Hereditary greasy seborrhoea "
The environment Meticulous details of internal and external surroundings must he documented: being confmed to inside the house, and the presence of rngs and carpets, expose the cat to a high level of house dust mite allergens. Old houses and frequent visits to the cellar and attic favour the multiplication of fleas and consequently flea allergy dermatitis. An outdoor country life predisposes to certain parasitic dermatoses (e.g. Otodectes otitis and tromhiculiasis), allergies (e.g. mosquito bite hypersensitivity), fungal infections (dermatophytosis) and viral infections (e.g. poxvuus infection reported in cats that hunt small rodents). If dermatological signs are worse when the cat is in certain locations, this may suggest atopic dermatitis. Any tips abroad or to different regions should be documented. Notoedric mange is prevalent in the French overseas territories, and parts of Italy, Switzerland, Spain, Slovenia and Croatia. Some systemic mycoses occur in particular geographical regions. The presence of other animals in the house and evidence of transmission to other animals or people: the presence of in-contact animals favours the development of certain dermatoses such as flea allergy dermatitis or contagious dermatoses like dermatophytosis, Otodectes otitis and cheyletiellosis. Evidence of transmission to man suggests dermatophytosis or a parasitic dermatosis like notoedric mange or cheyletiellosis. Changes in the environment: changes in the family situation (moving house, new furniture, new arrival or death of an animal or person) may cause behavioural disorders that can have dermatological manifestations.
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Development of the dermatosis Date of initial onset: knowing the date of onset allows the age of onset to be determined along with the duration of the condition. Acute or chronic development: Acute-onset dermatoses include cutaneous drug reactions and viral dermatoses whereas more gradually developing dermatoses include allergic dermatoses and turnours. Seasonality: conditions occurring more in autumn or summer include flea allergy dermatitis, atopic dermatitis, trombiculiasis, mosquito bite hypersensitivity or more rarely poxvirus infection. Initial nature and distribution of lesions: this information will help establish the extent to which the dermatosis has progressed. The owner should be asked precise questions: where were lesions first seen? What did initial lesions look like? The presence of pruritus, initially, or later in the development of the dermatosis: the distinction between a pruritic and non-pruritic dermatosis is arbitrary and oversimplified because a condition that is initially non-pruritic ma; later become pnuitic. here are five imp&ant aspects to be determined from the history: Did pnuitus develop before, at the same time as, or after the lesions appeared? How severe is the pruritus and how frequent is it? It is often described by the owner in a whole range of ways such as frantic, severe, constant, intermittent or occasional. How does pruritus manifest itself? Which parts of the body are affected? How does pruritus respond to corticosteroid therapy?
Prior and current therapy Establishing every minute detail of prior and current treatments is essential. This must include the name of the drug, dose, frequency and duration of administration, any side-effects, whether given as instructed, and clinical response obtained. If a cutaneous drug reaction is suspected, all treatments should immediately be stopped and the cause investigated.
Clinical examination ~~~~~~~~
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General examination A systematic general examination should he conducted. Methodical examination of the different organ systems should allow detection of general signs that might be associated with dermatological signs: for example, respiratory signs associated with atopic dermatitis, herpesvirus infection, herpesvirus-associated erythema multiforme or digital metastasis of a pulmonary adenocarcinoma; gastrointestinal signs associated with food intolerance; joint or renal signs associated with systemic lupus erythematosus; diabetes mellitus seen frequently with hyperadrenocorticism or the whole gamut of signs linked to cutaneous paraneoplastic syndromes (e.g. pancreatic paraneoplastic alopecia and paraneoplastic exfoliative dermatitis). In some cases, testing should be carried out for retroviruses.
uermatological examination Identification of lesions Dermatological diagnosis depends on the morphological identification of lesions '"". The dermatologist must identify and investigate primary and secondary lesions. Primary lesions make up the early lesions, representative of the dermatosis. They are sometimes transient and rapidly altered. Secondary lesions may develop spontaneously fro^ primary lesions. They may also arise as a consequence of scratching and licking, especially common in the cat, or following treatment. The identification and interpretation of these lesions is more difficult than in the dog. This is due to the dense coat of the cat and also because cats lick themselves a lot, both as normal grooming behaviour and as a sign of pruritus. There is no clear association between dermatosis and lesion: one particular lesion may suggest various different derinatoses and, conversely, one particular dermatosis may present in lots of different ways.
cal Guide
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Primary lesions Erythema refers to redness of the skin, diffuse or localised, which disappears when a piece of glass is pressed over it. Erythema results from vasodilatation in the superficial dermis '.1,'4,'i. This common lesion has little diagnostic significance: Generalised erythema may suggest atopic dermatitis, food intolerance (Fig. 2 : I), cutaneous drug reaction or epitheliotropic T cell lymphoma. Localised erythema should lead to suspicion of an infection or infestation (e.g. dermatophytosis (Fig. 2 : 2) or demodicosis), or, depending on its location, actinic or contact dermatitis. Purpura refers to a dark red, non-palpable spot which does not disappear when a piece of glass is pressed over it. It results from extravasation of red blood cells from dermal vessels 2,3.14,'5. Purpuric macules are called petechiae, when punctate or lenticular, and ecchymoses when more extensive (Fig. 2 : 3). Purpura is rare in the cat and should be considered a sign of disordered blood clotting (e.g. peripheral or central thrombocytopaenia) or other systemic illness. Platelet purpura occurs in thrombocytopaenia and vascular purpura in necrotising vasculitis that accompanies infectious illnesses (e.g. feline infectious peritonitis). A macule is a flat spot, with no infiltration, associated with a change in skin colour 2.'.'4.'s. Hyperpigmented macules arise from an increase in melanin pigmentation. Circumscribed areas of hypermelanosis may he congenital (e.g. lentigo) and caused by an increase in the number of melanocytes in the epidermal basal layer. They may also be acquired as in post-inflammatory melanin pigmentation (e.g. in pemphigus foliaceus or pancreatic paraneoplastic alopecia (Fig. 2 : 4)), and associated with melanocytic hyperactivity. Hypopigmented macules relate to a reduction (hypomelanosis) or absence of (amelanosis) melanin pigments. In the cat, the congenital, circumscribed hypo- or amelanoses (vitiligo) are classified separately from the generalised conditions (piebaldism, Waardenburg Syndrome and albinism).
A vesicle is a small (1-3 mm in diameter), translucent elevation containing clear fluid ','.'4.'5. Due to the extreme thinness of the epidermis, the vesicle is a fragile, transient lesion and therefore, rarely identified. Theoretically, epidermal vesicles are seen in for example, pemphigus vulgaris and poxvirus infection, whereas subepidermal vesicles are seen in epidermolysis bullosa and bullous pemphigoid.
A bulla is a large vesicle, greater than 3 mm in diameter2.3.'4.'3. A pustule is a raised, purulent spot, associated with an accumulation of neutrophils and modified keratinocytes i.'~'4.1*. Unlike in the dog, pustules are hard to identify, macroscopically, in the cat, as they are fragile and short-lived. Follicular pustules are centred around a hair and usually indicate bacterial infection (e.g. bacterial folliculitis (rare in the cat) and acne) (Figs 2 : 5,6), dermatophytosis or, very rarely, intra-follicular demodicosis. Non-follicular pustules are flat and independent of hair follicles. Also very fleeting, they are seen mostly in superficial pemphigus conditions (foliaceus and erythematosus). Both follicular and non-follicular pustules containing eosinophils are sometimes seen in allergic dermatoses, eosinophilic granuloma complex and notoedric mange. A papule is a small, raised circumscribed swelling associated with thickening of the epidermis or Papules are classified according to their location: epidermal, follicular, superficial dermis '~'~"~''. dermal. Epidermal papules are found in squamous cell carcinoma in situ (Fig. 2 : 7). Follicular papules are common in cats with miliary dermatitis and allergic dermatitis, in which case the infiltrate is made up mainly of eosinophils. In dermatophytosis and bacterial folliculitis, follicular papules often develop into intra-follicular pustules, progressing towards fumculosis and a granulomatous reaction. Dermal papules arise from localised infiltration in the dermis by inflammatory cells: eosinophils and mast cells in allergic dermatitis (Fig. 2 : 6), eosinophils in eosinophilic granuloma complex, and mast cells in urticaria pigmentosa. Papules sometimes join together to form plaques (eosinophilic plaques) (Fig. 2 : 8). Some dermal papules called dysmetabolic papules (Fig. 2 : 9) are associated with an intradermal excess of amorphous material which accumulates secondary to a systemic metabolic disorder. These papules are rare. They may be due to dermal accumulation of lipid (xanthoma), secondary to diabetes mellitus, or a primary lipid disorder (e.g. familial hypertriglyceridaemia).
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,.:..:
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Figure 2 : I :Generalisedfacial erythema in a cat withfood intolerance
Figure 2 :2 :Localisedpinnal eryihema in a cat with dermarophytosis caused by Microspomm canis
Figure 2 :4 :Multiple hypermelanotic macu.. ... paraneoplastic alopecia
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Figure3 :6 ;Pal~~~~(Iarpurtoles und papules in a ,L=,.,,.,,, dermantb
,.,
Figure2 :8 :Dermalp~pu.,,
,.u.iations
.. ..h pancr~
,.!ergy
in a cat withfoodiiitolerance
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Vegetations and verrucosities are raised, pseudoneoplastic lesions 2.'.'4,'i. Vegetations are cutaneous "cauliflower" or pediculated proliferations relating to a hypertrophic epidermis. Verrucosities are vegetations with a greyish keratotic appearance e.g. cutaneous horns associated with FeLV infection (Fig. 2 : 10).
A nodule is a firm, raised, mostly well-circumscribed lesion, involving the dermis or hypodermis 2,3.M.'5. Dermal nodules are associated with infiltration of the superficial or deep dermis by various inflammatory cells. They may be seen in deep mycoses (e.g. cryptococcosis (Fig. 2 : l l ) , histoplasmosis and sporotrichosis), specific bacterial infections (e.g. mycobacterial infection, feline leprosy, nocardiosis, actinomycosis and hotryomycosis), or various neoplastic conditions (e.g. carcinomas (Fig. 2 : 12), fihrosarcoma, mast cell tumour and lymphoma). Hypodermal nodules are less well circumscribed and seen in deep mycoses, specific bacterial infections or sterile nodular panniculitis associated with pansteatitis. Secondary lesions Scale refers to whitish flakes of keratin that break off from the thickened horny layer 2~J.'4~'5. This common lesion has only very slight diagnostic value. Scale is classified according to its size: pytiriasiform scales are small, thin and whitish and seen in allergic dermatoses, some parasitic dermatoses (e.g. cheyletiellosis and pediculosis), and some cases of dermatophytosis (Fig. 2 : 13); psoriasiform scales are broad and quite thick and found in cutaneous epitheliotropic lymphoma (Fig. 2 : 14), degenerative, mucinous, lymphocytic, mural folliculitis, herpesvirusassociated erythema multiforme, or paraneoplastic exfoliative dermatosis (Fig. 2 : 15). Epidermal collarettes are rarely reported in the cat (Fig. 2 : 16). Sclerosis is a lesion, often shiny, of the skin and subcutaneous connective tissue, relating to an alteration in the number of collagen and elastin fibres 2~J.'4~'*.It is rare in the cat and seen in morphea 6I,' (Fig. 2 : 17). Atrophy refers to thinning of the skin which can lead to persistent flaccidity and appearance of skin folds. It is due to a reduction in the number of structural elements in the epidermis and more especially, the dermis (collagen and elastin fibres) 2.3.14,'5 (Fig. 2 : 18). Atrophy is very hard to appreciate, given the thinness of cat skin. In some cases (e.g. dermatosparaxis or hyperadrenocorticism), atrophy may lead to skin tearing. Skin atrophy may also he seen in pancreatic paraneoplastic alopecia. Erosions and ulcers are defects involving the epidermis (erosions) or dermis and hypodermis (ulcers) 2,3.'4.''. Erosions, unlike ulcers, heal without scarring. These lesions have only slight diagnostic value. Erosions are common in the cat in pruritic dermatoses such as allergic dermatitis (Fig. 2 : 19), parasitic dermatoses, and skin conditions associated with behavioural disorders. Ulcers are rarer and may occur secondary to specific bacterial infections, deep mycoses, certain tumours, auto-immune dermatoses and certain dermatological manifestations of acquired systemic diseases such as acquired cutaneous hyperfragility syndrome (Fig. 2 : 20). Ulcers seen in squamous cell carcinomas are considered to be primary lesions. Crust is a mixture of blood, serum, exudate and/or pus which has dried at the surface of the skin, and to which scale and hair have adhered. It is usually secondary to rupture of a vesicle, bulla or pustule 2~1~'4~'i.Three types of crust are found in the cat: large spontaneously appearing crusts, usually thick and coalescing and common in auto-immune dermatoses such as pemphigus foliaceus (Fig. 2 : 21); crusts secondary to excoriation, which vary in size and location, seen in all pruritic dermatoses, especially allergic dermatitis; and punctafe crusts seen in miliary dermatitis (Fig. 2 : 22). Lichenification is skin thickening characterised by exaggerated superficial skin markings, generally associated with hyperpigmentation 2.3.'4,'5. This lesion is extremely rare in the cat, unlike in the dog. Lichenified lesions have been seen in atopic dermatitis " (Fig. 2 : 23). A comedone is a dilated hair follicle filled with sehum, keratinocytes and sometimes bacteria 2,3.'4.'i. In the cat, this rare lesion is seen in acne, Malassezia dermatitis (Fig. 2 : 24), idiopathic facial dermatitis and demodicosis. Sometimes, comedones are associated with accumulations of sebum surrounding the hair, known as follicular casts.
7. .
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Figure 2 :9 :Eosinophillc plaques
lurresy of B. Hubertj
........-.., ...J cat
Figure 2 :11 :Multrple dermal nodules in a cat w ~ t hcryptococcoszs
Figure 2 :12 :Dermal nodules, some of wl... wrth mult~cenrricsebaceous adenocarc~noma
Figure 2 :13 :Pytiriasiform scale and crust in a cat with Pea allera dermatitis and dermatophytosis caused by ~icrospommcanis
Figure2 :14: Psoriasiform scale in a cat with cutaneous epitheliorruprr T cell lymphoma
dermafiris (courresy of T. Olivry and C. Rivierre)
eryfhemarosus
'GWgu&re,E., Hubsn, B.& blabre, C. Vet. Dmnatol. 3, 1-12 (1992).
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Configuration of lesions Determining the configuration of lesions is much more difficult in the cat due to its dense coat. Nevertheless, the following arrangements may be recognised: punctate, lenticular, nummular (coin-shaped), annular, linear and arciform (ring-shaped) 14,' (Table 2 : 2). Lesion distribution Assess'ing the distribution of lesions is the h a 1 step in the dermatological examination ","" (Table 2 : 3). It ~rovi&sessential information as many conditions have specific distribution patterns (Table 2 : 4). They maialso he modified by ~ i w e v e r these , patterns may change as a dermatosis various treatments. The initial distribution pattern may be very different to the one seen in the consulting room. Table 2 :2 : Configuration of lesions "
punctate
lenticular
0 Large lesions nurnmular (coin-shaped)
indistinctly bordered
a
4-4.
indented
d
&
Jc'
v*-
map-shaped
s
annular
arcifom (ring-shaped)
0
Q,
part-bordered
C; -.,*.
linear
1
Very large lesions
:'
part-serpiginous
G/ !:-:.:>.: ,.---
rosette-shaped
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Hgure2 :17 :S:l.ler,~~L(In a COI W I Imbrpbro ~ (cou~lery ofE Bemrgnor,'
Figure 2 :18 :Alr'phy
Figure2 :19 :Erosionsandexcoriations on the pinna o f a cat wirhfood intolerance
Figure2 :20: Extensive ulceration in a cat with acquired hypefra&G,LJ syndrome
fohceus
Figure2 :22 :Punctate c r m s in a cat wrth m ~ b a r y d e r m t rassociated s withflea allergy
laferal pinno of a cat with atopic dermatitis
Figure 2 ;24 :Cmedonesnndfollicular casts on the chin of a cat with Malassezia dermatitis
ill
a cal hrld idrrqrnrc Oul~ing'rS)ndr~nrs
* ~msignor,E.,Pm. D.BrCar1atti.D.N. I. s d A n i m . P r c t 39.538-54C(1998).
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r~ghtprofile
ventral
dorsal left profile
nght profile
left profile
face
nght foreleg
nght hmdleg
left foreleg
left hmdleg
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FACE - Ponvirus infection - Herpesvirus infection - Herpesvirus associated erythema multiforme - Papillomavirusinfection - Bacterial folliculitis
-Bite abscess -Acne - Lepmsy -Atypical mycobacterial infection - Nocardiosis - Actinomycosis - Botryomycosis - Dermatophytosis - Malassezia dermatitis
- Candida albicans dermatosis - Subcutaneous mycoses - Sporotrichosis - Cryptococcosis - Histoplasmosis - Blastomycosis - Coccidioidomycosis
- Indolent ulcer - Eosinophilic granuloma - Superficial pemphigus - Pemphigus vulgaris - Bullous pemphigoid - Discoid lupus erythematosus, systemic lupus erythematosus - Cutaneous drug reaction -Auricular polychondritis - Pseudopelade - Hereditary epidermolysis bullosa - Vitiligo
-Bums -Frostbite -Actinic keratoses -Irritant contact dermatitis - Squamous cell carcinoma
- Multicentric squamous cell carcinoma in sifu
- Otodectic mange
-Basal cell tumour - Eibrosarcoma complex - Cutaneous epithelionopic T cell lymphoma - "Mastocytic" mast cell tumour - "Histiocytic" mast cell tumour
- Demodicosis - Trombiculiasis - Cheyletiellosis
- Pancreatic paraneoplastic alopecia - Paraneoplastic enofoliative dermatitis
- Leishmaniasis
- Degenerative mucinous lymphocytic mural folliculitis
- Atopic dermatitis
- Skin conditions associated with behavioural disorders
- Notoedric mange
-Food intolerance
- Mosquito bite hypersensitivity -Allergic contact dermatitis
FOOT - Ponvirus infection
- - Eosinophilic plaque
-Herpesvirus infection - Calicivirus infection - Herpesvirus-associatederythema multiforme
- Eosinophilic granuloma
-Bite abscess
-Cutaneous drug reaction -Plasma cell pododermatitis
- Bacterial paronychia
-Leprosy -Atypical mycobacterial infection - Nocardiosis - Actinomycosis - Botryomycosis
- Dermatophytosis - Malasseiia dermatitis - Candida albicans dermatosis
-Subcutaneous mycoses - Sporotrichosis - Cryptococcosis - Histoplasmosis - Blastomycosis - Coccidioidomycosis - Trombiculiasis - Demodicosis - Notoedric mange - Anahichosomiasis - Leishmaniasis - Atopic dermatitis
-Food intolerance -Mosquito bite hypersensitivity -Allergic contact dermatitis
- Pemphigus foliaceus
- Discoid lupus erythematosus, systemic lupus erythematosus - Congenital hypotrichosis - Pili torti
-Hereditary epidermolysis bullosa - Vitiligo
-Bums -Frostbite - Initant contact dermatitis - Squamous cell carcinoma - Trichofolliculoma - Fibmsarcoma complex
-Cutaneous epitheliohopic T cell lymphoma - Digital metastasis of a pulmonary adenocarcinoma -Pancreatic paraneoplastic alopecia
- Paraneoplastic exofoliative dermatitis - Vasculitis - Degenerative mucinous lymphocytic mural folliculitis
- Xanthomatosis
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Table 2 :4 : Examples of lesion distribution (continued from previous page) TRUNK i
- POXV~NS infection - Herpesvirus-associated erythema multiforme - Dermatophytosis
- Pseudopelade
-Cutaneous asthenia - Hereditary greasy seborrhoea
- Pancreatic paraneoplastic alopecia
- Cheyletiellosis - Otodectic mange - Notoedric mange
- Paraneoplastic exofoliative dermatitis - Hyperadrenocorticism
-Degenerative muchous lymphocytic mural folliculitis
-Flea allergy dermatitis - Food intolerance - Eosinophilic plaques
- Cutaneous epitheliotropicT cell lymphoma - Cutaneous metastasis of mammary adenocarcinoma - Multicentric sebaceous adenocarcinoma
- Pemphigus foliaceus
- Systemic lupus erythematosus
- Self-induced alopecia associated with behavioural disorder
TAU - Dermatophytosis - Seborrhoeaihyperplasia of the supracaudal organ - Self-mutilationof the tail associated with a behavioural disorder
REGION AROUND THE NIPPLES - Pemphigus foliaceus
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MUCOCUTANEOUS JUNCTIONS AND ORAL CAVITY
- Pemphigus vulgaris - Bullous pemphigoid - Hereditary epidermolysis bullosa
Differential diagnosis Taking a history and conducting a good clinical examination allows the clinician to formulate a differential diagnosis, consisting of at most 5 conditions listed in order of suspicion. These conditions can be rnled in or out by conducting carefully chosen diagnostic tests 14.
Diagnostic tests The choice of test depends on the precise differential diagnosis, ease of doing the test and the likely delay in getting the results. When a definitive diagnosis cannot be established following simple and rapid testing procedures, a further set of tests will be needed. In such cases, interim therapy is often indicated to relieve clinical signs and help point to a diagnosis 2". This may constitute a true therapeutic trial e.g. flea control when flea allergy dermatitis is suspected.
Simple diagnostic tests for immediate interpretation The tichogram (Table 2 : 5) is a detailed examination of hair involving tip, shaft and root '. About 20-30 hairs are mounted in liquid paraffin on a microscope slide and under a cover slip (Figs 2 : 25,26). They are examined microscopically (using average light intensity) at a magnification of x40, xlOO and x250. This procedure can reveal the following: 1) stage of the hair cycle (anagen or telogen) 2) condition of the hair tip (whether damaged) 3) state of the hair shaft (which can be altered in many ways including invasion by spores and hyphae in dermatophytosis, and production of follicular casts in acne and demodicosis)
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Pigwe2 :25 :Trzdtogram eprlanan of hairs
Figure 2 :26 :Trichogram. hairs are motwedm hqurdpr@n
Figure 2 :27 :Skin scrapmg a fold of skm rs held b e w e n rhumb and forej%gex The skin scraping should be t a k n m the same d~reetroni.e. pi-pendwlar to the futd ofsEn
Figure2 :28 :Tape stnp~pressrngrrunsparent sficky lope onto the skrn
Figure2 :29 :Coat brushing: skin debris is collected onto a large piece of white paper
Figure 2 : 30 :Coat br microscope slide under a cover slip
rtesy of C. Prost)
Figure 2 :32 :Wood's lamp examination: yeNow-greenishfluorescence associated with dermatophyte lesions caused by Microspomm canis (courtesy of G.TWilkinson)
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N o d proportion of telogen and anagen hairs; distal ends of hain not damaged
Normal coat
Normal proportion of telogen and anagen hairs; distal ends of hairs damaged
Allergic dermatitis Self-induced alopecia associated with behavioural disorder Cheyletiellosis Otodectic body mange
Hair shaft abnormalities
Dermatophytosis Pili torri Follicular dysplasia Trichorrhexis nodosa
Telogen hairs only, of normal appearance
Telogen efluvium (e.g. post-fever, -surgq) Pancreatic paraneoplastic alopecia Hyperadrenocotticism
4) various cuticular abnormalities (e.g. pili torti, follicular dysplasia and trichorrhexis nodosa). If there has been excessive licking, not only will the tips of hairs be damaged but fragments of ingested hairs will he found on faecal examination. Gross examination of the skin and hairs, with the help of a magnifying glass, can reveal various mites and insects la: Trombicula autumnalis larvae, Cheyletiella blakei, tick larvae and the louse Felicola subrostratus. The skin scraping is a diagnostic test that can give rapid results. A blunt scalpel blade is used to obtain scale and skin debris (epidermis, hair, etc.. .) for microscopical examination IS.To improve the quality of the sample, hairs should first be cut. A drop of liquid paraffm or chloral lactophenol should be placed on the scalpel blade and a fold of skin held between thumb and forefinger (Fig. 2 : 27). The skin scraping should he taken in the same direction, i.e. perpendicular to the fold of skin. An ample amount of the sample should then he placed on a microscope slide, to which is added a drop of liquid paraffi or chloral lactophenol. After mixing, a cover slip is applied ready for microscopical examination. The sample is first scanned at x40 and xlOO and then at x250 and x400 for parasite identification. Light intensity should be moderate to weak la.This procedure allows the following mites to he identified in different stages of their life cycle: Notoedres cati, Cheyletiella blakei, Otodectes cynotis, Demodex cati and Demodex gatoi. The louse, Felicola subrostratus can also be demonstrated. The tape strip test ("scotch test") allows the collection of parasites, at various stages of their life cycle, present at the surface of the skin or base of the hairs la.A piece of transparent sticky tape is pressed onto the skin after first clipping or cutting the hair with scissors (Fig. 2 : 28). It is then placed, sticky side down, ready for microscopical examination, as outlined for the skin scraping la. This procedure is indicated to demonstrate Cheyletiella blakei in its various stages of development. Coat brushings are carried out by placing the cat on a large piece of white paper and brushing the cat energetically, against the fur, with a surgical brush Is. Scale and cutaneous debris are collected, placed in chloral lactophenol or liquid paraffin (Figs 2 : 29,30) and examined microscopically as outlined for the skin scraping 18. This procedure is indicated to demonstrate Cheyletiella blakei, the louse, Felicola subrostratus, and fleas, especially Ctenocephalides felis felis. Combing with aflea comb can he camed out when looking for fleas and lice Is. Wood's lamp examination is a procedure that can be conducted early on in a mycolo y investigation 19. Wood's lamp is an ultraviolet lamp (Fig. 2 : 31) that emits a radiation of 3650 When exposed to ultraviolet light, hairs invaded by some strains of Microsporum canis give off a greenish fluorescence due to certain pigments (e.g. pteridin) present in the hyphae (Fig. 2 : 32). This long, detailed examination should be carried out in complete darkness, after first warming the lamp up for about 3-5 minutes. This procedure will detect about 50% of strains of Microsporum canis. False fluorescence, following application of certain topical agents, bluish colouration of scale, and yellowish colouration of crust should not he seen as indicative of Microsporum canislq.
i.
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c 2 : Diagnostic approach
Cytology can give rapid results and may help to suggest or even confim~a diagnosis 20,". Various techniques can be used depending on the type of lesion lC, (Figs 2 : 33,34) (Table 2 : 6). Smears should be air-dried rapidly before staining in order to limit damage to cells. Various stains are available including rapid stains (e.g. Diff-Quik), Giemsa stain and Wright's stain. These stains allow specific staining of cytoplasm, nucleus and micro-organisms. Staining of nucleus and nucleolus is not as good as that seen with the vital stains, hut good enough to distinguish neoplasia from hyperplasia lo. Diff-Quik cannot be used for metachromatic staining so mast cell granules will not all show up. The vital stains include haematoxylin and eosin, Papanicolaou and methylene blue. These stains give excellent detail of the nucleus and nucleolus, and allow appreciation of cellular architecture as well as some cytoplasmic granules and fungal elements. On the other hand, cytoplasmic structures and bacteria stain poorly with these products 20. Special stains can be used to identify particular cellular structures or microorganisms. Examples include Ziehl-Neelsen for mycohacteria and Sudan Red for lipid. Microscopical examination of smears should start with a low-power scan (x100) before more . is indicated in allergic dermatitis, detailed examination under high power ( ~ 1 0 0 0 )Cytology eosinophilic granuloma complex, pustular, erosive and crusting dermatoses (including autoimmune dermatoses, bacterial skin infections and deep mycoses), nodular dermatoses (inflammatory and neoplastic) and otitis externa.
Table 2 : 6 : Sampling procedures suitable for cytological examination of different lesional types
I
I
~ i r e c smear t
I
Impression smear
Erosions, ulcers, undersurface of crusts
Scraping
Erosions,ulcers, undersurface of crusts
Incision
Nodules
Fine needle aspirate
Nodules
I
Swab
I
Papules, pustules, vesicles, bullae, nodules and fistulae
I
Fistulae, buccal lesions, otitis extema
Additional tests Fungal culture is essential for specific identification of dermatophytes Iq. Culture media include Sahouraud's and Dermatophyte Test Medium (DTM). DTM is Sahouraud's medium with added phenol red, which changes colour rapidly, within 3-10 days, in the presence of a dermatophyte, giving a rapid indication of the likely diagnosis. Early colour change is followed by dermatophyte growth and production of alkaline metabolites which leads to the culture medium turning red (Fig. 2 : 35). An exception is seen in the case of Microsporum persicolor. Growth of this dermatophyte precedes the colour change by several days. A later colour change, after 2-4 weeks, is seen with growth of saprophytic fungi (e.g. Aspergillus spp. and Mucor spp.) or bacteria (Fig. 2 : 35). DTM is a good culture medium hut microscopical examination of the culture is necessary for specific identification. The lesion to be sampled should he disinfected with a spirited swab for 30 seconds to eliminate most of the contaminants, Hair and scale should be taken from the centre and edge of the lesion '" Cats suspected of being asymptomatic carriers should he brushed with a sterile carpet square or toothbrush (Fig. 2 : 36) which is then placed directly on the culture medium. The sample should he inoculated, under sterile conditions, at the peiiphery of the agar, using either a platinum loop or a pair of blunt forceps (Fig. 2 : 37). Incubation is slow (10-21 days) and is carried out at 25-27'C. Dermatophyte examination involves both macroscopic and microscopic culture examination. Colonies are examined microscopically according to Roth's flag method Iq(Figs 2 : 38,39) (Table 2 : 7). Microscopic dermatophyte i d e n t " is based on the type and arrangement of fruiting bodies (macroconidia and microc! Culture of other fungi must be done at a specialist laboratory. "
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Table 2 :7 : Microscopical examination of a section of fungal culture ''
Covers$ Drop of chloral lactophenol Shcky tape and sample of culhlre Drop of chloral lactophenol or methylene blue Shde
An elimination diet is the only way of diagnosing food intolerance (see chapter 11). lntradermal testing is very controversial in the cat 1"'~2'. The same allergenic extracts used in the dog can be used in the cat at the same concentrations. The test site should first be clipped. 0.05 ml of each allergenic extract is then injected intradermally. The test is read at 15 minutes and at 48 hours (delayed reactions are possible in flea allergy dermatitis). Interpretation is based on the same criteria as in the dog at 15 minutes. A reaction is considered positive if an erythematous papule, larger in diameter than the average diameter of the positive and negative controls, is present. Intradermal tests are often hard to interpret in the cat due to the small size of the positive control ".22~23. However, in some cats, a wide erythematous papule is seen at the site of the positive control or other extracts, as in the dog. In flea allergy dermatitis, a delayed reaction may be seen after 48 hours, with skin thickening or a small nodule at the site of injection of whole flea extract. Some allergens in low concentrations, will induce positive intradermal reactions in normal cats. These may be either irritant reactions or genuine positive reactions, there being a difference between clinical sensitivity and skin reactivity.
Further additional tests Bacterial culture and antibiotic sensitivity are less frequently indicated than in the dog. They are indicated only in recurrent pyoderma, paronychia, specific bacterial infections (which are rare), and suppurative otitis externa whenever cytology reveals a mixed bacterial growth (cocci and bacilli). If certain specific bacterial infections (e.g. mycobacterial infection or nocardiosis) are suspected, a specialist laboratory should be contacted. Skin biopsies should be carried out whenever the history and clinical examination suggest a dermatosis that requires histopathological diagnosis; when a reasoned diagnostic approach has not produced a diagnosis; or when apparently rational treatment has been unsuccessful They are also indicated for nodular or ulcerative lesions or for unusual or severe skin conditions. Primary lesions are normally selected for skin biopsy; older lesions affected by scratching, maceration, secondary infection and topical treatments should generally be avoided. Lesions in different stages of development should be biopsied. Different procedures involving excisional biopsy or punchbiopsy can be used. Biopsy punches in 4, 6 and 8 mm sizes are commonly available (Fig. 2 : 40). Excisional biopsy is preferred for large lesions (e.g. nodules), fragile lesions (e.g. pustules and vesicles) and deep lesions (e.g. panniculitis). Biopsy specimens are fixed in 10% formalin for standard histopathology 14. For electron microscopy or for some imrnunohistochemical procedures, specimens should be fixed by freezing in liquid nitrogen. 'Biopsies should be sent to a veterinary histopathologist interested in dermatology or to a veterinary dermatologist with a good knowledge of dermatopathology.
j4.
Blood tests (e.g. biochemishy, huematology and endocrine profiles; serology) are indicated in the investigation of certain conditions 2. Imaging techniques (e.g. radiology, ultrasonography and CT scanning) are necessary for diagnosing skin conditions associated with certain systemic illnesses and skin tumours.
www.vet4arab.co.cc 2 : Diagnostic approach
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.
-.
a microscope slide for staining and microscopical eramination
Figure2 :35 :Fungal culture using Dermarophyte Test Medium (DTMJ: the growth offungal colonies is revealed by the change in colour of the medium from yellow to red (lefr: sterile culture mediwn, centre: Micmostmr
is
Figure2 :36: Sreme toothbrush used to collect skin debris andinocu sample onto the fungal culture medium
ill dnnr rolhrw rioht rnntnminnnrol
Figure2 :5 ) :rungal culture: aplatinum loop is ued to inoculate k i r s at the periphery of the agar
Figure 2 :38 :Roth'sflag method: apiece ofsticky tape is used to remove a sectionfrom the centre of a colony
Figure 2 :40 :Skin biopsy using a 6 mm biopsy punch
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Practical Guide to Feline Demmlogy
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REFERENCES 1. Griffin, C. E. in Contemporary Issues in Small Animal Practice (ed Nesbitt, G.H.) (Churchill Livingstone, New York, 1987). I des carnivores (ed Guagukre, BE.)7-22 (PMCAC Editions, Paris, 1991). 2. Foumer, P. in Techniques diagnostiques ~ I dermatologie 3. Scott, D. W , Miller, W. H. &Griffin, C. E. Muller andKirk's SmaN AnimalDermatology, 5th edition (Saunders, WB., Philadelphia, 1995). 4. Mason, I. in Handbook of Small Animal Dermatology (eds Moriello, K. &Mason, 1.) 11-18 (Pergamon, Oxford, 1995). 5. Bond, R., Cums, C. E Ferguson, E. A,, Mason, I. S., & Rest, J. Vet Derm 11,35-41 (2000). 6. Paradis, M. &Scott, D. W. Feline Practice 18, 17-20 (1990). 7. Gamer, J. W., Davis, W. C., Prieur, D. J.,Baxter, J. & Norsworthy, G. D. J.Amei: Vet. Med.Assn. 166, 1103-1104 (1975). 8. Olivry Th., Dunston, S. M. & Marinkovich, M. P. Vet. Pathol. 36, 616-618 (1999). 9. Lopez, R., Ginel, P. J. & Molleda, J. M.and others E l . DermatoI. 5.27-32 (1994). 10. Vitale, C. B., Ihrke, P. J., Olivy, T, & Stannard,A. A, Vet. Dermatol. 7,227-233 (1996). 11. Bourdeau, P., Leonetti, D., Maroille, J. M. & Mialot, M. Rec. Med. 1/41, 164, 17-24 (1988). 12. Noli, C. & Scarampella,EProc. AAVD-ACVD, Maui, 65 (1999). 13. Power, H. T. Proc. AAVD-ACVD, Son Francisco, 45 (1990). 14. Alhaidari, Z. Prar. MPd. Chir. Anim. Comp. 23, 101-103 (1988). 15. Lemarchand-VenancibE & Saurat, J. H. Encycloptdle Mldico-Chirurgicale 12.220-A054 5.091-6 (1984). 16. Bensignor, E., Pin, D. & Carlotti, D. N. J, small Anim. Pracf. 39,538-540 (1998). 17. Gilbert, S., Pklaud, P. & Guagukre, E. Prat. MPd. Chli: Anim. Comp. 34, 15-31 (1999). 18. Bourdeau, P in Techniques diagnostiques en dermatologie des carnivores (ed Guagukre, E.) 43-58 (PMCAC Editions, Paris, 1991). 19. Guagukre, E., Carlotti, D. N, in Techniques diagnostiques en dermatologie des carnivores (ed Guagukre, E.) 77-84 (PMCAC Editions, Paris, 1991). 20. Marshall, C. in Techniques diagnostiques en dermatologie des carnivores (ed Guagukre, E.) 29-42 (PMCAC Editions, Paris, 1991). 21. Ferrer, L. Domingo, M. in Techniques diagnostiques en dermatologie des carnivores (ed Guagukre, E.) 99.106 (PMCAC Editions, Paris, 1991). 22. Carlotti D. N. in Techniques diagnostiques en dermatologie des carnivores (ed Gnagukre, E.) 127.138 (PMCAC Editions, Pais, 1991). 23. Carlotti, D. N. in Current Eterinary Tl~etopyXi (ed Kirk, R.W.)509512 (Saunders, W.B., Philadelphia, 1992). 24. Alhaidari, Z. in Techniques diagnosh'ques en dermatologie des carnivores (ed Guagukre, E.) 107-114 (PMCAC Editions, Paris, 1991).
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Ectoparasitic skin diseases Skin diseases caused by mites and insects are of prime importance in feline dermatology and enter into the differential diagnosis of many different conditions. Al[bough some are often suspected, others are less so because the signs associated with them are non-specific . Some fctoparasitic conditions may be the source of human infestations, unrecognised by either vet or dermatologist .
Notoedric mange Aetiopathogenesis Notoedric mange is caused by Notoedres cati, a mite from the family Sarcoptidae (Table 3 : 1). The mite lives in the epidermis ' and its life cycle is similar to that of Sarcoptes scabiei. The condition is highly contagious, especially by direct contact, to cats, dogs and man (causing a pruritic rash) Although notoedric mange is now rare in European countries like Great Britain, Germany, The Netherlands, France (excluding the overseas territories), it is still common in parts of Italy, Switzerland, Spain, Slovenia and Croatia, where it is either endemic or present in an epizootic state. Young animals and cats debilitated with retroviral infection are particularly susceptible '.
Clinical features Signs of notoedric mange appear initially on the face and pinnae and are characterised by hqr loss, erythema, scaling and thick crusts (a notoedric "helmet") "". With time, lesions spread to the limbs, abdomen and pen-anal region (Figs 3 : 1-4). Hyperpigmentation, lichenification and excoriations are then observed. Pruritus is variable (mild to severe)
Diagnosis Skin scrapings reveal numerous Notoedres mites - adults and immature stages (eggs, larvae and nymphs) (Table 3 : 1) (Fig. 3 : a). Faecal pellets are often seen.
Treatment Amitraz * (0.25% solution) can be given every 5 days for 4 - 6 weeks following local washing with a keratolytic shampoo '. Zvermectin * (200-400 pgkg), given once or twice (2 weeks apart), by subcutaneous injection, gives excellent results '. It should not he given to cats less than 4 months old. Chlorinated hydrocarbons and organophosphates are toxic in this species and should be avoided '. All in-contact cats should be treated. Ivermectin is the treatment of choice when groups of cats are affected. The environment should be cleaned thoroughly with an acaricidal agent that gives longlasting protection '.
* T?ispmiun is not iieensed for use in ule cat and isponribiiiq for is use falls on ule p-bing
veminar, surgeon
Pradcal Guide to Feline hnatology
I
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Sarcoptes scabiei var canis (Table 3 : 1) (Fig. 3 : b) is extremely rare in the cat, causing pruritus, alopecia, erythema, scaling and crusting on the face, neck and distal limbs. The parasite can spread to people causing a pruritic rash '.
Otodectic mange Aetiopathogenesis Otodectic mange, also referred to as otoacariasis or ear mite infestation, is the most common mite infestation in the cat, accounting for up to 25% of consultations in feline dermatology. It is caused by Otodectes cynotis, a mite from the family Psoroptidae (Table 3 : 1). Otodectes lives mainly in the external ear canal and more rarely, on the face (around the ears and on the lateral p'mnae), neck and body (dorsolurnbar region and tail base) '. Transmission is by direct contact and occurs mostly in the neonatal period. Young animals are, therefore, most susceptible Otodectic mange is endemic with a high morbidity. This mite is not host-specific and also causes otitis in the dog and ferret. Transmission to humans may cause pnuitus on the arms and trunk ',3.
Otodectes cynotis causes disease through its initant effects (mechanical and chemical) and also by induction of hypersensitivity reactions.
Clinical features Otodectic mange is characterised by otitis, usually bilateral and erythemato-ceruminous, with dry blackish, brown cerumen (Fig. 3 : 5). Pruritus is severe. Self-induced erosive lesions around the ears and aural haematomas are often seen '.I4. If the tympanic membrane is ruptured, vestibular syndrome is sometimes observed. Non-specific pruritic lesions on the face, neck and dorsolumbar region, presenting as miliary dermatitis or symmetrical alopecia, are typical (Figs 3 : 6-8) ",',"'. Sometimes, the body is affected without involvement of the ear canals '.
Diagnosis Microscopical examination of ear wax, mounted in liquid paraffin or chloral lactophenol reveals the presence of numerous Otodectes mites - adults and immature stages (eggs, larvae and nymphs) ' (Table 3 : 1) (Figs 3 : c,d). Skin scrapings, when the body is affected, reveals far fewer Otodectes cynotis &'.
Treatment Amitraz* (0,5%0in propylene glycol) can be applied twice weekly into the ear canals for 6-8 weeks, following ear cleaning '. Fipronil** in spot-on formulation is a very effective treatment for otodectic mange9. Two drops should be applied into each ear canal, on two occasions, two weeks apart, without prior cleaning. The rest of the pipette should he placed on the body to avoid wider cutaneous involvement.This treatment is extremely well tolerated. Ivermectin * (200-400 pgikg), given once or twice (2 weeks apart), by subcutaneous injection, gives excellent results I. It should not be given to cats less than 4 months old. Selamectin (6 mgikg) is very effective in the treatment of otodectic mange. It is applied, once, as a spoton onto the neck. Transient alopecia and local irritation at the application site have, in rare cases, been seen in cats. Acaricidal treatment of the whole body is necessary '. Treatment will sometimes fail due to reinfestation of the ears by mites present on the skin surface '. Current treatment involves either applying fipronil spray or spot-on over the body or subcutaneous injection of ivermectin at the dose given above. When groups of cats are affected, ivermectin is the treatment of choice.
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Figure 3 :1 :Eryrhema and crusting on the face and pinnae of a kitten with notoedric mange (courteq of 0.Cozette)
Figure 3 :2 :Same cat as in figure 3:l: alopecia and erythema around the elbow (courtesy of 0. CozetteJ
Figure 3 :3 :Thick crusts on the face andpinnae of a cat with notoedric mange (courtesy of J P Pages)
Figure 3 :4 :Interdigital crusting in a cat with notoedric ma, (courtesy ofB. Hubert) *
Figure 3 :5 :Erythemato-ceruminous otitis with dry, blackish cerumen in a cat with otodectic mange
Figure 3 :6 :Erythema and crusting on the medialpinna of a cat with otodectic mange: skin scrapings demonstrated aduh Otodectes in this reaion
Figure 3 :7 :Alopecia, erythema and erosionson the neck of a otodectic body mange
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O u a g u i ~E,..Hukrf 8.& Delabre, C. Vet Dematol. 3.1-12 (1992).
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~ n ins a cat with otodectic
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Aetiopathogenesis Cheyletiellosis is an underdiagnosed mite infestation which causes real problems in some catteries. It is caused by Cheyletiella blakei, a mite specific to the cat, from the family Cheyletidae (Table 3 : 1) .O' However, Cheyletiella yasgun' and Cheyletiella parasitivorax are sometimes found in the cat '.". Cheyletiellid mites live at the skin surface, feeding on cutaneous debris ','! External surroundings seem to play an important part in transmission as the parasites appear to be able to survive off the host for at least a month 'O. Cheyletiellosis is seen mainly in young cats (less than 1 year old) hut adults can be asymptomatic carriers lo. In catteries (especially involving Persians), it can be endemic with a high morbidity Its incidence may be similar to that of dermatophytosis in some colonies. Humans may be affected (pruritic rash on the m s and trunk) in 20-30% of cases 2.'0.
Clinical features Cheyletiellosis affects principally the head and trunk and is characterised by pruritus, sometimes marked, erythema, papules, localised or diffuse hair loss, scaling and crusting (Figs 3 : 9,lO). In the adult cat, cheyletiellosis can present as miliary dermatitis '.I,''.
Diagnosis Tape ships (scotch test) do not always demonstrate adult cheyletiellids (Table 3 : 1) (Fig. 3 : e) but eggs are readily found attached to hairs I.'. Better success can be achieved if this procedure is combined with coat brushings. Coat brushings enable the collection of scale, skin debris and parasites onto a piece of paper. The material is then examined microscopically.
Treatment Zvermectin * (200-400 pgkg), given once or twice (4 weeks apart), by subcutaneous injection, gives excellent results It should not be given to cats less than 4 months old. Fipronil ** in spot-on or spray formulation is also effective when given twice, 3 weeks apart. Other topical acaricides (e.g. amitraz) may also be used according to standard protocols '. When groups of cats are affected, ivermectin is the best treatment. Control of cheyletiellosis must include treatment of all in-contact animals, whether or not they are affected, and thorough cleaning of the environment '.
Trombiculiasis Aetiopathogenesis Trombiculiasis is a seasonal (summer and autumn) mite infestation caused by the 6-legged Trombicula autumnalis larva (Table 3 : I), a mite from the family Trombiculidae, which lives in rotting organic material '.I. Its life cycle lasts about 50-70 days I. Only the larvae are parasitic, affecting most animal species (e.g. dog, cat, man and poulby). In people, they cause very pruritic papular lesions on the limbs and mnk l,'. Trombicula autumnalis larvae cause disease through the proteolytic, irritant, and probably allergic effects of products in their saliva.
Clinical features Trombiculiasis occurs mainly on the head (base of the pinnae, Henry's pocket, neck) and feet (around the digits) and is characterised by erythema, excoriations, hair loss, erosions and crnsts ',IM(Figs 3 : 11-16). Pnuitus is very severe and persists long after the larvae have gone '. Systemic signs (e.g. fever) are sometimes seen '.
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Figure3 :9 :Pruritus andscaling in a Persian kiifen with cheyletiellosis (courtesy of Z. Alhaidaril
Figure 3 :10 :Pruritus and scaling in a Persian cat with cheyleriellosis
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Figure 3 :I1 :Erosive, crusting lesions at the base of the pinna in a cat with hambiculiasis (courtesy of E. Bensignor)
I
Figure 3 :13 :Very pruritic erosive lesions on the neck of a cat with trombiculiasis (courtesy of D. Smal)
Figure 3 :14 :Same cat as infgure 3:13: note crusting on the medial pinna (courtesy of D. Smnl)
Figure 3 :1.5 :Tmbieula autumnalis lawae in fhe claw fold of a car with trombiculiasis (courtesy ofD. Smd)
Figure 3 :16 :Trombicula autumnalis larvae in the interdigital space of a cat with trombiculiasis (courtesy of D. Smalj
Figure3 :12 :Tmmbicula autumnalis larvae in Henry'spocket (courtesy of D. Smal)
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Table 3 : 1 : Identification of the principal mites involved in feline skin diseases. (Techniques diagnostiques en dermatologie des carnivores, Bourdeau P. (editor Guagukre BE.)pp 43-58 (PMCAC Editions, Paris 1991)
Notoedres cati Cat (very rare), dog (extremely rare). Found in the epidermis. Roundish shape 200-24C mm. Short rostrum (square) - very short legs with suckers on long pedicels. Dorsal anus. Dorsally, 4-6 pairs of thick bristles; concentric cuticular ridges, rounded scales arranged transversely.
Cat (extremely rare), dog. Found in the epidermis. Oval-shaped 300-500 mm Short roshum (square) - very short legs with suckers on long pedicels (legs I and 2 in the male and legs 1.2 and 4 in the female) Terminal anus. Dorsally: 1 shield, 3 + 7 pairs of spiny bristles shaped like carpet tacks; Triangular scales arranged transversely
Cat and dog (very common). Found in the ear canal (rarely on the skin surface). Oval-shaped 450-630 mm. Short rostrum (pointed) -long legs with subsessile suckers. Males have poorly developed abdominal lobes with fdiform bristles. Females (often egg bearing) have a fourth pair of short legs (females appear to have only 3 pairs of legs); males and nymphs frequently seen Eggs sometimes seen alone (elongated ovoid shape containing the lama on which can the pointed rostrum and long legs can already be made out).
Figure 3 :c :Otodectes qnotis (copulating males and nymphs) (x40)
Figure 3 :d : Otodectes qnotis (adult female) xlOO
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Cat (occasionally man, dog and others). Found on the skin surface (rarely at the entrance to the ear canal). Oval-shaped hexagonal body 3W-5W p. A msverse groove separates two groups of legs (1-2 and 3-4). Long legs, each with a comb-shaped bristle (empodium) at the end. Very well-developed mshum with a dorsal M-shaped perirreme and two terminal pedipalps terminating ventrally in prominent, curved hooks. Species identificationrests on the shape of a broad-based, ovoid, sensory organ (solenidion) (3.5 pm) on genu I of the adult mite. Eggs: 120-130 pm, sometimes a cocoon of loose filaments.
Figure 3 :e :Cheyletiella blakel (x40) (courtesy of ENV Paras~tologyLaboratory, Lyon)
Trombicula (Neolrombicula) autumnalis (parasitic larvae)
I
Cat, dog, many other hosts mcludmg man. Found on the s h surface. Oval-shaped. Orange-red - colour 200-500 um. Pointed roshum with 2 lateral pedipalps terminating in claws. 3 pairs of long legs Dorsally: 1 pentagonal shield and 5 long, feathely bristles on the body and legs.
Figure 3 :f :6-legged lrombrcula aufumnalrs larva (x40)
Figure 3 :g :Demodex cari (x4W) (courtesy of D.N. Carlotti)
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Prosoma almost as long as Ule opisthosoma.
I
Figure 3 :h :Demodex gatoi (~400)(courtesy of D.N. Carlotti)
A Weal Guide m Feline kmat010gy
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Diagnosis The diagnosis is based on finding these 6-legged, orange-coloured larvae, either with the naked eye or with a magnifying glass. They can be identified on microscopical examination (Table 3 : 1) (Fig. 3 : f). Be wamed, these larvae are not always present at the time of consultation ',I.
Treatment Treatment is difficult and requires repeated application of acaricide. Pipronil** spray, 0.25%, applied monthly to the whole body, is moderately effective in the cat ". However, increasing the frequency (twice weekly) of spraying in larval predilection sites leads to much better efficacy (E. Guagukre, personal observations, 1998). Treating the external environment is possible but disappointing. Clearing out gardens and vegetation along with pesticide sprays is strongly advised '.
Demodicosis Aetiopathogenesis Feline demodicosis is caused by the excessive proliferation of 2 species of mite from the family Demodicidae: Demodex cati, a resident of pilo-sebaceous units ' and Demodex gatoi, a shorter mite that lives in the superficial layers of the epidermis ' I (Table 3 : 1). Their life cycle and mode of transmission are not well understood. Age does not seem to be a predisposing factor, although the "juvenile" form, seen in cats of less than 3 years, carries a better prognosis than the condition reported in cats older than 5 years, which is often associated with an underlying illness ','I. Examples of underlying illnesses include FeLV and FIV infection, diabetes mellitus, byperadrenocorticism, systemic lupus erythematosus and multicentric squamous cell carcinoma in situ '.".I4. Siamese and Burmese breeds seem to be predisposed '.
Clinical features The head and neck are the main areas affected, more rarely the trunk and limbs. Skin lesions are characterised by erythema, papules or pustules, localised or diffuse hair loss, scaling, erosions, ulcerations, crusting, comedones and hyperpigmentation '," (Figs 3 : 17-21). In the Persian cat, a paaicular clinical form (greasy facial seborrhoea) has been observed " (Fig. 3 : 22). Bilateral erythemato-cemminous otitis is often seen and may be the only clinical manifestation I,'' (Fig. 3 :23). Pruritus is variable but more common with Demodex gatoi infestation.
Diagnosis Deep skin scrapings can be used to demonstrate Demodex cati and Demodex gatoi in different stages of their life cycles ',' (Table 3 : 1) (Figs 3 : g,h). The possibility of an underlying disease must be investigated, especially when the condition is generalised '.'3,'4.
Prognosis and treatment The prognosis depends on theclinical form (the localised condition carries a better prognosis than the generalised form) and the underlying illness '.''.". The localised form can sometimes spontaneously resolve. Amitraz* (0.25%0solution) can be given every 5 days for 4 - 6 weeks, following local washing with a keratolytic shampoo ','I. This treatment is well tolerated. Antiparasitic macrocyclic lactones (ivermectin *, milbemycin *) could be used here. Control of the underlying illness must be instituted once the condition has been identified 'j.".
*This product ir not licensed far use in the cat and nspnsihility for i& use falls on f i e prescribing veterinary surgeon. This product is not licensed for this indication in f i e cs andresponsibility for i s use falls on the prescribing vetennary surgeon
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Figure 3 :17: C~rrularlesron of erythema and scalrng in a cat w ~ t k dernadicosrs (caused by Demodex gator)
'
Figure 3 :18 :Erythematous and erosrve blepkar rtrs in a cat wrth demodrcosrs (caused by Demodex catl)
Figure 3 : I9 : Seborrhoea and cellulitis on the neck of a cat with generalised demodicosis associated with FeLV infection (courtesy of D.N..CarlottiJ
of DN. Carlonil
Figure 3 :21 :Locahsed celluht~sin a wt w ~ t hdemodlcosrs
Figure 3 :22 :Greasy seborrhoeo on the neck of a Persran cat wrth demodcosis
Figure 3 :*J , ~ u , r r~d ~ as injgures 3 :W a n d 3 :20, eryfhematoceruminous otitis (coused by Demodex cati) (courtpsy of D.N.CarloftiJ
Figure 3 :24 ;Scoliiig oii tile Iatnvl yi,ma of u cut a'ith pediculuris: note thepresence afadult Felicola subrostratus
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Pediculosis Aetiopathogenesis Pediculosis is now rare in the cat and seen only in kittens or adults kept in poor conditions I.'. It is caused by Felicola subrostratus, a wingless insect of the suborder Mallophaga and family Trichodectidae (Table 3 :2). Its life cycle lasts, on average, 21-30 days and takes place entirely on the cat I. Felicola subrostratus is host-specific to the cat and therefore poses no risk to man. Clinical features The principal areas affected are the face, pinnae (Figs 3 : 24) and back. Non-specific skin lesions are characterised by a dull coat, scaling, papules and crusts. Sometimes, a true miliary dermatitis is seen. The degree of pruritus is variable 6. Diagnosis Diagnosis is based on finding lice and nits and identlfylng them microscopically (Table 3 : 1) (Figs 3 : ij).
Treatment Classic insecticide treatment (e.g. fipronil** given twice monthly for 4-6 weeks) generally gives good results. lvermectin * (200-400 pglkg), given once or twice (4 weeks apart), by subcutaneous injection, gives reasonable results '. It should not be given to cats less than 4 months old. When groups of cats are affected,ivermectin is the treatment of choice. The environment should also be cleaned thoroughly '.
Flea infestation Aetiopathogenesis Flea infestation is especially common in the cat. 95% of fleas isolated from cats are Ctenocephul~des felis felis. Depending on the cat's llfe style, other less specific species of flea may be found: Ctenocephal~descartis, Puler irritans,Archaeopsylla erinacei (hedgehog flea), Sp~lopsylluscuniculi (rabbit flea) and Echidnophaga galllnacea (bird flea) (Table 3 :2). Flea infestation may cause skin disease through the irritant, non-allergic action of flea saliva. Immediate and delayed hypersensitivity reactions to salivary antigens are often responsible for producing flea allergy dermatitis (FAD). ' Clinical features
Simplefka infestation may cause slight pruritus, a few papules and light scaling '. Flea allergy dermatitis (FAD)1s characterised by a pruritic dematosis affecting the rear half of the body. Clinical aspects are variable: symmetrical alopecia and miliary dermatitis. More rarely, FAD presents as eosinophilic plaques, linear granuloma or facial pruritus '. A seasonal pruritic dermatosis of the pinnae has been reported in Austraha and appears to be associated with Spilapsyllm cuniculi I.
Diagnosis Diagnosis of simple flea infestation is based on findig fleas and their faeces and identifymg them microscopically (Table 3 : 2) (Figs 3 : k). Treatment Hea control is now more straightforward, thanks on the one hand to the development of adulticides with enhanced residual activity that are virtually nou-toxic to mammals, and on the other hand to Insect Growth Regulators (IGR) which provide almost all we could wish for in an integrated conml programme. Strategy should involve selective use of several products, gven simultaneously or * 'hspodu~lanotlluns~dfor use 1" t h c c a t a n d ~ n s l b l h vfar w falkoa thepnscnbmg vehloary jwgaon ** Thls pmduet a ncd hcensrd far r h miteation m the oat and respaosibd~yfar as usc falls on be p-kng vctennar). mrgcon
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Table 3 : 2 : Identification of the principal insects involved in feline skin disease. 1c:hnlquta J~dgndslyucrzn d:rmaolog~c dcc :lmlvoro, BourJriu P rrd~turGuijuirc i: pp 43-Sh .PM(:A(: Edmnn\, Pv~s1991)
LICE Felicola subrostratus sh bands on the abdomen - 1 mm Large pentagonal head, truncated at the tip.
Figure 3 : i : Felicola subrostratus (adult) (x40) (courtesy of ENV Parasitology Laboratory, Lyon)
Figure 3 3 j : Felicola subrostrarus nit (~125)(courtesy of D.N. Carlotti)
FLEAS Ctenocephalides spn.
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Cat, dog, various mammals and sometimes man. Brownish. 1-3 mm rounded head with no fmntal tubercle - thorax well developed. Presence of 2 combs (ctenidia), one a horizontal comb on the head (genal comb) and the other on the prothorax (pronotal comb).
Cfenocepholidesfelis Head elongated in the female - 9 spines on the genal comb 5-6 notches on the tibia of leg Ill. Cfenocephalides canis Head rounded in both sexes - 8 spines on the genal comb, the first one much smaller - 8 notches on the tibia of leg Ill. Figure 3 :k :Ctenocep
felis (x40)
Pulex imlans Man, sometimes cat, dog and various mammals. Bmwnish - 1-4 mm - rounded head with no fmntal tubercle - thorax well-developed - no combs (ctenidia) I sub-ocular bristle and 1post-ocular bristle, both well-developed - 1 row of spines on the abdominal segments.
Archaeopsylla erinacei Hedgehog, rodents, mustelids (weasel family), cat. Brownish - 2-3 mm - shon head with no frontal hlbercle - thorax well-developed - 2 short spines.
Spilopsyllus cuniculi Rabbit, sometimes hair, fox, mustelids, cat. Brownish - 1-2 mm - angular head on the upper side - thorax well-developed - 2 combs - genal comb is oblique with 4-7 blunt spines, 2 ocular bristles.
Echidnophaga gallinacea Birds, dog, cat, various other mammals. Brownish - 1-1.5 mm - head at a slight angle with a well-developed occipital lobe - palps with one segment - laciniae strongly toothed -thorax short (less than the length of the first abdominal segment).
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successively, and the control of all stages, both parasitic and non-parasitic. Insecticide should be routinely associated with IGR, and mechanical control measures should not be forgotten. This new approach to flea control minimises the effects of inadequacies of any one insecticide, while maintaining efficacy and slowing down possible development of resistance. In practice, use of only one product, no matter how effective, will not provide long-term control of a flea population. Control strategy needs to he adapted according to the environment and clinical situation. It can only be successful if the benefits and limitations of each method are well-understood by both vet and owner.
Treatment of the animal Organophosphates and carbamates have now been rendered obsolete (whatever the presentation: systemic spot-on, drinkable solution with systemic action, collars, powders) by newer, more effective, more residual and less toxic products. Permethrin is a very effective, topical adulticide with excellent knock down and antifeeding properties. Use in the cat is the responsibility of the prescribing veterinary surgery, given the absence of a product licence for use in this species. The cat is particularly sensitive to permethrin toxicity and intoxication through overdosage is common. Its use is therefore not recommended. Fipronil is a very effective topical adulticide and comes either in a 0.25% spray or a 10% surfaceacting spot-on. Frequency of application depends on the formulation of the product (every 6 weeks for the spray and every 4 weeks for the spot-on) and the clinical situation (presence or absence of FAD). Advantages of fipronil include its great residual activity, low toxicity to carnivores and man, and possible use of the spray on cats aged 2 days or more. Its efficacy depends on good compliance by the owner (correct application given at the right frequency). Fipronil also has activity against certain non-parasitic stages (e.g. larval stages 1 and 2) 'j.
Imidacloprid is a very effective topical adulticide, used in a lo%, surface-acting, spot-on, and given every 3-4 weeks. Advantages include its residual activity, the fact that it is so safe for use in the cat and dog, and its possible use on kittens aged over 2 months. Moreover, imidacloprid is larvicidal against stage 1 larvae by virtue of squamous cells that become impregnated with it and get deposited in the general environment. Nitenpyram is a new adulticide which comes in 11.4 mg tablets. The particular advantage of this product is its extremely powerful knock down effect, within about 20 minutes. Frequency of application is variable (on average, once weekly), depending on whether fleas are present on the cat. Nitenpyram has no residual activity. There is no risk of toxicity in either cat or dog. Selamectin is a new avermectin, active against adult fleas. It is used monthly at 6 m&g in a spot-on formulation. The product becomes concentrated in the sebaceous glands and epidermal basal layer, and exerts its effects systemically. Advantages of selamectin are its residual activity, its low toxicity, its activity against certain helminths (e.g. toxocara cati and ankylostoma tubaeforme) and against Octodectes. Insect Growth Regulators (IGRs) interfere with insect growth and development and have the advantage of very low mammalian toxicity. IGRs include Juvenile Hormone Analogues (JHAs) and Chitin Synthesis Inhibitors (CSIs). All these substances play an important role, especially in prevention of flea infestation. Delay in onset of activity (at least a week) means that they cannot be curative. JHAs, such as pyriproxyfen, affect mechanisms associated with moulting. Pyriproxyfen persists for a considerable length of time (several months) and has ovicidal and adulticide activity (after a week). It comes in various formulations including collar, spray and surface-acting spot-on. CSIs (e.g. lufenuron and flufeuoxuron) affect chitin synthesis during moulting. Lufenuron prevents eggs from hatching, causing larvae to die and leading to an absence of adults emerging from the pupae. Lufenuron is given orally, every month, or by subcutaneous injection every 6 months. It is stored in the fat, then released into the blood ready for ingestion by the feeding flea. Treatment of the environment Control of non-parasitic stages and pre-emerged adults in the environment is vital as these stages make up 95% of the total flea population. Noting down all the potentially infested places (e.g. sleeping places, areas the animal walks through and car flooring) is the first step in a proper environmental control strategy.
www.vet4arab.co.cc 3 :Ectopmitic shin diseases Mechanical measures Mechanical measures like cleaning and vacuuming (remembermg, firstly, to remove cushions from armchairs and settees) are essential preliminary measures that have long been underestimated. Outside, damp, shady mas, frequented enough by cats and dogs to be contaminated by eggs and flea faeces (main food supply for the larvae), should be elmnaked. %
Chemical measures Insect Growth Regulators (e.g. methoprene, pyriproxyfen and flufenoxuron) act on non-parasitic stages. They come in vanous formulations. Foggers enable a large volume of product to be dispersed m the envuonment. h h a l cleaning is still necessary, in order to reach larval forms which are positively geotropic and negatively phototropic. In most cases, sprays must he used in association with foggers in order to treat the more inaccessible regions. Adulticldes, whether or not they are micro-encapsulated, stay on surfaces when sprayed in the environment. They do not penetrate carpets to reach the non-parasitic stages (especially cocoons). On the other hand, these adulhcides do kill adults that emerge regularly from their cocoons, before they are able to find a host. Most available environmental preparations, therefore, combine an adulticide with an IGR. Sodium polyborates (activated orthoboric acid) come in powder form and are used in Great Britain and the United States for environmental treatment. They work by abradimg the flea cuticle and then by desiccation. They have considerable larvicidal activity and a iery residual action (over a year) provided they are applied by specialist applicators 16. Control strategy
Prescribing the right flea control products requires good clinical knowledge and a thorough understanding of the parasite. The level of parasihc infestation determines the extent of the control programme which can range from s~mpleapplication of insecticide on the cat to intensive, combined therapy involving anlmals and envuonment, employing mechanical and chemical measures. Strategy must also be adapted to the animal's life style (e.g. where it goes, points of entry, presence of incontacts). If the surroundings are completely enclosed (e.g. a flat), the use of IGRs is justified and effechve. If the cat has FAD, flea control should he aimed at completely eliminating the parasite and preventing its re-appearance, by treabng the cat, in-contact annnals and the environment. Flea infestation In heavy infestations, it is best to eliminate most fleas rapidly with a topical insecticide, whatever its mode of action, or nitenpyram. To avoid permanent reinfestation, a residual insecticide should then be used in association with an IGR for at least 6 months. Other animals (dogs and cats) in the house should also be treated.
For the occasional or less severe infestation, any insecticide wlll be effective, provided it 1s used correctly. If the infestation persists, or if there are other animals in the house, IGRs should be prescribed. In some cases, treatment of non-parasihc stages in the environment is necessary. Flea allergy dermatitis (FAD] The first phase consists of beating the FAD. Even without symptomatic treatment, insecticidal treatment should provide rapid relief for cats being bitten by fleas, and remission from clical signs should be seen within 3 weeks. Here, the ideal insecticide should have arepellent and/or antifeeding effect, a knock down effect and a flushing effect. Using systemically-actingproducts (e.g. lufenuron) at this stage is pointless. Products with a good lmock down effect and rapid antifeeding action (e.g. pemethrin) are theoretically better than long-lasting residual products but m contraindicated in the cat due to their potential toxicity. Moreover, it has been demonstated in the dog that long-actingproducts with less marked knock down and antifeeding actions than permethrin are actually more effective. This efficacy is associated with a substantial, albeit more gradual, reduction in the level of infestation which falls below the allergenic threshold for signs to develop. This threshold varies from one animal @'another and does not usually consist of just one flea. Furthermore, the absence of sudden reinfestation contributes to clical remission. Whatever product is used, it is best to increase the frequency of applidation (e.g. fipronil should be given every 3 or 4 weeks). In addition to treating the affected cat, flea control must involve treating the environment and all in-contact animals. The use of products Tie fipronil or imidacloprid which have residual activity, also enables control of some non-parasitic stages in the environment.
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The second phase consists of long-term control of the infestation and preventing recurrence. Whatever treatment is proposed, flea control should be ongoing and applied all year round. Use of residual products (e.g. fipronil and imidacloprid), the frequency of which can he increased, will enable a number of fleas, below the allergenic threshold for signs to develop, to persist. IGRs on the animal (or in the environment) are also very useful after the start of the first phase of treatment.
REFERENCES 1. Guagukre, E. Pmt. MM. Chir. Anim. Comp. 28,211-223 (1993). 2. Scott, D. W. & Horn, R. T Vet. Ciin.N.Amer. 17, 117-144 (1987). 3. Foley, R. H. Comp. Cont.Educ. Pracl. Vet. 13,783-800(1991). 4. Scott, D. W. J A m e r Anim.Hosp.Assn. 16, 331-459 (1980). 5. Paradis, M. Comp. Conr. Educ. Pract. Vet. 20,459-484 (1998). 6. Scott, D. W., Walton, D. K.& Slater, M. R. Point Vit. 19,285-294 (1987). 7. Guagukre, E. Prat. Mdd. Chir Anim Comp. 27,705-708 (1992). 8. Scott, D. W. J.Amer'Anim. Hosp.Assn. 26,515-537 (1990). 9. Vincenzi, P. & Genchi, C. Proc. ESVD-ECVD, Pisa 177 (1997). 10. Bourdeau, P. Rec. Med. Vit. 164, 979-989 (1988). 11. Nullall, T, J., French, A. T., Cheetham, H. C. &Proctor, E J. I. J. small Anim. Pracr. 39,237-239 (1998) 12. Desch, C. E. & S1ewart.T. B. J M e d . Entomol. 36.167-170 (1999). 13. Guaguk~e,E. Plat. Mdd. Chir Anim. Comp 28, 31-36 (1993). 14. Medleau, L., Brow, C. A,, Brown, S. A. &Jones, C. S. J. Amer: Anim. Hosp. Assn. 24, 85-91 (1988). 15. Hunter, J. S. Proc. 4th Internarional Symposium on ectoparasiles ofpeh 83-84 (1997). 16. Dryden, M. W. Comp. Cont. Educ. Pract. Vet. 15,821-831 (1993).
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Dermatophytosis is a superficial fungal infection of the skin. It is caused by keratinophilic fungi of the genera Microsporum, Trichophyton and Epidermophyton. These fungi invade, inhabit and multiply in the stratum corneum and the keratin of hair and nails. Dermatophytosis (ringworm) is the most common infectious skin disease of cats '. It is clinically very variable, difficult to eradicate, and canies a substantialzoonotic risk. It is very important for veterinary surgeons to be familiar with this condition.
Aetiopathogenesis Causal organisms .Microsporn canis is the most common cause of feline dermatophytosis I". It is not part of the n m a l fungal flora of cats and its isolation indicates either an active infection or mechanical caniage of the organism on the hair coatz3.h rare instances, other organisms such as Trichophytonspp, or Microsporn gypseum may be isolated. Tricbophyton infedom are m e and occur following contact with rodents (usually asymptomatic carriers), horses, cattle or a contaminated environment. Trichophytan rubrum is a common cause of human dermatophytosis (e.g. tineapedis) and exposure of cats to infected people (e.g. while playing with the owner's feet) or contaminated surfaces may lead to dermatophytosis in the cat. Mimsporum gypseum is a geophilic organism and infection is most likely to result from exposure to fungal spores in the s o l
Mode of infeetion The naturally infective stage is the arthrospore, formed by segmentation and fragmentation of fungal hyphae. Cats become infected either by direct contact with an infected animal or by contact with a contaminated environment. The latter is an under-recognised reservoir of infection for both people and other animals. The number of spores needed to trigger dermatophytosis in a susceptible cat is unknown. Large amounts of infective material are present in homes and the environment of infected cats. Airborne spread of spores occurs readily and beating and ventilation material can easily be contaminated. Fomite transmission by contaminated collars, brushes, toys, hide boxes, transport cages, etc. may be considerable. Depending on ambient conditions, spores can remain viable for many months.
Predisposing factors When infective arthrospores contact a cat's coat, many factors influence whether or not successful infection occurs ?
Grooming behaviaur of cats is an important natural defence against infection; it can be difficult to establish experimental infection in cats which lick the inoculation sites. hterestingly, the first signs of dermatophytosis in kiaens often occur at, or around, the time they are separated from the queen. Additionally, lesions commonly occur on the face, an area that is difficult for young kittens to groom. The importance of grooming in mechanically removing spores may explain the common clinical observation that long-haired cats aremore susceptible to dermatophytosis. It is obvi&ly more difiicult for a longhaired cat to groom its coat as thoroughly as a shnrt-haired cat. Under optimal conditions, infective spores may germinate within 6 hours of adherence to keratinocytes '. Trauma to the skin may promote germination. Arthmspores cannot penetrate healthy intact skin and some type of trauma, even if only very slight, is necessw to facilitate infection. Other factors to consider that may predispose cats and kittens living in colonies to infection includemicrotrauma from other skin diseases, including those provokexj by fleas, lice, and mite infestations.
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Increased hydration and subsequent meration of the skin are very common factors in the pathogenesis of human infections, enhancing the ability of dermatophytes to penetrate the skin and favouring germination of spores. Natural barriers to dermatophyte infection include the 'desert-like' conditions of the epidermis and the fungistatic activity of sebum and certain factors in serum. Temperafure. Germination of spores is temperature-dependent. Sun-bathing may be protective and inhibit germination, Excessive bothing andgrooming may predispose cats to dermatophytosis by removing natural barriers to dermatophyte infection (fungistatic sebum and serum factors make up a chemical banier and superficial epidermal layers constitute a mechanical banier), and by increasing the humidity of the coat.
Risk factors These include bemg very young or very old, poor nutrition, the presence of ectoparasites, immunosuppression (e.g. retrovirus infection, neoplasia, corticosteroid therapy and chemotherapy). Living in a colony is another risk factor because of breeding activities and exposure to other cats at shows.
Immune response The immune competence of the host is very important in protection from dermatophyte infection. Recovery from dermatophytosis requires the development of an effective cellular immune response &'. Induction of anti-dermatophyte antibodies does not generally protect against infection. The lack of development of a cellular immune response may be a cause of chronic infection in some cats. These cats may develop tolerance to the dermatophyte. In addition, the fungal infection may produce enzymes that facilitate its survival. Once the fungal spores have evaded the host's natural defences, the infection establishes itself in the stratum corneum and hair follicles. Fungal hyphae proliferate down towards the hair bulb and produce keratinolyhc enzymes that aid penetration of the hair cuticle. Infection is supported only by anagen hairs; it will spontaneously'resolveif the hair goes into telogen or if the fungal infection c m o t keep an equilibrium between its downward growth and production of keratin.
Clinical features Feline dermatophytosis is very pleomorphic in its clinical presentation and should be considered in the diierential diagnosis of all feline skin conditions '.The highly contagious nature of this disease, as well as the public health consideration, furtber underscore the urgency to rule this disease out as quickly as possible. Pruritus is variable ranging from absent to intense. The most common lesioh is an irregular or circular patch of peripherally expanding hair loss with scale, crust and sometimes erythema. Hair loss can be very subtle, symmetrical or non-symmetrical, inflammatory or noninflammatory. Hairs are usually broken or frayed. The face (Figs 4 : 1-3) and distal limbs (Figs 4 : 4 3 ) are most commonly affected, especially in kittens, and lesions are often inflammatory and exfoliative. Other, sometimes very striking, clinical forms may be seen: exfoliative erythroderma, sometimes with lots of crusting around the mucocutaneons junctions on the face (eyelids, lips, nose) mimicking pernphigus foliaceus; keratinisation defects which may be generalised (Fig. 4 : 6) or localised (e.g. acquired tail seborrhoea which, in the Persian, should be distinguished from stud tail) (Fig. 4 : 7,8); generalised exfoliative dermatitis (Figs 4 : 9-11); chin acne; symmetrical alopecia (Fig. 4 : 12); miliary dermatitis (Fig. 4 : 13); paronychia (Fig. 4 : 14); kerion (very rare in the cat) (Fig. 4 : 15); and nodules (e.g. eumycetoma caused by Microsporum canis) seen in Persian cats and also in cats with FIV infection (Fig. 4 : 16) (E. Guagukre, personal communication, 1999). Dermatophytosis should never be considered a localised disease because spores spread rapidly, via the cat's grooming, over the whole body. In some cats with recurrent dermatophytosis, there may be an unrecognised, anatomical reservoir of spores, e.g. in the periocular area or in the facial folds in Persian cats.
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I :Erythmatow blepharitis with comedones in a Persian cat Fig, with demtophytosis caused by Microsporum canis
Figure 4 : 2 :Peripherally expanding patchof eqthema, scaling and hair loss inn kitten wiik demtophyiosis cawed by Microsporn canis
Figure 4 :3 :Erythema and alopecia o n the nose of a cat with dermatophytosis causedby Microsporumcanis. Note that the nasalplanum (which hasno hnirfollicl~s)is u&ected (courtesy ofDiV. CarlottiJ
Figure 4 :4 :Peripherally expanding area of scaling and alopecia on the distal limb of a cat with dermaiopkytosis caused by Minosporn canis
Figure 4 :5 :Multiple areus of peripherally erpanding hair loss on the distal limb of a cat with dermatophytosis caused by Micmsporn canis
Figure 4 : 6 :Localised keratinisation defect in a Persian cat with dermatopkytosis caused by Microsporn canis
Figure4: 7 :Keratinisationdefecton the tail ofa cat with demtophytosis caused by Microsporn canis
Figurn 4 :8 : Keratinisation defect on the tail of a Persian cat with dermatophytosis caured by Micmspomm canis
4 Practical Gude to Feline Drrmatalogy
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The term "asymptomatically infected cat" refers to a cat thatis truly infected with subclinical or very subtle lesions. The term "asymptomatic carrier" refers to a cat that is clinically normal and not infected, but positive on fungal culture. These cats, which mechanically carry the infective spores on their coat, can be either long-haired or short-haired but long hair predisposes cats to this fomite carriage. It must always be remembered that clinical cure may occur several months before mycological cure.
Diagnosis Diagnosis is based on Wood's lamp examination,microscopical evidence of fungal invasion of hair shafts, identification of the dermatophyte (genus and species) on fungal culture, andlor evidence of invasion of hair or keratin on skin biopsy '.
Wood's lamp examination Wood's lamp is an ultraviolet light with a wavelength of 3650 A, commonly used as a screening tool for dermatophytosis. Microsporum canis fluoresces apple-green in colour. Dust, scale and other non-fungal elements usually fluoresce bluish-white. A positive test is only suggestive, not diagnostic, of a dematophyte infection. Fluorescence only indicates the presence of fungal metabolites (pteridin) or altered substances in the hair, it does not prove that fungal arthrospores are present. Topical antifungal therapies and shampoos can affect fluorescence. Examination should be thorough and carried out in complete darhess. It may take several minutes for fluorescence to become visible to the clinician, probably because of the delay in human eyes adapting to the dark. This inexpensive test is very helpful in screening cats or kittens with clinical lesions, for selection of hairs to culture andlor examine microscopically. Screening of asymptomatic carriers or cats on therapy is time consuming. Only 50% of strains of Microsporum canis fluoresce and there may be more than one strain of Microsporum canis in any one colony. In a situation where infection has been confirmed and the strain fluoresces, Wood's lamp can be a useful tool to help monitor therapy but simultaneous fungal cultures are still needed.
Direct examination of hair and,scale This is a time consuming technique. Its use requires some training because numerous microscopic items can easily be confused with arthrospores. This test is easier if fluorescing hairs are used. Microsporum canis infections are ectothrix infections (spores formed on the surface of hairs) (Fig. 4 : 17) and, in most cases, hairs can be examined using liquid par&. Clearing agents such as potassium hydroxide (KOH), chloral lactophenol and Indian ink may also be used but care must be taken to avoid ~ a c t s . A technique using calcoflnor white and 10 percent KOH for the rapid identification of fungal elements in cats has been described. In both human and animal specimens, calcofluor white and KOH was found to be superior to KOH alone '. Calcofluor white is a textile brightener that binds to chitin and cellulose'and, under ultraviolet light, gives off an apple-green fluorescence. Broken or frayed hairs and scales taken from the margii of lesions are immersed in a few drops of a solution containing calcofluor white and Evans blue (1 : 9) and mixed with an equal volume of KOH. They are then examined under the microscope after 10-15 minutes. Although examination is enhanced if a fluorescent microscope is used, a standard light microscope and Wood's lamp are often sufficient.
Fungal culture Fungal culture is still considered the gold standard for diagnosing felme dermatophytosis as it allows genus and species idenfification of the causal organism. Toothbrush fungal culture is the most time and cost-effective technique for culturing cats. A sterile toothbrush (toothbrushes in their origmal packaging are mvcoloeicallv over the cat's bodv, andlor , u * sterile) , is nassed , . clinicallv susnicious lesions. The bristles we then stabbed in~oiungal cultuw nwdi3. There are now many comm&ialiy available brmds of fungal culrurc media (e.g. Sabouraud's Medium 2nd DermatophyteTest Medium) and $election should be based s h cultures are almost impossible on cost, shelf lieand ease of inoculation of the p l a t e s ~ ~ o o t h b ~fungal to inoculate onto media slants in glass jars due to the narrow mouth. 1
Fungal culture cannot distinguish between subclinically infected cats and healthy uninfected cats that are mechanically canying spores on their coat. AU cultures should be observed for at least 21 days. Cultures
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Figur~4:9:Generalrs~d ?x~,lrurrbp&,murrn, d~rnrotophylo!~~ crrur?d by Naosponm c3na
111
a P r ~ ~ l car un t~irh
Figure 4 :10 :Same cat as m fgure 4 9 after cl~ppinping- note the pny,he& erpanding q f ~ l ~ a hlarons ve
Figun 4 :I I :Dorsalunbar exfolzative dermantis in a cat with dmtophytosrs cawed by Mkmsporum cam
Figure 4 :13 :Gensralised mlllary dermatitrs i n a cat wrth dermfophytos~seausdby Micrasponwnc&
Figure I : 14 :PerpheralIy qnnding arm o f q t h e m nnd alopecia on the t p nnd m u l t i p l e ~ y c h i oid a snrwith demmphyrotts caused by
Figure4 :15 ;Kerron m ocaf wlthdennato~~sucmrsed~ Minaspamm canui lcounesy ofDN C@loniI
@re OZOIS
4 :16 :Nodule in a cat with a mycetomu mused by McmspoNm
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from cats with untreated infections are often positive within 5-10 days, although cultures from cats under treatment may take 21 days before fungal growth is seen. Grossly, colonies of Microsporum canis are pale yellow (buff) on Sabouraud's agar, with a yellow-orange pigment on the undersurface (Figs 4 : 18,19). However, all colonies should be examined microscopically, using Roth's flag technique, to demonstrate fruiting bodies (microconidia and microconidia (Fig. 4 : 20)). Although rare, dysgonic strains of Microsporum canis have been isolated, especially in colonies. These isolates of Microsporum canis do not show classic macroscopic or microscopic growth characteristics. Specifically, they do not change colour on DTM, they do not produce yellow-orange colouration on the undersurface of Sabouraud's agar and they do not produce fruiting bodies (spores). It is strongly recommended that any suspect colonies (i.e. pale yellow on top) showing atypical gross or microscopic growth be sent to a reference laboratory for subculturing and identification.
Skin biopsies Histopathological examination of skin biopsies can be carried out and will c o b a diagnosis of dermatophytosis in about 80% of cases. This procedure would appear to be particularly indicated in kerions and eumycetomas. Biopsies can be taken with a biopsy punch (6 mm diameter), from the centre of the lesion, or with a scalpel blade in deep lesions such as eumycetomas. Although classic stains (e.g. haematoxylin and eosin, safran) will often demonstrate fungal spores and hyphae (assuming a purplish colouration) in the hair follicles and epidermal keratin, more specific stains ( e . ~Periodic . acid-Schifn can help identification by staining fungi elements pink (Figs 4 1 2122). ~istop&olo~icalexamination of skin biopsies taken from typical clinical forms, will usually reveal a hyperplastic or spongiotic perivascular dermatitis. In kerions (Fig. 4 : 23), mycotic perifolliculitis, folliculitis and futunculosis can be found, and in mycetomas, a granulomatous panniculitis may be seen around the hyphae (Fig. 4 : 24).
Treatment Dermatophytosis will resolve spontaneously within a few months, in healthy, immune-competent cats, However, leaving the disease to resolve itself is rarely advised because dermatophytosis is both contagious and zoonotic. Therefore, the goals of therapy are to hasten recovev, minimise or prevent the spread of infection to susceptible hosts, and eliminate contaminahon of the environment.
'keatment of infected cats Cl~ppmgthe coat will remove infected hairs and minimise the risk of contagion. Clinical signs may worsen 7 to 10 days after clipping. Clipping is optional in short-haired cats with limited lesions. In these cats, infe,cfed hairs from the margin of lesions can be clipped with blunt-tipped scissors. A total body clip is strongly recommended in any cat with extensive lesions, or any long-haired catregardless of extent of lesions. In cats which are recovering, the coat constitutes a reservoir of fungal spores and can serve as a source of future infechon. Clipped hain should be collected in plashc bags and destroyed. Ideally, clipping should not be carried out m a veterinary c l i c , given the substantial risk of contaminating the environment. People doing the clipping must wear protective clothmg to be destroyed immediately after use.
In summary, clipping depends upon the severity of the infection. It is necessary in severely affected, animals but in cats with few lesions, it may do more ham than good. If the entire coat is clipped, the cat should definitely be treated with systemc antifungal therapy. Systemic treamzenrls tbe treatment of choice ",".
I
Griseofuvin is the initid drug of choice (V-50mgkg BID for themicrosized formulation, or 5-10 m a g SID if ultramicrosized), given orally for 6-8 weeks on average. It is absorbed better when admimtered in divided d d y doses and with fatty meals. Tne most common sideeffects (vomiting, dianboea and anorexia) can be avoided by dimding the dose into a greater number of applications or by slightly lowering the dose. Bone marrow suppression (neutropenia, anaemia, or pancytopenia) may occur in some patients. Severe neumpenic reactions have been reported in cats with dermatophytosis associated with FIV infection 'I. Griseofulvin should not he used in cats with mV. Ideally, all cats should be tested for mV before peofulvin is administered. If griseofnlvin is used inFIV-infected cats, once or twice-weekly blood counts are recommended. The use of griseofulvin is contraindicated in pregnant females.
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Figure 4 :17 :Infected hairs in chloral laciophenol Cc ecfofhrix imrion in one hair with another healthy hair (~250)(courtesy of ENV Parasitology Loborntop, Lyon)
F&R 4 :19 :Fungal culture of Micmspo~mcanis on Sabouraud's medium. The undersurface has a yellow-orange appearance
,.,.
Figrue 4 :21 :His logy ,:,n,;,,,: L..mlint fhe hair ,, presence of spores around the outside (stained wirh PAS, r250)
F&E 4 :18 :Fungal culture of Mi is on S medium. The top surface has a downy buflcoloured appearance
thick echinulate wolh undmade u p ~ f m o n cells y
,,,i
Fipre 4: 23 :Histdpafhologyofa kerion :notefunvlculosis with rupture of the basement membrane of the hair follicle, around an infected hair
kemtrn of o cat w~rhd ~ o p h ~ t o s caused l s by M~cmspomcanis, ossonared with FlV~$echon (statndd wrfhPAS, ~2501
canis : nofe fungal granuloma amund colonies of Microspo~umcanis (stained wifh PRS, ~ 2 5 0 )
d Guide to Fehe DematoIogy
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Table 4 : 1 : Type of hair invasion, fruiting bodies (spores), and arrangement of microconidia in the four main dematophytes 'O Ma : macroconidia, Mi : micmconidia
Dermatophyte
Microscopic culture morphology
Hair invasion I
MICROSPORUM GYPSEUM Ma
Mi
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4 :Dermatophytosis
Ketoconazole is a fungicidal azole drug, used in the treatment of dermatophytosis in the dog. It is not licensed for use in the cat. However, it has been used successfully to treat felme dermatophytosis in many European countries, at a dose of 10 m a g SID PO. Its absorption is improved when given in an acid pH, e.g. with food. Side-effects have been reported in the cat: liver problems (e.g. jaundice and elevation of liver enzymes), vomiting, diarrhoea, anorexia and neurological disorders. It may also be teratogenic and should not be given to pregnant females. Itraconazole is a v e y useful fungicidal drug. The recommended dose is 10 mgkg SID PO "J2, although a lower dosage (3-5 m a g SID PO) also seems effective ". Itraconazoleappears to be better tolerated by cats than ketoconazole. However, it has been associated with hepatotoxicity in dogs, and liver enzymes should be monitored regularly during therapy. Few side-effects have been seen in the cat, although one report of death due to hepatic necrosis has been reported. Hepatic necrosis appears to be dose-related and can occur in cats receiving more than 20 m a g SID over extended periods of t i e 'I. The use of itraconazole is also contraindicated in pregnant animals. Vaccination should only be considered an adjuvant therapy or an alternative to topical therapy ". One vaccine is commercially available in the USA for treatment of dermatophytosis in cats and kittens pel0-Vax MC-K, Fort Dodge Laboratories). Used alone, vaccination will not cure dermatophytosis, although experimental data suggest that it might reduce the spread of lesions. To date, no controlled studies have demonstrated that vaccination will protect against natural or challenge exposure 16. Local reactions may occur at the site of vaccination. Topical therapy is useful because it limits spread to other animals and reduces seedmg of the environment with infective material. In addition to clippiig, it is the most efficient way to loosen and remove infective hairs and cmsts from the skin. However, it takes a long time to cany out, especially where large numbers of cats are involved, and some cats will not tolerate topical therapy. Fythermore, clippiig combined with topical therapy can actually exacerbate lesions ".In vitro studies on cat hairs infected with Microsporwn canis have shown that the efficacy of many commonly used, topical antifungal preparations is questionable ". The antifungal lotion or shampoo should he applied as gently as possible in order ta prevent microtrauma to the skin and iatrogenic rupture of fragile hairs. The coat and skin should be dried as quickly as possible as moisture will cause maceration of the epidermis, compromising the natural protective barrier. Care should also be taken to keep young animals warm and prevent them from licking the a n t ' i a l solution. Solutions of lime sulphur (1 : 16 dilution) (available in the USA), 0.2% enilconazole and miconazole are very effective '','a. In a small clinical trial designed to evaluate safety, a group of Persian cats with dermatophytosis were treated twice-weekly with a 0.2% enilconazole solution I q . The coat was not clipped. Although there were anecdotal reports of toxicity, all cats tolerated the treatment well. Tne only side-effects seen were mild reduction in appetite and slight depression. In this study, cats required 8 to 10 weeks of twice-weekly dips before mycological cure was achieved. The manufacturers suggest that 2-3 weeks treahnent is enough. Enilconazole is not licensed for use in cats although it is widely used in Europe and Canada.
In rare situations, it may be necessary to treat only the kittens. These kittens should be removed from the queen, as soon as possible, and hand-reared. Alternatively, they could be separated from the queen at 4 weeks of age. Fungal cultures can be carried out at this age. If positive, topical therapy alone can be used until the kittens are 8 weeks old. Itraconazole can then be prescribed. Kittens should not be sold until fungal cultures have been negative on at least 2 or 3 successive occasions. Therapy must be monitored methodically. Dermatophytosis will usually resolve spontaneously within 60 to 100 days in a cat with a competent immune system. Treated cats often show clinical resolution within 4 to 8 weeks, but cats appear clinically normal long before they are cured mycologically. Cats should be treated until fungal culture, carried out weekly, is negative on two or three successive occasions. Fungal cultures should be started after 3 to 4 weeks of therapy. Wood's lamp examination can be used to screen for the presence oi absence of infection. However, the limitations of this procedure should be appreciated. Actively infected hairs tend to glow along the entire shaft or in the proximal region (towards the bulb). Hairs that are no longer infected may still fluoresce along the distal portion or just at the tips of the hairs. These hairs may or may not be positive on culture. False positive cultures can occur in cats that are clinically and mycologically cured, if they are living in a contaminated &vironment This is most likely in a breeding colony or cattery. Establishing the true status of these cats, asymptomatically infected or asymptomatic carrier, is difficult. In our experience, these cats frequently have fluctuating culture results, i.e. positive then negative. Additionally, the number of fungal colonies isolated from fomite canier cats is usually low (1 to 5 small colonies). If there is any doubt, the suspect cat should be isolated in a mycologically sterile cage for 3-5 days before being recultured to determine its true status. In many
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instances, a site visit and cultures of the environment can also he informative.
Environmental treatment A contaminated environment is an under-recognised reservoir of infection, particularly in multiple cat households, colonies and catteries. Decontamination should start with aggressive cleaning. AU possible fomites should be removed and destroyed, if possible. These include toys, bedding, cat scratching posts, brushes, etc. All organic material should also be removed, preferably by vacuuming. All surfaces will need to be vacuumed: ceilings, floors, walls, ledges, air vents, etc. Any place where cat hair or scale can accumulate is a potential source of infection. Next, these surfaces should receive a triple cleaning with an all-purpose, detergent solution that is safe to use around cats. Heating and air-conditioning appliances will also need to be cleaned and specialist cleaners may need to be called in. Care should be taken to ensure that there is adequate ventilation in the colony or cattery. Once cleaning has been completed, air filters can be fitted, which can be changed weekly to reduce future contamination. After the environment has been cleaned, an antifungal solution should be applied. These products will not work in the presence of infected organic material. Any surface that cannot be thoroughly cleaned should not be treated. There is no antifungal product effective against Microsporum canis following one application which also maintains a residual effect lo. Several applications lasting between 10 and 20 minutes are necessary to achieve optimal efficacy. According to one in vitro study using infected cat hair, household bleach in 1:10 or 1:100 solutions, chlorine dioxide, glutddehyde and potassium monoperoxysulphate are the most effective agentsz0.Enilconazole is also a very effective disinfectant and available as a spray or fogger*. Contaminated catteries or colonies should be cleaned every day and disinfected every other day. Most a n t i g a l disinfectants are irritating to the mucous membranes of cats and people. Therefore, cats should not be allowed contact with surfaces that are still damp. As spores are readily canied in the air and can stay infective for a long time, environmental decontamination should be continued for several months after the animals have been cured. If a colqny is open to visitors, accepts cats on breeding loan, or is involved in shows, these decontamination procedures should be performed routinely.
Preventing transmission to other animals and people Preventing transmission to people and other cats in colonies is also important. Fungal cultures should be performed on all cats to c o h infection. Clinically affected cats should be isolated. In a colony, it is better to assume that all cats are infected. It is actually rare for infection to be limited to just a few cats. Treating only selected animals usually results in the colony becoming seeded with asymptomatic carriers. Cats should not he shown, sold, or sent on breeding loans. No new animals should be accepted into the colony, which should he closed to outside visitors. Long-haired cats should be clipped and treated topically once a week and vaccination may or may not be indicated for all cats. These measures may not be feasible in large establishments. Systemic antifungal treatment is recommended for all cats (except pregnant queens which should not be heated before the kittens are horn) and should be continued until fungal culture, carried out weekly, is negative on two or three successive occasions. Although Wood's lamp examination may be helpful in monitoring therapy, fungal culture is more reliable for giving the colony the all-clear. Contact between cats should be limited. Animals should not be allowed to wander freely and should be restricted to their cages. Providing thorough flea control and addressing all other causes of pruritus is also important as pnuitus will cause damage to the skin, facilitating penetration of spores. In addition, scratch'mg cats shed more hairs into the environment. Finally, fleas, themselves, are capable of harbouring and transpotting fungal spores.
dreventing recurrence Once dermatophytosis has been eliminated from a colony, the infection may be re-introduced by contact with infected cats, contaminated fomites, or part of the environment that was incorrectly treated. A negative fungal culture should be obtained from all new cats before introducing them to the colony. While awaiting results, these cats should be isolated. At shows, cats should, when possible, remain in their cages and these should be covered to prevent airborne spread of spores.
* fogger not available in UK, mslator's note.
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REFERENCES !
1. Foil, C. S. in I?tfectious Diseases of the Dog and Cat (ed Greene, C. E.) vol. 2,362-370 (Saunders,W. B., Philadelphia, 1998). 2. Moriello, K. A. & DeBoer, D. I. Amer. J. Vet.Res. 52,602-606 (1991). 3. Sparkes, A. H., Werrett, G. & Stokes, C. R. J small Anim. Pract. 35,397-401 (1994). 4. DeBaer, D. I. & Moriello, K. A. J. Vet. Microbial. 42,289-295 (1994). 5. Ajabre, S., Richardson, M.D. &Scott, E. M. Clin. Exp. Dermarol. 18,231-237 (1993). 6. Sparkes, A. H. Aspects offeline dermatophytosis and the immune response to Microsporum canis (PhD thesis, Department of Clinical Science, University of Bristol, Bristol, 1993). 7. DeBoer, D. J. & Moriello, K. A. J. Vet. Med. Mycol. 31, 121-132 (1993). 8. DeBoer, D. 1.&Mo%llo, K. A. Comp. Cant. Educ. Pract. Vet. 17, 1197-1203 (1995). 9. Carlotti, D. N.& Couprie, B. Prat. Me'd. Chir. Anim. Comp. 23,450457 (1988). 10. Haldene, D. I. M. &Robe$ E. Diagnostic Microbiology and Infecriolrr Diseases 13,337-341 (1990). 11. DeBoer, D. I. & Moriello, K.A. Comp. Cont.Educ.Pract. Vet. 17, 1471-1481 (1995). 12. Moriello, K. A. & DeBoer, D. I. J. Amer Vet. Med. Assn. 207,439-444 (1995). 13, Shelton, G. H., Grant, C. K, Lineberger, M. L. &Abkowitz, I. L. J. Vet. Int. Mcd. 4,317-319 (1990). 14. Carlotti, D. N. Point VLt., 29,681-689 (1998). 15. Medleau, L., Jacobs, G. 1.&Mark$ M. A. J. Vet. Int Med. 9, 39-42 (1995). 16. DeBoer, D. I. & Moriello, K. A. Vet. Dermaiol. 5,47-55 (1994). 17. DeBoer, D. I. & Moriello, K. A. J.Amer. Vet. Med Assn, 207,52-57 (1995). 18. Paradis, M., Dejaham, C. & Page, N. Can. Vet.J 38,379-382 (1997). 19. White-Weithers, N. & Medleau, L. J Amer. Anim. Hasp. Assn. 31,250-253 (1995). 20. Moriello, K. A. & DeBoer, D. J. in Advances in Veterinav Dermatology, vol. 3 (eds Kwochka, K. W., Wdlemse, T. & von Tschamer, C.) 309-318 (Butterworth-Heinemam Oxford, 1998).
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L. Ferrer - A. Fondati
Deep mycoses Deep mycoses are caused by the growth and proliferation of saprophytic fungi that normally live in the soil, vegetation or decomposing organic matter, within subcutaneous connective tissue and internal organs. Most of them are considered oppormnistic pathogens. In man, they cause diseases in neutropenic or immunodeficient individuals '. The link between deep fungal infections and the immune system still requires clarification in veterinary medicine, although the majority of cases probably arise following a reduction in the cell-mediated immune response. Fungi entering the individual subcutaneously,following a break in the epidermis, are responsible for subcutaneous mycoses, whereas those that are inhaled cause systemic mycoses. Systemic mycoses occur initially in the lungs before disseminating via the lymphatics and blood, to other internal organs and the s h . Clinically, subcutaneous mycoses are characterised by the presence of one or multiple nodules, located mainly on the abdomen, and an absence of systemic signs. Systemic mycoses present similarly on the face and also on the distal limbs and nasal mucosae. The cat is affected systemically and lymphadenopathy, respiratory, nervous, ocular and bony signs may be present. It is important to be aware of deep mycoses as they enter into the differential diagnosis of many feline dermatological conditions. Prognosis is always guarded. Although deep mycoses are rarely contagious to man, some of them, such as sporotrichosis, histoplasmosis, blastomycosis and coccidioidomycosis are highly zoonotic.
Subcutaneous mycoses Aetiopathogenesis
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Subcutaneous mycoses are rare opportunistic infections caused by the multiplication of ubiquitous saprophytic soil fungi. They are charactensed by dermal or subcutaneous pyogranulomatous kions following traumahc inoculation of Tun@ into the skin. Fungi responsible for subcutaneous mycoses belong to various taxonomic groups. Theclasslficatiou of these mycoses is not clear, but one system has teen put forward by Foil %.
- Mucormycosis (zygomycosis) caused by fungi of the generaRhizomucor andMortierella among others, - Hyalohyphomycosu caused by fungi of the genera Fusarium and Paecilomyces among others, - Phaeahyphomycosis caused by fungi af the genera Alternana, Blpolons, Cladosportwn, Exophtala, Moniliella, Phialophora, ScoIecobasrdium and Stempbllium amoug others,
- Dark-grain, ewnycoric mycetoma caused by fungi of the genera Curvularta and Madmella among others, - Pythiosis caused by Pythrm
inridiosum.
Clinical features MucannycosismdhyaEohyphomycosisarerarely descnied in the cat TrEy involve sy~temicsignsmore than subcutaneous lesions. Phaeohyphomycosis i s more c o d y seen in the cat than the dog. It manifests clinically as nodules (Figs 5 :I$), usually s o m , on the face and distal limbs, withvariable ulcerahon and draining tracts. The brain, nose and cornea may also be affected.
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Dark-grainfungal mycetoma resembles phaeohyphomycosis.It can be distinguished by the presence of blackish granules in the exudate, which make up the fungal colonies. Pythiosis is a subcutaneous mycosis caused by a pathogenic (and non-saprophytic) member of the class Oomycetes, Pythium insidiosum. The infective agent is an aquatic zoospore which is motile in warm water and at-cted to plant and animal tissues. Zoospores are only viable in this environment and the geographical distribution of this illness is therefore limited to the tropics. Infection is rare in the cat and probably follows contact with infected water. Subcutaneous, ulcerated nodules on the abdomen and distal limbs have recently been described in this species '.
Diagnosis The diagnosis of subcutaneous mycosis is based on the history and, mainly dermatological, clinical signs (nodules, variably ulcerated, on the face and/or abdomen, non-responsive to antibiotic treatment). The presence of grains in the exudate strengthens the clinical suspicion, although some deep bacterial and dermatophyte infections can also produce grains '. Cytological and histopathological examination of deep samples and fungal culture are the most useful diagnostic tests.
Cytological examination of exudate or jine-needle aspirate from lesions may demonstrate fungal elements. Histopathological examination of skin biopsies can reveal hyphae in the dermis. Phaeohyphomycosis and dark-grain fungal mycetoma are characterised by the presence of large (2-6 pm in diameter), septate and pigmented hyphae in dermal and subcutaneous pyogranulomas * (Figs 5 : 3,4). In phaeohyphomycosis, fungal colonies take the form of small pigmented yeast inclusions called Medlar bodies 4 m o s i s is characterised by the presence of an eosinophilic infimatory infiltrate which may be nodular or diffuse, granulomatous or pyogranulomatous, dermal or subcutaneous with foci of necrosis. Pythium insidiosum hyphae are broad (4.5-5.5 p in diameter), sometimes septate, with irregular branches, but are not pigmented. Hyphae do not stain with haematoxylin and eosin (H and E). They stain poorly with Periodic Acid-Schiff PAS), but well with silver stains (Gomori). Immunohistocbemical techniques can be useful for identifying fungal structures. Fungal culture of deep biopsies, placed in suitable transport medium, can be used to identlfy the genus and species of the fungus involved. It should be performed by a specialist mycology laboratory. The fungi that cause phaeohyphomycosis and dark-grain fungal mycetoma grow easily on Sabouraud's agar at 25°C. Growth may take three weeks, and enrichment media are sometimes necessary to aid identification. Pythium insidiosum grows on blood agar at 35-37'C. Diagnosis depends on seeing motile zoospores, which can require sophisticated culture techniques. Serology (ELISA) can also be used successfully in the diagnosis of pythiosis in the cat. Other diagnostic tests, including FeLV and FIV screening, should be performed routinely.
Wide surgical excision of nodular lesions is, where possible, the treatment of choice. Amputation is sometimes necessary when a distal limb is affected by pythiosis. When surgery cannot be carried out effectively in phaeohyphomycosis or dark-grain fungal mycetoma, oral itraconazole (5 mgkg BID) can be used but must be continued for three months beyond clinical resolution. In most cases, complete remission is impossible or only temporary. Pythium insidiosum is poorly sensitive to cowentional antifungal treatment as its plasma membrane does not contain ergosterol, site of action of the azole derivatives. Many treatments have been tried with little success, notably the azole derivatives and amphotericin B.
Sporotrichosis Aetiopathogenesis Sporohichosis is a ubiquitous mycosis caused by Sporothrix schenckii, a dimorphic, saprophytic soil fungus, found commonly in rotting plant matter. The portal of entry is typically a skin wound, in particular a scratch or bite fmm an infected'cat. The disease is therefore more common in eniue male cats that live outdoors. Siamese cats seem predisposed.
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Figure 5 :I :Ulcerated nodule on a metacarpal footpad ofa cat with phueohyphmycos~~ (courfeqofD W Scott)
2 :Nasal nodule in a cat with phaeohyphomycosis
Figure 5 :3 :Pyogranulomntous nodule in the deep dermis, associated withphaeohyphomycosis (HE stain, X 1Wj
Figure 5 :4 :Prgfnenfedfungal elements (t) surrounded by a pyo$runulamtow reaction associafed wuh phaeohyphomycosts (HE smm, X 250)
Figure 5 !5 :Ulcers on rhe nose a d face of n cot wuh spomtr~chosis (courtcq ofGH MullernndD W ScoffJ
Figure 5 :6:Ulcers nndcrusrin$ on theface of a cat with spmfr~chom (courfesyofG H Muller a d D W S&*
Figure 5 :7 :Deep ulcerations on the drstal sporotnchosrs (courtesy 4D.W Scott)
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Figure 5 :8 :Sporothnx schenckix urtrucelldnr and extracellukzr, cigar-shaped yens& 1-4 p i long (Dg-Qwk siam, x 400) (courtesy of D w Scott)*
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Clinical features The disease can present in three clinical forms: cutaneous, cutaneolymphatic and systemic '. It is likely that the clinical form reflects the cat's immune response, the localised form relating to an immune system that is only slightly disordered. However, most affected animals present with internal lesions on necropsy. Dermatological signs are characterised by ulcerated nodules on the head (Figs 5 :5,6),tail base and limbs (Fig. 5 : 7). Extensive necrosis occurs which may also affect muscle and even underlying bone. With grooming, cats may spread fungal organisms over the entire skin surface. The disease fquently becomes generalised, via the lymphatics, and causes pulmonary, renal, digestive and central nervous system lesions. Fever is often seen.
Diagnosis Diagnosis is based on the history and, mainly dermatological, clinical signs (ulcerated necrotic nodules on the face. tail and limbs. followine a bite or scratch, and nou-responsive to appropriate antibiotic treatment). kytological and'hi~to~ath~logical examination of deep skples and G g a i culture are the most useful diagnostic tests. . -
Cytological examirrationof exudae and histopathologicalexamination of deep samples usually reveals . . very large numbers of fungal elements. Sporothrix schenckii is a very pleomorphic yeast. Its most typical form is cigar-shaved,2-4 um long and either intracelular or extracellular (Fig. 5 :8). On histopathological examinafion, t h e e E ~ t i l cell k wall of Sporothrix schenckii, and the fragmented cytoplasm may give the impression of a capsule. Special stains (PAS, Gomori) will differentiate Sporothriw schenckii and Cryptococcus n e o f o m m . In the cat, the inflammatory a t r a t e is granulomatous with epithelioid macrophages and lymphocytes. Immunofluorescent techniques are sometimes useful when demonstrating and/or growing the fungus is difficult. Fungal c u b e of deep tissue samples can be used to isolate and identify the fungus. Sporothrix schenckii grows as a yeast on blood agar at 37'C and in mycelial form on Sabouraud's agar at 2S°C. Microscopic examination of colonies reveals branching, filamentous hyphae, with piiform conidia and rosette-shaped conidiophores.
Treatment is based on the use of oral itraconazole (5 mgkg BID) for at least two months. Oral potassium iodide (20 m&g BID), with food, can also be used and must be continued for at least one month beyond clinicireso6tiin. oh ever, iodide derivatives are not always well tolerated in cats and may cause sideeffects (e.g. depression, vomiting, anorexia, hypothennia and cardiac insufficiency).Antibiotics are also desirable when there is secondary bacterial infection.
Risks for public health Feline sporotrichosis is very contagious to man, probably because of the large number of fungal elements nresent in infected tissues. Man can become infected following a bite or scratch from an affected cat, or s therefore, always be wom if 'even by direct contact with infected tissues or body fluids. ~ G v e should, sporohichosis is suspected. The most common form in man is the cutaneolymphatic form. The extracutaneous form, which stws in the lungs, before becoming systemic, is rare but can be seen in immunosuppressed patients 8 .
Cryptococcosis Aetiopathogenesis Cryptococcosis is a systemic mycosis caused by an encapsulated saprophytic fungus, Cryptococcus neoformans. Although there are other species, Cryptococcus neoformans is the only one that can grow at 37'C and consequently the only one that is pathogenic. Cryptococcus neoformans is a round yeast-like fungus, 3.5-7 pm in diameter, capable of forming a thick heteropolysaccharide
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~ 5 : 9 : P e ~ u l c e r 1 n a ~ ~ c s h o n h a i r c ~ w i r h c ~ m 0 ~ m s i sFigaYcS: 10 :Nasal ulcer ina ilomesl~cshort hair cotwith crypfococcosis (couflesyofB. HuheY (connesyof4. Hubert)
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.?sionsniiw , ,;ts asinvolve in Figure ,. ..,@er two months-withb.. the whole of the lateral sideoftheface
S~amesecat with ctpt~~occosis
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Figuw 5 :13 :'Ulceron the upper lip @a cat with cr)ptococcosh (couiesy 0fD.W Scott)
crypfococcosis
Figure5 :15 :Fineneedieaspiratefmma lymphnode oftbe! cGrn F~gugure 3 14. wcuolatedmocwphagesand numerow clustersofcf)pfococcr(D@-
Figure 5 :I6 :Cytology mm-bu.sedb&~ng o note the th~ckcapsule (Indun I& stam, x ION)
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capsule (1-30 pm). This capsule is responsible for the virulence of this fungus and explains its resistance to desiccation. It is not a true yeast as a phase of sexual reproduction (mycelial form) can be demonstrated under laboratory conditions 9. Cryptococcosis in man and animals is caused by two varieties of Cryptococcus neoformans: Cryptococcus neoformans var. neoformans (3 serotypes: A, D and AD) and Cryptococcus neoformans var. gattii (2 serotypes: B and C). In man, in Europe, North America and Japan, most strains correspond to Cryptococcus neoformans neoformans whereas in Central and South America, Africa and Australia, Cryptococcus neoformans ganii is the most prevalent strain lo. There is little information regarding the relative importance of the two varieties in the dog and cat. One recent Australian study has shown that out of 27 cats, Cryptococcus neoformans neoformans was isolated in 21 animals and Cryptococcus neoformans gattii in the other six ". Pigeon droppings, and soil that has been contaminated by them, contain a reservoir of Cryptococcus neoformans. This fungus lives in birds' intestines where it utilises creatinine as a source of nitrogen. Cryptococcus neoformans gattii has only been isolated from soil around Eucalyptus trees. The majority of cases are caused by the inhalation of cryptococci which are then spread via the blood to the nasal cavity, lungs and other organs, especially the nervous system, lymph nodes, eyes, kidneys and skin. More rarely, animals such as man are infected via the skin 12. The development and spread of the infection are strongly dependent on the host's immune system. Cell-mediated immunity is most important in preventing and eliminating the infection. Most people affected are immunosuppressed (e.g. by AIDS, corticosteroid eeatment or other immunosuppressive treatments). In the cat, no epidemiological studies have been carried out although immunosuppressive illnesses such as FIV and FeLV infections, and lymphoma, may be predisposing factors. However, an underlying illness is rarely demonstrated in cats with cryptococcosis. No age, sex or breed predisposition has been demonstrated although in some studies, Siamese and Abyssinian cats are well-represented ".
Clinical features Cryptococcosis is the most common systemic mycosis in the cat.
Systemic signs (e.g. respiratory, neurological and ocular) are common and varied. Sneezing, sniffing and a haemorrhagic, seropumlent discharge are often seen. The lungs are rarely affected. Neurological signs, including depression, passing out, turning round in circles, pressing against the wall, ataxia and paresis, vary according to which pm of the central nervous system is affected. The most common ocular signs are anterior uveitis, blindness due to detached retina, chorioretinitis and panophthalmia. Dematological signs involve single or multiple nodules, ulcers and draining tracts, affecting mainly the face (the nose is affected in about 70.80% of cases ") (Figs 5 : 9-13), p'mae and footpads. Peripheral lymphadenopathy is often seen (Fig. 5 : 14).
Diagnosis Diagnosis is based on the history and suggestive clinical signs (e.g. multicentric nodular lesions affecting mainly the face...), cytology, histopathology, identification of circulating antigens and fungal culture.
Cytological examination of fine needle aspirates from lesions reveals pyogranulomatous or granulomatous inflammation with numerous pleomorphic yeast-like organisms (Fig. 5 : 15). Fungal elements have the appearance of spheres surrounded by a bright refiactile halo which stains particularly well with Indian ink (Fig. 5 : 16). Narrow-based budding is common. Histopathological examindon of skin biopsies reveals either a pyogranulomatous or granulomatous reaction, rich in fungal elements (Fig. 5 : 17) or sometimes, in immunocompromised individuals, the presence of yeasts with no real granulomatous reaction. Special stains (Gomori, mucicmine red) are useful for identifying these yeasts (Figs 5 : 18,19). A latex a g g l u t i h n test can be used to detect capsular antigens. It is a very sensitive (more than 90%) diagnostic procedure that is quick and easy to use ". Currently available tests detect all serotypes and can be performed on serum, urine or cerebrospiial fluid (CSF). In the cat, antigenic titres correlate with the
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Figure 5 :17 :Uemral gmnalomtuus mu 'rrun ~~lthcn w h ~ c~ mh he seen
Figurr 5 :18 :Profire numbers uf cryptorocn I+, ~ilihinihe dermis hrrh no nwrled gramlonrrrulo reuriion m J L ~ I!I ~ i c~pivcoccoris h and Flt'infeciiun, nore r h rhirkness ~ ofif12~-upsakof r11m)eacr; 1P.4.7 rrarn.
Figure 5 :19 :Profuse numbers of cryprococci within the dermi o marked granulomatous reaction in a cat with cryptococcosis and FIV infection (Mucicarminestain, x25Oj (courtesy of J P Magnol)
Figurn 5 :20 :C~yptococeusnwfonnans m culture -
Figun 5 :21 : Ulcerated nodule on the face of a Persian cat with histoplasmosis (courtesy of S.W. White)
Figure 5 :22 :Same cat as In F i g w 5 21, ulcerafd nodule onrhe dorsd aspect ofthe metucarpus (courtefy 4fS.W. Wkrte)
3 :Difisepyogranulomatous reaction in the dermis withfungal Fig elementspresent (+), inassociationwith histoplarmosis(PASstoin,x100)
Figure 5 : 2 4 : Close-up view ofFigure 5 :23. Spherules and enhspores
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white colonies (courtesy ofB Hubefl
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+j are clearly visible when srained with PAS (PAS stain, x250j
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severity of the iUness. High titres are seen with systemic illness. Titres can also be used to assess response to treatment and to give a prognosis. The prognosis is good when the antibody titre is going down, whereas a high titre after treatment indicates that the cat is still infected. Fungal culiure of exudate, tissue samples, CSF or urine can be used to isolate and identify these yeasts on Sabouraud's agar at 25°C and 37°C.They form creamy, white colonies from between 48 hours and 6 weeks (Fig. 5 :20). Amplifiah'on techniques (polymemse chain reaction (PCR))are used in man to detect Cryptococcus neoformans.
Treatment The mtment of choice is oral itraconazole (5-10 mglkg SID or BID) continued for at least 2 months beyond clinical resolution. Oral fluconazole (5-15 mgkg SID or BID) can be used when the central nervous system is affected. Oral flucytosine (50 mglkg TID) and intravenous amphotericin B (0.1 to 0.5 mglkg, three times weekly) are now used a lot less frequently. Voriconazole, a new broad spectrum antifungal triazole agent may be an alternative therapy in years to come 16. For lesions restricted to the skin or nasal mucosae, response to treatment is usually good.
Histoplasmosis Aetiopathogenesis Histoplasmosis is a systemic mycosis caused by the dimorphic fungus, Histoplasma capsulalum. In its mycelial form, this fungus is a saprophyte of humid, nitrogen-rich soils. The disease is endemic in the Mississippi, the Missouri, the Ohio valleys, and many parts of the tropics. It has also been reported sporadically in other parts of the world, notably Europe". The accumulation of this fungus in house dust and interior plant soil may explain the emergence of this disease in cats kept in flats. The disease usually affects young cats less than 4 years old. Persian cats and females appear predisposed. The route of infection is the respiuatory tract. Infective fungal elements enter the host via the respiuatory tract. Here, they change into yeasts before spreading to internal organs via the lymphatic system and blood. Immunodeficiency does not seem to be involved in the development of this disease la.
Clinical features Histoplasmosis is the second most common systemic mycosis of the cat. The primary lung form is responsible for a granulomatous pneumonia (causing dyspnoea and tachypnoea), frequently associated with other systemic signs such as depression, anorexia, weight loss, fever, pallor of mucous membranes, generalised lymphadenopathy, hepatomegaly and splenomegaly. Histoplasmosis may also cause neurological, ocular (uveitis and chorioretinitis) and bony signs. Dermatological signs are rare and characterised by nodules or ulcers on the face and limbs (Figs 5 : 21,22).
Diagnosis Diagnosis is based on the history, systemic (respiratory, neurological and ocular) and sometimes Cutaneous signs, cytology, histopathology and fungal culture. Cytological and histopatthological examination of deep samples (cutaneous nodules, lymph nodes, bane marmw or lungs) can be used to identify many fungal organisms. Histoplasma capsulatwn appears as a round yeast, 2-4 pm in diameter, with a basophilic centre and a bright halo. It can frequently be seen phagccytosed by innammatory cells. Special stains (e.g. Gomori, PAS) on histopathological preparations help to identify the organism within a granulomatous or pyogranulmtous innammatoy reaction. hunofluoresceut techniques are sometimes necessary when using histopathological examination to identify fungi. Fungal culiure can be used to isolate and identify Histoplasm capsulatum which grows as a yeast on blood agar at 30°C or at 37"C,or in mycelial form on Sabouraud's agar at 25°C.Mycelial forms represent a serious source of potential infection for people, a fact which alwaysjustifies using specialist laboratories in case of suspicion. Anaemia and hypercakaemia are often seen in systemic forms.
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Treatment Oral itraconazole (10 mgkg SID or BID), given for at least two months beyond c h c a l resolution, is necessiuy. For senous systemic forms, ~traconazolecan inibally be grven in associahon with intravenous amphotencin B (0.25-0.5 mgkg, three tunes weekly) untd a c o m b i dose of 4-8 mgkg has been reached. Amphotencin B must not be given if the patient has an associated renal insufficiency. Oral fluconmle (2.5-5 mgkg SID or BID) is an alternative therapy when there is ocular and neurologcal mvolvement. Treatment must be contmued for at least two months beyond chnical resolution. Response to treatment is usually good when there are pulmonary signs.
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Blastomycosis
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Aetiopathogenesis Blastomycosis is a systemic mycosis caused by the saprophytic dimorphic fungus, Blastomyces derma~idis.Tht infective mycelial form of Blastamyces dermatidis lives m sandy, acid soils clam to water. The disease is endemic in the Mississippi, the Missouri and Ohio valleys and in some parts of westem North America ". Blastomycosis has not beenreportedin cats inEurope. Abyssinian and Havana cats appear p r e m e d . Infective forms enter the hostvia the respuatary tract and transform into yeasts inpu1mom.p tissue where they provoke initial lesions Thediseasecanthen be spreadvia thelymphaticsand blood into other organs including the sldn Involvement of lymph nodes, kidneys, gastrointeshnaltract, eyes, wvous sysbm and skin has been reported. Cats seem to have n a h d resistance to the disease.
Clinical features SI@S v a q according to the organ affected. Systemit signs (depresfion, weight loss, respiratory, neurological and ocularsigns) are common hatological lesionspresent as mdhple ulcerated nodules. Diosis Diagnosis is based on the history, ptemic (respiratory, neurological and ocular) and sometimes dermatological signs, cytology, histopathology and fungal dtw.
Cytological and hisfopathologiculexamidon of deep samples does not always allow identification of Blastomyces derntab'dis as these fungal organisms vary in number in lymph nodes, lungs and slan. Special stains (e.g. Gnmori, PAS) help to demonstrate the Organism within small pyograndomas, s m d e d by epithelioid macrophages and mulfinucfeate giant cells. Blastomyces dermatl'dis appears as a round or oval yeast, 5-20 pm m diameter, usually extracellular and often with braad-based budding. Immunoflumscent techniques are sometimes neeessay when using histopathological amhation to identify fungi. It is charattmised by athick mfractile, doublecoutoured cell membme. Conhimtion of the diagnosisis made easier by the use of immundogical techniques on tissue sections. Fungal culture can be used to isolate and identify Blast~irgcesdermtidis w W grows as a yeast on b l d agar at37'C andinmycelial form on Sabouraud's agar at25 "C Mycelial forms represent a &DU~ source of potential infection for people, a fact which always justifies using spechlistlaboratories in oase of suspicion. Serology (ELIMI tasting is m n t l y being ednated and may m the&diagnosis of blastomycosis in t beat.
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A muderate non-regenerativ~mtaemia md hypergZobuIlnaemia are o h seen in systemic forms.
Treatment Oral itraconazole (5 mgkg SID or BID), given for at least two months beyond clinical resolution, is necessary. For serious systemic forms, itraconazolecan initially be given m association with intravenous amphottricin B (0.25-0.5 m a g , three times weekly) unii a combii~doseof 4-8 mglkg has been reached. Aqhotericin B must not be given if the patient has an associated r e d msuftlciency. Oral fluconazole (2.5-5 a& SID or BID) is an alternative therapy when there is ocular and neumlogical involvement. Treatment must be continued for at least two months beyond clinical resolution. The prognosis is generally good except whenneurological andsevere pulmonary forms rnpresent.
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Coccidioidomycosis Aetiopathogenesis Coccidioidomycosis is a systemic mycosis caused by the saprophyhc dimorphic fungus, Coccidioides immitis. This fungus has the distinction of heing found in a "specialised ecological niche", the Sonoran basin zone. Low rainfall, low altitude and a sandy alkaline soil characterise this geographical zone, which connects the South Western United States, Central America and South America. This disease has not yet been seen in Europe. Infective conidia enter the organism via the respiratory tract and transform in pu1mon;uy tissue into large sphemles which contain numerous endospores. Once the endospores are released, they give rise to a new sphemle at body temperature. Spherules are resistant to phagocytosis, although endospores are chemotactically attracted to neutrophils and are easily phagocytosed. Spread of the disease via the lymphatics and blood leads to chronic systemic lesions affecting bone, eyes and skin.
Clinical features Signs are characterised by systemic effects (anorexia, weight loss...), locomotor signs (lameness), ocular signs (uveitis...) and ulcerated or fistulous cutaneous nodules. Affected cats rarely present with respiratory signs.
Diagnosis Diagnosis is based on the history, systemic (locomotor and ocular) and dermatological signs, cytology, histopathology and fungal culture.
Cytological and histopathological examination of deep samples reveals, in most cases, a pyogranulomatous dermal reaction (Fig. 5 : 23). It does not always lead to identification of Coccidioides immitis, due to the low number of rnicro-organisms in lesions. Cytological preparations obtained from lymph node aspirations, tracheobronchial lavage or draining tracts in the skin must be stained with Papanicolaou stains or PAS (Figs 5 : 23,24). With Papanicolaou stain, endospores appear reddish brown with a yellow cytoplasm and a purple or black membrane. PAS or Gomori stains are preferable for examination of histopathological preparations. Extracellular spberules (10-200 pm in diameter) are seen, but the endospores (2-5 lun in diameter) are usually heing phagocytosed. Confumation of the diagnosis is made easier by the use of immunological techniques on tissue sections. Fungal culture can be used to isolate and identify Coccidioides immitis which grows as a yeast on Sabouraud's agar at 37'C and in mycelial form on Sabouraud's agar at 25 "C. Mycelial forms represent a serious form of potential infection for people, a fact which always justifies using specialist laboratories in case of suspicion. The role of a serological test in the diagnosis of coccidioidomycosis is currently disputed, even though immunoglobulins IgM and IgG (anti-fungal) have been detected by precipitin and complement fixation tests respectively. A moderate non-regenerative a w m i a and hyperglobuliwmia are often seen.
Treatment Oral ketoconazole (10 mgkg SID or BID), has long been the treatment of choice. New azole derivatives (itraconazole and fluconazole, 5-10 mgkg SID or BID), given orally, are very effective and cause fewer side-effects. Whatever treatment is given, recmnce is common.
REFERENCES 1. Samuelson, J. in Robbins Pathologic Basis of Diseases (eds Cotran, S.R., Kumar, V. & Collins, T.) 3 2 9 4 2 (Saunders, W.B., Philadelphia, 1999). 2. Foil, C. S. in Infectious Diseases of the Dog and Cat (ed Greene, C.E.) 420-430 (Saunders, W.B., Philadelphia, 1998). 3. Thomas, R. C. &Lewis, D.T. Comp. Cont. Educ. Pract. Vet. 20.63-74 (1998). 4. Scott, D. W. Miller 11, W. H. &Griffin, C. E. Muller & Kirk's Small Animal Dermatology, 5th edition (Saunders, W.B., Philadelphia, 1995).
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www.vet4arab.co.cc 5 : Deep mycoses 5. Yager, I. A. & Wilcock, B. P. Color Atlas and Text of Surgicql Pathology of the Dog and Cat (Wolfe Publishing, London, 1994). 6. Rosen, T.& Overholt, M. Int. J.Demtol. 3596-98 (1996). 7. Rosser, E. J. & Dunstan, R. W. in Infectious Diseases ofthe Dog and C m (ed Greene, C.E.) 399402 (Saunders,W.B., Philadelphia, 1998). 8. Vieira-Dias, D., Sene, C.M., Or&fice,E, T m m , M. A. G. & Hamdan, J. S.Mycoses 40, 197-201 (1997). 9. Jacobs, G. 1.& Medlau, L. in Infectious Diseases of the Dog and Car (ed Greene, C.E.) 383-390 (Saunders, W.B., Philadelphia, 1998). 10. Criseo, G. & Gallo, M. Mycoses 40,95-100 (1997). 11. Malik, R., Wigney, D. I., Muir, D. B., Gregory, D. J. &Love, D. N. J. Med. Vet. Mycol. 30, 133-144 (1993). 12. Ng, W. E & Loo, K. T.Amer. J. Dermatopathol. 15,372-377 (1993). 13. Davies, C. &Troy, G. C. J. Amer. Anim. Hosp. Assn. 32,380-391 (1996). 14. Gerds-Grogm, S. & Dayell-Hart, B, J. Amer. Anim. Hosp. Assn. 33, 118-122 (1997). 15. Jacobs, G. J., Medleau, L., Calvert, C. & Bmwn, J. J. Vet.Int. Med. 11, 1 4 (1997). 16. Wolf, A. M. in Infectious Diseases of the Dog and Cat (ed Greene, C.E.) 378-383 (Saunders, W.B., Philadelphia, 1998). 17. Polak,A. Mycoses41, 1-30 (1998). 18. Legendre, A. M. in Infectious Diseases of the Dog and Cat (ed Greene, C.E.) 371-377 (Saunders, W.B., Philadelphia, 1998). 19. Green, R. T in lnfeczious Diseuses of the Dog and Cat (ed Greene, C.E.) 391-398 (Saunders, W.B.,Philadelphia, 1998).
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Bacterial dermatoses Bacterial dermatoses, also called pyodermas, are rare in the cat despite being so common in the dog1-". The main reasons for this are perhaps the small number of bacteria on the skin and coat of the cat and also the importance of grooming in cats i.6. Bacterial skin infections are most often secondary to trauma, bites or scratches and resolve easily with suitable antimicrobial treatment. On the other hand, some specific bacterial infections, possibly secondary to a systemic illness (e.g. retrovirus infection), can be difficult both to diagnose and to treat.
Aetlopathsgemsis Abscems are SQB tisSue M c t i m , caused by the iafmduc&on of bacfnia inta ~ h c u ~ ~ s wmctive tissue, writh a bite or scmklh The bacteiarespansible belong to resident ad flora. They m#y be &&tativr: m obligamy anaerobes, indudmg gram n%;.grivebacilli &u6ha~ Pasteurditz m~tt~tac&,Frrsabactmua spg,, spimehaetes and &cam-pmitive eoaf, in particular 8-haemolyfis streprowmi !Entiremales are p & b ~u m of their ggres%ive qaturs.
Clinical features Der@a@log&al &s
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Sj&emic & h 6 s u ~ h afever?an~rexia~letkargy~ an(ir&onal I y m p W n ~ t h are f almoslinvari&ble.
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an the bistoiy and c h i a d &a$. Cyni1o@cal ex&atim df pup* ba@&I c u k and antibide &tivity, and saeming Eor retrwiru8e.san:necessrvy in reeurrent
w, Treatment surghl &&wge artdflushing w@ mm6e:s o ? ~ m such Mof6eKidine 10.5%1, dilute povidoneio$ine a 3%kydr@gmp ~ r i d eis, necessary in the majodty of casm. craffjniw~aial &abwH invoIves the use of bm;td m m .;mtibioties for about 10 days. P e e k mltwidn is frequently kkted, penieiu"as am .the antibiotic of choi6e. W h ame+m@~ hacreriaitm preseflt+plitidmpin is a good &iw df ~ K a t i (libla c 6 : 1). S@e& A6
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A Weal Guide to %line Dermatology
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Table 6 : 1 : Main antimicrobial agents used in feline dermatology im: intramuscular; po: oral; sc: subcutaneous; iv: intravenous; SID: dose given once daily; BID: dose given twice daily Penicillin G Clavulanate-potentiatedamoxycillin Oxacillin Cephalexin Cefadroxil Enmfloxacin Marbofloxacin Clindamycin Lincomycin Trimethoprim-sulphadiazine Trimethoprim-sulphamethoxazole Doxycycline Minocycline Tehacycline Gentamicin Rifampicin Clofazimine Dapsone
im PO, SC PO PO Po PO, SC
100 000 U I kg SID, BID 12.5 to 25 mg I kg BID 11to35mglkgBID 20 mg I kg BID 20 mg I kg BID 5 to 20 mg I kg SID
PO PO
2to5mglkgSID 5.5 mg I kg BID 20 mg / kg BID 15 to 20 mg I kg SID, BID 15 to 30 mg I kg SID, BID 5 t o 11 mglkgSID,BID 5 to I1 mg I kg SID, BID 10 to 30 mg I kg BID 4 mg I kg SID 10 to 20 mg I kg BID 2-8 mg I kg SID 1 mg I kg SID
PO
PO Po PO PO Po iv PO Po Po
Superficial pyoderma Aetiopathogenesis Superficial pyoderma is rare but probably underdiagnosed Id. It usually follows an underlying dermatosis (allergic dermatitis, auto-immune dermatoses, demodicosis etc ...), systemic illness (e.g. retrovirus infection) or immunosuppressive treatment (e.g. corticosteroids and antimitotic therapy). The bacteria most frequently isolated are Staphylococcus aweus, Staphylococcus simulans and Staphylococcus intermedius
Clinical features Superficial pyoderma is characterised clinically by non-specific papules, pustules and, more rarely, epidermal cellarettes Id. It may sometimes assume the appearance of a miliary dermatitis, an erosive or ulcerative dermatitis (Fig. 6 : 2) or lesions of the eosinophilic granuloma complex I.
Diagnosis Diagnosis is difficult because bacterial skin infection cannot be diagnosed with certainty on clinical examination alone. Whether lesions are caused by infection or by the underlying illness, is also impossible to tell.
The skin smear is the first diagnostic test to try. Impression smears are useful when dealing with erosive and ulcerative lesions. For papular, papulo-crustous and crusting lesions, adhesive tape preparations are preferable. Adhesive tape is applied to the lesion, removed, and then placed on a slide to which a drop of stain (e.g. lactophenol blue, methylene blue or blue Diff-Quik stain) has been added. The preparation is then examined microscopically under oil-immersion. Interpretation is difficult. If cytology reveals lots of neutrophils and intracellular cocci, bacterial infection is present. If neutrophils, keratinocytes and lots of extracellular cocci are seen, pyoderma cannot be diagnosed with certainty hut a therapeutic trial with an oral antibiotic is justified. If cytology demonstrates only keratinocytes and extracellular bacteria (cocci), even in large numbers, pyodema cannot be diagnosed. In this case, the decision to start antibiotics is very subjective and depends on the number of bacteria, the type of lesions present and the experience of the clinician. Note that improvement, and even resolution of lesions, following systemic antibiotic therapy, does not necessarily confirm a diagnosis of pyoderma.
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Histopathological examination of skin biopsies may be consistent with bacterial infection and also an underlying dermatosis. This procedure may reveal intraepidermal pustules containing degenerate neutrophils, perifolliculitis, or mural or interface folliculitis compatible with bacterial infection. Special stains may be used accordmg to the differentials '. Bacterial culture should he routine in cases of recurrent pyoderma or when multiple species of bacteria are seen on cytology.
A search for an underlying dermatosis or systemic illness should always be conducted and the condition identified where possible.
Treatment Systemic antimicrobial therapy is the treatment of choice. The majority of staphylococci responsible for pyoderma in the cat, are resistant to penicillin, amoxycillin and ampicillin, The most effective antibiotics are clavulanic acid-potentiated amoxycillin, cephalosporins (e.g. cephalexin and cefadroxil), emofloxacin, marbofloxacin and clindamycin. Trimethoprimpotentiated sulphonamides are often used in Europe and the United States (Table 6 : I), although in Australia, strains of Staphylococcus infermedius are very commonly resistant to these la.Antibiotics should he given for a minimum of 3 weeks and should be continued for at least a week beyond clinical resolution. Paste preparations are particularly useful, firstly because they are easy to administer and secondly because they can generally be given in one daily dose. Antibacterial shampoos are rarely used because cats have a reputation (often unjustified) for not liking being washed. However, shampoos, when it is possible to apply them easily, form a very effective adjunctive therapy. A 2.3% chlorhexidine solution is one example. For localised pyoderma, local application of an antiseptic containing 0.5% chlorhexidine is often useful. Treatment of the underlying cause, when identified, is essential to prevent or limit recurrence.
Superficial juvenile pustular dermatitis Supemcia1 juvenile pustular dermatitis is a bacterial skin infection of the cat caused by Pasteurella multocida and various beta-haemolytic streptococci. No underlying cause has been identified. Dermatological signs are characterised by non-follicular pustules associated with epidermal cellarettes, mainly on the dorsal neck and trunk. Systemic signs are rare. Pasteurella multocida or beta - haemolytic streptococci may be isolated on bacterial culture. Histopathological examination of s k i biopsies demonstrates the presence of non-follicular pustules containing lots of degenerate neutrophils. Treatment involves giving a suitable antibiotic for about 3 weeks.
Bacterial paronychia Aetiopathogenesis Bacterial paronychia 1s particularly common in the cat. Various bactena have been isolated from witbm lesions, including Staphylococcus spp., Streptococcus spp., Pseudomonas spp., and Protevs spp. Multiple bacterial paronychia should lead to suspicion of an underlying demtosis or systemic illness (e.g. rebovtrus infecuons, systemic lupus erythematosus) " 12.
Clinical features Dermatological signs are characterised by painful and swollen nail beds (Fig. 6 : 3). Pus, varying in colour and sometimes with a nauseatrng smell caused by the bacteria, is also present around the digits. Multiple digits and several feet are very often affected " 12. Systemic signs vary according to the underlying illness
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A RacacalGuide to Feline ~ 0 1 0 g y
Diagnosis The diagnosis is based on appearance of the lesions. The differential diagnosis includes other causes of paronychia (e.g. dermatophytosis, cryptococcosis, pemphigus foliaceus) and digital metastasis of a pulmonary adenocarcinoma.
Cytological examination of pus usually reveals evidence of colonisation by different types of bacteria. Bacterial culture should be carried out routinely. The underlying cause must always be looked for and identified.
I'rognosis and treatment The prognosis is always dependent on the underlying cause ".12. Treatment is difficult. Surgical treatment involves ablation of the affected nails followed by twice daily antiseptic washes. Antibiotic therapy is the treatment of choice and should be based on antibiotic sensitivity testing. Fluornquinolones (e.g, enrofloxacin and marbofloxacin) are particularly indicated (Table 6 : 1). Duration of treatment has to be long, from several weeks to several months and must be continued for several weeks beyond resolution. Recurrence is common.
Acne Aetiopathogenesis Acne is a primary keratinisation problem, resulting in secondary infection of areas rich in sebaceous glands ',", Signs of acne are the same as those described for demodicosis, Malassezia dermatitis, even contact dermatitis (e.g. associated with plastic food bowl) or dermatophytosis ",'< Various bacteria, including Pasteurella multocida and beta-haemolytic streptococci, can be isolated from within infective foci ".
Clinical features Dermatological signs are cbaracterised by comedones, follicular casts (Fig. 6 : 4), papules, pustules and furuncles on the chin and sometimes the upper lip. Rarely: marked swelling of the c h i is seen .4I.'' If comedones and follicular casts are present, acne should be considered, whereas if they are absent, an eosinophilic granuloma should f i s t be suspected.
Diagnosis The diagnosis is based on clinical examination and exclusion of other causes (demodicosis, Malassezia dermatitis, dermatophytosis) by appropriate diagnostic tests.
Cytological examination of pustular contents demonstrates varying numbers of intracellular and extracellular bacteria, degenerating neutrophils and macrophages ". Histopathological examination of skin biopsies reveals dilated, keratin-filled hair follicles, perifolliculitis, folliculitis and furunculosis. Marked fibrosis is often seen in chronic cases 14.
Treatment Appropriate systemic antibiotics are not always successful in treating acne ". Clindgnycin appears to us to be the antibiotic that gives the best results (Table 6 : 1). Treatment should be given for 4-6 weeks and continued for at least one week beyond clinical resolution. Benzoyl peroxide shampoos (2%), applied 1 to 2 times daily, may give good results but care should be taken to rinse thoroughly in order to avoidipossible local initation 'I.
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Muuirocin pel (2%) is effective in the treatment of feline acne ". This eel is used twice dailv for 3-6 weeks. ~beiesibnsshould not be licked for 5-10 minutes after application. Nephrotoxicity c'aused by the excipient polyethylene base is unlikely to develop provided only small amounts of the product are applied each time.
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F i p 6 :1 :Abscess on the distal limb, caused b~ Pastewella multocrda
-,.,..- ...- --.....,..-, ...fectionn
Phofo 6 :4 :Multiple comedones and follicular casts in a cat with acne
Figure 6 :5 :Multiple abdominal draining tracts in a cat with atypical mycobacterial infection caused by Mycobacterium formihim
Figure 6 :6 :Same cat ns in Fig. 6 :5. Multiple draining tracts on fhe abdomen
composed mainly of neumphils, surmunding visually empry vacuoles (HES stain: haemntarylin, eosin s o f m x 4W) ( c o w e v of M. Mialot)
Figure 6 :8 :Atypical mycobacterial infection:pyogranulomn surrounding a vacuole containing acid-fist bacilli (Ziehl-Neelsen srain, x 1000) (courtev of M. Mialof)
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Figure 6 :2 :Secondary p y o d e m in a cat with atopic d e m n n s
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Radical Guide to Feline kmatology
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Other topical antimicrobial agents, such as chlorhexidine used in a 3% shampoo or a 0.5% lotion are also beneficial Synthetic retinoids can also be used ",". Topical tretinoin (0.01-0.05%), given once daily until resolution, is sometimes initant 'I. Oral isotretinoin (2-5 m@g SID) can be given but side effects (increased pnuitus, dry mucous membranes, conjunctivitis, and raised liver enzyme levels) have been reported in cats given systemic synthetic retinoids 'I.
Atypical mycobacterial infections Aetiopathogenesis Atypical mycobacterial infections are rare ubiquitous infections, caused by facultative pathogenic bacteria of the genus Mycobacterium, excluding those causing tuberculosis and feline leprosy. The main organisms involved are Mycobacterium chelonei, Mycobacterium fortuitum, Mycobacterium phlei, Mycobacterium smegmatis and Mycobacterium thermoresistible,all of which live in the soil '.'' 18. Entry into the organism often occurs via contamination of bites, scratches and other wounds by these bacteria. Retrovirus infections could predispose to the development of these atypical mycobacterial infections. Their pathogenicity seems to be increased in the presence of lipids, which could perhaps explain the very high incidence in cats of lesions on the abdomen I.
Clinical features Dermatological signs are characterised initially by alopecic, erythematous, firm,slow-growing nodules. Within several weeks to several months, these develop into subcutaneous abscesses. They are sometimes painful (pyogranulomatous panniculitis), ulcerated or accompanied by subcutaneous draining tracts (Figs 6 : 5, 6). When draining tracts are present, attempts to find a foreign body by surgical exploration lead to wound breakdown and recurrence. Main areas affected are the abdomen and inguinal regions, although other parts of the body may also be involved 3.'6-'8. Systemic signs (fever and anorexia) are rarely seen.
Diagnosis The diagnosis is based on lesion distribution, suggestive or even diagnostic, skin biopsies and possibly identification of the mycobacteria responsible.
Cytology of nodular contents (fine needle aspirate) and of pus reveals a pyogranuloma. Acid-fast bacilli can sometimes be seen within neutrophils when preparations are stained with Ziehl-Neelsen. Histopathological examination of skin biopsies, taken from nodules or draining tracts, is essential. Excisional biopsies are preferable to punch biopsies because the biopsy must go deep enough to include the deep dermis and panniculus. Histopathology is characterised by nodular dermatitis or diffuse andlor pyogranulomatous panniculitis (Fig. 6 : 7). Granulomas, made up of neutrophils, surround visually empty vacuoles (lipid vacuoles) in which acid-fast bacilli may be seen with the use of special stains (e.g. modified Ziehl-Neelsen or Fite-Faraco) ' (Fig. 6 : 8). Bacterial culture for atypical mycobacteria needs to he carried out on skin biopsies taken under aseptic conditions. Epidermis and dermis should be dissected away. The deep dermis and panniculus should be preserved in sterile gauze soaked in sterile water before sending to the laboratory. Culture is performed on special media (blood agar, Lowenstein-Jensen medium or Stonebrink medium) at 37°C. Cultures grow rapidly but species identification is often difficult ',I7. Molecular biological techniques (e.g. amplification) can now be used to identify mycohacteria. A methodical search for an underlying illness (e.g. retroviral infection) should be routine.
Prognosis - Treatment The prognosis must he guarded, given the frequency of recurrence, but may now he improved thanks to the use of long-term specific antibiotic therapy. Treatment is based on surgical excision associated with prolonged antibiotic therapy. Many
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I 6 : Bacterial dermatoses
antibiotics have been used in the treatment of atypical mycobacterial infections: kanamycin, gentamicin, amikacin, tetracyclines, potentiated sulphonamides and emofloxacin '. In our experience, oral doxycycline (5 mgkg SID for 6-8 weeks), selected from antibiotic sensitivity testing, is the antibiotic treatment of choice. This can be followed by broad surgical excision and cutaneous reconstruction techniques 18. From the time of surgical excision, intravenous injections of gentamicin (4 m a g ) should be given every 8 hours for 3-4 days. Oral emofloxacin (5-20 m a g SID) can then be given for 2-4 months (Table 6 : 1).
Feline leprosy Aetiopathogenesis Felme leprosy is a rare and mainly cutaneous infechon, probably caused by Mycobacteriwn lepraemurium, the agent of leprosy in rats 19. Penetration of naturally infected tissue causes skin lesions w i t h 2-5 months. The condition may also be transmitted by rat bites, and possibly by mosquitoes, fleas and hcks Feline leprosy is a ubiquitous condition reported in the United States, Canada and Australia as well as in Great Britain, the Netherlands and France. No breed or sex predilection has been seen. However, feline leprosy is reported mainly in cats aged between 1 and 3 years >. j.
Clinical features Dermatological signs are characterised by single or multiple, ulcerated or non-ulcerated alopecic nodules, seen mainly on the face, limbs and sometimes the tnmk (Figs 6 : 9,lO). Ulcers and draining tracts may be seen 19a0.
Systemic signs are rare. Regional lymphadenopathy is seen in some cases. Syatemc involvement is extremely rare in the cat '.
Diagnosis The diagnosis is based mainly on lesion distribution and suggestive skin biopsies.
Histopathological examination of deep skin biopsies usually reveals a "lepromatons" reaction, characterised by a granulomatous dermatitis, rich in macrophages and giant cells (Fig. 6 : 11) and numerous intracellular well-stained bacilli, arranged in strips (Fig. 6 : 12). Much more rarely, a "tuberculoid" reaction is seen, characterised by the presence of epithelioid granulomas, surrounded by lymphocytes, with only a few bactena in the centre ",ll. Bacterial culture is difficult and often negative on standard mycobacterial culture media. In vltro growth is very slow (about 3 months). Special media (e.g. Ogawa egg yolk medium and a medium emched in cytochrome C and alpha-ketogluratate) can be used >. Molecular biological techniques (e.g. amplification) can now be used to identify mycobacteria
Treatment Surgical excision is probably the treatment of choice for single nodules although post-surgical recurrence may be seen.
Oral clofahine (2-8 mgkg SID) glves good results It comes as a capsule which may need to be punctured to allow correct dosage. Gloves should he worn when handling the capsules due to the red colouration of the antibiotic. Treatment may stain the skin and mucous membranes orangy-red. Following use of this product, a moderate Increase in the level of hepatic enzymes has been reported in the cat. "'.
Other combination therapies involving dapsone ( 1 m a g SID), c l o f a z ~ and e rifamp~cin(10-20 m a g BID), given orally, are sometimes necessary in cases refractory td'standard treatment " (Table 6 : 1).
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A Pradcd Guide to Wine Damatology
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Nocardiosis Aetiopathogenesis Nocardiosis is a very rare skin infection caused by filamentous bacteria of tbe genus Nocardia. Colonies form grains within pyogranulomatous reactions. These bacteria are aerobic, gram-positive and partially acid-fast soil saprophytes. Various species may be isolated including Nocardia asteroides, and more rarely Nocardia caviae and Nocardia brasiliensis Pathogenesis is poorly understood. Infection may occur via a scratch or bite. In immunosuppressed cats, infection may arise by inhalation and spread to other organs.
Clinical features Dermatological signs occur mainly on the face, distal limbs (Fig. 6 : 13) or abdomen. They are characterised by ulcerated lesions, draining tracts and pus containing white and yellowish grains '.I Systemic signs are common and relate to underlying illness: pyrexia, regional lymphadenopathy, dyspnoea (if pyotborax), etc...IJ.
Diagnosis The diagnosis is based on lesion distribution, suggestive skin biopsies, and identification of the bacteria by bacterial culture. Cytological examination of grains reveals filamentous bacteria arranged in stars. ~ i s t o ~ a t h o l o ~ iexamination cal of deep skin biopsies reveals a nodular or diffuse dermatitis and/or a pyogranulomatous panniculitis with or without grains. Colonies of Nocardia spp. appear partially acid-fast when stained with modified Fite-Faraco l. Bacterial culture is performed on skin biopsies taken aseptically and inoculated onto aerobic media. Antibiotic sensitivity testing should be conducted.
Prognosis - Treatment The prognosis is guarded, depending on the presence of an underlying illness. Treatment is difficult. Broad surgical excision of the lesion and debridement, involving curettage and antiseptic flushing, are possible in some cases. Therapy based on antibiotic sensitivity testing is essential. Oral trimethoprim-sulphamethoxazole(30 m a g BID) is given until lesions have resolved and for one month after. Other antibiotics such as penicillin G (100,000 IUkg SID), given by intramuscular injection over 10 days, may be used (Table 6 : 1)
Actinomycosis Aetiopathogenesis Actinomycosis is a very rare skin infection caused by filamentous bacteria of the genus Actinomyces. Colonies form grains within granulomatous reactions. These bacteria form part of the resident bacterial flora in the buccal cavity and intestine. They are gram-positive, anaerobic and non-acid-fast. Pathogenesis is poorly understood. Infection occurs mainly via wound contamination (e.g. bites and scratches). In immunosuppressed cats, infection may arise by inhalation and spread to other organs. Apparently, the condition is not dependent on immunosuppression of the host.
Clinical features Dermatological signs occur mainly on the face, neck and tmnk and are characterised by variably circumscribed abscesses, draining tracts (Fig. 6 : 14) and pus, containing yellow sulphur grains. Systemic signs generally reflect the degree of systemic involvement.
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Figure 6 : 9 :(ilcerotednodular lesion rn a cat wrth leprosy (courrexy of P IhrkeJ
Figure6: 10 :Multiple nodules, becomrngulcerated m a cat with lepr~xy (courtesy of 0.Cozette)
Figure 6 iI 1 :Leprosy. drffus~,granulomatous dermatitis (many macmpha$es and grant cells are present) nr a cat w ~ t feiine h lepmsy (HES stain,x 100) (corutesy of 0 Cazene)
Figuure 6 :I2 :Leprosy: very large numbers of intracellular, acid-fosr bacilli in macrophages and giant cells (Ziehl-Neelsen stain, x 1000) (courtesy of 0.Cozefte)
Figure 6 :13 :Drgital ulcers rn a rat with nocardiosrs (courtesy of T Ohvry)
F~gure6 :14 :Mulnplefislulous sor es ~na cat wrth actrnomycosls
Figure6: 15:Drgrtalulce1s wtthyellow grarorns (n a cat wrthbot~omycos~s
Fi-6: 16: Botryomycosir:pyogranulomafausdermatitis, wirhin which are bacterial colonies surrounded by a Splendore-Hoepplireaction
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A Pl;lctieal Guide to F e l h ~ 1 o g y
Diagnosis The diagnosis is based on lesion distribution, skin biopsies, and identification of the bacteria by anaerobic bacterial culture.
Cytological examination of grains reveals filamentous bacteria Histopathological examination of deep skin biopsies reveals a nodular or diffuse dermatitis and/or a pyogranulomatous panniculitis in which grains are seen in about 50% of cases. These basophilic grains are surrounded by a Splendore-Hoeppli reaction. Bacteria are not always clear on standard stains.
Prognosis and treatment The prognosis is guarded, given the very high incidence of recurrence ' Treatment requires broad surgical excision, where possible, or debridement with curettage and antiseptic flushing. This treatment must be accompanied by very long courses (3-4 months) of antibiotics, based on sensitivity testing. Penicillin G (100:OOO IUkg SID or BID), given by intramuscular injection, may be continued for one month after clinical resolution (Table 6 : I).
Botryomycosis Aetiopathogenesis Botryomycosis is a ubiquitous and under-diagnosed skin infection, caused by non-filamentous bacteria. Colonies form grains within pyogranulomatous reactions. Various agents are responsible (Staphylococcusspp., Streptococcus spp., Pseudomonas spp., Proteus spp. and Actinobacillus spp.) and sometimes they may be found in combination. Pathogenesis of these lesions is poorly understood. Bacteria entering subcutaneous connective tissue via a wound (e.g. bite or scratch) probably trigger a hypersensitivity reaction and an alteration in the destructive role of lencocytes. Retrovirus infections might sometimes predispose to botryomycosis j.
Clinical features Dermatological signs are often chronic and occur mainly on the limbs. They are characterised by single or multiple, ulcerated or non-ulcerated, alopecic nodules, containing small white or yellow grains (Fig. 6 : 15). Ulcers or draining tracts may sometimes be seen. Systemic signs vary according to the presence of an underlying illness (e.g. retrovirus infection)
Diagnosis The diagnosis is based on lesion distribution, skin biopsies, and identification of the bacteria by bacterial culture.
Cytological examination of grains (after crushing) reveals very large numbers of non-branching bacteria. Histopathological examination of deep skin biopsies reveals a pyogranulomatous dermatitis, within which there are bacterial colonies surrounded by a Splendore-Hoeppli reaction, composed of polysacchatides and glycoproteins around the bacterial colonies pig. 6 : 16). Bacterial culture is performed on skin biopsies, taken aseptically, and inoculated onto various media. Antibiotic sensitivity testing should be conducted.
Prognosis and treatment The prognosis is variable, depending on the presence of an underlying illness. Treatment requires broad surgical excision, where possible, or lesion debridement with curettage and antiseptic flushing. This treatment must be accompanied by antibiotic therapy, based on sensitivity testing (Table 6 : 1). Most antibiotics penetrate these lesions poorly.
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REFERENCES 1. Scott, D. W. J. Amer. Anim. Hosp. Assn. 16, 331-459 (1980). 2. White, S. D. J. Amer. Anim. Hosp. Assn. 27, 141-146 (1991). 3. Scott, D. W., Miller, W H. &Griffin, C. E. Muller & Kirk's SmaNAnimal Dermatology, 5th edition (Saunders W. B., Philadelphia, 1995). 4. Medleau, L., Rakich, P. M., Latimer, K. S. &Grant, J. B. Vet. Med. 86,807-811 (1991). 5. Devriese, L. A,, Nzuambe, D. & Godard, C. Vet. Microbial. 9,279-285 (1984). 6. Hall, I., Campbell, K. L. In Consultations in Feline I n t e r ~Medicine l 2 (ed August, J. R.) 233-240 (Saunders, W. B., Philadelphia, 1995). 7. Hart,B. L. & B m t t , R. E. J. Amer. Vet. Med. Assn. 163,290-292 (1973). 8. Medleau,L. & Blue,J. L. J.Amer Vet. Med.Assn. 193, 1080-1081 (1988). 9. Lloyd, D. H., Lamport,A. I. & Feeney, C. Vet. Dermarol. 7,171-175 (1996). 10. Mueller, R. S., Bettenay, S. V., Lording, P. & Dell'Osa, D. Aust. Vet. Pract. 28, 10-13 (1998). 11. Guagukre, E., Hubert, B. BiDelabre, C. Vet. Dermatol. 3, 1-12 (1992). 12. Scott, D. W &Miller, W.H. Comp. Cont. Educ. Pract. Vet. 14,449-457 (1992). 13. Rosenkrantz, W. S. Vet. Med. 86.504-512 (1991). 14. White, S. D., Bourdeau, P. B., Blumstein, P. and others Vet. Dermatol. 8, 157-164 (1994). 15. Power, H. T. & Ihrke, P. J. in Current Veterinary Therapy XI1 (ed Bonagura, I. D.) 585-590 (Saunders, W. B., Philadelphia, 1995). 16. White, S. D., Ihrke, P J., Stanna4A.A. andothers. J.Amer Vet. Med.Assn. 182, 1218-1222 (1983). 17. Kunkle, G. A. in Infectious Diseases of the Dog and Cat (ed Greene, C. E.) 567-569 (Saunders,W. B., Philadelphia, 1990). 18. Malik, R. Hunt, G. B., Goldsmidt, S. E., Martin, P.,Wigney, D. I. &Love, D. N. J. smaNAnim. Pracr. 35,524-530 (1994). 19. Kunkle, G. A. in Infectious Diseases of the Dog and Car (ed Greene, C. E.) 569-572 (Saunders,W. B., Philadelphia, 1990). 20. McIntosh, D. W. Can. Vet.J. 23,291-295 (1982). 21. Mundel1,A. C. Vet. Clin. N.Amer. 20,1541-1556(1990).
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E. Guaguere - J. Declercq
I Viral dermatoses Viral dermatoses are a developing field in feline dermatology. They are underdiagnosed because of difficulties in identifying the causal virus, but new investigative procedures (e.g. electron microscopy, immunohistochemistry and viral amplification) have enabled these new dermatoses to be cbaracterised. An understanding of them is important as they enter into the differential diagnosis of many different conditions. They also represent a major zoonotic risk for man.
Poxvirus infection Aetiopathogenesis Poxvi~usinfection IS a vual dermatosi~caused by cowpox virus, an oahopox virus, and has been reported in many species, notably the cat '! Seen for the first time in Great Britain I, poxvirus infection is reported regularly in the Netherlands ', Belgium, Austria ', Germany ', Italy ' and now France Not all strains of poxvirus isolated in the cat are identical and they seem to vary according to their geographical origin. In Great Britam, the virus isolated in the cat is the same as the cowpox identified in other species. However, this has not been verified in other countries 9.
In almost every case, poxvirus infection has been seen in rural hunting cats I,". Infection occurs mainly through contact with rodents (e.g. voles and field mice) and sometimes with cattle. The increased mcidence in summer and autumn (very pronounced in Great Britain) relates to when these rodents are most active and also their breeding season g. The route of infection of cowpox virus 1s percutaneous and sometimes oronasal "O. The latter route is responsible for a milder form of the disease, which is why cats in contact with an affected cat will sometimes seroconvert, but rarely show clinical signs of infection. After infection, the virus undergoes local replication and produces the pnmary lesion. It then spreads via the lymphatics to cause multiple secundary lesions 9. Clinical features Dermatological signs are characterised fmtly by a solitary lesion on the head, neck or forelimbs I8 ". This lesion is an erythemams macule which ulcerates rapidly (Fig. 7 : 1). With~nabont 10 days, many secondary pnuitic lesions, including macules, papules and nodules (0.2-2 cm m diameter), appear all wer the body @g. 7 : 2,3). They are initially erythematous, becoming ulcerated. About 20% of cats have ulcerations in the oral cavity and on the tongue (Fig, 7 :2) Systemic signs may be present. These include depression, anorexia, pyrexia, conjunchvitis and respiratory signs 9. In most cases, these secondary lesions resolve spontaneously w i t h 3-8 weeks '.Secondary bacterial Infection or concurrent F N infection can lead to developmentof systemic signs, - including pneumonia which may sometimes prove fatal 9. Laboratory tests Impression smears, stained with May-Grunwald-Giemsa may %veal the iutracytoplasmic eosinophilic inclusion bodes characteristic of pox viruses (Fig. 7 :41, but this procedure should only be undertaken by a very competent cytologist 56. $.
Histopathological examination of skin biopsies, taken from the margin of recent lesions, reveals hydropic degeneration of keratinocytes and cells of the follicular outer root sheath, the presence
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within these cells of characteristic intracytoplasmic eosinophilic inclusion bodies, microvesicles and epidermal necrosis which is sometimes extensive (Fig. 7 : 5-7) Is".
Electron microscopy of skin biopsies reveals virus particles with an average size of 310 x 240 nm and a helical symmetq characteristic of orthopox viruses (Fig. 7 : 8) ',". This procedure will detect virus in only 75% of cases ". Viral isolation on cell culture or emhryonated hen's egg chorioallantoic membrane is possible, hut specialist laboratories are needed 5,6,8,". Serology (viral neutralisation, haemagglutination inhibition, complement fixation and ELISA) cannot be used to distinguish this poxvirus from other orthopox viruses."~'S~i This is because of the close antigenic relationship between the different orthopox viruses. However, the persistence of antibodies 6 months after infection makes retrospective diagnosis possible '.
Treatment-Prevention Purely symptomatic treatment for secondary bacterial infection involves a 2-3 week course of antibiotics and local antiseptic agents. Getting the cat to eat is also necessary and sometimes quite difficult, due to the painful oral lesions. Corticosteroids are contraindicated and may lead to development of systemic signs '-". Prophylactic measures are important Given the risk of transmitting the condition to another cat, the sick cat should he isolated. The virus is quite resistant to ambient temperature and humidity and so the external surroundings will sometimes need to be cleaned with household bleach. The risk of zoonotic transmission is very real, particularly for immunodeficient people, children and the elderly. In order to reduce the risk of contamination, the owner must, therefore, follow certain precautions (e.g. wearing gloves when handling the cat) '".
Feline infectious peritonitis Feline infectious peritonitis is a systemic viral illness caused by a coronavirus. It is particularly common in certain cat colonies. Systemic signs are varied (e.g. ascites, pleural effusion, hepatitis and uveitis). Skin signs are rare but should he looked for. They are associated with vasculitis caused by deposition of viral antigens in blood vessel walls, detectable by direct immunofluorescence. Skin lesions occur mostly on the face (Fig. 7 : 9), pinnae, neck and anus (Fig. 7 : 10) and are characterised by areas of oval or linear, well demarcated, nonpnuitic, non-painful, punched-out necrosis and ulcerations l2. Histopathological examination of early lesions, taken before the necrotic stage, reveals an interface hydropic dermatitis and a vasculitis 12. Definitive diagnosis is difficult hut is based on epidemiology, clinical signs and serum protein electrophoresis which reveals hyperproteinaemia with a marked increase in R and y fractions. Serological tests available are not very reliable. The prognosis is very bad as the condition is always fatal.
Papillomavirus infection Papillomaviruses infect epithelial cells and cause development of benign tumours or papillomas. In some circumstances, viral infection can cause malignant transformation of cells. Multiple, hyperplastic plaques, induced by a papillomavirus, have been seen in old Persian cats " and in other cats, one of which was FIV-positive ". These lesions, which are sometimes hyperpigmented, occur mainly on the trunk.Histopathology shows epidermal and follicular infundibular hyperplasia, dysplastic keratinocytes, koilocytosis and intracytoplasmic inclusion bodies '"". Electron microscopy reveals viral particles suggestive of papillomavirus 'I. Immunohistochemical studies have confinned the presence of papillomavirus antigen within lesions ". Papiilomaviruses also seem to be implicated in the development of multicentric squamous cell carcinoma in situ (Bowen's disease) 16. Immun~hi~tochemicalstudies using rabbit anti-bovine papillomavirus polyclonal antibodies have demonstrated the presence of papillomavirus antigens in 45% of cases of squamous cell carcinoma in situ 16. These are seen mostly in cats aged more than 10 years "20 and some of them have been reported to he FIV-positive (Figs 7 : 11,12)18,".Clinically, they are characterised by papules, nodules, and even hyperkeratotic and hyperpigmented plaques which can sometimes become
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7 : Vial dermatoses
Figure 7 :1 :Ulcerative lesions on the upper and lower lip of a cat with poxvirus infection
Figure 7 :2 :Ulcerative lesions on the tip of the tongue of a cat with poxvirus infection
Figure 7 : 3 : Ulcerative, circumscribed, confluent lesions on the abdomen of a cat withpoxvirus infection
:inophilic Photo 7 :4 :Impression smear - note intracytopias inclusion bodies (-+) in the keratinocytes (poxvirus infection) (Dlq Quik, x 1000)
Figure 7 :5 :Histopathology - note severe hydmpic degenerationof many keratinacyfes, and introcytoplasmic eosinophilic inclusion bodies in the keralinocytes(pm'minfection1 I fH&E.x2501 fcouffemof.? De~orcel
Pigure 7: 6 :Histopafhoiogy - note iwacytopiasmic e~sinoPhilicinclusion baiies inthe keratinoqtes (poxvirus infectio) ) (H & E, ~ 4 0 0(courtesy ) of F. Degorcel
Figure 7 : 7 . ......, athology - note lntracyfoplasrmceosmophlhc rnclusron bmiies m the cells of thefdlrcularouter mot sheath (poxv~rusmfaftronJ(H & E, x 400) (courtesy of F.Degorce)
Figure 7 :8 :Paralleleprpedic, mndndndgedvlralpartrcles wnh helrcal symmetq ~harocterrsh'cof orthopox viruses
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ulcerated. Lesion distribution is multicentric but involves mostly the face, shoulders and limbs The diagnosis is based on histopathological examination of lesions which reveals moderate to severe epidermal dysplasia with loss of polarity, variations in the association between nucleus and cytoplasm, variable mitotic figures, isolated dyskeratotic keratinocytes and an absence of rupture in the basement membrane 11-20
Retrovirus infections Retrovirus infections are the most serious and most common viral illnesses of the cat. They are caused by two retroviruses: the leukaemia virus (FeLV) and the feline immunodeficienc~virus (FIV) . . 22. Although human immunodeficiency virus (HIV) is responsible for many, varied skin proMems in man 'I, FeLV and FIV are much more rareiy associated with skin disease in cat;.
Skin diseases caused directly by FeLV virus A giant cell dermatosis has been reported in FeLV-positive cats. This is a pruritic dermatosis of the face (e.g. eyelids, area behind the ears, chin and lips), pinnae (ulcerative otitis), neck and sometimes trunk, characterised by alopecic, scaling and crusting lesions (Figs 7 : 13,14) ". Systemic signs (anorexia, lethargy, weight loss) were seen. The cats died or were euthanased within 4 months. Histopathology of skin hiopsies revealed syncytial-type giant cells in the epidermis and follicular outer root sheath. Some of these contained up to thirty nuclei and had abundant eosinophilic cytoplasm. In these areas, there was local absence of keratinocyte maturation along with dyskeratosis of keratinocytes, and sometimes of giant cells (Figs 7 : 15,16). Immunohistochemical studies ulhng gp70 antiserum demonstrated the presence of gp70 antigen in all cats, solely in the areas containing giant cells. Immunohistochemical studies from the skin of FeLV-positive cats without the giant cell dermatosis, did not demonstrate gp70 antigen in the skin. The FeLV virus may have induced a neoplastic alteration of the keratinocytes, by recombination with host oncogenes. The presence of many dyskeratotic keratinocytes is also a sign of neoplastic alteration 14.
Epidermal horns may also be seen in FeLV-positive cats 21,26. These homs, single or multicentric are found mainly on the footpads (Figs 7 : 17) and sometimes on the face. Histopathology reveals severe, compact orthokeratotic hyperkeratosis (Figs 7 : la), and in some cases, dyskeratosis and epidermal multinucleate giant cells. Treatment involves surgical excision. These homs resemble other keratinisation disorders such as acquired ichthyosis or Reiter's syndrome seen in human AIDS patients 13. These hyperproliferative dermatoses might be the consequence of the same pathophysiological mechanism. It is unknown whether stimulation of keratinocytes is caused directly by the virus or by cytokines released by monocytes or T lymphocytes infected by the HIV virns 23. Vasculitis associated with FeLV infecabn has recently been dmcribedn. It is characterised by severe necrosis (Fig. 17 : 19) of the p i i a e and tip of the tail (Fig. 7 :20). Systemic signs (e.g. pallor of the mucous membranes) may also be seen. Histopathology of pen-lesional skin biopsies reveals leucocytoclastic vasculitis and evidence of vascular thrombosis (Figs 7 : 21,22). Immnnohistochemistry using gp70 antibodies demonstrates the presence of the gp70 antigen in the skin and in many blwd vessels, both damaged and healthy. This suggests that the necrosis of the p i i a e and tail $ is probably due to an immnnecomplex vasculitis".
Dermatoses induced by B lymphocyte activation In feline retrovirus infections, humoral immune system derangement leads to B lymphocyte activation 2',22. This can sometimes cause plasma cell infiltration in the mouth (plasma cell stomatitis), footpads (plasma cell pododematitis) and the pinnae (plasma cell chondritis). It should, however, be noted that none of these skin and mucous membrane plasma cell proliferative lesions is related specifically to feline retrovirus infection. As a general rule, plasma cell infiltration should be treated as a chronic reaction pattern that may arise in response to various different antigens (bacteria, viruses, etc...)
Plasma cell stomatitis is characterised by painful proliferative lesions on the palatoglossal folds and arches. It causes anorexia, halitosis, excessive salivation and weight loss, often with associated gingivitis and stomatitis. These proliferative lesions have a tendency to ulcerate and
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Figure 7 :9 :Skin necrosis of theprefemporal region in a caf wifhfeline infectiousperitonitis
Figure 7 :10 :Same caf as infigure 7 :9 - note skin necrosis around anus and genifals
Figure 7 : 11 :Hyperkeratoticplaques on the malplanum of a cat with multicenfric squamous carcinoma in sihl (Bowen's disease) (courtesy of E. Bensignor)
Figure 7: 13 :Scalrngandcrushng on theface of a cat wth a giant cell demalos~sassociafed wrth FeLV mnfectmn (courfesy of D.W Scoftj
Figure 7 :15 :H~stopathology- nofe many apoptotic kerafinocyfes (+j (giant cell dermafosisj (H & E, x 250) (courfesy of D. W Scoff)
Figure 7 : 14 :Same cat as rnfgure 7 . 13 - nofe scalrng and crusting on the trunk (courtesy of D W Scott)
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L Raaical Ouide to Feline Dermatology
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bleed. In some studies, FIV infection has been found to be a predisposing factor (15.30% of cases were FIV-positi~e)'~.This was not true for FeLV infection (less than 6% of cases were FeLV-positive) ". Lesions are similar to those seen in plasma cell gingivitis in many HIV patients ''. Failure of the immunological barrier of the oral cavity may be induced by certain viruses (e.g. FIV and Calicivirus) and pathogenic periodontal bacteria (e.g. Porphyromonas spp.), often present in huge numbers in periodontal disease. This failure could explain some features of the pathophysiology of plasma cell stomatitis. It has recently been reported that odontoclastic resorptions were more common in FIV-positive cats 'O.
Plasma cell pododermatitis is rare " and usually starts with marked pain in one or more metacarpal or metatarsal footpads. These swollen footpads are soft and painful in the centre, causing lameness. With time, swellings, which ulcerate and bleed at the slightest touch, develop on one or more metacarpal or metatarsal footpads and/or digits (fig. 7 : 23). The older the lesions are, the more likely they are to develop secondary infection. Cats are sometimes affected systemically with pyrexia, listlessness, anorexia, anaemia and peripheral lymphadenopathy. Plasma cell stomatitis is sometimes also present. In one recent study of 18 cases of plasma cell pododermatitis, nearly 50% of cats were FIV-positive ' I . In another study, lesions of plasma cell pododermatitis were found in 6 out of 9 cats with natural FIV infection ll. FIV-immunoreactive cells have been found in the inflammatory infiltrate of a cat from which it was possible to take frozen sections. Plasma cell chondritis is extremely rare '""and is characterised by an often symmetrical, painful swelling of the pinnae, followed by reduction in size and healing (Fig. 7 : 24). In the initial phase, systemic signs (pyrexia etc ...) are seen. Some of these cases have been found to be FeLV or FIV-positive '>.j6.
When there is plasma cell infiltration, irrespective of where it occurs inthe body, biochemistry profiles often reveal hypergammaglobulinaemia. Histopathology initially reveals, an almost pure plasmacytic infiltration, with Russell bodies, followed later by a mixed cellular infiltrate (lymphocytes, neutrophils and eosinophils) ".
Opportunistic skin infections associated with T cell immunosuppression There are no studies proving the existence of opportunistic skin infections associated with FeLV and FIV 21~22. Only a few isolated cases of association between retroviruses and reputedly opportunistic infections in man have been published. However, some studies do attempt to show an association between certain clinical manifestations and status of one or other of the retroviruses ". The development of opportunistic skm infections is related to an already advanced cellular immunosuppression. The medical prognosis for a particular condition is no more severe in a cat with FIV and / or FeLV infection than in a cat without these infections, in that there are no signs of immunodeficiency connected with derangement of cell-mediated immunity '.
Mycoses make up the main group of opportunistic infections linked to FeLV or FIV (Table 7:l) Few studies on the fungal skin flora of cats carrying retroviruses have been conducted. It is universally true, however, that more fungi (genera and species) are carried by cats with a positive retroviral status The incidence of Microsporum canis carriage varies in different studies from 10% - 75%. These substantial differences arise because of the diverse nature of the populations tested 38~'9. No study has shown that superficial and deep (subcutaneous and systemic) mycoses (Table 7:l) are more common in retrovirus-positive cats. The very most that can be said is that they are clinically more severe and richer in fungal elements, and that they resolve more slowly or even incompletely. This applies even to superficial mycoses. Although a causal relationship between retroviral status and subcutaneous and systemic mycoses has not been proven, once these mycoses have been diagnosed, testing for retroviruses should he routine ". j8.
Multicentric bacterial paronychia is very common in retrovirus-positive cats, especially those that are FIV-positive Stained smears taken from the digital region show several species of intracellular and extracellular bacteria (cocci and bacilli). The prognosis is often guarded. j'.
Deep bacterial skin infections are regularly encountered in retrovirus-positive cats and are characterised clinically by multiple nodules or true deep abscesses with draining tracts. They can be found in various locations ". Histopathology points towards a particular aetiological grouping (Table 7:l). Identification of the causal bacteria is not always easy and often requires the help of specialist laboratories
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Pipure 7 : 17: Ep~dermalhorns on a metacarpalfoolpad of a cat lnfected with FeLV
Figure 7 : 18 :H~sfopathology- note e p ~ d mhyperplasra l andthzckness of the horny lager o f n cut with epidermal horns assoc~atedwrth FeLV rnfechon (H & E, x 100)
Figure 7 : 19 :Necrosis ~ t h the m pinnae o f a cat wrth FeLV-assoanted vascul~ns
Figure 7 :20 :Same cat as In figure 17.19 - note necmsls of the tip of the tail
Figure 7 :21 :H~stopathology- lemcytoclashc wscuhhs and j o f a large thrombus m a btood vessel of a cat w ~ t hFeLVassocmted vascuhhs (H & E, x 250)
Figure 7 :22 :Immunohistochemistry - notepresence of antigen gp70 within the vascular wall of damaged and healthy blood vessels of a cat with FeLV-associated vasculitis (AEC stain, x 250)
Figure 7 :23 : Swellrn~ . , footp~ pododermatitis and FIV ~nfection
Figure 7 : 24 :Pinnal swelling and scarring in a cat with plasma cell chondritis and FIV infection
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cat wrth plasma cell
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Parasitic dermatoses like notoed~ic'~ or demodectic mange", which are clinically very severe and usually involve large infestations, can be seen in retrovirus-positive cats (Table 7:l). Diagnosis by skin scraping is easy. The prognosis is very guarded especially for feline generalised demodicosis ".
Retrovirus I skin tumour relationship The relationship between retroviruses and tumours has been the focus of many studies 2',". Generally speaking, tumours associated with retrovhses seem to be mostly lymphoid tumours and, less
Table 7 : 1 : Oppomnistic skin infections seen in FeLV andlor FIV-positive cats MYCOSES3'-" 1 -Superficial mycoses - Geueralised dermatophytosis caused by Microsporum canis 2 . Deep mycoses - subcutaneous - Eumycetoma caused by Microsporum canis - Mucormycosis Rhizomucor spp., Mortierella spp. - Hyalohyphomycosis
Fusarium spp., Paecilomyces spp. - Phaeohyphomycosis
Alternoria spp, Bipoloris spp, Cladosporimn spp, Curvularia spp., Exophiala spp, Monilielia spp, Phialophora spp, Scolecobasidium spp and StemphyNium spp.
- Pythiosis
Pythiwn insidiosum 3 -Deep mycoses .systemic - Rhodotorula infection Rhodororula mucilaginosa - Cryptococcosis
Cryptococcus neoformans
- Histoplasmosis
Histoplasma capsulatum - Sporotrichosis
Sporothrix schenckii
BACTERIAL SKIN INFECTIONS "4 I - Bacterial paronychia 2 -Atypical mycobacterial infection
.Mycobacterium fortuitum
- Mycobacterium chelonae - Mycobacterium smegmatis
3 - Nocardiosis Nocardia asreroides 4 - Actinomycosis - Actinomyces spp. 5 - Botryomycosis Staphylococcus spp. -Streptococcus spp. - Pseudomonos spp. - Proreus spp. - Actinobacillus spp.
-
-
PARASITIC SKIN INFECTIONS "," 1- Notoedric mange
.Notoedres cati
2 - Demodicosis Demodex cari - Demodex garoi
-
commonly, myeloid turnours, carcinomas and sarcomas. However, no prospective study has been conducted to investigatean associationbetween retroviruses and cutaneous lymphomas in cats, which otherwise are rare. Multicentic squamous cell carcinoma in situ (Bowen's disease) has been reported in FN-positive cats This seropositive state might help reinfo~ethe local immunodeficiencywhich allows Demodex cati to multiply locally within tumours lo.
-
www.vet4arab.co.cc 7 : Viral dermatoses
ue 7 :25: Ulcemtivefacial lesions in a cat with herpesvim dermatitis (courtesy 0fD.W. Smtt)
Figure 7 : 26: Hisfapathology - note intronuclearinclusion bodies in the keratimytes (+) (herpesvirus dermatitis) (H & $ x 250)
Pigwe 7:27: Hisfdpathology- note inlranuclear inclusion bodies in the kerarinocyres (herpesvirus dermatitis) (H & E, x 250)
Figure 7 : 28 :Histopathology - note markedfollicular necmsis (herpesvirur dermatitis)(H & E, x 250)
Figure 7 :29 :Erosive lesions of the tongue andpalate of a cat with herpesvirus-associatederythema multiforme (courtesy of B.A. Atlee)
Figure 7 :30 :Erythematous, emsiue, facial lesions in a cat suspected of having herpesvirus-associated erythema multiforme
Figure 7 :31 :Same cat as infigure 7 :30 - e ind ulcerative lesions of the face and neck of a cat with herpesvirus-associated erythema multiforme
Figure 7 :32 :Same cat as in Figures 7 :30,31 - erythematous, scaling and crusting lesions on the trunk of a cat suspected of having herpesvirus-associated erythema muitiforme
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Herpesvirus infections Dermatological manifestations of herpesvirus infections (feline herpesvirus 1) have long been described in the cat. Signs are chmcterised by a facial and nasal dermatitis (Fig. 7 : 25) involving vesicles, ulcers and crusts, and stomatitis #.Histopathological examination of biopsies reveals necrotic, ulcerative and crusting lesions, along with a mainly eosinophilic dermal infiltration and intranuclear amphophilic inclusion bodies in keratinocytes and follicular outer root sheath epithelial cells (Figs 7 : 26-28). The nuclei of these cells exhibit margination of chromatin and the cytoplasm assumes a foamy appearance. Oral lesions are identical but with some degree of hyperplasia. Ultrastructural examination has enabled the isolation of viral nucleocapsids (100-125 nm) compatible with a herpesvirus. Amplification PCR techniques have documented the existence of herpesvirus I within lesions *. A dermatosis compatible with herpesvirus-associatederythema multiforme has recently been reported in the cat a. Skin signs appeared 10 days after the classic signs of a herpesvirus infection (respiratory signs and conjunctivitis) and involved a generalised erosive and exfoliative dermatosis (Figs 7 :29-32). Histopathological examination of biopsies revealed massive parakeratotic hyperkeratosis, isolated necrotic keratinocytes and lymphocytic satellitosis. The illness seemed to resolve favourably within a few weeks.
REFERENCES 1. Petit, E. RevueMid. Vit. 148,3-18 (1997). 2. Thomsett, L. R. in Current Veterinnq Therapy M (ed Kirk, R.W.) 605-606 (Saunders, Philadelphia, 1986). 3. Baxby, D. Vet. Rec. 104, 175 (1979). 4. Egberink, H. E J. Vet. Med. 33,237-24C (1986). 5. Nowohly, N. Wiener TierartzlicheMonatsschrifi 81,362-369 (1994). 6. Munz, E. and others J. Vet. Med. B 39,209-225 (1992). 7. Eondati, A. & Grivetto, V. Qund. Dermatol. 4,23-25 (1997). 8. Groux, D., Degorce-Rubiales,E 81 Capelli, I. -L. Prat. Mid. Chir Anim. Comp. 34.215-229 (1999). 9. Bennett, M. and others J. small Anim. Pract. 31, 167-173 (1990). 10. Bennett, M. and others Vet. Rec. 118, 387-390 (1986). 11. Bennett, M. and others J. small Anim. Pract. 26,653-661 (1985). 12. Scott, D. W., MillerJr, W. H. &Griffin, C. E. inMuller & Kirk's SmaNAnimlDermatology, 5"edition (Scott, D. W.,Griffin, C.E. &Miller, W.H.), 469483 (Saunder;, W B., Philadelphia, 1995). 13. Carney, H. C. I. Vet.Diagn.1nvest. 2,299 (1990). 14. Clark, E. G. Proc. AAVD-ACVD, San Diego 56-57 (1993). 15. Egberink, H. E Vet. Microbial. 31, 117-125 (1992). 16. Leclercq, S. M., Clark, E. G. & Haines, D. M. Proc. AAVD-ACVD, Nashville 125-126 (1997). 17. Rowland, P., Affolter, V., Suner, S. & Miller 11, W. H. Vet.Pathol. 29,440-444 (1992). 18. MillerJr, W H.,Affolter,V., Scott, D. W. & Suter, S. Vet. Dermatol. 3, 177-182 (1992). 19. Baer, K. E. & Helton-Rhodes, K. Vet. Pathology 30,535-543 (1993). 20. Guaguhre, E., Olivq, T., Delverdier-Poujade,A., DCnemlle, P., Paghs, 1.-P & Magnol, I. -P. Vet. Dermoial. 10, 61-67 (1999). 21. Hartmann, K. & Knft, W Revue Mid. Vit. 145, 191-197 (1994). 22. Hartmann, K. Vet.J. 155, 123-137 (1998). 23. Achten, G., A n d 6 I., Clumeck, N., De Maubeuge, I., Goens, I. &Parent, D. in EncyclopidieMidicaie et Chirurgicale 12680,AlO(Elsevier, Paris, 1989). 24. Gross,T. L., Clark,E. G., Hargis,A. M., Head, L. L. & Haines, D. M. Vet.Dermato1.4, 117-122 (1993). 25. Gross, T. L. Ihrke, P. I. & Walder, E. J. Veterinary Dermatopathology (Mosby Year Book, St Louis, 1992). 26. Scolt, D, W.J. Amer Anim. Hosp. Assn. 20,537-564 (1984). 27. Declercq, I., Maenhout, T. Vet. Dermatol. Personal communication (1999). 28. Kwowles, I. D., Gaskell, R. M, & Gaskell, C. I. Vet.Rec. 124,336-338 (1989). 29. White, S. D., Rozychuk, R. A. W. & Janik, T. A. J. Amer Vet.Med, Assn. 200, 1377-1380 (1992). 30. Hofmm-Lehmann, R., Berger, M., Sigrist, B., Schawalder,P. & Lutz, H. Vet. Immunol. Immunopathol. 65,299-308 (1998). 31. Guagubre, E., Hubert, B. &Delabre, C. Vet.Dermato1. 3, 1-12 (1992). 32. Guagukre, E. & PrClaud, P. Personal communication (1999). 33. Simon, M. and others Vet. Pathol. 30,477 (1993). 34. Scott, D. W. J. Amer Anim. Hosp. Assn. 23,255-274 (1987). 35. Bunge, M. M. J Amer. Anim. Hosp. Assn. 28,203-206 (1992). 36. Guaguhre, E. Prat. Mid. Chir Anim. Comp. 27,557-563 (1992). 37. Shaw, S. E., Robertson, I. D., Robinson, W. E, Alexander, R. & Sutherland, R. 1. Aust. Vet. Pract. 20, 194-198 (1990). 38. Sierra, P. Flare fongique et ritrovirosesfdines - risultats dune enqugte mycologique (Thbe de doctorat vCtCrinaire, Maisons-Alfort, 1997).
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39. Mancianti, E, Gianelli, C., Bendinelli, M. & Poli, A. J Vet. Mud. Mycol. 30,257-259 (1992). 40. Greene, C. E. Infectious Diseases of the Dog and Cat (Saunders, Phyladelphia, 1998). 41. Bourdeau, P., Hubert, B. & Magnol, J. -P. Rec. Mid. VI/. 168,91-96 (1992). 42. Guagukre, E.Prat. Mid. Chir. Anim. Comp. 28,211-223 (1993). 43. Guagukre, E. Prat. Mid. Chir. Anim. Comp. 28,31-36 (1993). 44. Hagis,A. M., Gim, P. E., Mansell, J. E. K. L. & Caber, R. L. Vet. Dermatol. 10,267-274 (1999) 45. Olivry, T. Personal communication (1999).
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The cat flea: applied biology Cats and their environment are frequently infested with fleas, and eradication of these fleas can be a long and onerous task. Fleas are a major nuisance because they cause or transmit various illnesses to man and his pet animals. The species most frequently incriminated is Ctenocephalides felis felis, the cat flea. Numerous advances relating to the biology and control of cat fleas have been made over the last ten years.
Medical and veterinary importance Ctenocephalides felis is responsible for the transmission of murine typhus. This illness is transmitted via contamination of a wound, by faeces or crushed particles of parasites infected by a rickettsia, Rickettsia typhi. It is not h-ansmitted by bites. It is characterised clinically by headaches, shivering and skin eruptions, and, less frequently, by effects on the kidneys or the central nervous system '. Murine typhus affects humans and many small mammal species, particularly rats and mice. It is endemic throughout the world, but seems more frequent in South America (Argentina, Brazil, Chile, Columbia) which has a thud of the cases reported world-wide. Traditionally, the causative vector is the oriental rat flea, Xenopsylla cheopis. However, Ctenocephalides felis seems to be equally implicated. Typhus is observed in the United States along the coasts of the south-east, the south-west and the Gulf of Mexico. In southern California, it seems that transmission occurs via opossums and cat fleas 2. Ctenocephalidesfelis has recently been cited as the cause of transmission between cats of Bartonella henselae, the bacterium responsible for cat scratch disease in humans ). Immunocompetent patients with cat scratch disease have painful lymph nodes and a fever that resolve with appropriate antibiotics. Immunosuppressed patients can present with serious complications (e.g. bacillary angiomatosis), which can be fatal. Over and above its role in the transmission of viral and bacterial disease, Ctenocephalides felis is the cause of severe nuisance and dermatitis in humans and in animals. Flea allergy dermatitis (FAD) is an immunological disease in which hypersensitivity states are produced, following injection of antigens present in flea salivary glands. This ubiquitous disease is the most common dermatosis in cats and one of the major causes of selfinduced symmetrical alopecia and miliary dermatitis '. A similar dermatosis, papular urticaria, is frequently seen in humans. Fleas are haematophagous insects responsible for anaemia in major infestations, especially in young animals. This has been reported in dogs, cattle, goats and sheep, but also in cats I. Sometimes severe blood loss can lead to death. Cat fleas can also transmit some intestinal parasites. Dipylidium caninum is one of the most common intestinal helmintbs of dogs, cats, and rarely children. It develops as an immature form (cysticercoid) in the fleas of cats, dogs and humans. The flea larvae ingest the eggs which develop into cysticercoids in the body of the flea. When grooming, dogs and cats can swallow the infested fleas and the cysticercoids are then released.
Species of flea encountered
.,.
Although many species of flea have been reported in cats, only Ctenocephalides felis felis (Fig. 8 : I), Ctenocephahdes canis, P u l a irritans and Echzdnophaga gallinacea " are seen in sufficient numbers to be
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considered important parasites. Cats in the United States are infested mainly with Ctenocephalides felis '". Van'ous studies canied out in Europe: also show Ctenocephalidesfelis to be the species most frequently found in cats.
Reproduction and host associations Adult Ctenocephalidesfelis begin to feed almost as soon as they are on their host. Droppings are observed 8 to 9 minutes after the staa of the blood meal lo.Since feeding begins so quickly, currently available insecticides cannot kill all the fleas before they have started to feed. Products with insect repellent properties can, nevertheless, reduce the size of the blood meal. Newly emerged, unfed males and females are similar in size. Once feeding begins, size differences quickly become apparent (Fig. 8 : 2). The volume of blood ingested by males is unknown, but female Ctenocephalides felis can take up 13.6 pl of blood per day ". After rapidly passing through the digestive tract, the blood is excreted and dries within a few minutes to fonn blackish droppings or characteristic long tubular spirals (Fig. 8 : 3). Droppings dispersed in the environment become an essential food item for the larvae. Reducing the amount of faeces in the environment could reduce future flea populations. This can be achieved by washing of vacuuming the areas where the animals spend most of their time, in piuticular their sleeping and resting places. Consumption of blood is necessary for the reproduction of Ctenocephalidesfelis. Copulation takes place after the fleas have fed and egg laying s t a s 24 to 48 hours after the fmt blood meal (Fig. 8 : 4) '2,'3. Females stay on their host and lay their eggs in the fur; the eggs then fall off into the environment. As reproduction is closely l i e d to the host, the flea's life cycle can be interrupted at host level. To achieve this, treatment must prevent reproduction of the fleas by using an adulticide with residual activity. Fleas are then killed within 24 to 36 hours, before they can reproduce. Reproduction can also be stopped or diminished by the administration of systemic or topical insect growth regulators. If reproduction is not interrupted, the females produce 40 to 50 eggs per day at maximum lay rate, averaging 27 eggs per day over 50 days, and can lay for over 100 days 14. The maximum lay rate occurs during the eight last hours of the scotopbase 'I.
The host's grooming activity significantly reduces this reproductive potential. Substantialreduction in egg laying and longevity - . of adults is observed when fleas are placed on cats living in metabolic cages with no restriction on host grooming ",16. In addition, fleas feeding on allergic cats lay few& eggs than flea; feeding on non-allergic cats". Allergic cats can take in and eliminate up to 25% of their fleas per day, through ingestion and permanent scratching. Hence, a cat with FAD may present to the vet with few, or even no fleas at all in its coat.
Stages in the environment Ctenocephalidesfelis eggs are pearly-white, ovoid with rounded ends, and 0.5 mm long (Fig. 8 : 5). The eggs fall from the fur and accumulate in areas where the animals spend most of their time, in particular the sleeping and resting areas 18. Regular cleaning of these areas can si@~cantly reduce the number of fleas by removing the eggs and immature stages.
The eggs generally hatch within 1 to 6 days, depending on the temperature and relative humidity (RH) (Fig. 8 : 6). Around 70% of eggs hatch at 16°C and 70% RH, with the success rate rising up to 92% RH IP. Nearly all the eggs hatch when the RH is greater than 50% at 27°C. However, at 37', only 40% of eggs hatch when RH is 75%.
Larvae Larvae develop in sheltered microhabitats with a moderate temperature, high RH, and an available source of faecal blood (Fig. 8 : 7). The duration and success of development depends on the temperature and humidity. The larval stage generally lasts 5 to 11 days but can last 3 weeks depending on the presence of food and the environmental conditions 19. Consequently, when environmental
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Figure 8 :4 :Crenocephalidesfells laying eggs on a cat: numerous eggs are produced m 20 mulures
Figure 8 :3 :Several female Cknm rite subsranrial aniourlt ojfaeces emitted
F~gure8 5 Ctenocephalld and smooth
24 hours afer hatching) and hatching)
uu
loid appear ance,pearly-white
third stag; larva-(w) (5 days after
Figure 8 :6 :Fii 11 r t q r lawn newly emerged from the egg
Figure 8 : 8 :( sur&unded by debris
:s felis cocoon: note the silky fibres
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A PracM Guide m Elk h a t o l o g y
conditions are optimal, flea populations can grow rapidly within a fortnight. Larvae are very sensitive to desiccation. Exposure to RH of less than 33% is fatal. Larvae are capable of resisting a temperature of 27OC if the RH is greater than 50% ".At 50, 55 and 65% RH, the percentage of surviving larvae capable of developing, increases (24,77 and 91% respectively) As humidity is a critical factor for larval survival, the areas where RH is high must be monitored carefully. Survival and development of fleas is more hazardous out of doors than indoors. Less than 60% of larvae survive at a temperature of 35°C ". They do not develop in areas exposed to sunlight and only survive out of doors if RH is higher than 50% for several consecutive days, or in microhabitats with elevated RH 2 ' . Areas outside which are favourable for the development of Ctenocephalidesfelis are characterised by RH higher than 50% and a temperature of between 4 and 35°C '. The areas showing maximum larval development are near to sleeping and resting places. W.A. Osbrink (personal communication, 1993) observed that less than 15% of larvae placed in a carpet moved more than 20 centimetres before pupation. These data are in accord with previous observations which show that the first stages of development do not move far from the point of hatching The dispersion of immature stages is principally linked to the behaviour of the host. Larvae show positive geotropism and negative phototropism, resulting in development at the base of carpet fibres, under furniture and around skirting boards 18. Out of doors, larval activity is restricted to the upper few millimetres of the soil U. Flea larvae are protected from most of the adult insecticides applied indoors, probably because they develop at the base of carpet fibres where the treatment cannot reach them.
Pupae Following a short pre-pupal period, the larva matures into a pupa, usually within a silk cocoon. The cocoon is ovoid, around 0.5 mm long and whitish (Fig. 8 : 8). The silk fibres are sticky and soon surrounded by debris from the environment. Cocoons can be found in soil, in vegetation, in carpets, under furniture and in the animals' sleeping areas. Larvae which have been disturbed are able to come out of their cocoon and spin a second one or develop as naked pupae 23.". Studies on the formation of cocoons by Cterlocephalidesfelis larvae show that the larvae need to align themselves along a vertical surface to spin a cocoon successfully ". Less than 3% of larvae are able to spin a cocoon at 28°C and 80% RH in an environment without any vertical objects. However, more than 95% of these larvae develop successfully as naked pupae, showing that the cocoon is not essential for pupation or for moving to the adult stage. The pupal stage can last from 6-7 days to several weeks. The pupal stage is the most resistant immature stage to desiccation, with around 80% of pupae emerging as adults at 27'C and 2% RH ". At 24.4"C and 78% RH, adult Ctenocephalidesfelis begin to emerge 8 days after the start of pupation and all the fleas will have emerged within13 days The cocoon does not present a barrier to insecticides 25. The survival of pnpae in houses treated by insecticides is not due to the protection conferred by the cocoon but due to a lack of penetration of the insecticide into carpets. In the wild. the primary function of the cocoon could be to prevent predation by various arthropods ".
Pre-emerged adults in the cocoon Adult Ctenocephalides felis can stay quiescent in the cocoon for 140 days at ll°C and 75% RH ''. When eggs are laid in the autumn, the emergence of adult fleas can he delayed for 20 to 30 weeks 27"8. The ability to survive in the cocoon for prolonged periods of time is very important for a species like Ctenocephalides felis, with hosts that are often mobile. Emergence from cocoons is favoured by an increase in temperature and mechanical factors. Ctenocephalidesfelis can complete its development and emerge in a minimum of 13 days and a maximum of 300 days, depending on temperature and environmental stimuli. Nevertheless, in most cases, Ctenocephalidesfelis completes its development and emerges within 3 to 5 weeks. It is common to see adult fleas reappear, several days after treating carpets with aerosols or sprays. Fleas can continue to emerge from their cocoons for 4-6 weeks after an insecticide and insect growth regulator has been applied to the environment. This resurgence is attributed to pupae and pre-emerged adults beine nresent in their cocoons at the time of treatment. Vacuuming stimulates the emergence of adult fleas and decreases the period of infestation in as much as some newly-emerged fleas are eliminated by the vacuum cleaner.
www.vet4arab.co.cc 8 : The cat flea: applied biology
Search for a host by the adult Adult Ctenocephalidesfelis rely onvisual and thermal stimuli to find their host 19. Certain factors such as age of the flea and the level of C02 modify their ability. Ctenocephalidesfelis is more sensitive to light rays of wavelengths between 510 and 550 nm (green light) than to light of wavelengths between 650 and 700 nm '03'. A yellow-green filter of 515 nm wavelength is twice as attractive to adult Ctenocephalidesfelis than white light ". The responsiveness of fleas to light rays explains why fleas are found in large numbers in passage ways, at the entrance to dog kennels, and by doors and windows. This response to light is the reason behind the use of light traps to capture fleas. Although Ctenocephalidesfelis orientate themselves and move spontaneously towards a light source, this tropism is notably increased when the light source stops suddenly and temporarily. In one report, an intermittent light trap allowed collection, within 20 hours, of 77% and 57% of fleas released at 4.1 and 8.5 metres respectively from the trap ". The short interruption of light produced by the trap could be mimicking the shape of a host moving around, the trigger for the jumping reflex, In addition to visual stimuli, thermal stimuli are extremely important in acquiring a host 29. In a given area, adult fleas make clear distinctions between heated targets and those maintained at ambient temperature. Positive phototropism and also negative geotropism, improve the chances of success in host acquisition. Newly emerged fleas move towards the surface of carpets, rugs or vegetation where they are more likely to encounter a host. They can survive for several days before taking a blood meal. Their survival is strongly correlated to ambient temperahlre and humidity. In air with saturated humidity, 62% of adult Ctenocephalidesfelis can survive for 62 days, whereas, in a cold and dry environment, only 10% of fleas survive for 20 days 2'. At 22.5"C and 60% RH, only 5% of Ctenocephalidesfelis survive for 12 days '.
Alternative hosts The reappearance of fleas, several weeks ormany months after qnmnt eradication of an infestation Is aproblem regularly enmuniered by owners who treat their infested animals. The prolonged survival of preemergedadults &the lack of penetration of insecticides into carpets may explain many of the reinfestations that occur within several weeks to W h s after the treatment. Neve&elm, other explmatiom are necessary to mount for the annual reappearance of infestations in tempera climates. Although ceftain species of fiea pass theii winter months as pupae or adults off their host, no stage of Ctenoeephalidesfelis can survive for 10 days at 3 O C or for 5 days at -l°C. h u a l recurrencemay be connected with the large variety ofhose of Ctenacephalidesfelis. Thisflea can be harboured by many wild mammals: coyote, folt, polecar, various rodents, coypu, opossum and ferretJ. These alternative hosts,some of which live in close proxunity to man and his pet anunals, can be permanent # o m of re-infestation. Elimination of certain wild mammal species in urban areas may reduce the number of repeated infestations of Ctenocephnlidesfelis.
Conclusions The eggs and larvae of the cat flea cannot swive major climatic variations, particularly in temperature and humidity. Hence, areas suitable for the development of Ctenocephalides felis are generally limited. In most households, only a small proportion of eggs develop into adults. Flea populations survive due to a high reproductive capacity, the large range of hosts available and because of the strong association between the flea, the host and its restingareas. A large percentage of immature stages can survive, if temperature, relative humidity and l S a l food reserves are optimal. In these conditions, an explosion in flea populations can be observed to the detriment of man and his pet animals.
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REFERENCES I. Azad, A. E AnnunlRwiovs ofEntomology 35,53-569 (1990). 2.Adams, W H.,Emmons, R. W. &Bmoks, 1. E. h e r . J. Tmp. Med. Hyg. 19,311-318 (1970). 3. Foil, L.,Andress, E., Freeland,R. L., and others J Med. Entomol. 35,625-628(1998). 4. Halliwell, R. E. W. Camp. Conr. Educ. Pract. Vet. 1,367-371 (1979). 5. Dryden, M. W. & Rust, M. K. Vet. Parasitol. 52,I-19 (1994). 6.Amin, 0.M. J. Med. Entomol. 13, 179-192 (1976). 7. H m a n , D. A,, Halliwell, R. E. W. & Greiner, E. C.Vet. Parasitol. 23,135-140 (1987). 8. DTyden, M. W.Evaluation of certain parameters in the bionomics of Ctenocephalidesfelisfelis (Bouchd 1835) (MS. Thesis, M u e University, W. Lafayette, Indiana, 1988). 9. Painter, H. I? & Echerlin, R. I? Krginia J Sci. 36, 114 (1985). 10. Dryden, M. W. Blood c o m q t i o n andfeeding behavior of the catflea, ~tenocephnlidesfelis felis (Bouchi 1835) (PhD dissertation, M u e University, West Lafayette, Indiana, 1990). 11. Dryden, M. W. & Gaafar, S. M. J Med Entomol. 29,394-400 (1991). 12. Hudson, B. W. & Rince, EM. Bulletin of rhe WorldHealth Orpizarion 19,1126-1129 (1958). 13.Aldn,D. E. Relationship between feeding and reproduction in the cat flea, Crenocephalidesfelis (Bouchd) (MS. Thesis, University of Florida, Gainesville, Florida, 1984). 14. Ihyden, M. W. Vet. Parasitol. 34, 117-122(1989). 15. Rust, M. K. J Med. Entoml. 29,242-245 (1992). 1 16. Osbrink,W. L. A. & Rust, M. K. J.Med. Entomol. 21,727-731 (1984). 17. McDonald, B. J., Foil, C. S. & Foil, L. D. Vet. Dermtol. 9,75-79 (1998). 18. Bymn, D. W. Aspects of the biology, behavior, bionomics, andcontml ofimmature stages of the catflea Crenocephalidesfelis felis (Bouchi) in the domiciliary environment (Ph. D. Dissertation,V i a PolytechnicInstiNte and State University, Blacksburg, Virginia, 1987). 19. S i l v e r n , J. &Rust,M.K. JMed.Entomo1. 18,78-83 (1981). 20. Bruce, W. N.Annals ofthe Entomological Society ofAmerica 41,346-352 (1948). 21. Silverman, J. &Rust, M. K. Envimn. Entomol. 12,490495 (1983). 22. Kern W. H., Jr Pest Management 10,20-22 (1991). 23. Silverman,J. &Rust, M. K. Annals of the Entomological Society ofAmerica 78,763-768 (1985). 24. Dryden, M. W. &Smith, V. J Med. Entomol. 31,272-277 (1994). 25. Dryden, M. W. & Reid, B. J Econ. Entomol. 89,421427 (1996). 26. S i l v e r n , J. & Appel, A. G. Proc. Entomol. Soc. Washington 86,660-663(1984). 27. Olsen, A. AnnualReport (Danish Infestation Laboratory, Lyngby, Denm* 1990). 28. Metzger, M. E. &Rust, M. K. J Med. Entomol. 34, 173-178 (1997). 29. Osbrink, W. L. A. &Rust, M. K. Annals of the EntomologicalSociety ofAmerica 78,29-34 (1985). 30. Cmm,G. E., Knapp, E W. & White, G. M. J Med. Entomol. 11,88-94 (1974). 31. Dryden, M. W. &Broce, A. B. J. Med. Entomol. 30,901-906(1993).
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M. W. Vroom
1 Flea allergy dermatitis Flea allergy dermatitis (FAD) is the most common pruritic dermatosis in the cat." A diagnosis of FAD cannot be eliminated by the absence of fleas or flea faeces because allergic cats can remove fleas from their coat by grooming. FAD should be suspected when self-induced, principally dorsolumbar, alopecia, miliary dermatitis or, more rarely, eosinophilic plaques or linear granulomas are present. Allergy testing has little diagnostic value. Treatment initially involves rigorous flea control for the affected cat, in-contact animals and the environment. When antipmritic treatment is necessary, the use of corticosteroids produces immediate improvement. Innnunotherapy is, currently, of no benefit.
Aetiopathogenesis Numerous studies on the immunopathogenesis of FAD have been publisbedin the guinea-pig, man and the dog, but it is difficult to extrapolate these to the cat. Saliva from the flea Ctenocephalidesfelis felis contains numerl could be a major ous allergenic proteins, one of which, a high molecular weight protein, d e s i p a t e d ~ f e 1, allergen in the dog '.In the dog, FAD is due to an immediate type 1 hypersensitivity reaction with a late-phase reaction and a delayed cutaneous basophii hypersensitivity reaction. In the cat, the immunopathogenic mechanisms of FAD are still unknown. Some authors report only immediate intrademal reactions whereas others also mention delayed reactions 45,6.
Clinical features FAD is seen in cats of every age, sex and breed
' ~ 7 ~ 8 . 9 . ' o . It can be seasonal or non-seasonal depending on the geographical region. Signs are often the result of cutaneous self-trauma and generally involve the caudal half of the body (hack and caudomedial thighs) (Figs 9 : 1,2). Pruritus is constant and sometimes even severe. The clinical picture is variable, involving,symmetrical alopecia, broken hairs (Figs 9 : 3,4), scaling, papules, little crusts which feel'diary to the touch, or crusts of a hue miliarydermatitis (Figs 9 : 5-7). More rarely, FAD presents as eosinophilic plaques (Figs 9 : 8,9), linear granulomas (Fig. 9 : 10) or facial pruritus. Unlike in the dog, the cat with FAD rarely presents with secondary bacterial infections. As cats tend to groom themselves very thoroughly, it is often difficult to demonstrate fleas or flea faeces. Owners sometimes describe weight loss and restlessness in affected animals ".
Diagnosis History Historical factors, suggestive of FAD, are of the utmost importance in both establishing a diagnosis and instituting treatment.
Thepresence of in-contact dogs or cats in the environment is an impo&idement of the diagnosis and, as infestation in the cat is often inapparent, these animals may help permanently maintain the flea population. An in-contact cat, even if treated for fleas, constitutes an important risk factor for recurrence l2 The seasons offlea development are very variable, depending on geographical region and environmental conditions. Peaks may occur between March and October. However, increased pruritus in winter does not rule out FAD and may be due to a rise in ambient temperature of the habitat ').
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In massive infestations involving contamination of the environment with immature stages, cat owners may be bitten by young adult fleas emerging from their cocoons in search of a host ". Papular lesions are seen, particularly on the limbs, ankles, trunk, waist and even the m s " (Figs 9 : 11-13). Pruritus can vary signijicantly from one place to another depending on the population density of fleas present in the environment. Corticosteroid responsiveness is a feature of all inflammatory dermatoses. FAD is initially responsive to corticosteroids although this becomes less marked with time. Response to insecticidal treahnent must be noted precisely. A definite response is an important part of the history. If response is partial or non-existent, the possible reasons for treatment failure must be investigated: underdosing, lack of treatment of the environment or in-contact animals I*.
Clinical examination FAD should be considered before any other pruritic dermatosis when a cat is presented with miliary dermatitis, self-induced alopecia or certain types of eosinophilic granuloma complex (principally eosinophilic plaques). A full allergy differential diagnosis, must of course be constructed.
Demonstration of fleas Demonstration of fleas or their faeces is difficult, sometimes impossible. Cats with flea bite allergy nibble and lick themselves more than other cats, effectively removing fleas from their bodies. The search for adult fleas is usually canied out in the perineal and inguinal regions and under the c h i 16. Even thorough inspection is often unrewarding but using a flea comb can help considerably. Combing for a few minutes after applying an insecticidal spray is probably the best way of demonstrating adult fleas. If neither adult fleas nor eggs can be found, it may be possible to demonstrate flea faeces. These small. pieces of debris are reddish brown and shaped like commas or fragments of plates (Fig. 9 : 14). After careful combing, the collected faecal droppings are placed on a damp piece of blotting paper. The droppings are made up of haemoglobm crystals which readily dissolve to form reddish brown stains. Flea faeces can be examined under the microscope to reveal their characteristic shape and colour (Fig. 9 : 15). This can convince the owners that their pet really does have fleas and also that flea droppings are nice to look at! This search only proves worthwhile in relatively massive infestations or in a cat which grooms inadequately (e.g. when animal is tired, depressed, obese...). The most obvious sign of a heavy environmental burden of young adult fleas is human infestation with "carpet fleas" i.e. young adult fleas, recently emerged from their cocoons. Eventually, eggs and larvae can also be seen on the animals' bedding. Segments of Dipylidium caninum around the anus or even in the environment, are a sign of infestation by Ctenocephalides felis felis ',".
Differential diagnosis The differential diagnosis of FAD includes all pruritic dermatoses: allergic skin disorders (food intolerance, atovic dermatitis), infestation with Otodectes cynotis, Chqletiella blakei or lice, Felicola subrosfratus and ~ino~nathus'setosus, and also pruritus associated with behavioural disorders. Sometimes, diagnosis is made difficult by the possible association of FAD with one of these other dermatoses ' . ' . 5 , 6 . Histopathological examination of skin biopsies is of no major benefit, revealing only an inflammatory dermatosis with variable eosinophilia. Blood eosinophilia and anaemia are sometimes reported.
Allergy testing Diagnosis of FAD by intradermal testing has been at the heart of the veterinary fascination with allergy and dermatology and yet paradoxically, the poor reliability of this procedure, especially in the cat, has actually discouraged many practitioners.
Allergenic extracts of Ctenocephalides felis felis Whole body extracts of Ctenocephalidesfelisfelis, obtained by grinding up fleas and extracting the protein, are used in both diagnosis and immunotherapy. They contain a mixture of proteins of various molecular weights. Studies looking at whole body extracts and salivary gland extracts separated into fractions onto polyacrylamide gel have revealed about 15 fractions of 14-150 kD 18-'2. The composition of whole body extracts, and therefore antigenicity, is variable which poses problems of repro-
www.vet4arab.co.cc 9 : Flea allergy dermatitis
R i p 9 :1 :Self-induceddDrsolumbaralopecia in a Persian cat with FAD
Figure9 :2 :Self-induceddorsolwnbar alopecia iliaiii papules arepresent
Figure9 :3: Self-induced alopecia invoivingflonks, abdomen and iateroi rliiglis
igure 9 croscoplc examination broken hairs (x 100)
Figure 9 :.
Figure 9 :6 :Same cat as in figure 9 :5 - lots of crusts ondj are present
~ollm~barmiliary der-maritis
Figure 9 :7: Cervical miliary dermatitis in cat with FAD -papules, lots of crusts andself-induced lesions are presenr (courtesy of D.N. Carlotti)
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ducibility in both diagnosis and treatment =,-. Some Ctenocephalidesfelis felis antigen fractions have now been produced by genetic engineering 19,22. These reagents may allow development of better diagnostic tools offering.enhanced reproducibility, especiallyin vitro but also in ~ivo-"'~.
Intradennal testing Intradermal testing kits contain non-standardised whole body extracts of Ctenocephalides felis felis, ready to use at a concentration of 0.1% WN. The protocol for using flea extract is exactly the same as for the aeroallergens. Reactions are read at 15-20 minutes and 48 hours after administration. At 20 minutes, any clearly erythematous reaction with a diameter greater than the average of the positive (histamine) and negative (diluent) controls is considered positive (Fig. 9 : 16). If the reaction around the injection site of the flea extract is "negative" at 20 minutes, it is re-examined at 48 hours. At that time, the presence of just a palpable swelliig can be interpreted as a positive result. In practice, intradermal testing in the cat is often hard, even impossible, to interpret. Furthermore, in the absence of studies comparing normal animals with those with FAD, the diagnostic value of this test is unknown. Most reactions are seen at 20 minutes, those at 48 hours seem much rarer ".
Laboratory tests No serological test has to date been validated for use in the cat I. With regard to FAD diagnosis, two appro ache^ are promising: the in vitro hasophil degranulation test and serological tests using an alpha recombinant chain of the human FceRI receptor. However, the incidence of sensitisation in normal cats is so great that the positive predictive value of this test is very poor ". Allergy testing in the cat is, therefore, very unrewarding. A positive allergy test does not confirm FAD. Equally, a negative test does not rule it out 6.
Treatment Treatment is based mostly on flea control for the affected cat, in-contact animals and the environment. Efficacy relies on the owner having a good understanding of the flea control programme. The life cycle and flea habits must he carefully explained to the owner along with the circumstances in which FAD appears (i.e. injection of flea saliva into the skin). Antipruritic treatment is often necessary to give immediate relief to the cat (and the owners!). It may be needed for long periods in cats which have marked pruritus despite well-conducted flea control.
Short-acting corticosteroids (prednisone, prednisolone or dexamethasone) can be given at usual anti-inflammatory doses. They produce few side-effects when given over a short period. Cats with severe pruritus must be treated with dexamethasone, often more effective but associated with more rapid onset of side-effects. When pruritus has sufficiently subsided, prednisone or prednisolone should again be prescribed at a dose of 0.25-0,5 mg/kg BID. For prolonged use, oral, alternate-day, corticosteroid therapy, is preferable to parenteral administration, despite being harder to administer to some cats. Antihistamines are sometimes useful. Chlorpheniramine (0.5-1 mgkg BID) and hydroxyzine (2 mgkg BID) are most commonly used in the cat. Several weeks treatment may be needed to achieve a satisfactory response and the concomitant use of corticosteroids during the first few weeks is therefore desirable ". Syntheticprogestagens (e.g. megoestrol acetate) are no longer in vogue given their severe side-effects: pyometra, diabetes mellitus, gynecomastia, mammary hyperplasia or adenocarcinoma, polyuria and polydipsia, ohesity, behavioural changes and increased arterial pressure. Zmmunotherapy using whole body extracts of Ctenocephalides felis felis is not effective la. This could be due largely to the poor allergenic quality of whole body extracts. Trials with purif~edfractions or recombinant antigens could, in future, offer new treatment opportunities.
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9 :Flea allergy dermatitis
Figure 9 :9 :Entcmtve eosinophilicplaquer in a cat wrth FAD
Figure 9 : 10: Linear gronrrlomn in a cot wrth FAD
Figure 9 :11 :Ctenocephalides felis felis biting a man
Figure9 :12 :Hypersensitivity to the bites of Ctenocephalides felis felis on a lady's legs - many papules are present (courtesy ofR:Rzeznik)
..., .,the
PigtueB :13: Hypersens~.
bites of Ctenocephalides fehs fells
on the nrms of a child - marry papule ate present (courtesy of R
Figure 9 :14 :Flea faeces on a PeAra..
.-...rth FAD
Rrezruk)
Figure 9 :15 :Mrcrarcoplc appearance offleofaeces
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) : 16 :I n t r a ~ reactions to whole body extracts , ~ ~ n o c e ~ h a l ifelis d e sfelis. Note the similar sire of thepositivereactionat20
F
minutes (erythemafourpapule, P) and the positive conml (hismine,Hi
iRaaid Guide to Peline Dermamlogy
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REFERENCES 1. Scott, D. W. Miller Jr, W. H. & Griffin, C. E. Muller & Kirk's SmaNAnimal Dermatology, 5th edition (Saunders, W.B., Philadelphia, 1995). 2. Willemse, T., Vmom, M., Mol, I. & Rijnberk, A. Amer. J. Vet. Res. 54,69-72 (1993). 3. McCall, C., Hunter, S., McDemott, M., Stedman, K., Weber, E. & Wassom, D.Proc. ESVD-ECVD, Maastricht 156 (1998). 4. Halliwell, R. E. W. & Goman, N. T. Veterinary Clinical Immunology (Saunders, W.B., Philadelphia, 1989). 5. Sousa, C. Vet. Clin.N.Amer 25,814-831 (1995). 6. Lewis, D. T., Ginn, l? E. & Kunkle, G. A. Vet. Dermatol. 10,29-37 (1999). 7. Prilaud, P. Les Dermites Allergiques du Chien et du Chat (Masson, Paris, 1991). 8. Gross, T. L. Ihrke, P. I. & Walder, E. J. Veterinary Dermatopothology (Mosby Year Book, St Louis, 1992). 9. Buerger,R. G, inKirk's CwrentVeterinaryTherapyXII, SmaNAnimalPractice(eds Bonagua, D.J. &Kirk, R.W) 631-634 (Saunden, W.B., Philadelphia, 1995). n, 10. Ddnemlle, P. Prat. Mi'd. Chir Anim. Comp. 28,433-449 (1993). 11. Kwochka, K. W. & Bevier, D. Contemporary Issues in Small Animal Practice, Dermatology (Churchill Li\,ingstone, New York, 1987). 12. Guagukre, E. & Martignoni, L.Proc. Novartis International Symposium, Birmingham (1998). 13. Silverman, J. &Rust, M. K. Envimn. Enromol. 12,490-495 (1983). 14. Teillac, D. in Allergologie Pidiatrique (eds Paupe, J., Scheinmann, P. & De Blic, J.) vol. 2,430-434 (Elarmnarion Midecine Sciences, Paris, 1994). 15. Rust, M. K. & Dryden, M. W. Annu. Rev. Entomol. 42,451-473 (1997). 16. Pdlaud, P. & Guagukre, E. Prat. Mid. Chir Anim. Comp. 33,373-387 (1998). 17. Thompson, R. C. A,, Meloni, B. P., Hopkins, R. M., Deplazes, P. & Eynoldson, J. A u t r Vet. J. 70,268-270 (1993). 18. Slacek, B. & Opdebeek, J. P.Ausfr Vet. J.70,313-314(1993). 19. Greene W. K., Camegie, R. L;, Shaw, S. E., Thompson, R. C. & Penhale, W. J. Parasite Immunol. 15,69-74 (1993). 20. Halliwell, R. E. W., Preston, I. E. & Nesbitt, G. H. Vet. Immunol. Immunopathol. 17,483-494 (1987). 2 1 : ~ c ~ e o S. n , E. & Opdebeek, I. P. Int. J. Parositol. 24,259-263 (1994). 22. Frank, G. R., Hunter, S. W., Stiegler, G.L., Wallenfels, J. & Kwochka, K. W. in Advances in VeterinaryDermatology, vol. 3 (eds Kwochka, K.W., Willemse, T. & von Tschamer, C.) 201-212 @utterworth-Heinemam, Oxford, 1998). 23. Cook, C. A,, Stedmm, K. E., Frank, G. R. & Wassom, D. M. in Advances in Veterinary Dermatology, vol. 3 (eds Kwochka, K.W., Willemse, T. & von Tschamer, C.) 494 (Butteworth-Heinemann,Oxford, 1998). 24. Prilaud, P. Proc. Congres National de la CNVSPA 3,89-91 (1993). c 25. Bevier, D., Rose, B. I., Kunkle, G. A. & Mondesire, R. Comp. Cont. Educ. Pract. Vet. 19s. 17-23 (1997). 26. Pdlaud, P. Proc. ESVD-ECVD, Pisa 170 (1997). 27. Messinger,L. M. Vet. Clin.N.Amer. 25,981-1005 (1995). 28. Kunkle, G. A. & Milcarsky, J. J. Amer. Vet. Med. Assn. 186,677-680 (1985). l..,
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- S. Gilbert
I Atopic dermatitis Atopy is a condition involving a hereditary predisposition to the development of hypersensitivity reactions to environmental antigens. It can cause respiratory, digestive, ocular and dermatological signs with atopic dermatitis being one of the possible clinical manifestations. There is a tendency to assume that any animal in which sensitivities to aeroallergens (airborne allergens) are demonstrated is atopic and, therefore, that any cat with a pruritic dermatosis and positive intradermal test reactions to aeroallergens has atopic dermatitis Sensitisation to airborne allergens, whether demonstrated by intradermal testing or by serological methods, occurs in many normal cats and is, therefore, not synonymous with atopy '. If the same criteria used in other species are applied to cats, the term "atopic dermatitis" should be reserved for a discrete clinical entity involving corticosteroid-responsive pruritus of the face and feet and a genetic component, indicated either by the cat's family history or breed predisposition '(Table 10 : 1).
Types of allergens Aeroa&rgens: The most commonly incriminated airborne allergens are the house dust mites, Allergies to human scale, pollens and moulds are muchless especially Demtophagoides farinae common. Cmss- actions can occur between house dust mites and parasitic mites like Otodectes cynoils and this could, in part, explain the incidmce of apparent sensitivity to house dust mites in n o d cats S.
Food &%ens: Foodstuffs can act as allergens and trigger an atopic condition, as in dogs and people 9. The most eommonly incriminated foods, depending on local feeding habits are beef, lamb, chicken, fish, dairy products, eggs, soya, cereals, gluten and certain additives "". Fleas Strictly speaking, fleas are not allergens in themselves but can exacerbate pre-existing hypersensitivity and even stimulate a Th2-type immune response through the action of superantigens present in the insect's saliva ').
Immune response Inflammatory i n f i h t e in allergic dermatitis It is likely that CD4t T-lymphocytes are the dominant force in directing the immune response in allergic d e d t i s . The predominant cell-types found in skin biopsies taken from non-inflamed skin are lymphacytes and mast cells whereas, in biopsies from lesional skin and eosinophilic granuloma complex lesions, eosinophlls are usually the most common inflammato~ycells 2. Langerhans' cells, more numerous in the epidermis of lesional skin, could play an essentid role in the development of skin lesions I*. Allergen-specific IgE production ,. Unlike in the dog and man, no difference in allergen-specific prod&tion has been demonstrated between atopic and non-atopic cats, whichever technique has been used ? Concenkations of Dermatoplragoidesfarinae - specific IgE do not correlate with results of either intrademal or passive cutaneous anaphylaxistests, which suggests that there may be more than one type of IgE, each with different roles and affinities.
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Table 10 :1 : Evidence for and against the existence of atopy in cats
EVIDENCE FOR EPIDEMIOLOGY None
EVIDENCE AGAINST No breed or family predisposition documented; no lines of atopic cats described to date
CLINICAL FEATURES
.
Asthma
Few cases suppofled by provocation tests orresponse to desensitisation
Dermatoses resembling atopic dermatitis
Rare in the cat
Other pruritic dermatoses
Other causes possible: behavioural problems, flea bite hypersensitivity
BIOLOGY Sensitivity to house dust mites Incidence of food intolerance Inflammatory infiltrate composed of CD4t cells producing IL 4 in lesional skin.
THERAPY Favourable response to immunotherapy Control of experimentally induced asthma with cyclosporinA.
Similar incidence to that of normal animals livino in the same surroundings
Impossible to demonstrateme allergy; results of challenge often unconvincing.
-
Only open studies performed, with variable group sizes; efficacy not proven to date. -
Factors favouring an ZgE response Whether or not an animal develops cl'mical signs of atopy depends partly on the environment in which it lives. Normal cats, raised in laboratories, have significantly lower levels of Dermatophagoides farinae - specific IgE than either normal or atopic cats living in more natural conditions '. Endoparasitism (e.g. Toxocara cati) and, to a lesser extent, vaccinations (involving live attenuated viruses) have been shown to favour IgE production in experimental sensitisation models involving orally administered antigens, but this was not, in these studies, accompanied by clinical signs of atopy 'I.
Clinical features The age of onset of clinical signs ranges from 6 months to 8 years although most cases involve young cats aged between 6 months and 3 years ',I6. Signs can involve the skin and/or the respiratory tract. Pruritus, initially non-lesional, is constant and sometimes very intense. It can he seasonal or non-seasonal 2S"~"~"~'8. The dermatological signs most commonly associated with atopy are self-induced alopecia (Fig. 10 : I), miliary dermatitis (Fig. 10 : Z), certain types of eosinophilic granuloma complex (mainly eosinophilic plaques) (Figs 10 : 3,4) as well as pnuitus, erythema, erosions and crusting on the face and neck (Figs 10 : 5-8) 19"'. More rarely, the clinical picture resembles that of dogs and humans with atopic dermatitis, i.e. facial erythema, bilateral erythematous otitis (Fig. 10 :9), pododermatitis, licking of the feet, lesions in the axillary and inguinal regions, (Figs 10 : 12,13) and keratinisation abnormalities 6L0. Pruritus and lesions can be either localised or generalised. Lymphadenopathy can occur in chronic cases of miliary dermatitis and eosinophilic plaques U 1 . Lichenification, secondary pyoderma and Malassezia dermatitis (Fig. 10 : 14) are rarely described in atopic cats Respiratory signs in atopic cats are variable (0 to 50%) and include rhimitis, chronic cough suggestive of allergic bronchitis, and dyspnoea associated with an asthmatic wheeze. Bilateral, erythematous blepharoconjunctivitis is sometimes seen.
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Pigrrre 10 :I :Selfinduced aiopecio on the foreirrnb of a cat with an allergy m house dust mires
Figure10 :2 :Same catas inFigure I0 :I:, faciaimiiiaq dermatitislesions.
Figure I0 :3 :Abdmmal e o s m p h d ~ c p l ~inn e s catallergicro home
Figare 10 :4 :Eosinophilic plaques in the axilia in a car allergic to house dust mites
dust mties
Figure 10 :5 :Excoriations second
zciaiprurirus in an atopic cat
Figure 10 :6 :Extensive facial uicemtion secondary to faciaiprurirus in an atopic cat
Figure 10 : 8 :Alopecia, lichenification, erythema and excoriation secondary to cewicofacialpruritus in an atopic cat
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A M e a l Gude m F h e Dermatology
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Diagnosis The aim of an allergy investigation is to determine the allergens responsible for the cliical signs of atopy. This first involves taking a detailed history to narrow down the list of possible allergens. Without this information, interpretation of allergy testing is impossible. The main purpose of allergy testing is to select allergens for inclusion in an immunotherapy course and put in place allergen-avoidance measures (e.g. dietary restriction, flea control and avoidance of airborne and contact allergens).
Restriction/challenge tests Avoiding the causal allergen is only really practical for food allergens and flea infestations. A cat suspected of being atopic should always be put on an elimination diet for a period of 3 to 8 weeks, depending on clinical response, although such a diet can be difficult to enforce if the animal lives outside. Flea control measures must always he adopted because flea bite hypersensitivity is a contributory factor in the development of pruritus and also because flea infestation can increase the chance of sensitisation to other allergens. If pruritus is significantly reduced following flea control, it is reasonable to assume that flea allergy dermatitis is associated with the atopy
Intradermal testing Intradermal testing is often unrewarding in cats and is the subject of much controversy. The allergenic extracts are the same as those used in the dog and they are given at the same concentrations. The test site must first be gently shaved. Then, 0.05 ml of each extract is injected intradermally. The test is read at 15 minutes and interpreted in the same way as in the dog, i.e. a reaction is considered positive if an erythematous papule develops around the injection site, with a diameter greater than the mean diameter of the positive and negative controls. Intradermal testing can he difficult to interpret in cats because the positive control reaction is often very weaki (Fig. 10 : 15). However, in some cats, large, erythematous papules, similar to those seen in dogs, can develop at both the positive control and test extract sites (Fig. 10 : 16). Some allergens, at low concentrations, can induce positive intradermal reactions in normal cats. These may be either irritant reactions or genuine positive reactions, there being a difference between clinical sensitivity and cutaneous reactivity I .
In vitro laboratory tests Serological testing To date, no serological test has been properly evaluated in the cat. These procedures use anti-feline IgE (either natural or chimeric) antibodies or anti-human FceRI antibodies, the DNA sequence of the IgE binding site for its high affinity receptor (FcERI) being apparently very similar in man, dog and cat 2'. With some laboratories, it can be impossible to find out the type and specificity of their antisera. Correlation with intradermal test results, when known, is very poor I.'. Moreover, serum concentrations of allergen-specific IgE (paaicularly for Dermatophagoides farinae) in normal cats are comparable to those in cats with atopy-like dermatological signs "'. However, immunotherapy based on serological testing is just as successful as that based on intradermal testing suggesting that the degree of correlation between the two techniques does not necessarily indicate how reliable each of them is. Cellular tests The direct basophil degranulation test used in humans and dogs has been adapted for use in the cat $. A patient's basophils are mixed in vitro with different concentrations of the test allergen - if the animal is allergic, there will be significantly fewer basophils than for the negative control. Results are expressed as maximum percentage degranulation or activation. A considerable amount of fresh blood is needed for this test so its use is generally very limited. It represents one of the most interesting approaches in allergy diagnosis because it demonstrates both an IgE-dependent reaction and activation of target cells while dispensing with the problems of quality and specificity of the immunological reagents. The indirect basophil degranulation test is much easier to perform in the normal practice situation. Feline anaphylactic antibodies are heterocytotropic and bind human and horse basophils which can therefore be sensitised and activated in vitro. Although the correlation between the results of this test and intradermal testing is variable '6,",ii, its diagnostic value remains as questionable as that of serological testing. In a prospective study involving 99 cats with eosinophilic granuloma complex lesions, there was no difference in the incidence of sensitisation to either the house dust mite
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Figure 10 :9 :Bilateral erythematou otitis in an atopic cat
Figure 10 :10 :Bilateral fore-limb interdigital pododermatitis in an atopic cat
Figure I0 :11 :Erythema of the ungualpad in an atopic cat
Figure 10 :I2 :Self-induced alopecia of an'llae, i n g u i ~ regions l and extremities in a cat allergic to house dust mites
Figure 10 :13 :Erythematousplaques in the aillae of an atopic cat
Figure 10 :14 :Malassezia dermatitis secondary to atopic dermatitis
Figure 10 :15 :Uninterpretable innadermal test
Figure 10 :16: Positive intradermal test reactions (+) mite extracts.
to house dust
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Dermatophagoides farinae or the flea Ctenocephalides felis felis between normal and affected cats. The incidence of sensitisation to these two allergens was between 25 and 30 % in both groups 14.
Practical diagnostic approach Felme atopy remains essentially a clinical diagnosis - the interpretation of intradermal testing k i n g difficult and the concentration of allergen-specific IgE being similar in normal and atopic cats. Haematology and histopathology are of no use in establishing a diagnosis of feline atopy - blood eosinophilia is very variable and histopathological changes are non-specific '. Given that allergy tests are not very reliable and that atopy, in fact, often co-exists with other conditions, it is vital to cany out avoidance measures (e.g. diet and flea control) before considering either intradermal or in vitro allergy tests. As in the dog, the aim of performing these tests is purely to select allergens for immunotherapy.
Treatment Treatment depends on the severity of the condition, its duration and the possible presence of other allergic skin diseases.
Allergen avoidance In practice, only food allergens can really be avoided. Avoidance of aeroallergens is only practical if the allergens concerned are in a limited area from which the allergic cat can be excluded. The most important allergens for cats in Europe are house dust mites and although various measures aimed at reducing their number can be recommended, these are only likely to be effective if combined with other procedures: very regular ventilation of the cat's surroundings, frequent aeration of duvets, mattresses and blankets, use of a vacuum cleaner fitted with special filters (with a pore size of under 0.3 pm), treatment of resting areas with a combination of insecticides and insect growth hormone regulators and steam cleaning of sleeping areas 26.
Anti-inflammatory medication Anti-inflammatory medication, given either alone or in combination with other treatments, is very useful in the symptomatic control of atopy in the cat. Corticosteroids are usually well tolerated by cats and are still the symptomatic treatment of choice. They can be administered orally (prednisolone or prednisone, 1 to 2 mgikglday, for 5 to 10 days, then every other day) ' or parenterally (methylprednisolone acetate, 5.5 m a g or 20 mglcat, given by subcutaneous or intramuscularinjection or triamcinolone acetonide, 5 mglcat, given subcutaneously) '. Parenteral administration is sometimes preferable because many owners find it very difficult to give their cat tablets. Used early on, corticosteroids give good results but with time, they tend to become less effective. Side-effects can occur (e.g. weight gain, polyuria-polydipsia, diabetes mellitus, iatrogenic Cushing's syndrome with fragile skin and urinary tract infections) and they should, therefore, only be used when other treatments are unsatisfactory.
Megeshol acetate is still widely used as an anti-inflammatory agent in feline dermatology. Its antiinflammatory activity is comparable to that of the corticosteroids but because side-effects are common and severe (as well as being the main cause of diabetes mellitus in cats, it can cause iatrogenic Cushing's syndrome, behavioural problems, weight gain and gynecomastia), its use should be avoided 17. Antihisfamines are very useful in the treatment of allergic skin disorders in the cat. The most commonly used antihistamine (HI blocker) is chlorpheniramine (2-4 mglcat given orally, BID) with improvement reported in 73% of cases Its main advantage is the low incidence of side-effects (e.g. lethargy, vomiting and weight gain). Hydroxyzine (12.5 mglcat given orally, BID) is sometimes used in cats but is potentially teratogenic. Cyproheptadine (2 mglcat BID) can also be used; this drug also has serotonin antagonistic effects but side-effects (e.g. polyphagia, sedation, behavioural problems and vomiting) occur in 50 % of cases ". Essential fatly acids of the omega-3 and omega-6 series have been reported to produce improvement in 50 to 75% of cats with miliary dermatitis
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10 : Atopic dermatitis
Immunomodulators Immunosuppressive therapy is sometimes necessary.
Chlorambucil(0.1 to 0.2 mgnig SID) can be useful in cats ". It is usually well tolerated but is only indicated in cases which have not improved with aggressive corticosteroid therapy (prednisone, 2-3 Cyclosporin A has been successfully used at high doses (5 m a g BID) to treat experimentally induced feline asthma 3'. Trials using a lower dose of 5-8 m a g SID for 4 weeks, then every other day, have produced very encouraging results in the treatment of corticosteroid-refractory eosinophilic granuloma complex lesions and cervicofacial pruritus (E. Guagukre, personal communication). Immunotherapy Allergen specific immunotherapy (also called hyposensitisation or desensitisation) is considered the thera~vof choice for lone-term treatment of feline atow 6,m,". The m t ~is identical l to that used in the dig with allergenic extracts bemg either aqueouiir alum-precipitated. Most studies have been based on quite short follow-up periods (6-10 months) with varying degrees of improvement seen in 67 to 100% of cases 6. When the follow-up period has been longer (one to three years), success rates are lower In a multi-centre study involving over 80 cats, definitive cure was reported in only 12 % of cases ". All reports published to date have been open studies, often involving small, clinically heterogeneous groups making it difticult to judge whether this therapy is effective in the cat. The practical difficulty of recruiting enough suitable cases is such that there is unlikely to be an early answer to this. Furthermore, the logistics of immunotherapy are quite demanding (initially one injection per week) and its safety profile (risk of inducing fibrosarcoma?) has never been evaluated. Immunotherapy is, therefore, an option but should only be used as a last resort, once avoidance measures have proved ineffective. j3.
REFERENCES 1.Rcedy, L.M.MiU4,W. H.& W i s e , T. A l l q i c Skin Disemes ofDogsandCnrs &aPhiaddphi& , 1997). 2 Soon D. W. M b r Jr, W. H.BGnffin,C,E.MuUer di Kirk's S d A n m r a l Dernzabilog~5th ednm 484626 (SannderszWB.,Phil&elphh 19951. 3. GilW S. &HdheU,B.E W. Vet. I m n ~ L . I m m m o p ~ f h 63,235-252 ot (1998). 4. G i i n , S.,Maud, P. & GuaguS~E. Prd. Mid. Ckk A m Camp 94,15-31(1999). 9, PrQau4F',LesDermitesAUergiquesdu Chienst& Char @fasson, h i s , 1991). 6.C~lattl,D. N. & Pros& C.Point VCr 20,1772184 [198933 7 Eostq A, P. & O'Dair, H Vet Dennorol. 4,111-115(1993). 8. SaridanwhJ&, M~N.,Koutina$,k E, Gioulckas,D.,Leontides, L. & Polyzopoulou, 2. Vet.Dermml. 10,89-94(1999). 9. Guagub, E.& Wlnd, P . M . M u . Chk Anim, C w . 33,389407 (1P98). 10. Markwell, P. I., m a d , W.G.,Jones, B.R.,Hate, I. G. 5 .Wills,J, in Advances ifa Veterinmy Dmn@oh@, vdl, 3 (eds Kwwhka, K.W., W111me, T. & von Ts~hmer,C.)493 fButtmc&~&Heham Oxfanl, 1998). 11. Gua&re,E. Pmt. Med. Chrr,A n i . Camp. 28,451464 (1%). 12.Ws,S.&Paradix, M Le MCdec~nV&!unred~ Quibec24,15-20 (1'3941. 13. P$av%, P. Allergologie Can~ne(Mason, Paris, 1599). 14,Ram&,P,,W e ~ - M e m D., . Goldsdrmidt, M.H., MWIC.A., Willemse, T, &Murphy, Cr. E. EAm J. Path01 151,927-932(1997). 15. GilW S. &&&We& R. E. W.PrroeAAVD.AAClD, Sun Anfado 105-106(199Q. 16 Rust, C in Advmes m Ve&tkary D ~ ~ i vd. o & 3 (eds ~ Kwocfika, K.W., Will-, T. & von Ts~hamw,C) 516-517 (8uttewoah & Hememam, Odord, 1958). 17 WhiteWhae S. 0. &Sequoia, D. J,Amer. Vet.Med Assn. 194,69%695 (1984. 18. CwIOm,D. N.,R6ay,I. & Rosf C.Vet. Dermntol, 1,55-62 (1990). 19 Smn, D. W.J. Amec Anim. Hosp Assn. 20,537-564 (1%). 20. Ham&R. E W. J.Amer.Anb Hasp, Awn. 33,282-288 (1597). 21. Pawet, H.T & Ihrke) P. J. Vet Chn.N.Amer 23,833-850(1995). 22 Wlaud, P. & Gua&~, fi. Prnt Mid Ckir Anim. Conyr 33,373-387 (19%). 23. E~ster,k P. Ver. AU Clrn Immwol. 5, 103-109 (19971, 24. Wlaud, P.P m . ESVD-ECW, PPiSa 170 (19971, 25. Pdlaud, P., Boiteau.h & Daahanps, E.Ptnf. Mdd CMI:Aam. Comp 38,3g7-391(1993). 26 Laur, C.,B~daf,E & Gu&h,L Rezfr ANqel, 37,208205 0947). 27 Church,D B ,W&@~II, D L, Emslie, D k & Middleton, D. 1. Res V& Set* 56,175-118 (1594).
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28. Miller, W. H.&Scott, D. W. J. Amer Vet. Med. Assn 197,67-70 (1990). 29. Scott, D. W., Rothstein, E., Beningo, K. E. &Miller Jr, W. H. Can. Vet. J . 39,634-637 (1998). 30. Harvey, R. G.Vet.Rec. 128, 326-329 (1991). 31. Helton-Rhodes, K. H,in Kirk's Current Veterinary Therapy XI1 (eds Bonagura, D.J. & Kirk, R.W.) 581-584 (Saunders, W.B., Philadelphia, 1995). 32. Padrid, P.A., Cozzi,P. & Leff,A. R.Am, J Respir. Crit. Care. Med. 154, 1812-1818 (1996). 33. Bettenay, S. V. in Advances in Veterinary Dermatology. "01. 3 (eds Kwochka, K.W., Willemse, T. & von Tschamer, C.) 517-518 (Butterworth & Heinemann, Oxford, 1998).
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The term food allergy refers to all the clinical manifestations of hypersensitivity to mgested allergens. However, in the vast majority of cases, neither identification of the actual allergen responsible nor elucidation of the exact immunological mechanisms involved is possible so it may he wiser to use the term food intolerance','. Moreover, certain kinds of clinical problem may be associated with the ingestion of foodstuffs but without any evidence of any causal immunological reaction: food can contain phmacologically active substances (e.g. histamine which induces vasodilatation); metabolic reactions due to some kind of enzyme deficiency (e.g. lactase) are common; and both fungal toxins (in dried, poorly prepared or inadequately preserved food) and plant toxins (e.g. tannins and alkaloids) can elicit non-immunological reactions2. The incidence of food intolerance in cats is difficult to establish with any precision because it depends on both the definition of food intolerance and to what extent the possibility of food intolerance is considered in the diagnosis. In a recent study, 6% of all dermatoses in cats were attributed to food intolerance but this figure cannot be taken as definitive because challenge testing was not routinely undertaken. Food intolerance represents the third most important cause of feline hypersensitivity'.'.
Few studies of the immunopathogenesis of feline foodmtolerancehave been conducted so most immunological data are extrapolated from the human field.
Food allergens Any foodstuff is potentially allergenic but, in practice, a finite number of ~ngredientsare involved. The actual list varies aceording to local feeding habits in countries where the animals live. In cats, the most common food allergens are beef, lamb, m~lk,fish, tinned food and dried food. Less commonly, &hieke& gluten and addihves can also induce reactionP. The foodstuffs most likely to be allergenic are those which contain the most protein and those which are most commonly fed. The cat will often have been eating the foodstuff in question for a long time and the more a particular protein has been consumed, the more likely are the chances of inducing hypersensitivity % The . exact nature of allergenic proteins in cats has never been studied. It is likely that many foodstuffs are also responsible for non-immunologically based Intolerance. Certm fish contain high levels of histamine, ag. tnna and any dried or inadequately preserved fish, Shellfish~ommonallergens in humans-have not often been identified as allergens in cats even though they are a common ingredient in "cat treats". Nevertheless, shellfish may induce non-specific histamine release1 9. Most of the mmmonly suspected additives are haptens (small molecules which m oonly allergenic when conjugated with a carrier protein), and hypersensitivity to this type of antigen has never been demonstrated in cats. Many of the additives used m the human foad industry like benzoates and f a m i n e are never used in cat food; however, the use of others is v?Iflespead, including sodium bisulphite, monosodium glutamate, azo-dyes, $odiumnitrite, spices, sodiumalgiiate, vegetable gums, propylene gIycol and ethoxyq~in'~, Storage mites in m m c i a l , dried cat food could be a major source of oral sensitisation for carnivorous m a l s . In dogs, allergy to storage mites is common although in crib it has never been possible to demonstrate that the sensitivity is specific to forage mites and not due to cross reaction
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with house dust mites or mites present in food.
Immune response The most common immunological response involved in food allergy is probably a Type I immediate hypersensitivity althoughType Ill (Arthus) reactions andType N (delayed) hypersensitivity may also occur. Immediate responses appear within minutes or hours of ingestion of the allergen whereas delayed responses take several hours or days. Defence mechanisms to prevent development of food allergy include the protective gastrointestinal mucosa and immune tolerance maintained by cellular immunity associated with the digestive tract ". The mucosal barrier excludes most ingested allergens although it is permeable to peptides and small proteins, especially if there is any kind of inflammation, e.g. due to viral or parasitic infection. Although no exact mechanisms have been demonstrated in cats, it is assumed that local and systemic IgA eliminates potential allergens and that any defect in this defence would predispose an animal to possibly damaging hypersensitive reactions. Food allergy can develop along with other kinds of allergy, e.g. flea allergy dermatitis, atopic dermatitis, etc...".
Clinical features
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Food allergy is a non-seasonal dermatosis with no age, breed or sex predilection. Age of onset varies between 3 months and 11 years with most studies showing a mean age of 4 to 5 years. There is no breed predilection although two different studies have shown a higher incidence in Siamese cats. It is usually believed that food allergy is more common in cats than in dogs although it is impossible to carry out meaningful epidemiological studies because allergic dermatitis is poorly defined and the means of investigating feline allergies are limited. As it is easier to carry out an elimination diet and control flea allergy dermatitis in the cat than it is to perform intradermal allergy testing, food allergy is usually considered the most likely differential in this species (unlike in the dog) after flea allergy dermatitis.
Dermatological signs Clinical signs are not specific although varying degrees of non-seasonal pruritus (either generalised or localised) have been reported in over 90% of cases C6,'5-". Response to corticosteroid therapy was good in almost 50% of cases 4'1. In some studies, corticosteroids have been found to be less effective although these were either reeospective studies of chronic cases or involved doses similar to those used in dogsl.4,%14~I6, Food allergy often manifests in cats as a pruritic dermatosis of the face (cbeilitis and bilateral blepharitis) andneck with erythema, papules, erosions and crusts (Figs 11 : 1-9). Bilateral erythematoceruminous otitis, pododermatitis and perianal inflammation are sometimes observed (Figs 11 : 10, 11) ',". Food allergy can also present as miliary dermatitis (Figs 11 : 12), generalised scaling or symmetrical alopecia (Fig. 11 : 13), each of which carries a detailed differential diagnosis. In addition to the other clinical presentations, all the entities of the eosinophilic granuloma complex should be considered, e.g. indolent lip ulcers (good markers, according to some dermatologists) (Fig. 11 : 14) and eosinophilic plaques, wherever they occur1a.Urticaria and secondary bacterial or fungal infections (e.g. Malassezia dermatitis) seem to be relatively rare in cats.
Gastrointestinal signs The incidence of gastrointestinal involvement, which may or may not be associated with dermatological signs, is underestimated. In a series of 17 cases 6, gastrointestinal involvement (e.g. vomiting and-intermittent diarrhoea) was observed in 30% of the animals. Most cases of recurrent lymphoplasmacytic colitis, c'ommon in cats, seem to be related to food intolerance in this specie^'^.
www.vet4arab.co.cc 11 : Food Intolerance
Figure 11 :1 :Faciaiprur cat with food allergy
Figure 11 :2 :Same cat as in Figure 11 : 2, erythema on the lateral pinnae
Figure 11 :3 :Same cat as in Figures 11 :I - 2, lesions of miiiary dermnritis
Photo 11 : 4 :Facial prurifus, erythema, scaling and crus Persian cat with food allergy
Figure 11 :5 :Erosions around the skin behind the ears in a cat with food allergy
Figure 11 :6 :Same cat or in Figure 11 :5, biephamconjunctivitis
Figure 11 :7 :Severe facial pruritus and very crusty lesions in a Perslan cat with food allergy (sardines)
Figure 11 :8 :Same cat as in Fi, : 7 seen after clipping, showing severe erosive and ulcerative lesions on theface
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Diagnosis In practice, establishing a definitive diagnosis can be difficult and requires a rigorous approach. The animal's history must be thoroughly reviewed, including the cat's living and eating habits, and the diet itself, especially with respect to protein and carbohydrate sources. The physical examination should be methodical. Food intolerance should always be considered in an animal with a non-parasitic pnuitic dermatosis.
Differential diagnosis The differential diagnosis is that of all pruritic dermatoses, including initially the ectoparasitic infestations (e.g. cheyletiellosis, notoedric mange, trombiculiasis and pediculosis.), other causes of allergic dermatitis and dermatophytosis. Facial involvement entails a more detailed diagnostic approach to rule out auto-immune dermatoses and certain viral infections'.. .
Diagnostic tests Hematological profiles (differential count, etc.) are worthless; at best they might reveal nondiagnostic eosinophilia. Histopathological examination of skin biopsies does not provide any specific inf6rmation, but "sually reveals pe&ascular inflammation with varying numbers of eosinophils and mast cells, indicating allergic dermatitis in genera L4,6.
Elimination diets The next stage is to instigate an elimination diet, the aim of which is to give the cat one or more foodstuffs which it has never eaten before. Although this sounds simple, in practice it can be fraught with problems both because these days, commercial cat foods contain a wide variety of different proteins and because owners often find it difficult to make their cat follow a strict diet; prior to settling on a diet, it is crucial to assess the owner's motivation. Before the effects of an elimination diet can be properly evaluated, all secondary and concomitant skin problems must be controlled, e.g. flea allergy dermatitis and secondary infections (although these are rare in cats). Certain preliminary guidelines are important: the food must he offered on a plate (avoid plastic or metal), toys should be taken away and, in theory, no treats, vitamins, mineral supplements or drugs should be given during the time of the diet. Prescribing corticosteroids cannot always be avoided and, in this case, the special diet can be started immediately but, for proper assessment of its effect, it should be prolonged for at least two weeks following the end of the drug course ',"'.
The choice of foodstuffs should take into account the cat's normal eating habits. The choice of diet needs to be a joint decision, taken with the owner, and the cat's eating habits should not he changed too rapidly. The new diet should therefore he introduced gradually, over the course of 4 to 5 days. It should also be given at the same times and correspond to about the same total amount of food as given previously. It must include a relatively lean protein source (lamb, chicken, turkey, horse, duck, rabbit or game), offered either cooked or raw, together with boiled vegetables (potatoes, tomatoes, lentils, etc.). A response can he observed by the end of the third week (Figs 11 : 15,16) but may take up to 10 weeks for the diet to have any effect '6,'0. Commercial, hypoallergenic cat food based on lamb, chicken, duck, rabbit, game or catfish and rice is not usually recommended for diagnostic purposes because some cats are sensitive to the additives used in such preparations. However, these products are very easy to use and may sometimes have their place. If no response is observed, it does not necessarily mean that the cat does not have any kind of food allergy. In this case, a traditional elimination diet should be instigated ". If only a partial response is observed, there may be other, concomitant skin problems (and it should be checked with the owner that the diet was rigorously followed). If no response is seen within 10 weeks, the diagnosis should be reviewed. Feeding a cat commercial food ensures a balanced diet-a recent study on hypoallergenic diets prescribed by American vets revealed that 90% failed to provide the officially recommended daily intakes for adult animals 'O.
Challenge tests The principle of the challenge test is to reintroduce, at regular intervals, each of the former foodstuffs for a period of one week and monitor for reappearance of signs. This is a demanding process which is often rejected by the owner, does not absolutely prove that any particular foodstuff is responsible, and gives no information on mechanism. However, this approach can be useful because few allergens
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Figure 11 :9 :Erosions, exconahoris andfacralprurrfus m a Earopean dornesnc shorthair cat wrrhfood allergy (be@
Figure 11 : 10 : Same cat as in Figure 11 : 9 , erythematous ~ododermafifis
Figure 11 :I1 :Same cat us in Ft~ures11 9-10, peranal erythema
Figure 11 :12 :Severe miliaiy dermatitis in a domestic short haired cat with food allergy (beef)
Figure 11 :13 :Se@mduced aiopecro on the abdomen of a domesbc short harr rat wrthfoodallergy
Figure 11 :14 :indolent ulcer on the upper lip of a domestic short hair cat with food allergy (milk)
Figwe 11 :15 :Some cat as rnfgure I1 14, eruslons and ulrerafmons on upper and lower Ips
zme cat as in Figures I1 :14-l5,3 weeks afer starting Fii an elimination diet.
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tend to be involved; just one or two account for over 90% of cases 4-6,'5. The vast majority of cats do not relapse when the former foodstuff is reintroduced-this may be due to a change in the immune response with time or, more likely, because eating very digestible food for a while gives the intestine time to re-establish normal permeability.
Allergy tests Allergenic extracts derivedfrom food allergens Commercially available extracts of animal-derived food allergens (e.g. beef, milk, fish and eggs) are of very variable allergenicity hut give satisfactory results. In contrast, studies in humans have shown that extracts of plant-derived food allergens need to be native and prepared immediately before use; laboratory preparations are inactive ". However, it has never been possible to exmapolate these findings to cats. There are no published data on what concentrations of these extracts should be used in cats.
Diagnostic value of inhadermal testing and in vitro IgE testing Intradermal skin testing 1'-21, in vitro IgE testing ''" and cellular testing have no value in the diagnosis of food allergy -.in cats. A particular foodstuff cannot be excluded on the basis of a negative result and asymptomatic sensitisation is common '. These tests are theoretically useful in &an medicine because they are helpful in establishing a more acceptable elimination diet, i.e. a more varied diet can be prescribed once certain important potential food allergens have been eliminated. Even so, opinions are divided on this approach which could get it seriously wrong =. It has been stated that "an elimination diet should always be well-constructed and never put together on the misleading basis of a few positive in vitro test results".
In veterinary medicine, such an approach is defmitely worthless because we can impose as strict a diet as necessary for a period of weeks without any serious problem. Nevertheless, this has not stopped certain companies from promoting food allergen-specific IgE assays to diagnose food allergy. This commercially appealing approach often goes down well with owners. Whatever the outcome, the change in diet is often associated with clinical improvement, if only because the new diet is more balanced or more digestible than the former one. In this way, food intolerance can be misdiagnosed as food allergy.
Treatment Hypoallergenic diets The only acceptable, effective way of treating food intolerance is by eliminating the foodstuff(s) responsible. However, this must not adversely affeci the nutritional balance of the diet. Hypoallergenic diets cannot be prolonged for more than 3 weeks without risking skeletal damage 26, unless vitamin and mineral supplements are included. Therefore, owners can either feed their animals a balanced home-prepared diet based on the hypoallergenic diet or give very digestible commercial products.
Symptomatic therapy Corticosteroids (1-2 m@g prednisone SID, orally) are effective especially in the early stages. Antihistamines are ineffective. Some reports have recommended chlorpheniramine (4-8 mdanimal BID, orally).
Treating secondary infections Secondary skin infections are rare but, in cats with gastrointestinal symptoms, it is important to control bacteria in the small intestine by prescribing a suitable antibiotic (metronidazole) ' in order to break the vicious cycle of sensitisation followed bithe aggravation of gastrointestinal lesions leading to exacerbated dermatological signs.
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REFERENCES 1. Scott, D. W. Miller Jr, W. H. &Griffin, C. E. Muller & Kirk's Small Animal Dermatology, 5th edition (Saunders, W.B., Philadelphia, 1995). 2. Guagukre, E. & Pdlaud, P. Prat. Med. Chir Anim. Comp. 33,389-407 (1998). 3. Denis, S. & Paradis, M. Le Midecin Vitirinaire du Quebec 24, 15-20 (1994). 4. White, S. D. & Sequoia, D. J. Amer Ver. Med. Assn. 194,692-695 (1989). 5. Carlotti, D. N., R h y , I. & Prost, C. Vet. Dermatol. 1,55-62 (1990). 6. Guagukre, E. Prat. M4d Chir. Anim. Comp. 28,451-460 (1993). 7. Markwell, P, I., Guilford, W G., Jones, B. R., Hate, J. G. & Wills, J. in Advances in Veterinary Dermatology. vol. 3 (eds Kwochka, K.W., Willemse, T.& von Tschamer, C.) 493 (Butterworth & Heinemanu, Oxford, 1998). 8. Guilford, W. G. J. small Anim. Pracad. 35,620-624 (1994). 9. Moneret-Vauhin, D. A. in Allergologie. vol. 3 (eds Charpin, J. & Vervloet, D.) 349-365 (Elammarion M6decine Sciences, Paris, 1992). 10. Roudebush, P. & Cowell, C. S.Vet. Dermatol. 3,23-28 (1992). 11. Kamphues, J. J Nutr. 121, S165 (1991). 12. Roudebush, P., Gmss, K. L. & Lowry, S. R. Vet. Dermatol. 5,69-74 (1994). 13. Gilbert, S. & Halliwell, R. E. W. Proc. AND-ACVD, San Antonio 105-106 (1998). 14. Scott, D. W. J. Amer Anim. Hosp. Assn. 23,255-274 (1987). 15. Rosser, E. J. in Advances in Veterinary Dermatology. vol. 2 (eds ihrke, PJ., Mason, I. &White, S.D.) 33-39 (Pergamon, Oxford, 1993). 16. Wills, 1. M. Vet. Med. 87,884-892 (1992). 17. Medleau, L., Latimer, K. S. & Duncan, J. R. J.Amer. Vet. Med. Assn. 189,692-693 (1986). 18. Power,H. T. & Ihrke, P. J. Vet. Clin.N.Amer. 25,833-850 (1995). 19. Nelson,R. W.,Dimperio,M. E. &Long,G. G. J.Amer Vet.Med.Assn. 184, 1133-1135 (1984). 20. Moneret-Vautrin,D. A,, Kanny, G., Rance, E. & Dutau, G. Revj? Allergol. 36,239-244 (1996). 21. August, J. R. J.Amer.Anim. Hosp.Assn. 18,157-163 (1982). 22. Kunkle, G. A. &Homer, S. J.Amer. Vet. Med. Assn. 200,677-680 (1992). 23. Jeffers, G. Proc. AAVD-ACVD, San Antonio 76-79 (1998). 24. Mueller, R. S. &Tsohalis, J. Vet. Dermatol. 9, 167-171 (1998). 25. Dutau, G., Frand, E, Juchet, A,, Eeji, S., Nouilhan, P. & Bdmont, E Rev.fi.Allergo1. 35,429-439 (1996). 26. Roudebush, P. & McKcever, P. J. Vet. Dermotol. 4, 1-4 (1993).
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I K. Mason - G. Burton
1 Eosinophilic granuloma complex Despite much recent progress in feline dermatology, the eosinophilic granuloma complex (EGC) remains poorly understood and is still a source of treatment failure. It presents in three different forms: indolent ulcer, eosinophilic plaque and eosinophilic granuloma Id. These three entities are grouped together because they can be seen concomitantly or successively on the same animal. Thus, clinically and histopathologically distinct entities which are expressions of a reaction pattern in response to various triggers, can he found on the same animal. EGC is, therefore, not a disease nor a diagnosis in itself 2,'. Other variants, such as mosquito bite hypersensitivity and familial forms that do not form part of this classic triad, have been described
Aetiopathogenesis Theories on the causes of the EGC are particularly numerous: viruses ', genetic background ", bacteria lo, autoimmune disease "I2, parasites 25" and allergies 211.41314.
The role of eosinophils and mast cells As a general rule, the skin of a cat has a tendency to react via the intervention of numerous mast cells and eosinophils ". Eosinophils are often implicated in inflammatory reactions of epithelium and are found in inflammatory infiltrates in the respiratory tract, alimentary canal, skin, eye and sometimes in the bladder 215'6. Ther presence is often interpreted as indicating allergic reactions or parasibc (e.g. helminth) infestabons 'i'5'4 It now seems that the eosinophil plays a wider role in the inflammatory reaction, beyond the context of parasites or allergy lS. Furthermore, there exists in the cat a hypereosinophilic disease, which could be caused by either neoplashc medullary dysfunction or an absence of downregulation of an allergic or anti-parasitic reaction.
In the cat, mast cells are often associated with eosinophils in epithelia and they play a central role in the chemical attraction and activahon of eosmophils. Once mast cells are sensitised, they can become hyper-reactive and degranulate at the slightest stimulus (pressure, trauma etc...). Mast cells and eosinophils, which release proteolytic enzymes and pro-mnflammatory mediators, are responsible for collagen necrosis. A peripheral macrophage reaction follows. These foci can have a specific strnctural organisation, which has Ied to them being called palisadmg granulomas 2"1"".'4. The collagen necrosis behaves like a foreign body and may calcify and be eljminated across the epidermis up to the skin surface. Essentially, the lesion presents as a raised ulcer with characteristic whtish collagen necrosis m its centre (Fig. 12 : I). By this stage, even elimination of the cause will not necessarily produce rapid resolution and any secondary bacterial mfection, mechanical of chemical initation or allergic shmulation may exacerbate the process.
Causes The main causes of the EGC are allergic and parasitic, sometimes complicated by bacterial infection. A genetic predilection has been demonstrated in some cases a". Proliferative diseases, involving neoplastic or non-neoplastic eosinophils, might explain some rare, or clinically similar, variants of the condition (Table 12 : 1). The evidence for allergic and parasitic causes is undeniable. Allergic causes include food allergy,
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atopy, flea allergy dermatitis and, in some geographical areas, mosquito bite hypersensitivity. All these allergic diseases generate pruritus that can affect skin and sometimes the buccal cavity. The cat's tongue is made up of hard, abrasive, filiform papillae. Consequently, although licking can relieve the sensation of pruritus, the tongue can also cause tissue destruction just as claws do when a cat scratches. Excessive licking may also he associated with behavioural disorders. Genetic causes of the EGC have been demonstrated in a colony of specific pathogen free cats '".This familial predisposition already been reported ".
Table 12 : 1 : Aetiology of the eosinophilic granuloma complex Allergies Aeroallergens Flea bites Mosquito bites Food Intestinal parasites Chemicals Irritant substances (contact)
Foreign body reactions mite or insect particles Bacterial infections (secondary to allergy) Genetic background Parasites Cheyletiella spp. Otodectes cynotis Notoedres cati Idiopathic
Clinical features Indolent ulcer The indolent ulcer, also incorrectly called eosinophilic ulcer, is an ulcerated lesion of the upper lip, which, most commonly, extends either side of the philtrum (Figs 12 : 1-5) or the hard palate (Fig. 12 : 4). It varies in size from 5 mm to more than 5 cm in length. It is not unusual for the ulcer to start opposite a canine tooth (Fig. 12 : 5). At the beginning, erythema appears on its own, followed by a well-circumscribed area of ulceration, reddish brown in colour, alopecic and glistening. The border is slightly raised, revealing a central sphacelus (Figs 12 : 1,2). This lesion is generally non-pruritic and non-painful. Palatine lesions (Fig. 12 : 4) can affect small arterioles and produce haemorrhages. However, as the cat swallows the blood, these go mostly unnoticed 1",5. Regional lymph glands are sometimes enlarged. Clinically similar lesions seen at the lip commissure, on the gums, tongue, palate, pharynx and chin are usually eosinophilic granulomas. No breed predilection has been observed. However, females may be predisposed.
Eosinophilic plaque Eosinophilic plaques are alopecic, raised, erythematous, erosive and ulcerated lesions, varying from small poorly defined erosions to large well-circumscribed plaques (Figs 12 : 6-10). Favoured sites are the abdomen, inguinal region, medial and caudal thighs, neck and interdigital spaces. Lesions are associated with constant licking, nibbling and scratching.
dosinophilic granuloma Also called linear granuloma because of the linear shape of one of its common forms, the eosinophilic granuloma is a pinkish, scaly lesion involving intact skin and variable alopecia (Figs 12 : 11,12). These lesions are not pruritic and are very often asymptomatic. The classic form appears in young cats (aged 6 months to 1 year), usually on the caudal thighs. This form can regress spontaneously ','. Other parts of the body such as the flanks are sometimes involved. Based on histopathological criteria, there are two other variants, an ulcerated, proliferative, oral form with whitish foci of collagen
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12 : Eosinophilic granuloma complex
Figure 12 :1 :Indolent ulcer on the upper 11p note central sphacelus (courtesy ofD N Carlottl)
Figure 12 :2 :Indolent ulcer- on the upper- lip extending either side of the philtrum (courtesy of D N . Carlotti)
Figure 12 :3 :Indolent ulcer on the upper lip (courtesy of T Olivry)
Figure 12 :4 :Indolent ulcer on the hardpalate: these lesions can affect a palatine artery and cause sign$cant bleeding
Figure 12 :5 :Indolent ulcer starting opposite the two canrnes
Figure 12 :6 :Eosrnophhc p l a q w appearrng during the summer and autumn lntradennal testing showedposinve reactions after 15 mmutes to grass pollens, weedpollens and brtrng rnsects
Figure 12 :7 : V Pe.ttrn,r,e ~ ~u~rnuphrlrcplayucr un thc ubflomcn o f a car v.rrlt hjpere~jrnuphil,~ rydrome (rounes) oiJ P. Jlagnol,
Figure 12 :8 :Eosinophilic plaque in the palmar space of a cat with atopic dermatitis
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necrosis, associated with dysphagia (Fig. 12 : 13) and another form characterised by a firm, rounded and often asymptomatic swelling of the chin (Fig. 12 : 14). These two variants can affect cats of any age.
Atypical forms Mosquito bite hypersensitivity Mosquito bite hypersensitivity is characterised mainly by papular, erosive, crnsting and depigmenting eruptions on the nose (Figs 12 : 15-17) and p ' i a e pig. 12 : 18). The footpads may become swollen with fissures and scale (Fig. 12 : 19). Peripheral lymphadenopathy and moderate fever associated with blood eosinophilia are commonly seen. No age, breed or coat colour predisposition has been noted. Lesions appear in spring and summer when conditions (e.g. humidity, warmth, marshy regions) favour insect development. Signs tend to regress in winter. Other clinical forms, indolent ulcers (Fig. 12 : 20), oral granulomas (Figs 12 : 20,21), cutaneous plaques and eosinophilic keratitis due to mosquito bites are seen, in the absence of typical papular and scaling lesions on the ears and distal limbs. These lesions regress when the cat is kept in a mosquitofree environment 3,6,'8.
Familial forms Familial forms of EGC have been reported only in lines of specific pathogen free cats, aged between 4 and 18 months (average 10 months). All the clinical forms of the EGC have been obsenred Peripheral lymphadenopathy and blood eosinophilia have also been seen. No allergic or infectious cause has been demonstrated in these cases. Lesions usually occur in spring and summer, suggesting an association with the reproductive cycle or time of year. However, no link has been established with the sexual cycle, nor with sernm concentration of sex hormones a.After the age of 4 years, these lesions stop developing ",I.In one study, 21 out of 24 cats descended from these animals, presented with lesions without sex predisposition '. In natural conditions, the juvenile forms of linear granuloma that regress spontaneously in adulthood, could be compared to this familial form 4,SS.
Since the various forms of the EGC are reaction patterns with different causes, a thorough diagnostic approach is needed.
History Historical and clinical details suggesting allergy are seasonality of lesions, exacerbated grooming, self-induced alopecia, miliary dermatitis, and erythema and oedema of the face, ears and eyelids, associated with other EGC lesions. The age of the cat is important, with genetic forms appearing in animals of less than 2 years.
Clinical examination Indolent ulcer The lesion is sufficiently characteristic for a diagnosis to he made. If the ulcer is not associated with other EGC lesions but is associated with seasonal excessive grooming or miliary dermatitis, an allergic cause must be considered. Indolent ulcers are often associated with flea allergy dermatitis but also with allergy to aeroallergens and food items.
Eosinophilic plaque In areas most commonly affected (abdomen, thighs), clinical diagnosis is straightforward and can be confnmed by cytology (presence of eosinophils) (Fig. 12 : 22). The aim of the clinical examination is to find other lesional types. If the plaque is associated with other EGC lesions, a more thorough diagnostic investigation - involving flea control, elimination diet, intradermal testing, having the cat in a restricted area, and antibiotic therapy - is necessary.
www.vet4arab.co.cc 12 :Eosinophilic granuloma complex
Figure 12 :9 : Ulceraied eosinophilic plaques in a cat wlrh a fwd allergy to lmnb
Figure 12 :11 :Eosinophilic granu and thorax (courtesy o f Z Alkaidari)
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Figure I2 :10 :Same cat as in Figure 12: 9. Recurrence of lesions following reinnoduction of lamb meat afer resolution of lesions: note resolution and appearance of new lesions at the back of the knee
Figure 12 :12 :Eosinophilic granuloma (linear)on the lateralforelimb (courtesy of Z. Alhaidari)
Figure 12 : . ,~smophrlrc granulomas on the plate The whrfish appearance is connected wrth collagen necrosis (courtesy of DM. Carloni)
Figure 12 :14 :Eosinophilic granuloma on the chin
Figure 12 :15 :Hypersensitivity to mosquifo bites: depigmentation, erosions ami crust on the nose fineluding nasalplanurn), note mosquito on the lesion
Figure 12 :16 :Hypersensitivity to mosyuuo u6cn. wvr,rry uzrrrurrd lesions on the nose (including nasal planm), note mosquito on the lesion
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Eosinophilic granuloma The lesion is sufficiently characteristic for a diagnosis to be made. In a young animal, a linear form is suggestive of a limited familial form. With other forms, histopathological examination allows confirmation of the diagnosis, the histopathological features being characteristic. Chin lesions, which are generally asymptomatic, can sometimes he associated with a mosquito bite allergy dermatitis in its non-pruritic granulomatons form. Extensive oral lesions or an association of the three clinical forms (for example indolent ulcer, plaques and oral granulomas) on the same animal often pose difficulties in aetiological diagnosis.
Histopathological diagnosis In order to eliminate all other differential diagnoses, histopathology is necessary in the following circumstances: when several clinical forms of EGC, especially oral ulcerated lesions, occur on the same animal; when appearance or distribution of lesions is atypical (back, face); and when there is a poor response to standard treatment (Table 12 : 2).
Indolent ulcer Histopathology is of little value, unless biopsies are taken from fresh, peripheral lesions. Histopathological features are poorly specific (superficial, hyperplastic, ulcerated, neutrophilic, perivascular dermatitis) and vary according to the stage of lesion. A recent ulcer (48 to 96 hours old) is characterised by a cellular infiltrate composed mainly of eosinophils. An ulcer that has .been developing for between 3 days and 3 weeks will also show collagen degeneration. In an old chronic ulcer, the predominant features will be a cellular infiltrate rich in mononuclear cells and neutrophils, and dermal fibrosis; an eosinophilic infiltrate and collagen degeneration are seen much more rarely ','.
Eosinophilic plaque Histopathological lesions are characterised by epidermal parakeratosis and acanthosis (with ulcerated areas lined with fihronecrotic tissue), spongiosis and eosinophilic, intra-epidermal vesiculation. Dermal lesions involve mainly eosinophilic cellulitis but mast cells and plasma cells can also he found. Eosinophilic folliculitis is also sometimes seen
Eosinophilic granuloma Histopathological lesions are characterised by a palisading granuloma rich in inflammatory cells (macrophages, giant cells) around foci of collagenolysis (Figs 12 : 23,24). Eosinophils and mast cells are also present
Mosquito bite hypersensitivity Histopathological lesions have the same features as those described earlier for the classic forms of EGC 6,18.
Differential diagnosis Although the differential diagnosis list for indolent ulcer, eosinophilic plaques and linear granuloma is small, it is often much larger for the atypical forms (Table 12 : 2).
Allergy diagnosis For the clinical forms associated preferentially with allergies, the differential allergy diagnosis is based on successive trials to eliminate a cause at each step: control of flea infestation, elimination diet, placing the cat in an environment free of mosquitoes etc.. However, when several clinical forms are observed on the same animal or when large or buccal granulomas are present, an inverse sequential allergy work-up may be indicated. This consists of eliminating all the possible causes in one go, over a period of 4 to 8 weeks, while preventing the cat from grooming. The cat is hospitalised in a mosquito-free place, treated for fleas, given antibiotic therapy and fed an elimination diet. It also wears a buster collar. Two or three anti-flea treatments are recommended along with use of a flea comb to check efficacy of treatment. Intradermal testing should then be carried out to demonstrate a possible allergy to house dust mites, pollens or insect bites. Using this protocol, plaques and some granulomas will get better within one or two weeks, but calcified granulomas regress a lot more slowly taking one to two months. Once lesions have disappeared, the buster collar is removed and each suspected cause is tested in turn. If no relapse is seen, antibiotic
www.vet4arab.co.cc 12 : Eos~noplul~c granuloma complex
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figure 12 :17 :H)pe~rrnririvrgro mosqu~fobites: ulcerario~rcon rhe no,r (inrl~tdingr ~ n iplankm,, ~l larer~lpitmdeand jorelimk
Figure 12 :18 :Same cat as in Figure 12 :17: in addition to previous lesions, note the presence of ulceratedpapules on the medial pinnae
Figure 12 :19 :Same cat as m figures 12 :17,18~m a r k d swellmng @ the fompads
Figure 12 Hypersensirivitg to mosquifo bites: indolent ulcer and lingual eosinophilic granulomas
Figrrre 12 :21 :Hypeisens~f~v~ty io mosquito htes oral eostnoph~lrc granulomas
Figure 12 :22 :Cytolog~nrlsmear of an aosimph~licplaque note that only arsrnopluls are present (stonred wrth RAL,x 1MO) (courtesy of D N Carf~flr)
FigunM :23 :Histopafholog~calsection ofan eosrrwphrlic granuloma' note central collagenolys~sflanked mmocMphages artaged in a pdrsade (pal~sad~ng granuloma) (stainedwlthH a n d E , x 2 0 (covrfesy o f J P Magml)
Figure 12 : 24 :Hrslopatholog~calsectton of a lmgual eosinoph~ltc granuloma w ~ t ha fragment of rnsect leg (starned w ~ t hH and E, x 200)
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Tableau 12 : 2 :Differential diagnosis of the different forms of the EGC Indolent ulcer Squamous cell carcinoma Mast cell tumour Excessive grooming in lactating queen Herpesvirus or calicivirus infection Cryptococcosis Eosinophilic plaques Cutaneus epitheliotropicT cell lymphoma Mast cell tumor Squamous cell carcinoma Cutaneous metastasis of mammary carcinoma Demodicosis Poxvirus infection Subcutaneous mycoses Systemic mycoses Idiopathic ulcerative dermatosis Mycobacterium infection Chronic abscess Xanthoma
Oral granulomaslulcers Squamous cell carcinoma Fibrosarcoma Lymphosarcoma Pemphigus vulgaris Plasma cell stomatitis Vial stomatitis (hevesvirus or calicivirus) Plaques and granulomas of the digits Plasma cell pododermatitis Bite abscess Tumours Contact dermatitis Herpesvirus or calicivirus infection Poxvirus infections Mosquito bite hypersensitivity Dermatophytosis Pemphigus foliaceus Food allergy Notoedric mange Demodicosis
treatment may be contmued and the previous diet reintroduced (Figs 12 : 9,lO). If, after one week, there has been no relapse, some fleas, gathered either with a comb or bred specifically, can be placed on the cat. Reappearance of lesions, excessive licking, nibbling or scratching are considered diagnostic of the suspected trigger. This diagnostic procedure is lwgrhy, restrictive and onerous and requires understanding and rigour on the part of both the owner and the vet. However, it is sometimes necessary when dealing with long-standing or recurrent forms of the condition.
Treatment Treatment has often been l i i t e d to the use of anti-inflammatory drugs without taking into account the aetiology and the possibility of treating the cause ".I9
Aetiology-based treatment Aetiology-based treatment is essential and reduces the frequency of recurrence. It is based on draconian flea control measures for flea allergy dermatitis, a hypoallergenic diet for food intolerance and possibly immunotherapy for atopic dermatitis 2,9,'1.
Symptomatic treatment Symptomatic treatment is always necessary whether or not a cause has been demonstrated.
Corticosteroids represent the most widely used first line of treatment in the form of methylprednisolone acetate, given by intramuscular injection (4 mgkg repeated every 2 to 3 weeks and given a maximum of 3 times) or oral prednisone or prednisolone (1-3 mgkg SID for 4 weeks and then on alternate days) 9. Antibiotics may be used in the symptomatic treatment of indolent ulcers which respond well to the following antiicrobial agents: nimethoprim sulphur (30 mgikg BID), cephalexin (20 mgkg BID), doxycycline (10 mgkg SKI) and claavulanic acid-potentiated amoxycillin (12.5 mgkg BID). Antibiotics should certainly be given as a first line of treatment and even constitute a long-term solution which is preferable to giving cmticosteroids. Response of some ulcers to antibiotics does not
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necessarily confirm a bacterial cause as many antibiotics also have anti-inflammatory properties ','".
Megestrol acetate is also used in the treatment of some intractable forms of EGC at a dose of 2.5 - 5 mglcat, orally, every 48 hours, until resolution. The dose can then be reduced (2.5 - 5 mg every week or every two weeks). However, side-effects (diabetes mellitus, polyphagia, mammary hyperplasia, pyometra, behavioural disorders and hyperadrenocorticism) are such that this treatment is best avoided in cats ' , I 9 . Cyclosporin (5-8 mg/kg SID) given orally, has recently been used with success for intractable, corticosteroid-resistant forms of EGC (eosinophilic plaques, indolent ulcers and oral granulomas). Improvement is seen withii two weeks. Treatment is then continued at the same dose for 2 weeks before reducing the frequency to alternate days. No side-effects have been seen la. Other medical therapies have been proposed, either to be given alone or along with oral corticosteroids. These include chlorambucil (0.1-2 m a g SID or every 2 days) given orally and cyclopbosphamide (1 mgkg SID) given orally, 4 days out of 7. These therapies are not devoid of sideeffects and serum biochemistry and haematology profiles should be taken regularly. Chrysotherapy (aurothioglucose, 1 mgkg, by intramuscular injection, once weekly until remission, then once monthly) has sometimes been beneficial in the treatment of indolent ulcers '. Radiotherapy, laser therapy and surgical excision have been used with success in some cases of indolent ulcer 9,2'. However, given the lack of severity of these lesions and the fact they tend to be painless, it is important to discuss the condition with owners and to avoid tlying every available intensive therapy just for the sake of resolving an ulcer. The role of such therapeutic options as antimitotic therapy and radiotherapy is questionable '.
REFERENCES 1. Langford, L. W. & Sdby, L A. Vetermary Medec~ne/Smalih1m1 C l i n m 7 4 665667(1979j. 2 Rosenkranh, W. S. hCureuVerennory Dernznfdpgy (eds Griffin, CB.,Ewochka, &W.& M a c W 4 R . W . ) 319-324@50sbyYearBook,St Louis, 1993) 3. W@mmn, G, T. &Bate, M. 1.J.Amer.Anim Hosp A m . 20,325-331 (1984). 4. Scott,D. W,J Amer A m . Kosp Assn 12,261-Z0 /1976). 5. Rosdm%W.S. Vet. F e u 1,29-31(1989J 6. Mason, C. V. & Evw,A 0.J. Amsr Vet.Med edsn. l98.2086-208811991). 7. Neufeld, J L ,Bumn, L. 8r J e f f e ~K. R Ikt Pafhol. 17,97-99 (1980). 8 Rower,H. T. Proe AAVD.ACVD, San F r d n ~ f ~ o(1990) 45 9. Power, H. T.& Ihrke, I? J. Vet.Clin. N.Amer 25,833350 (1995). 10. Russell, R G.,Slatturn, M. M.& A W i f z , I. Vet P~ntlti.25,249-250 (1988). 11. Gelberg, H.B., Lewis, R. M,Felsburg, P. J. & S&, C k A m J. Vet, Res. 46,263-265(1985). 12 Howard, E B. B Jannke, C,C.Amer J &t. Ctin Pathal 221.26 11958). 13. McDwgal, B. L. M&n VFet Pmcf.67,639-633 (1986). 14. Reedy, L.U J.Amer.Adrn Kosp.Assn. 18,618-623 (1982). Is.Nman, T.B , Cohen, 5. G & Ottesen,E. A, Allergy Pmc.9,641447 (1988). 16. Weller, P. F. Currdnr Oprnion III I m n o t ~ & 685.90 ~ (1994). 17. koa, D.W J Am.Anim, H~osp,Assn.16,33f-459(19801. 18, Nagata, M. & Wda, T Vef. Dexmatol 8,lP-26 (1997). 19. Romantowski, 1 J Amer. Vef.Md.Assn. 194,700 7M. 11989). 20, Guagn&e, E,,MIaud, P. Observnfionspersonnellesnoapublides (1999). 21. Manning, T.0. $em,Vet Med Sug 3,%6211(1987).
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T. Willemse
I Auto-immune dermatoses Auto-immune dermatoses are rare. They are characterised immunologically by the deposition of autoantibodies at various levels of the epidermis (pemphigus) and basement membrane (bullous pemphigoid) or immune complexes within the basement membrane (lupus erythematosus). An understanding of them is important as they enter into the differential diagnosis of many different conditions. The pemphigus complex consists of several forms: pemphigus vulgaris (PV), pemphigus foliaceus (PF) and pemphigus erythematosus (PE). PE could be a benign form of PF or a form intermediate between pemphigus and lupus erythematosus Bullous pemphigoid (BP) has just recently been identified in the cat I. Discoid lupus erythematosus and systemic lupus erythematosus are encountered only exceptionally 1,2,4.
Aetiopathogenesis Pemphigus Pemphigus dermatoses are characterised by intraepidermal fissures caused by loss of cellular adhesion in the epidermis. Their incidence is very low in the cat, although PF is the most common form. In some animals, drug administration (e.g, amoxycillin, cnnetrdine, sulphonamides) may act as a trigger 12. No age, breed or sex pred~lectionhas been reported although as a general rule, these dermatoses are seen more often in middle-aged and older cats '>. The antigens responsible are desmosomal glycoproteins of the cadberin group of intercellular adhesion molecules Is. In dogs, the desmosomal cadherm involved in PE is desmoglein 1 (Dsg 1, molecular weight 148-150 kD). In man and the dog, the antigen involved in PV is desmoglem 3 (Dsg 3, molecular weight 130 kD). In the cat, the target antigens have not yet been characterised, but are most likely to he similar in ongin and molecular weight. Desmogleins are associated with a desmosomal plaque protein called plakoglobln which plays an important role m cellular adhesion. There seems to be a heterogeneity in the compositron of desmosomes at different levels of the epidermis, which could explain why acantholysis (the process associated with loss of desmosomal cohesion) occurs suprabasally in PV and relatively more superficially in PE. Antibody binding is seen at all levels of the epidermis in all forms of pemph~gus.Antibodies could provoke cell separation in the area where the target antigen is the main adhesion molecule I
The trigger factors are not clearly established. Immunogenetic studies m man have shown an association between pemphigus and major histocompahbllity complex HLA-DR4. It is well estabhshed that drugs with a sulphydryl group may directly trigger acantholysis. Ageing and alteratron of the immune system also contribute to development of auto-immune msease through loss of tolerance to auto-antigens and through cross-antigenicity between these auto-antigens and external agents such as viruses'.
Bullous pemphigoid ., BP has recently been reported in two adult cats, one a European, the other a Hnnalayan l. Immunological studies have demonstrated the presence of IgG auto-antibodies both m the serum and fixed within the basement membrane, directed agaurst the epitope NC16A of the antigen BP180, or colIagen XVII, of molecular weight 180 kD. Collagen XVII is a major constituent of hemidesmosomes '.
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Lupus erythematosus In lupus erythematosus (LE), tissue damage is the result of the deposition of type UI immune complexes in the epidermal basement membrane and other organs (in the systemic form) Both systemic (SLE) and cutaneous (discoid - DLE) forms of the disease are rare. No age or sex predilection has been reported but Siamese, Persian and Himalayan cats seem to be predisposed. Ultraviolet (UV) rays, live attenuated viral vaccines and genetic factors could be predisposing. However, only the influence of UV light has been demonstrated 2",7. UV rays could provoke cellular lesions with enhanced expression of intercellular adhesion molecule 1 (ICAM-1) and auto-antigens by keratinocytes. These could lead to auto-antibody production, immune complex deposition and antibody-dependent cytotoxicity of keratinocytes '. These immune complexes could also be responsible for vasculitis lesions seen in the kidneys and other organs.
Clinical features Pemphigus vulgaris is characterised by involvement of the oral cavity and mucocutaneous junctions (lips, nostrils, eyelids, vulva, prepuce, anal region). Primary lesions are vesiculobullae, which due to their extreme fragility, develop rapidly into erosions, ulcers, collarettes and crusts. Rarely, these primary lesions transform into pustules. Cats are almost always affected systemically ' . I . Pemphigus foliaceus produces exclusively cutaneous lesions, initially localised to the nose and pinnae (Figs 13 : 1,2). More rarely, onychomadesis, paronychia and footpad lesions (hyperkeratosis and ulcers) may be seen (Fig. 13 : 3). Multiple nail bed lesions with a creamy exudate are very suggestive of PE. Primary lesions are mainly vesiculobullae or pustules which due to their fragility, develop into erosions, ulcers, scales and crusts. In most cases, the reason for consultation is the appearance of crusts. In exceptional cases, PE presents as large crusts, arranged in a serpiginous pattern on the abdomen, inguinal regions and axillae (Figs 13 : 4 3 . As a general rule, development is slow except for the ventral form. The cat is often affected systemically I,'. Pemphigus erythematosus resembles PF with photosensitive lesions being found on the face and pinnae l a (Figs 13 : 6,7). Bulbuspemphigoid is a localised dermatosis in the cat, characterised by vesicles, erosions and crusts in the oral cavity, around the lips and on the pinnae '. Discoid lupus erythematosus generally affects the face and pinnae and sometimes the footpads " (Figs 13 : 8-12). Lesions are sometimes photosensitive and resemble those seen in PF, with the exception of pustules which are never seen in DLE. Pruritus is variable. Systemic lupus erythematosus is clinically extremely variable. Systemic signs include fever, anaemia, glomeruloneplnitis, polyarthritis and sometimes ulcerative stomatitis (Figs 13 : 13-15). About 20% of cats with SLE present with skin lesions including erosions, ulcers, crusts mainly on the face (nose, eyelids, lips and pinnae) and feet '. Paronycbia and ouycbomadesis may also be seen. One case of a cat with both DLE and SLE has been reported '.
Diagnosis
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Pemphigus The diagnosis is based on the history (age of onset of lesions, response to prior therapy, etc ...), climical examination, cytology of smears, histopathology of biopsies and in rare cases direct imunofluorescence 1~2~6~a, This last procedure is usually unavailable, expensive and of very limited diagnostic value. Pemphigus is normally diagnosed from clinical information and histopathology.The determination of antibody titres against Dsgl and Dsg3 in order to differentiate between mucosal dominant PV, mucocutaneous PV and PF, as done in humans 'is not yet available for cats.
Cytology ofpustular contents can be very suggestive of pemphigus. If many pustules are present, multiple smears can be made, revealing lots of rounded acantholytic keratinocytes arranged either
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13 :Auto-iiune demtoses
F@re I3 :I :Crusflmg and emslons around rke lrps, and on the chin and nose in a car witkpemph~gwlfolaceus
Figure i3 :2 :Bilaieral pinnal cruding in a cat wiih pemphigus foliaceus
Figure 13 :4 :Numerou pernphrgus fohaceus
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pustules on tke abdomen of a cat wrth
Figure 13 :5 :Same cat us in&ure 13.4 wrth pustules, crusts and cellarettes
Figure N :6 :Small c r u b and eroswns on the bridge of the nose and nasalplanum in a cat withpemphigus erytkemntosus
Figure 13: 7:Pustules and crusts on the edgr of fhepinna tn a cat wrtk pemphrgus erythemntosus
Figure 13 :8 :Crusting on theface and neck m a cat wi erytkematosus*
.J I lupus ~
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singly or in groups (rafts). In PF and PE, non-degenerate neutrophils are also common (Fig. 13 : 16). If there are few pustules, histopathology of skin biopsies is preferred to cytology '".
Histopathological examination is the diagnostic procedure of choice. Using this procedure, @e different types of pemphigus can be distinguished Although definitive diagnosis is sometimes impossible, multiple biopsies from lesions like pustules often does allow a diagnosis to be made. Hospitalisation may he necessary to enable biopsies to be taken at the most appropriate time. I n pemphigus vulgaris, the characteristic lesion is a suprabasal cleft or vesicle caused by acantholysis.
The basal cells remain attached to the basement membrane and look like a "row of tombstones". Vesicles contain few inflammatory cells. Dermal lesions are non-specific I n pemphigus foliaceus, typical histopathological features include subcorneal intraspinous pustules,
and ~ustulesin the hair follicle outer root sheath. In these pustules, acantholytic keratinocytes, arranged singly or in clumps, may possibly be associated with nowdegenerate neutrophilsand sometimes eosinophils. Acantholytic keratinocytes have eosinophilic cytoplasm, well-defined borders and a viable nucleus which differentiates them from necrotic keraiiocytes I n pemphigus erythematosus, histopathological findings include subcomeal pustules containing
acantholytic keratinocytes, similar to those seen in PF, and a moderate lichenoid reaction. Along the basal layer, hydropic and apoptotic keratinocytes are common, along with lichenoid interface dermatitis and pigmentary incontinence. Inhaspinous and mural follicular pustules tend to be more common than subcorneal lesions
The differential diagnosis should initially include dermatophytosis, demodicosis and notoedric mange. Further diagnostic tests (e.g. elimination diet, FIV serology, antigen capture for FeLV) should then be carried out depending on the history, presence of pruritus and the appearance and distribution of the lesions
Bullous pemphigoid Diagnosis is usually based on clinical features and histopathology. For the time being, direct and indirect immunofluorescent techniques remain only clinical research tools I.
Histopathological examination is the diagnostic procedure of choice. It reveals changes very compatible with BP: demo-epidermal clefting and eosinophils within the resulting vesicles '. The differential diagnosir should include all the facial, oral, erosive and ulcerative dermatoses.
Discoid lupus erythematosus The diagnosis is usually based on clinical features and histopathology.
Histopathological examination is the diagnostic procedure of choice. It reveals changes very compatible with DLE: a lichenoid inflammatory infiltrate, consisting of lymphocytes and plasma cells which may also extend into the hair follicles and adnexae. In addition, hydropic degeneration an& apoptosis of basal layer keratinocytes and the follicular infundibulum may be seen. The differential diagnosis should include all the facial, pedal, erosive, ulcerative and crusting dermatoses.
Systemic lupus erythematosus The diagnosis is usually based on clinical, histopathological and immunological features.
Histopathological examination of skin biopsies reveals very compatible lesions. They are similar to those seen in DLE, but lvm~hocvtes . & . are the predominant cell type .. in the lichenoid infiltrate. There is also a thickening of the basement membrane. A necrotising and leucocytoclastic vasculitis may be associated with the interface dermatitis. Other diagnostic procedures including haematology and biochemistry profiles and antinuclear antibody (ANA) testing are necessary.Yet more diagnostic tests, relating to non-dermatological signs, may be indicated. These might include cytology of synovial fluid and lymph nodes, histopathology of hustle biopsies and elec~omyelography(EMG) The differential diagnosis should include all the erosive, crusting, facial and generalised dermatoses.
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Fig~igure13 :9 :$mail crusts on lhepinna ofa cat w ~ t hdrsco~d1quS erytkemafosllf
Figure 13 :10 :Vesicles andpapules on thepinna of a cat with discoid lupus eryfhematosu*
Figure 13 :11 : Ulceraflon~dong the pinnd ma~#ns of a Mf wifR drscoi luprrs erythemafosus
Figure 13 :12 :Thickening of the footpads in a cat with discoid lupus eiythematosus
Pigure 13 :13 :Stm'f~sand gt_"'.+". in a cat wirk Systemic Lupus eryrkmiosus
Figure 13 :14 :Crusting and erosions around the eyes and on the ears in a cat with systemic lupus eryrhematosu
Figzire 13:lf :Polymthnt~si n p cat wrthsysfem~clupus eryfhen...(courtesy of 6 Hubert)
Figure 13 :16 :Smear showing numerous acantholytic keratinocytes (+j and neutrophils in a cat with pemphigus foliaceus (stained with D@-Quik, x 250)
* Wilki"s~;TBKueman,l P YILDammol 1,19-M(1989).
A M c a l Guide m Feline tol logy
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Prognosis-Treatment
P e m p h i g u s PV is the form of pemphigus for which the prognosis is gravest despite immunosuppressive doses of corticosteroids and supportive therapy. With PF and PE, the prognosis is good in the majority of cases although most cats require life-long therapy la. Corticosteroids are the treatment of choice. Although topical corticosteroids can sometimes be useful, this option is usually impractical. Oral prednisone or prednisolone (2-4 m a g SID) will normally induce remission. Once improvement has been seen, altemate day therapy should be given. It is important to use the lowest possible dose that will control the dermatosis so as to reduce the risk of side-effects. Sometimes, PF and PE do not respond to prednisolone. In such cases, dexamethasone may produce spectacular regression In cases where corticosteroid therapy does not give satisfactory results, chlorambucil or gold salts may be used. Azathioprine is contraindicated in cats because of serious toxic side-effects resulting in irreversible and fatal leucopaenia and thrombocytopaenia La,'o. Chlorambucil (0.1 m&g SID or 0.2 mgkg every other day) is an orally administered alkylating agent which can be given alone or along with corticosteroids. Although less toxic than other akylating agents, haematology profiles should be monitored every 2-4 weeks because of possible bone marrow suppression. Gold salts (chrysotherapy) may be useful in cats which do not respond to other treatments or wdich exhibit unacceptable side-effects to them lo.Cbrysotherapy bas been shown to be effective in feline pemphigus. The initial dose of aurothioglucose is 1 m a g given by intramuscular injection. This is followed by weekly injections (provided there are no side-effects) at 1 m&g until remission is seen. The interval between injections is gradually extended until only one injection is given each month for 6 months. About 25% of corticosteroid-resistant cats respond to chrysotherapy Cats undergoing therapy with gold salts should be monitored clinically, and with blood tests, for side-effects including, in particular, renal, haematological and dermatological (e.g. toxic epidermal necrolysis) disease '. In PE, the cat should avoid exposure to sunlight in addition to receiving medical treatment. In cases where a drug is suspected of being a trigger for the condition, this and all chemically-related products should be avoided.
Bullous pemphigoid Prognosis is variable. Treatment involves oral immunosuppressive doses of corticosteroids (e.g. prednisolone 2 m a g BID) until resolution of lesions. The dose is then given on altemate days. Clinical remission lasting more than six months without treatment has been seen in one out of two reported cases I.
Discoid lupus erythematosus Prognosis is usually good. Topical corticosteroids and avoidance of sunlight are sometimes suffuient If not, oral corticosteroids or chlorambucil can be given, using the doses for pemphigus.
Systemic lupus erythematosus The prognosis is very guarded. Systemic immunosuppressive treatment should always be suggested even though response to this treatment is very variable and often poor.
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REFERENCES 1. Scott, D.W., Miller Jr, W.H. & Grifb, C.E. Muller &Kirk's Small Animal Dermatology. 5th edition (Saunders, W.B., Philadelphia, 1995). 2. Wdemse, T. Clinical Dermatology of Dogs and Cats. 2' edition (Elsevier - Bunge, Maarssen, 1998). 3. Olivry, T., Chan, L.S., Xu,L. Vet. Pathol. 36,328-335 (1999). 4. Wfflemse, T. & Koeman, LP.Vet. Dermatol. 1, 19-24 (1989). 5. Wakelin, S.H. & Wojnarowska,E in Skin Immune System (SIS) - Cutaneous immunology nndClinicallmmunodermato1ogy(ed Bos, J.D.) 445-460 (CRC Press, New York, 1997). 6. Suter, M.J., De Bmin, A. & Wyder, M. and others inAdvances in Veterinafy Dermatology. vol. 3 (eds Kwochka, K.W., Wfflemse, T. & von Tschamer, C.) 321-337 (Buttenvorth & Heinemann, Oxford, 1998). 7. Bos, J.D. & De Rie, M.A. in Skin Immune System (SIS) - Cutaneous Immunology and Clinical Immunodermatology (ed Bos, J.D.) 471-478 (CRC Press, NewYork, 1997). 8. Yager, J.A. & Wdcock, B.P. Color Atlas and Tert ofSurgico1 Pathology of the Dog and Cat (Wolfe Publishing, London, 1994). 9. Amagai, M,, Tsunoda, K., Z i n s , D., Nagai, T. & Nishikawa, T. J. Amer Acad Dermatol. 40,167-170 (1999)
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Dermatological manifestations of systemic diseases Dermatological manifestations of systemic diseases are starting to be documented in the cat, although their pathogenesis is not always understood. They are very diverse clinically and relate to various systemic illnesses. Their diagnosis is important as these skin lesions enter into the differential diagnosis of many different conditions. They also appear before the underlying illness. Unlike in the dog, endocrinopathies very rarely cause skin lesions in the cat. Spontaneous and iatrogenic Gushing's syndrome are very rare, spontaneous hypothyroidism is exceptionally rare, hyperthyroidism produces a few non-specific changes in the skin, and dermatological signs associated with sex hormone imbalance are now hotly disputed. On the other hand, the cat has a whole range of systemic disease-associated dermatological lesions, all of its own.
Pancreatic paraneoplastic alopecia Aetiopathogenesis Pancreatic paraneoplastic alopecia (PPA), described only in the cat, mainly affects aged animals I-'. No breed or sex predilection has been reported. The mechanisms to explain the association between skin lesions and the internal tumour, a pancreatic or biliaq adenocarcinoma, metastasised to the liver, are not understood. It is oossible that neoolastic cells produce cytokines responsible for follicular atrophy. Immnnohistochemical markers have to date, not revealed anomalies in insulin, glucagou, adreno-corticotropichormone (ACTH) or somatostatin production '.
Clinical features Dermatological signs, which precede systemic signs associated with the tumour, are very suggestive of PPA. They are characterised by the sudden appearance of abdominal alopecia. The face, limbs and flanks are subsequently affected (Figs 14 : 1-4). Hair loss is total; the skin adopts a characteristic shiny hue, sometimes with black spotted pigmentation (Fig. 14 : 3). Footpads may undergo dermoepidermal separation, which can be very painful. Concomitant Malassezia dermatitis may also be seen '. Systemic signs are not very specific (abdominal dilatation, poor condition, depression, weight loss, anorexia), worsen rapidly and are fatal '".
Diagnosis The diagnosis is based on the appearance of skin lesions associated with severe systemic signs, suggestive skin biopsies, and abdominal ultrasound. Histopathological examination of skin biopsies reveals almost complete absence of stratum comeum (hence the shiny appearance of the skin), marked telogenisation of hair follicles, follicular atrophy and moderate, non-specific dermal penvascular inflammation '" (Fig. 14 : 5). Y&sts of the genus Malassezia are sometimes seen in the remaining stratum cornem or hair follicle infnndibulum '. Haematology and serum biochemistry profiles reveal slight, non-specific changes, which are not even suggestive of pancreatic or biliary tumours.
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Abdominal radiography does not identify the primary pancreatic tumour, although localised mineralisation of the duodeno-pancreatic region can he seen. Radiographs of the lungs may demonstrate possible metastasis. Ultrasound scanning allows pancreatic and biliary turnours to be visualised, and especially hepatic and biliary metastases. This procedure requires excellent quality equipment (7.5 MHz or 10 MHz) and an experienced operator. An ultrasound-guided needle aspirate may suggest the origin of the tumour. CT scanning of the abdomen is very useful in demonstrating the tumour and its metastases. Necropsy generally reveals neoplasia which has already metastasised to the liver, peritoneum and lungs (Fig. 14 : 6). The primary tumour is often a pancreatic, or more rarely a biliary, adenocarcinoma. The differential diagnosis must include spontaneous and iatrogenic Cushiug's syndrome, causes of symmetrical alopecia, telogen effluvium and superficial necrolytic dermatitis.
Prognosis - Treatment The prognosis is very poor. In the absence of visible metastasis on radiography and ultrasound, an exploratory laparotomy may be indicated. Temporary resolution of PPA, following partial pancreatectomy, with improvement in general condition and hair regrowth has been seen, confirming the paraneoplastic nature of the cutaneous lesions I. All other cases reported have died very soon after diagnosis, due to the generalised distribution of the tumour ','".
Superficial necrolytic dermatitis A dermatosis resembling superficial necrolytic dermatitis (SND) in the dog has recently been described in two female, 11-year old cats, in relation to a pancreatic tumour one with and one without metastasis.
Dermatological signs were characterised by alopecia, non-pnuitic erythema, erosions and crusts. In one case, the dorsal skin was thickened and fissures seen over the thorax *. In the other case, the alopecic skin was shiny around the axillae l. Histopathology of skin biopsies revealed lesions compatible with SND seen in other species (man, dog) and was characterised by parakeratotic hyperkeratosis and intraepidermal oedema. Necropsy in both cases revealed a pancreatic adenocarcinoma, one without metastasis and the other with hepatic and mesenteric metastasis 6. The many similarities between SND and PPA suggest that these two dermatoses could be dermatological expressions of the same pathological process.
Acquired cutaneous hyperfragility syndrome Acquired cutaneous hyperfragility syndrome (ACHS) is a rare dermatological syndrome characterised by skin fragility leading to skin thinning and spontaneous non-haemorrhagic and non-painful tearing.
Aetiopathogenesis ACHS is often idiopathic, although the underlying cause must always be looked for and treated where possible. Underlying causes include spontaneous Cushing's syndrome (very rare in the cat), iatrogenic Cushing's syndrome caused by excessive use of corticosteroids (rare) or megestrol acetate (more common), diabetes mellitus, hepatic lipidosis', and cholangiocarcinomas. No age, breed or sex predilection has been reported. Pathogenesis is unknown. Severe metabolic disorders could exacerbate a subclinical cutaneous asthenia and thus trigger ACHS.
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Figure 14 :1 :Pancreatic paraneoplastic alopecia: note shiny app;.::..::::: of the skin
Figure 14 : 3 :Pancreatic paraneoplastic alopecia: note shiny appearance of the skin and the presence of black pigmented macules on the abdomen
Figure 14 :4 :Pancreatic paraneoplastic alopecia. note almost generalised shiny appearance of the skin
Figure 14 :5 :Pancreatic paraneoplastic alopecia, note epidermal, follicular and adnexal atrophy (H andE, x 100) (courtesy of T. Olivfyj
Figure 14 :6 :Pancreatic paraneoplastic alopecia, note pancreatic tumour and hepatic metastases (courtesy of B. Atlee)
Figure 14: 7 :Acquired cutaneous hyperfragility syndrome in a cat with hepatic lipidosis
Figure 14 :8 :Idiopathic acquired cutaneous hyperfragility syndrome, presentfor several months in a cat which has already had several suture repairs.
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Clinical features Dermatological signs are characterised initially by skin thinning, followed by spontaneous tearing on minor trauma (restraint, scratches, injections...) (Figs 14 : 7,s). These tears often extend to become very large. At the edge of these tears, the skin is extremely thin, l i e cigarette paper. Bleeding and pain are usually absent. Systemic signs vary according to the underlying illness
Diagnosis The diagnosis is primarily clinical because the appearance of the lesions is very unmistakable. The search for an underlying illness should always be conducted using specific diagnostic tests (ACTH stimulation test, blood glucose, etc....).
Histopathology of skin biopsies reveals marked epidermal and dermal atrophy. The epidermis is composed of only one layer of keratinocytes. Collagen fibres are few and pale 9. Hair follicles are very small. However, taking skin biopsies is very difficult as adipose tissue often separates from the dermis. The differential diagnosis must include cutaneous asthenia, a term which refers to a group of congenital collagen and elastin disorders seen in young animals.
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Prognosis 'Ikeatment The prognosis is very guarded. There is no specific treatment. Wounds can be sutured but healing is difficult. The underlying illness must be treated.
Paraneoplastic exfoliative dermatitis Aetiopathogenesis Paraneoplastic exfoliative dermatitis (PED) is a dermatological paraneoplastic syndrome associated with development of a thymoma "". Regression of skin lesions after removal of the tumour confirms the paraneoplastic nature of the dermatosis. PED is seen mainly in adult or aged cats (older than 10 years. No breed or sex predilection has been reported. The pathogenesis is not clearly understood. In man, there are many paraneoplastic immunological syndromes associated with thymomas but it is only recently that an exfoliative dermatitis has been linked to this type of tumour 15. PED is probably caused by an auto-immune cell-mediated process. When thymomas occur, immature auto-reactive T lymphocytes could be responsible for attacking keratinocytes. The presence of cytotoxic CD8tT lymphocytes in the lesional epidermis supports this hypothesis ".
Clinical features Dermatological signs appear early on and precede the systemic signs. They are characterised by a non-pruritic, very erythematous dermatitis becoming exfoliative, initially on the head, neck and pinnae and eventually over the whole body 'O-". (Figs 14 : 9-1 1). Bacterial and fungal (e.g. Malassezia dermatitis) infections may complicate the picture ". Sometimes, skin lesions are the only clinical manifestation. Systemic signs linked to thymoma development include coughing, dyspnoea and quite non-specific signs (anorexia, lethargy, muscle weakness) la".
Diagnosis The diagnosis is based on the appearance of skin lesions, identification of a thoracic tumour and skin biopsies.
Histopathology of skin biopsies is characterised by an interface dermatitis with hydropic
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Figure 14: 9 : Paran~opla~nc e ~ f ~ l t r r drtmanrir ne norr ayrhema and nwrkrl i;rI!ng o!! fbefacr ( C O U ~ 0~ fPTI Olivry, ).
Figwe 14: 11 :Same cat as in Figures 14 :9 and 14 :10: note alopecia andpsoriasiform scaling on the neck (courtesy of T. OlivryJ
Figure 14 : 13 : Paraneoplastic exfoliative dermatitis: thoracic in front of radiograph (lateral view): note region offluid density the heart, suggest in^ a tumour (courtesy of T. Olivry and C. Rivierre)
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Figure I4 :10 :Some i a f or rn Figure 11 9 n6te eqthzmo and rcalmg p,oriastjorm on rbe las~,alpl,lna(Coerfer) ,f 'I.Olllr?
kyperplasia, dermal lymphoplasmytic infiltration, keratinocytes and absence of sebaceous glands (cou
surgery: note multiple cysts within the tumour (courtesy of T. Olivry and C. Rivierre)
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theface andears, and the v e v inflamedappearance of the skin (courtesy of T. OIivq and C. Rivierre)
Figure 14. Jame cat as in Figure 14 :15: resolution of skin lesion? 5 months after surgery (courtesy of T Olivty and C. Rivierre)
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degeneration of basal cells, apoptosis of keratinocytes, pockets of satellitosis and a lymphocytic dermal inflitrate '"'3 (Fig. 14 : 12). Absence of sebaceous glands was reported in one case ".
Thoracic radiography c o n h s the presence of a mediastinal mass compatible with a thymoma (Fig. 14 : 13).
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Ultrasound scanning of the tumour reveals a hyperechogenic mass or the presence of lots of hypoechogenic regions (multilobular cystic mass). Ultrasound-guided samples can he obtained for cytology. Cytology of needle aspirates demonstrates a very rich population of small mature lymphocytes, mast cells and eosinophils Id. Histopathology of the tumour usually reveals a benign thymoma lo-"(Fig. 14 : 14). Blood tests can show a very significant increased level of creaiiine phosphokinase (CPK) suggesting an associated polymyositis like that seen in man li, and my~glohiiuriae~~. The differential diagnosis must include all exfoliative dermatoses (cheyletieUosis, dermatophytosis, allergic dermatitis, cutaneous drug reaction, herpesvirus-associated erythema multifome, autoimmune dermatoses, lymphocytic folliculitis and epitheliotropic T cell lymphoma).
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Prognosis Treatment The prognosis remains guarded although complete surgical removal of the thymoma and sternal lymph nodes has produced resolution of the thymoma and skin lesions withim a few months (on average 4-5 (Figs 14 : 15, 16).
Paraneoplastic pruritus Paraneoplastic pnuitus in association with an oral epidemoid carcinoma has been demonstrated in a 13-year old cat 16. This generalised pnuitus, affecting mainly the distal limbs, was characterised clinically by selfinduced lesions (alopecia, excoriations and crusts). Complete regression of pruritus was observed 5 days after removal of the tumour and persisted for 2 months. Local recurrence of the tnmour led to reappearance of pnuitus.
Degenerative mucinous lymphocytic mural folliculitis Degenerative mucinous lymphocytic mural folliculitis (DMLMF), also called sebaceous pseudo-adenitis refers to a group of dermatoses, which are probably all different, that manifest lymphocytic mural folliculitis, detectable on histopathol~gy'"'~.
Aetiopathogenesis Aetiopathogenesis is not understood but immunological mechanisms are thought strongly to be involved No breed or sex predilection has been reported but DMLMF affects mostly middle-aged or older cats.
Clinical features Dermatological signs are characterised by diffuse alopecia, with easily epilated hairs, and severe scaling on the head, limbs and trunk (Figs 14 : 17-19). Bilateral ceruminous otitis is very often seen. Pruritus is variable"-'8. Systemic signs are not very specific (lethargy, dehydration...).
Diagnosis The diagnosis is based on clinical appearance of the skin lesions, systemic signs and skin biopsies.
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nphocytic mucinous degenerative mural folliculitis: Figw note diffuse alopecia and intense scaling on the face, limbs and trunk (courtesy of T. Olivryl
Figure 14 :18 :Same car as in Figure 14 : 17: close-up of the face (courtesy of T OlivryJ
Figure 14 :19 :Same cat as in Figures 14 :17,18: note difise alopecia and scaling on the trunk (courtesy of T. Olivry)
Figure 14 :20 :Lymphacytic mucinous degenerative mural folliculitis: note lymphocytic mural folliculitis and the granulomatous reaction around the sebaceous gland (H & E x 400) (courtesy of T.OlivryJ
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Figure 14 : 21 : hyperadrenocorticism: note pendulous abdomen and fruncal alopecia
tears (acquired cutaneous hypeeagility syndrome) afier iwo days hospitalisation
* Guagu&n,E., Hubcn.B.& Ihlabre. C. Vli Dermolol. 3. 1-12 (1992).
Figure 14 :22 :Hyperadrenocorticism in a cat: note skin atrophy and prominent subcutaneous blood vessels (courtesy of D.W. Scott)
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Histopathology of skin biopsies is diagnostic and reveals mainly a mononuclear cell infiltration along the hair follicles and in the sebaceous glands, responsible for their destruction (Fig. 14 : 20). Follicular mucinosis 1b18and hydropic interface dermatitis are sometimes seen. The differential diagnosis must include all exfoliative dermatoses (cheyletiellosis, dermatophytosis, allergic dermatitis, cutaneous drug reaction, herpesvirus-associated erythema multiforme, autoimmune dermatoses, paraneoplastic exfoliative dermatitis and epitheliotropic T cell lymphoma).
Prognosis - Treatment The prognosis is very grave. The condition is invariably fatal for no precise reason. Response to corticosteroids and synthetic retinoids is very variable.
Hyperadrenocorticism Spontaneous hyperadrenocorticism, also called spontaneous Cushimg's syndrome, involves a collection of clinical signs, supported by diagnostic test results, relating to excessive cortisol production by the adrenal glands. This syndrome is rarely seen in the cat'"'.
Aetiopathogenesis Spontaneous hyperadrenocorticism may be pituitary-dependent (80% of cases) or adrenal-dependent (adrenal tumour) (20% of cases). In over 50% of cases, this type of hyperadrenocorticism is associated with diabetes mellitus. No breed or sex predilection has been seen hut the condition mainly affects animals aged between 7 and 15 years (average age: 10 years)1521.
Clinical features Systemic signs are a constant feature and involve polyuria-polydipsia (90-loo%), polyphagii'(80100%) and abdominal enlargement (70.95%) (Fig. 14 : 21). The presence of diabetes mellitus that is non-responsive to insulin should lead to suspicion of hyperadrenoc~rticism'~~~', Dermatological signs are not always seen. Truncal alopecia is only seen in 60 to 80% of cases (Fig. 14 : 21). Skin atrophy is often marked (Fig. 14 : 22). A cutaneous hyperfragility syndrome, seen in 15 to 30% of cases, is a dermatological expression of hyperadrenocorticism peculiar to the cat (Fig. 14 : 23).
Diagnosis The diagnosis is based on the combination of the suggestive systemic and dermatological signs and the results of adrenal function tests.
Serum biochemistry profiles. These are non-specific and often show hyperglycaemia, sometimes marked. Serum alkaline phosphatase (SAP) levels are very rarely raised due to the absence of adrenocortical-induced SAP in the cat. Hormonal assays are also hard to interpret in the cat, given the small number of cases of hyperadrenocorticism documented. Adrenal function tests used in the dog can also be employed in the cat. The ACTH stimulation test (blood samples taken at T 0, T 0 t 1 hour or T 0 + 45 minutes, and T 0 + 75 minutes after the intramuscular injection of 0.25 mg ACTH) will confirm an abnormally high response in 80% of cases of hyperadrenocorticism. The urinary cortisol creatinine ratio (UCCR) could be used in the catz0since it is elevated (50-270 x lo4) in all the cases of hyperadrenocorticism studied. In normal cats or cats with other illnesses, the values range from 0.6 - 75 x lo4 20~2'. The low dose dexamethasone suppression test (0.01 mgkg N ) will diagnose most cases of hyperadrenocorticism in the cat lq1O. Some authors have proposed a dose of dexamethasone of 0.1 mgkg2'. The high dose dexamethasone suppression test (HDD) (0.1 mgkg IV '9,m or 1 mgkg2') will theoretically differentiate between pituitary-dependent hyperadrenocorticism and an adrenal tumour but there have been too few cases of hyperadrenocorticism described in the cat to be able to assess the
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diagnostic value of this test.
New medical imaging techniques will probably be used in the future for diagnosing spontaneous hyperadrenocorticism in the cat. Ultrasound has not been fully evaluated. CT scanning of six cats with pituitary-dependent hyperadrenocorticism (PDH) revealed a macroadenoma in four casesz0.
Treatment Medical treatment is difficult and poorly documented. 06-DDD does not seem to produce side-effects '9,2', but this product has never been used successfully in the cat ". Ketoconazole does not seem to suppress cortisol production in the normal cat and its use has been disappointing =. Metyrapone (65 mgikg BID or TID), given orally, inhibits adrenal 11 R-hydroxylase and blocks the conversion of ll-deoxycortisol to cortisol. It has been successfully used in one cat which became controlled within 24 hours with resolution of its diabetes". Taking into account the rapid effects on cortisol secretion and therefore on resistance to insulin, the animal should initially he hospitalised to prevent hypoglycaemia or an Addisonian crisis. L-deprenyl has not yet been used in the cat. However, it deserves to be tried given the importance of the pars distalis in this species, and its probable, more frequent involvement in feline pituitarydependent hyperadrenocorticism. A dose of 1-2 mgkg SID could be proposed. Surgery seems to be the current treatment of choice, both for adrenal tumours and for PDH. For PDH, bilateral adrenalectomy with supplementation of mineralocorticoid and glucocorticoid is performed. It seems that post-operative management is easier in the cat than in the dog. Out of five cats treated with this regime, three were cured, one remained diabetic and one was lost to follow up2'.
Cutaneous xanthoma W o r n a s are cutaneous or yellowish subcutaneous lesions associated with an ammulation of lipid in subcutaneous connective tisue. In the cat, they are mostly idlopathie, butmay be cawed by familial bypetchylomicronaemia, spontaneous diabetes mellitus, or prolonged xlmhtration of megestrol acetate.
Clinical features Dermatological signs are chxacterised by papules, plaques or yellowish cutaneous or subcuraneous nodules, resembling candle-uax (Fig. 14 : 24). These non-pruritic lesions have no pred~lectionsitFd. Systemic Signs vary a m lipid deposits) may be seen.
to ihe.underlying cause, Ocular s i p s (associated with inmcomeal
Diagnosis The diagnosis is based on appearance of skin lesions and skin biopsies. Ifa xanzhoma is present, a search should always be conducted for an underlymg systanic illness.
EIIstoputhology of skin biopsies reveals typital lesions chatacterised by rhe presence of foamy histiocytes associated with multinucleategiant cells; Touton cells. Sudan red can be used to stain lipid within the histioctyes.
A blood lipid pro@ (e.g. cholesterol, triglyceriides, lipoprotein electr&horesis, chylomicrons and lipoprotem lipase) should be carded out.
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Prognosis Treatment The prognosk and treatment depend on the underlying systemic illness. A low-fat diet has, in some
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REFERENCES 1. Brooks, D. G., Campbell, K. L., Dennis, 1. S. & Dunstan, R. W. J.Amer Anim. Hosp. Assn. 30,557-563 (1994). 2. Pascal-Tenorio,A,, Olivry, T., Gross, T. L., Atlee, B. A. & Ihrke, P. 1. Vet. Dermatol. 8,47-52 (1997). 3. Hodson, S., Griffon, D., Nuttall, T. J., Hill, P. B. & Withbread, T. J. Proc. ESVD-ECVD, Maastricht 164 (1998). 4. Godfrey, D.R. J. small Anim. Pract. 39,394-396 (1998). 5. Patel, A,, Withbread, T J. & McNeil, P. E. Vet. Dermatol. 7,221-226 (1996). 6. Runge-Hams, U.Proc. ESVD-ECVD, Maastricht, I75 (1998). 7. Diquelou, A. Prat. Mdd. Chir Anim. Comp. 26, 151-158 (1991). 8. Regnier, A. & Pieraggi, M. T.J. small Anim. Pract. 30,419-423 (1989). 9. Gross, T. L. Ihrke, P J. & Walder, E. 1. Veterinary Dermatopathology (Mosby Year Book, St Louis, 1992). 10. Loveday, R. K. J. South aj? Vet. Assn. 30, 33-34 (1959). 11. Carpenter, 1.L. & Holzworth, I. J Amer. Vet. Med. Assn. 181,248-251 (1982). 12. Scolt, D. W.,Yager, 1. A. &Johnston, K. M. Feline Practice 23, 8-13 (1995). 13. Forster-van Hijfte, M. A,, Cultis, C. E &White, R. N. J. small Anim. Pract. 38,451454 (1997). 14. Rivierre, C. & Olivry, T.Prat. Mid. Chir. Anim Comp. 34,531-537, (1999). 15. Holder, 1. Clin. Exp. Dermatol. 22,287-290 (1997). 16. Paterson, S. Proc. ESVD-ECVD, Maarhichf 163.164 (1998). 17. Declercq, 1.Vlaams Diergeneeskd Ejsckrifr 64, 177-180 (1995). 18. Gross, K. L. & Olivry, T. Proc. ACVP (1997). 19. Nelson, R. W., Eeldman, E. C. & Smith, M. C. J Amer Vet Med.Assn. 193,245-250 (1988). 20. Meyer, H. P. & Voorhout, G. Proc. ESVD-ECVD, Maastricht 69-72 (1998). 21. Ze~be,C. A. in Current Veterinary Therapy X (ed Kirk,R.W.) 1038-1042 (Saunders, Philadelphia, 1989). 22. Henry, C. J., Clark, T.P.,Young, D. W. & Spano, J. S. J. Vet. lnt. Med. 10, 123-126 (1996). 23. Willard, M. D., Nachreiner, R. F. &Howard, V. C. Amer. J. Vet. Res. 47,2510-2513 (1986). 24. Daley, C. A,, Zerbe, C. A,, Schick, R. 0. &Powers, R. D. J. Amer Vet. Med. Assn. 202,956-960 (1993). 25. Jones, B. R. Feline Practice 16.7-10 (1986). 26. Grieshabert, T.L. and others J.Amer Anim. Hosp. Assn. 27,509-512 (1991). 27. Kwochka, K. W. & Sholt, B. G. Comp. Cont.Educ.Pract. Vet. 6, 185-191 (1984). 28. DCnerolle, P. Prat. Mid. Chir Anim. Comp. 27,549-554 (1992).
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E Delisle - P. Devauchelle
1 Skin tumours Tumours of the skin and its adnexae are some of the most diverse and common tumours seen in the cat. Such a large variety is possible because the skin is made up of lots of different components, each of which can potentially form a tumour. We can therefore see epithelial tumours which involve the malpighian layer, the adnexal sebaceous or sweat glands and hair follicles; tumours of the melanin synthesising system; mesenchymal tumours developing in the dermis or subcutaneous connective tissue; tumours derived from lymphoid tissue; and finally, nerve and vascular tumours. The majority of skin tumours in the cat are primary, with secondaq tumours occurring much more rarely '. Skin tumours make up 20 to 30% of all tumours (only lymphoid tumours are more common). Their high incidence is matched by their severity with the ratio of malignant to benign tumours being 3: 1 in the cat and only 1:2 in the dog. Although epithelial and mesenchymal tumours are equally represented, the different types of tumour do not occur at the same frequency. Four of them, squamous cell carcinoma, basal cell tumour, fibrosarcoma and mast cell tumour, make up about 70% of skin tumours in the cat. The relative frequency of these four types of tumour is cul~entlychanging. Although epithelial tumours have long been the most common, mesenchymal tumours, especially fibrosarcomas, have now taken over the top spotzd.
Squamous cell carcinoma Squamous cell carcinomas (also called epidemoid carcinomas) are epithelial tumours derived from keratinocytes. When the tumour remains smctly localised in the epidermal layer and hair follicles, it is referred to as being non-invasive or in st&. However, when it passes through the basement membrane and invades the underlying dermis, it becomes known as invasives.
Aetiology In catg, the invasive stage is preceded, in most cases, by an in situ stage, which itself follows a precancerous lesion associated with solar dermalosis (actinic keratosis). It is highly likely that exposure to sunlight is involved in the development of these tumours, which occur typically in sparsely-haired or hairless areas of unpigmented skin such as the p h l marg'is, eyelids, nasal planum and lips. White cats are 14 times more Iikely than pigmented cats to present with squamous cell carcmoma. There is no breed or sex predisposition for this tumour but most affected cats are aged between 9 and 12 years'.
Clinical features These tumours involve mainly the face, and more precisely the tips of the ears, the eyelids, nose and nasal planum, and hps (Figs 15: 1-7). Multiple and/or bilateral tumuurs are not uncommon. Local development is slow. Actinic keratosis of the pinna is characterised by erythema followed by scaling and crusting. The lesion becomes surrounded by a waxy crust and foms an indurated plaque. When the area around the eyelids is affected, wythematous and erosive lesions CM he seen. No matter where it oecurs, squamous cell carcinoma is usually characterised by a deep ulcer covered with crust. It can also be associated with raised lesions but this is less common5.
Development - Prognosis After a period of growth in st&, the tumour breaks through the basement membrane and invades the
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underlying dermis. It then acquires metastatic potential, although spread to other organs and lymph nodes is rare and occurs slowly. Two cases of paraneoplastic hypercalcaemia have been reported6.
Diagnosis The diagnosis is histopathological. The histopathology of actinic keratosis is characterised by epidermal hyperplasia, enlarged keratinocytes and sometimes pronounced rete ridges. Although these ridges are always lined by an intact basement membrane, they are made up of atypical epithelial cells (e.g. very basophilic nucleus, two nuclei, large nucleolus or nucleus, increased mitotic activity, dyskeratotic cells). Sometimes, there is inflammation, increased vascularisation and hyalinisation of collagen fibres in the underlying dermis '. The histopathology of squamous cell carcinoma is characterised by proliferation of anastomosing and branching cords invading the dermis. These are made up of polyhedral epithelial cells, joined by spinous bridges, with atypia and variable mitotic activity. These epithelial cells undergo collective keratinisation with the development of horn pearls or individual dyskeratosis. A severe, fibrous stromal reaction is often seen. A histopathology-based grading system (Broders) has been devised to give an accurate prognosis. The percentage of differentiated (keratinised) cells is assessed: the higher the score, the more aggressive and malignant the lesion. Very undifferentiated forms (fusiform or round cells) are difficult to differentiate histopathologically from fibrosarcoma in cats.
Treatment Initial treatment involves early, extensive surgery. The average survival time following pinnal amputation is 2 years, and after excision of the nasal planum, 8 months a (Figs 15 : 7,8). Radiotherapy (e.g. implant radiotherapy, cobalt therapy) can be used initially on small lesions, lesions that are nonoperable due to their size or location (Figs 15 : 9,10), or as adjunctive therapy after incomplete excision. The prognosis then varies according to the size of the lesion and how invasive it is (average survival time is 9 to 53 months depending on the stage) 9-'0. New therapies such as photodynamic therapy and proton therapy, have been carried out in a small number of cases with encouragingresults '. Systemic (adriamycin, mitoxantrone), or local (cisplatin), chemotherapy has been used selectively with variable results "-".Synthetic retinoids have been of little benefit in cats with pre-cancerous lesions".
Multicentric squamous cell carcinoma in situ (Bowen's Disease) A particular form of multicentric squamous cell carcinoma in situ is seen in the cat, the appearance and development of which are comparable to Bowen's disease in man ' i 1 8 . The aetiology is unknown although papillomaviruses seem to be implicated in 45% of cases 19. The condition is seen principally in cats over 10 years of age '5-'8. Quite a number of cases have been described in FIV-positive cats I6l8. Clinically, it is characterised by papules, nodules, and hyperkeratotic and hyperpigmented plaques which can become ulcerated (Figs 15: 11-14). The distribution of lesions is multicentric but involves mainly the face, shoulders and limbs Diagnosis is based on histopathology which reveals moderate to severe epidermal dysplasia with loss of polarity, variations in the association between nucleus and cytoplasm, variable mitotic index, isolated dyskeratotic keratinocytes and no rupture of the basement membrane '5-18 (Fig. 15:15). In some cases, Demoden sp. mites can he seen in the hair follicles within lesions (Fig. 15:16). Various therapeutic options have been proposed but it seems that synthetic retinoids, notably acitretin, given orally at a dosage of 1 mgikg BID until remission of lesions and then on alternate days, gives variable results depending on FIV retroviral status 18. This treatment requires regular monitoring: Schirmer tear testing every 2 months, and measurement of serum cholesterol, triglyceride and hepatic enzyme^'^.
Basal cell tumour (basal cell epithelioma) Basal cell tumours are epithelial tumours showing cytological characteristics of cells of the epidermal basal layer, i.e. cells which have not undergone epidermal differentiation and not, therefore, linked by spinous
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15 : Skin Tumours
Figure 15 :1 :Actinic keratosis on the eyelids, onepinna and the nasal planum (courtesy of P. Ddnerolle)
Figure 15 :3 :Actin~ckeratosis on the lefl ear and squamous cell carcinoma on the right ear
Figure I5 :4 :Squamous cell carcinoma on the right ear: note the deep ulcer covered with crust
Figure 15 :5 :Squamous cell carcinoma on the eyelids
Figure 15 :6 :Squamous cell carcinoma on the nasal planum
F i g w 15 :7 :Squamous cell carcinoma on the uasal planum before surgical removal of the uasalplanum (courtesy of C. DelabreJ
Figure 15 :8 :Same cat as m F~gure15 7, huo months after removal of the nasal planum (courtesy of C Delabre)
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bridges. Several types can be distinguished histopathologically (cystic, adenoid, ribbon, solid, medusa head), but the development and prognosis of the different forms are the ~ a m e ~ . ' ~ .
Aetiology Basal cell tumours are more common in the cat than in the dog and make up 11-26% of all skin tumours in this species 3 P . Their development does not seem to be dependant on sunlight. They occur in older cats with no sex or breed predisposition. Clinical features Basal cell tumours are most often characterised by a single lesion of 0.5 to 3 cm in diameter, on an area of pigmented skin. It is sometimes pigmented, taking on a bluish grey colour. This might suggest a melanoma although melanomas are rare in the cat. A site preference for the head and neck is sometimes reported, but the whole skin surface is susceptible. Multicentric forms occur very rarelyz0.
Development - Prognosis The tumour remains strictly localised. The prognosis is, therefore, good if treated appropriately.
Diagnosis The diagnosis is histopathological. Histopathologically, basal cell tumours are characterised by the proliferation of cords of basaloid epithelial cells coming from the basal layer of the epidermis. These cords can present in several patterns, sometimes within the same tumour. A classification system based on these patterns, bas been devised. This system is strictly morphological and generally gives no indication of prognosis except perhaps for basosquamous types. Types of basal cell tumour include trabecular or solid, cystic, ribboned or medusa head, pigmented, keratinising, granulai cell, clear cell, basosquamous and fusiform cell'.
Treatment Surgical excision is the treatment of choice. Radiotherapy can also be used if size or location of the lesion or recurrence lead to surgery being unsatisfactoryi0.
Feline fibrosarcoma complex Epidemiology Tumours belonging to the "feline fibrosarcoma complex" are currently the most common tumours in the cat (12 to 41% of skin tumours) "U. In France, the average age of cats with fibrosarcoma is 9.6 years, but with a 95% confidence interval of 3.2 to 16 years, an unusually wide range for naturally occurring tumours. The age of cats with fibrosarcoma bas sometimes been shown to have a bimodal distribution, with one peak seen at around 6 or 7 years of age and a second peak at around 10 or 11 years ". However, the age range of cats with injection site fibrosarcomas is significantly very different to that of cats which develop fibrosarcomas at sites where injections are not normally given. Aetiology The aetiology of feline fibrosarcomas has been a matter of great controversy due to the suggestion that vaccination injections might increase the relative risk of developing a fibrosarcoma ",". This theory is based on: epidemiological data showing an increase in the incidence of feline fibrosarcomas correlated with the frequency of vaccinations (in particular the anti-rabies vaccination); a lowering of the age of cats with fibrosarcoma; and a change in the sites affected by the tumour (previously the distal limbs and head, now the injection site region)",26. clinical data showing an increased incidence of post-vaccination focal granulomatous panniculitis. Fibrosarcomas occur most commonly at the injection site region4.
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15 : Skin Turnours
rnoma on the nasalplanwn: note the
Figure 15 : 10 : Same cat as in Figure 15 : 9, five weeks after radiotherapy
Pigure IS : 11 : Squamous cell carcinoma ln sltu note the hyperkeratonc and prgmented plaque m rhe pre-femporal regron (courfeqof T Olivryi
Figure 15 : 12 : Squamous cell carcinoma m s~tu. nore the hyperkerafottcand encrustedplaqueon the lateralprnna (courfesyo f P D6nerolleJ
Figure 15 : 13 : Squomous cell carcinoma in sltu. nate the hyperkeratohc and encrustedplaqueson the sides of the nose (courresy of E Bensrgnorj
Figure 15: 14: Squamous cell carernoma In situ note the deep ulcerofed appearance of the amour In rhw case,pmgressron towards a squamous cellcarcinomn can be seen (courtesy of P D4nerollej
Figwe I$ :1.5 :Sqcell canrnoma m situ note the neoplasnc pml!ferahon wrlhfn the epidermis In one place f j, a breach of the h m t &me can be seen (H&E,x 100) (courtesy@T OlrwyJP
Figure 15 :16 :Squamous cell cgrcmoma m slhl Note the presence of (I numerousDemodex m ffiehaafollicles occurring intralesionaliy+ (H&E, ~ 2 5 0(courtesy ) of T Olcvryj
Figure 15 :9 ;Squnmous c in"aS.
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histopathological data: aluminium has been found in macrophages in some fibrosarcomas (aluminium hydroxide is the main adjuvant of many vaccines); injection site fibrosarcomas have a significantly different histopathological appearance; post-vaccination reactions to the rabies agent have been induced e~perimentally~~; data from comparative pathology: in humans, chronic inflammation linked to foreign bodies, infections or to aluminium-containing bone implants can lead to sarcoma development. Although it is very likely that vaccination injections do induce neoplastic transformation, it is hard to know if they are the sole cause, or whether any injection of initant or allergenic substances could he involved. Some authors also point the fmger at injections of long-acting therapeutic products. This wider theory suggesting that cancer may be linked to chronic inflammatory phenomena is not new, either in the experimental field (chemo- or radio-induced tumours) or for naturally occurring tumours (e.g. appendicular osteosarcomas at the site of previous fractures, oesophageal osteosarcomas and infestation by Spirocerca lupi, intra-ocular sarcomas and eye trauma). The cancer-causing mechanism associated with either vaccination or therapeutic injections is complex and involves inflammation and oncogenes. In the cat, a possible role of viral oncogenes FeLV or FeSV (Feline Sarcoma Virus) has been eliminated following a study involving a series of injection site fibrosarcomas in which these oncogenes were undetected by PCR (Polymerase Chain Reaction). On the other hand, a rare form of viral-induced multicentric fibrosarcoma occurs. This fibrosarcoma is caused by the FeSV virus which mainly affects young animals. FeSV is defective in genes permitting its replication. It therefore has to "borrow" the genes required for its replication from the FeLV virus (cats with viral-induced fibrosarcoma must have been infected by FeLV 17).
Clinical features Tumours of the "feline fibrosarcoma group" are characterised clinically by subcutaneous, firm, nodular or multi-nodular lesions. They are non-painful (except when very large andlor have infiltrated into deeper structures) and initially non-ulcerated (Figs 15 :17-21). They occur most commonly at injection sites: the interscapular region, dorsal neck, thorax, lumbar region and thighs (Figs 19 :1921). Involvement of the face and distal limbs, previously described as classic, is now rare (Figs 15 : 17,18). The speed of development of fibrosarcomas is very variable. Nodules can remain small for a very long time or may rapidly double in size. It seems that this growth may accelerate in line with the number of surgical excisi~ns~'.~. Grauulomatous panniculitis is a non-neoplastic lesion, seen usually in the weeks following a vaccination or other injection. Injections of anti-rabies vaccine " or long-acting therapeutic agents are most commonly involved. Clinically, it is cbaracterised by the sub-acute or chronic development of an erosive or ulcerated, painful area at injection sites, particularly in the interscapular region lg.
Development - Prognosis Fibrosarcomas, malignantfibrous histiocytornas and other similar sarcomas are very aggressive locally and show frequent post-surgical recwence. Metastasis, usually to the lymph nodes or lungs, is uncommon and seen in only 10 to 15% of cases. When it does occur, it is usually a long time after the development of the initial tumour.
Fibromatoses never metastasise but very frequently recur or develop in another place . Grauulomatous panniculitis can evolve towards a neoplastic form.
Diagnosis The diagnosis is histopathological. At present, there is no one recognised classification system. The British and Americans recognise the following histopathological types: fibrosarcomas, malignant fibrous histiocytomas, extra-skeletal chondrosarcomas and osteosarcomas, myofibroblastic sarcomas and rhabdomyosarcomas '. The terms used by most French pathologists are slightly different: true fibrosarcomas, malignant fibrous histiocytomas, undifferentiated sarcomas, extra-skeletal osteosarcomas and chondrosarcomas and fibromatose~~~.
True jibrosarcomas Currently, true fibrosarcomas constitute about 30% of the feline fibrosarcoma complex. They are very cell-rich tumours, made up of fusiform cells in a herringbone pattern within a discrete collagenous
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Figure 15 :1 7 : Digitalfibrosarcoma
Figure 15 :18 :Fibrosarcoma on a disral limb: note the very invasive appearance of the tumour (courtesy of B. Hubert)*
Figure 15 :19 :Fibrous histiocytoma on a distal limb (courtesy of JJ. Legrand)*
Figure 15 :20 :Invasivefibrosarcom~on the back and lumbar region
Figure 15 :21 :Ulceratedfibrvsarcomn on the back and lumbar region
Figure 15 :22 :Iridium implarti on afibrosarcoma on the back of a cat
Figrcre 15 :23 :'Mastocytic' mast cell tumon- on a distal limb: note the firm, fairly well-delineated nodule (courtesy of D. Fritz)
Figwe 15 :24 :Mult~cenfrzc'mastocy~c'mast cell ixmour on theface
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stroma. Cellular pleomorphism is marked: neoplastic cells are fusiform with an elongated nucleus and frequent nuclear atypia. There are numerous mitotic figures, and necrotic or haemorrhagic foci are common.
Malignant fibrous histiocytomas (MFH) Malignant fibrous histiocytomas make up about 60% of the tumours of the feline fibrosarcoma complex. These tumours are very polymorphic, with differences occurring not only between tuinours but also within the same tumour. MF'Hs are characterised by the combined presence of mesenchymal and histiocytic neoplastic cells within a relatively abundant collagen stroma. Sub-types of MFH have been recognised in relation to the presence of multinucleated giant cells (MF'H with giant cells) or abundant myxoid stroma.
Fibromatoses Fibromatoses are subcutaneous mesenchymal tumours characterised by well-differentiated fibroblastic proliferation associated with a dense collagenous stroma. Unlike in true fibrosarcomas, the fusiform cells have few nuclear atypia, and mitotic figures are rare. This neoplastic tissue can cause fibrosis and scarring. Some people distinguish nodular fibromatoses from the expansive growth of infiltrating fibromatoses. Careful histopathological examination of connective tissue and the fascia close to the fibroma, often reveals many subclinical neoplastic foci, sometimes quite far away from the macroscopically visible tumour. Hence, the high frequency of post-surgical recurrence with this type of tumour despite the weakly aggressive histopathological appearance of fibromatoses.
Other types Many other mesenchymal tumours occur suhcutaneously in the cat: undifferentiated sarcomas, osteosarcomas, chondrosarcomas, haemangiosarcomas, rhahdomyosarcomas, haemangiopericytomas and neurofibrosarcomas. These tumours are generally more similar in biological behaviour to the feline fibrosarcoma complex than their names would suggest. For example, subcutaneous haemangiosarcomas in cats metastasise no more than malignant fibrous histiocytomas, and in any case, much less than splenic haemangiosarcomas. Some anaplastic carcinomas can re'semhle undifferentiated sarcomas due to the fusiform appearance of their cells. Only immunostaining techniques with anti-cytokeratin and anti-vimentin antibodies will characterise precisely the embryonic origin of tumour cells. In essence, immunostaining of carcinomas is cytokeratin positive and vimentin negative, while immunostaining of sarcomas is cytokeratin negative and vimentin positive. Other monoclonal antibodies can then be used to determine more precisely the phenotype, and therefore the degree, of tumour cell differentiation. Only these immunostaining techniques will allow classification to develop".
Granulomatous panniculitis Granulomatous panniculitis is typically a well-circumscribed, subcutaneous, granulomatous, inflammatory reaction, consisting of a central necrotic area, invaded and surrounded by mononuclear cells (macrophages, lymphocytes, plasma cells) often in association with eosinophils. Cytoplasmic inclusions of greybrown amorphous material are often seen in macrophages infiltrating this lesion. This material could be a residue of non-absorbable adjuvant used in some vaccines. Granulomatous panniculitis could reflect a particular sensitivity of cats to vaccine adjuvants or slow-release excipients. If so, and this has never been proven, it could be a pre-cancerous lesion for tumours of the feline fibrosarcoma complex29.
Therapy is based on very wide surgical excision sometimes associated with other local or general treatments such as radiotherapy and chemotherapy respectively. Locally aggressive tumours require a combination of surgery and radiotherapy in order to reduce local recurrence. The aim of chemotherapy is to limit distant metastases. Immunogenotherapy is still experimental but preliminary results are encouraging.
Surgery Surgery is still the main treatment for feline fibrosarcomas. Early intenrention and wide surgical removal are both essential. In practice, if surgery is performed when the tumour is already large, removal will be difficult and therefore probably incomplete. Best results are obtained on tumours smaller than 1 cm3: any subcutaneous neoplasm on a cat must be removed and analysed as soon as
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possible. Fibrosarcomas are rarely encapsulated and frequently invade the muscles and adjacent fascia. All the muscle or adjoining fascia from which the tumour has developed should be removed. With interscapular fibrosarcomas, it is sometimes necessary to perform a partial scapulectomy, along with removal of the dorsal spinal processes (often the site of local recurrence).
Radiotherapy Radiotherapy, in association with surgery, is especially indicated for highly proliferative tumours and for those that are very prone to post-surgical local recmence. True fibrosarcomas, malignant fibrous histiocytomas and all soft tissue sarcomas with high mitotic indices seem to be good indications for additional radiotherapy. On the other hand, fibromatoses or sarcomas with a low proliferation fraction are not such good indications for radiotherapy. Factors limiting the use of radiotherapy in feline fibrosarcomas are their relative resistance to X-rays of doses less than 60 Gray, and the tendency of these tumours to develop close to healthy radiotherapy-sensitive tissues (lungs, spinal cord, liver and intestine). These technical factors immediately rule out the use of cobalt 60 radiotherapy (except in special cases). Side-effects following irradiation with such a high dose of cobalt therapy would be too severe.
Cobalt 60 radiotherapy In practice, cobalt 60 radiotherapy is used on feline fibrosarcomas in two situations: firstly, when wishing to reduce the size of a large tumour in order to facilitate its surgical removal, and secondly, if the tumour recurs in an area already irradiated. Doses in the order of 15 to 30 Gray are then used. Administering a soft tissue equivalent (bolus) allows the dose to be concentrated on the skin surface, limiting the skin-sparing effect, which in this situation can be a disadvantage. Interstitial radiotherapy (brachytherapy) Interstitial radiotherapy or brachytherapy is of great interest in the treatment of feline fibrosarcomas. Gamma rays emitted by iridium 192 are much less energetic than those emitted by cobalt 60. This results in faster absorption and less penetration. This technique therefore enables a total dose of 60 Gray to reach the chosen site, while limiting exposure of adjacent structures. Radioactive iridium implants are inserted subcutaneously at the site of surgical excision and left in place for as long as is necessary to deliver a total dose of 60 Gray on the treated site (Fig. 15:22). The best long-term results are obtained when brachytherapy is carried out within three weeks of fust-time, wide surgical excision of small tumours with a high mitotic index. In these ideal conditions, an average of over 24 months without recurrence can be obtained.
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Chemotherapy
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Tumonrs of the feline fibrosarcoma complex rarely metastasise (less than 15% of cases) and when they do, the process is slow. In addition, soft tissue sarcomas are not very sensitive to chemotherapy, either in human or veterinary medicine. The role of chemotherapy is therefore controversial. That said, chemotherapy, as an adjunct to surgery, can be given for lesions with a high mitotic index, but there are no recent publications on chemotherapy of feline fibrosarcomas. Adriamycin (25 mg/m2, given on 5 occasions over 3 weeks by intravenous drip in isotonic sodium chloride) is the drug with the greatest activity against fibroblastic tnmours in humans, and can be used for this purpose in cats.
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Non-specific immunomodulators Non-specific immunomodulators which were frequently used about twenty years ago have now been abandoned in veterinary medicine due to their weak activity. In the United States, only acemannan, an extract of Aloe Vera, is authorised for the treatment of various solid tnmonrs; however, its role is controversial.
Zmmunogenotherapy
In human medicine, the use of cytokines such as interleukin 2 or gamma interferon seems particularly promising, but toxicity, when given systemically, renders their use hazardous. The use of genetically modified cells to produce cytokines overcomes the problem of toxicity: VERO cells (derived from monkey kidneys), genetically modified to produce human interleu@ 2 (hIL2) have been used. Injected into the excision site, these VERO-hL2 cells behave like "pumps" manufacturing human interleukin 2. The release of interleukii 2 activates and stimulates the multiplication of immunocompetent cells in the tumour site, a certain number of which are specifically directed against tumour antigens present in the removed tumour. One study reveals a statistically significant reduction in recurrence, and even an improvement in overall survival, in cats treated with surgery + brachytherapy t VERO-hIL2 when compared to cats treated with surgery t brachytherapy only ''.
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Mast cell tumour Mast cell tumours arise from the many mast cells present in the dermis. Less prevalent than in the dog, they nevertheless represent the fourth most common type of skin tumour in the cat (4 to 21% of all skin tumours). Visceral mast cell tumours are also seen.
Epidemiology - Aetiology Mast cell tumours occur mostly in older cats (9 years old, on average) without any breed or sex predisposition. There seems to be no association between cutaneous and visceral forms which usually develop separately.A "histiocytic" mast cell tumour has been described in young Siamese cats (aged less than 4 years). Their aetiology is unknown".
Clinical features Clinically, "mastocytic" mast cell tumours are usually characterised by a single, firm,well-delineated dermal nodule on the face (pen-orbital area), neck (in more than 50% of cases), or distal limbs (Fig. 15:23). Multicentric forms are seen (Fig. 15:24). The "histiocytic" mast cell tumour, seen in the Siamese, often consists of several large masses on the head and neck3'.
Development - Prognosis Not all authors agree on the behaviour of feline mast cell tumours. Some consider these tumours to he aggressive whereas others see them as carrying a more favourable prognosis. The "histiocytic" mast cell tumour, seen in the Siamese, carries a good prognosis and can spontaneously regress.
Diagnosis The diagnosis is histopathological. "Mastocytic" mast cell tumours are characterised histopathologically by dermal andlor subcutaneous sheets of round, independent cells with a central nucleus and granular cytoplasm, eosinophils and lymphoplasmacytic cells. Tumour cells are mostly well-differentiated and grading is less important in establishing prognosis than in the dog '. "Histiocytic" mast cell tumours are characterised histopathologically by dermal andlor subcutaneous sheets of round independent cells with a central nucleus and a sparsely granular cytoplasm. Metachromatic staining is weak and cells are histiocytic in appearance. Eosinophils and lymphoplasmacytic cells occur as in the "mastocytic" forms7.
Treatment When there is only one tumour, surgery is the treatment of choice, but further tumours may develop at additional sites and clinical monitoring is therefore advised. For multiple well-differentiated mast cell tumours, palliative excision can be performed on lesions whose growth would not be satisfactorily checked by medical treatment (corticosteroids and vincristine). For recurrent andlor large tumours, radiotherapy has been shown to be effective when used alongside surgery and chemotherapy.
Other tumours Ceruminous gland tumours Ceruminous gland tumours, also called ceruminomas, develop from the cemminous glands. These modified apocrine sweat glands are not attached to hair follicles and are distributed over the cutaneous lining of the external ear canal. They can undergo neoplastic transformation which may be benign (adenoma) or malignant (adenocarcinoma). Adenocarcinomas are more common than adenoma~'~~'. The clinical picture is that of a chronic suppurative otitis extema, usually unilateral. Auroscopic examination of the ear canal reveals the presence of single or multiple, pink or pigmented, ulcerated or non-ulcerated, sessile or pedunculated nodules which can vary considerably in size from a few
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millimetres to several centmetres (Figs 15: 25,26). Cemminomas can cause destruction of the parotid region. Other clinical signs (e.g. head tilt, Homer's syndrome, facial paralysis and vest~bularataxia), indicating middle or inner ear involvement, may or may not be associated with signs of otitis extema. Recurrent or bilateral lesions are common. In adenocarcinomas, metastasis to the regional lymph nodes occurs in 15 to 20% of cases7.". Although cemminomas are small, surgical excision and histopathology allow malignancy to be determined and appropriate therapy established (e.g. more radical surgery or supplementary radiotherapy). For large lesions (greater than 5 mm), early extensive surgery (ablation of the ear canal and bulla osteotomy) is recommended. If involvement of the middle or inner ear is suspected, a CT scan will reveal the extent and feasibility of surgery. Surgery is difficult and the one year post-surgical survival rate is low (30%). However, in one study involving 16 cats treated with ear canal ablation and bulla osteotomy, the average survival time was 42 months and the 1-year survival rate was 75%. Additional radiotherapy can improve the prognosis In one study involving 6 animals, all were still alive after 39 months3'. j2.
Cutaneous epitheliotropic lymphoma Cutaneous epitbeliotropic lymphoma, also called mycosis fungoides, is rare in the cat "". It affects mainly animals over 10 years of age. No breed or sex predisposition has been reported. Skin lesions are very variable and are characterised initially by often pruritic, generalised erythema and scaling, followed by self-induced erosive lesions (Figs 15:27,28). Sometimes, these lesions can become really crusty. In this clinical stage, there are few systemic signs. The condition evolves slowly, over several months or even years, towards a multi-nodular form with lymph node hypertrophy (even spreading into the viscera) in the terminal phase (Figs 15:29,30). The diagnosis is histopathological. Histopathological examination of skin biopsies reveals a lichenoid infiltration in the superficial dermis, of medium-sized, irregular, polymorphic, lymphocytic cells (T lymphocytes) with irregular cerebriform nuclei. The tumour proliferates along the basement membrane at which it nibbles away. Intra-epidermal cavities filled with tumour cells (Pautrier's microabscesses) can be seen. The immunophenotype of the neoplastic T lymphocytes is CD4+, contrary to that observed in the dog. Various treatments have been proposed (corticosteroids, multiple chemotherapy, synthetic retinoids, radiotherapy), but none has produced satisfactory control.
Melanoma Cutaneous melanomas are rare in the cat 3536, ocular melanomas being more common in this species. They are usually seen in cats averaging between 8 and 11.5 years of age. There is no breed or sex predisposition. Most pigmented cutaneous nodules in cats are basal cell tumours. Lesions develop mainly on the ears, tail and limbs, and are characterised by small, pigmented, sometimes ulcerated, slow-growing nodules. The prognosis is usually favourable after surgical excision although metastasis to regional lymph nodes and viscera has been seen in some cases. For skin melanomas, there appear to be no histopathological criteria on which to base an accurate prognosis.
Cysts Cutaneous cysts are well-delineated, follicular or non-follicular cavities encased in the dermis. They are lined with a well-differentiated malpighian epithelium and contain keratin and possibly hairs and sebaceous and sweat secretions.
Epidermal cysts contain greyish or brownish pasty material. They can release keratin into the dermis causing a marked inflammatory reaction with cellulitis and sometimes fistula formation. The prognosis is good after surgical excision, but this is sometimes difficult because of the inflammation. Multiple cysts become a real problem because they are often accompmred by diffuse cellulitis in the cat. Follicular cysts are formed when obsmction of a follicular opening causes dilatation of a follicle. They contain keratin and glandular secretions'.
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Cutaneous metastases Cutaneous metastases of mammary adenocarcinomas Cutaneous metastases of mammary adenocarcinomas occur ventrally and are characterised clinically by sub-acute development of numerous, erosive, painful papules or plaques '. The diagnosis is histopathological. The differential diagnosis includes eosinophilic plaques. The prognosis is very poor. Only palliative therapy can be proposed as and when required.
Digital metastases of pulmonary adenocarcinomas Digital metastases of asymptomatic pulmonary adenocarcinomas are seen in the cat They are characterised by nodular, ulcerated, painful, single or multi-digit lesions which often cause ouychomadesis (Fig. 15 : 31). Radiographic examination reveals severe osteolysis of the phalanges of affected digits (Fig. 15 : 32). Thoracic radiography confirms the presence of an often asymptomatic pulmonary tumour. A biopsy of the osteo-cutaneous lesions reveals major infiltration of phalangial bone by tumour tissue consisting mainly of tubular structures lined by a prismatic epithelium, with, in the most differentiated cases, a pseudo-stratified epithelium consisting of ciliated cells and mucous caliciform cells. The pathogenesis of this particular metastasis remains unknown. Metastasis to the digits could be l i e d to the rich vascularity of the feline footpad. Pulmonary adenocarcinomas in the cat may metastasise to other locations apart from skin, including bone, muscle, eyes and kidneys. The prognosis is poor in the short term and treatment can only be palliative.
REFERENCES 1. Bostock, D. E. Br. Vet. J. 142,506-515 (1986). 2 Dom, C. R. J. Amer Anim. Hosp. Assn 12,307-312(1976). 3. Mialot, M. & Lagadic, M. Rec. Med. Vit. 166,937-947 (19%). 4. Millm, M. A., Nelson,S. L. &Turk, 1. R. Vet. Pathol. 28,389-39s (1991). 5. Ruslander, D., Kaser-Hotz, B. & Sardinas, J. C. Comp. Cont. Educ. Pract. Vet. 19, 1119-1129 (1997). 6. Klausner, 1. S., Bell, E W. & Hayden, D.W. and others J.Amer. Vet. Med A m . 196,103-105 (1990). 7. Gross, T. L. Ihrke, P. 1. & Walder, E 1.Veterinay Dermutopafhology w h y Year Book, St Louis, 1992). 8. WiUuav, S. 1. &Straw, R. C. J. Amer Anim. Hosp. Assn. 26,219-222 (1990). 9. Carlisle. C H. & Gould, S. Vet. Rndiol. 23, 186-192 (1982). 10. Theon, A. P.,Madewell, B. R. & Sheam V I. J. Amer Vet. Med. Assn. 206, 991-996 (1995). 11. Evans, A. G., Madewell, B. R. & Smdard, A. A. A. Amer J.*er.Res. 46,2353-2557 (1985). 12. Mauldin, G. N., Matus, R. E. & Pahlaik; A. K. J Vet. Int. Med. 2,6045 (1988). 13. Feaston, A. E., Leach, M. W. & Higgins, R J. J. Amer. Vet. Med Assn. 202, 1261-1265 (1993). 14. Theon, A.,'F VanVechten, M. K. &Madewell, B. R. J. Amer Vet. Med. Assn. 57,205-210 (1996). 15. Baer, K. E. & Heltan, K. Vet. PPofhi. 30,535-543 (1993). 16. Miller Jr, W, H., Affolter, V A. & Swtt, D. W. Vet.Demtal.3, 177-182 (1992). 17. Rawland, P., Affolter,V., Sutter, S. &Miller Jr, W. H. Vet. Pathol. 29,440 119B)). 18. Gnagusre,E., OlivryryT., Delverdier-Poujade, A,, Denerolle, P.,Pag&, 1. -P.& Magwl, J:P. Vet. Dermtol. 10, 61-67 (1999). 19. Lecleq, S. M., Clark, E. G. & Haines, D. M. P m . AAVD.ACVD, Nashville 125-126 (1997). 20.Ditte13,R. W. & Walsli, K. M. Vet. Pothol. 21,51-56 (1984). 21. Hendriek, M. I.,Shofer, F. S. & Goldschmidt, H, M. J. Amer. Vet. Med. Assn. 205, 1425-1429 (1994). 22. Weigand, C. M. & Brewer, W. G. Comp. Cont. Educ. Pmcr. Vet. 18,869-875 (1996). 23. Macy, D. W.& Bergman, P.1. Feline Practice 23,N-27 (1995). 24. Kass, P. H., Barnes, W. G.,Spangler, W. L., Chomel, B. B. &Culbetstbn, M. R. J. Amer. Vet.Med. Assn. 203,396405 (1993). 25. Hendrick, M.J. & Goldsdunidt, H. M. J, Amer. Vet. Med. krsn. 199,968 (1991). 26. Hendriks, W. H., Goldschmidt, H.M., Shofer, E. S., Wang,Y. & Somlyo, A. P. CancerResearch 52,5391-5394(1992). 27. Goldschmidt M. H. & Shofer,P. S. Skin tumors of the Dog and Cat (F'ergamon Press, NewYork, 1992). 28. Magnol, 1. P., Eoumel, C., Jaland,P.Y., Marchal, T. & Devauehelle, P.Potnf V6t. 22.43-50 831-838 (1991). 29. Hendrick, M. 1,& Dwgan, C A. J. h r . Vet. Med. Assn. 198,304.305 (1991). 30. Quintin-Colonna, E, Devauchelle, P., Radclizi, D., etal. Gene Therapy 3, 1104-1112 (1996). 31. Game, E M. & Lingeman, C. H. Vet. Pathol. 7,517-530 (1970). 32 Theon, A, P., Barthez, P. X,Madewell, B. R. & Griffey, S. J. Amer. Vet.Med Awn. 205,566-569 (1994).
I
www.vet4arab.co.cc 15 : Skin Turnours
Figure15 :25: Cerminorrr glandcamnoma lnvadrng the external ear note severe ulceranons
Figure 15 :26 :Vety invasive ceruminous gland carcinoma on the eat (courtesy of M. Mialot)
Figure 15 : 27 :Eprtheliotroprc lymphoma m a S~amesecot note erythema and scahng
Figure 15 : 28 : Epitheliotropic ljmphoma in a Siamese cat: note erythema and scaling
Figure 15 :29 :Multrceni~icepitheliofropic bmphoma (nodulurformj
Figure 15 :30 :Multicentric epltheliotropic lymphoma (nodularform)
Figure 15 :31 :Digital detastasis of an asymptomatic pulmonary odenocarcinoma: note nodular and ulcerated appearance (courtesy of S.W. White)
Figure 15 :32 :Radiographic appearance of digital melastases of an asymptomatic pulmonary adenocarcinoma: note severe phalangial osteolysis
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33. Marino, D. J., MacDonald, I. M., Matthiesen, D. T.& Patnaik, A. K. J. Amer: Vet. Med. Assn 204,54-58 (1994) 34. Baker, I. L. &Scott, D. W.J. Amei' Anim. Hosp. Assn. 25, 97.101 (1989). 35. Tobey, I. C. J Amer. Vet. Med. Assn. 204, 606-609 (1994). 36. Miller 11, W. H., Scott, D. W. &Anderson, W I. Ver. Dermarol. 4, 19-26 (1993). 37. Estrada, M. & Lagadic, M. Prat. Mid. Chir. Anim. Comp. 27,791-795 (1992). 38. May, C. & Newsholme, S. I. J. smaNAnim. Pracr. 30,302-310 (1989).
www.vet4arab.co.cc E. Guaguere - Z. Alhaidari - J. Fontaine
1 Genodermatoses Genodermatoses are rare, although they constitute a developing field in feline dermatology. In recent years, investigative procedures such as electron microscopy and immunohistochemistry have led to the identification of new genodermatoses. It is important to be familiar with these as they enter into the differential diagnosis of many different dermatoses. Genodermatoses affect the epidermis and its adnexae, the melanogenesis system, the dermo-epidermal junction and the dermis.
Hereditary greasy seborrhoea Aetiopathogenesis A hereditary greasy seborrhoea has been described in the Persian, the Himalayan and the Exotic Shorthu '. Thls genodermatosis, the mode of Inheritance of which is autosomal recessive, is very common in Canada and, to a lesser extent, the United States. In Europe, it is seen in animals descended from Canadian and American cats. No sex or colour predisposihon has been documented.
Clinical features Dermatological signs appear, in severe cases, from 2 days of age and are charactensed by a greasy, matted coat. Keratosebaceous deposits cover the skin and proximal hairs. There is progressive alopecia and bilateral ceruminous otitis is often seen. In milder cases, signs appear later from about the age of 2 months. The coat then appears dull and keratosebaceous deposits are less severe ' (Fig. 16 : 1).
Diagnosis Dlagnos~sis based on the history, appearance of skin lesions, and suggestive histopathology from skin biopsies.
Histopathology of skin biopsies reveals orthokeratotic hyperkeratosis, papillomatosis (sometimes severe), and nuld penvascular dermatitis '. The digerential diagnosis should include primarily cheyletiellosis, dennatophytosis and Malassezza dermatitis. Prognosis and treatment Theprognosis, dermatologically,is very guarded. In severe cases, these cats leave greasy deposits m their environment. Many colonies rapidly euthanase affected cats '. Topical freafment involves frequent application (up to once or twice a week) of keratomodulating shampoos (with no rebound effect) contaming, for example, salicylic acid and sulphut Tar is toxic to cats and shampoos containing it should be avoided. In severe cases, frequent cllpping is often necessary. Synthetic retinoids have not, to our knowledge, been used for this condition, but deseme to be tried. provlded their side-effects ' are taken into account.
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Congenital hypotrichosis has been reported in the Birman 2,' (Fig. 16 : Z), Burmese l , Devon Rex ' and Siamese l . Generalised congenital hypotrichosis has even been investigated in certain breeds like the Sphinx 4. The mode of inheritance is autosomal recessive. No sex predisposition has been documented. A few kittens in the litter are usually affected. Cats are born hairless or with a fine downy coat which falls out during the first weeks of life. Sometimes, a fine coat will develop in the first few months ' (Fig. 16 : 3). Other ectodermal abnormalities (e.g. absence of whiskers, claws or tongue papillae) may be associated with this condition in the Birman '. In the Burmese, the thymus has been reported absent '. Microscopical examination of a group of hairs demonstrates exclusively small, fine, secondary hairs (Fig. 16 : 4). Histopathological examination of skin biopsies reveals an absence or reduced number of hair follicles, or hair follicle hypoplasia Similar abnormalities occur in the sebaceous and sweat glands. There is no specific treatment. Topical treatment with highly emollient, keratomodulating shampoos and preparations containing essential fatty acids can improve skin quality.
Follicular dysplasia Follicular dysplasia has been reported in the Cornish Rex *. It was described in a 10-month old female tricolour (blue, white and beige) which had presented at birth with no hair on the tail and caudal thighs. At 8 months, it subsequently developed non-inflammatory, bilaterally symmetrical alopecia on the back, face, neck and ears. Alopecia did not appear to be linked to any particular colour. Histopathological examination of skin biopsies revealed dysplastic primary hair follicles and secondary follicles that resembled the tentacles of an octopus. Hair shafts were absent, dysplastic, malformed or very irregular in shape. The demarcation between cuticle, cortex and medulla was not very distinct. Melanin deposits, of varying size and shape, caused cuticular deformities. No sebaceous or pen-follicular melanosis was observed. Accumulation of melanin appeared to be linked to the Maltese allele carried by the cat and is not diagnostic of the disease.
Hair dysplasia has been reported in the Abyssinian breed 2,6 and is characterised by onion-shaped bulges in whiskers and primary hair shafts. These structural deformities, the cause of which is unknown, render hairs very fragile leading to fracture. Histopathological enamination of skin biopsies reveals no follicular abnormality.No spec@ treatment has been reported.
Pili torti is a congenital, structural hair abnormality of kittens which consists of a flattening and rotation of the hair shaft of secondary hairs only. It causes excessive fragility and leads to fracture of secondary hairs '. Signs involve virtually generalised hypotrichosis, twisted or coiled hairs, seborrhoea, ceruminous otitis, accentuated skin folds which impart a pleated appearance to the skin (Figs 16 : 5-8), pododermatitis and paronychia '. Sometimes, ocular abnormalities (e.g. hlepharitis, corneal opacity and bilateral cataracts), osteoporosis and poor growth are seen. The cat usually dies very early (C. Hugnet and E Degorce, personal observations, 1998). Pili torti may be a genetic marker for a general ectodermal dysplasia. Microscopical examination of hairs reveals twisted, rotated or fractured hairs (Figs 16 : 9,lO). Histopathological eramination of skin biopsies confirms these abnormalities (Fig. 16 : 11). Melanin aggregates are sometimes noted in hairs and hair follicles (Figs 16 : 11,12) hut this seems to be linked to caniage of the Maltese allele and is in no way diagnostic ofpili torti (C. Hngnet and E Degorce, personal observations, 1998).
Genetic abnormalities in melanin pigmentation The process by which melanin pigmentation is genetically predetermined is very complex Melanocytes are specialised cells which synthesise melanin pigments in specific organelles called melanosomes. Melanin
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Figure 16 :1 :Heredrtary greasy seborrhoea in a 6-month old Perstan krtten note the greasy coat
Figure 16 :2 :Congenital hypotrichosis in a litter of Birman kittens. One of the kittens has a normal coat (courtesy of P. Bourdeau)*
Figure 16 :3 :One of the cats in Figure 1 6 2 : note downy appearance of the coat once the cat has become adult (courtery of P Bourdeaul*
Figure 16 :4 :Hair microscopy: only sn~all,v e v j n e secondary hairs are present ( x 40) (courtesy of P. BourdeauJ*
Figure 16 :5 :Vtually generalised hypoti accentuation of skin folds, seborrhoea and bilateral corneal opacio in a cat with pili torti (courtesy of C. Hugnet)
Figure 16 :6 :Same cat as in Figure 1 6 5 : note seborrhoea and accentuation of skin folds in the pedal extremity
F i g m l 6 : 7:Same cat as in Figure 1 6 5 : note ventral hypotrichosis and
F i g u ~ I 68: :Same cat a. ... ..,- ....5 : note associated erythematoceruminous otitis (courtesy of C. Hugnet)
seborrhoea (courtesy of C. Hugnet) Bourdesu, P,Leoneni, D., Mamale, I.-M. 81 Mila M. Re<. Med. Ye!. 164 17-24 (1988).
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pigmentation involves a number of steps. Precursor cells, called melanoblasts, develop in the neural crest and migrate dorso-ventrally and cranio-caudally towards the areas where they differentiate (skin, eyes, meninges and internal ear). In these sites, melanoblasts must survive and proliferate before differentiating into melanocytes which will synthesise melanosomes and melanin pigments to be functional. During these steps, the melanocyte utilises products made by many specific genes (e.g. transmission factors, growth factors, structural proteins and specific enzymes). A mutation at any level can disrupt melanogenesis and lead to hypopigmentation
Melanocytopenic hypomelanoses and amelanoses Melanocytopenic hypomelanoses and amelanoses are characterised by the absence of melanocytes, following faulty melanoblast development in the neural crest or inability of melanoblasts to survive in their main sites.
Waardenbura Syndrome ~ a a r d e n h u r ~ ~ y n d r oisman e extensive melanocytopenic hypomelanosis transmitted as an autosomal dominant trait. In the cat. this svndrome demonstrates complete penetrance for hair and skin acbrornia and incomplete penetrance f& degeneration of the intemal earwhich causes deafness IN! A genetic mutation has not yet been identifed in the cat. Degenerative lesions of the intemal ear appear at the end of the first week of the cat's life and result from an absence of endolymph secretion. Clinically, this syndrome is associated with a white coat, iridal hypocbromia or heterocbromia and deafness (Fig. 16 : 13). Piebaldism Piebaldism is an extensive melanocytopenic hypomelanosis transmitted as an autosomal dominant trait 9. It is not considered a pathological abnormality in the cat. Multicoloured, white coats are considered quite acceptable. Vitiligo Vitiligo is a well-circumscribed melanocytopenic amelanosis which is transmitted as an autosomal dominant trait with incomplete penetrance in man and as an autosomal recessive trait in the cat. Vitiligo is a polygenic disease in which different mutations simultaneously affect several genes, resulting in melanocyte death or increased risk of melanocyte death. In cats, the Siamese is particularly predisposed '"". The pathogenesis of vitiligo has not been determined. Vitiligo may be the consequence of an autoimmune process directed against one of the components of the melanin system, causing progressive melanocyte destruction. According to the neurogenic theory, vitiligo might be secondary to release of a neurochemical catecholamine-derived mediator capable of interfering with normal melanocyte activity and inhibiting melanogenesis. Another theory, the 'melanocyte self-destmction theory' proposes that a mechanism that normally protects the melanocyte from cytotoxic damage by products of melanogenesis becomes ineffective in certain, genetically predetermined cells. These theories are not necessarily mutually exclusive and, because of the chemical attack, melanocytic antigens may come into contact with Langerhans' cells and trigger an immune reaction ". Clinical signs are characterised by the progressive development of more or less symmetrical, achromic macules on the mucocutaneous junctions of the face (nose, lips and eyelids) (Fig. 16 : 14). This depigmentation, which is not accompanied by any inflammation, sometimes involves the footpads (Fig. 16 : 15), claws and coat (leucotrichia). It develops slowly and unpredictably ",''. Diagnosis is based on the history, appearance and distribution of the lesions, and suggestive histopathology. Histopathological examination of skin biopsies reveals an absence of melanocytes and the presence of melanin in the dermis and hair follicles of affected areas. Ultrastructural microscopy confirms the destruction of melanocytes 'O,". Prognosis is guarded, given the chronic progression of vitiligo. No specific treatment has been successful in the cat
Melanopenic hypomelanoses Melanopenic hypomelanoses are characterised by a functional melanocyte defect, the mode of transmission of which is autosomal raessive.
Oculo-cutaneous albinism The only types of oculo-cutaneous albinism (OCA type 1) that have been described in the cat are those associated with mutations on the albino locus of the gene coding for tyrosinase. The most
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Figure I6 :9 :Hall mrcroscopy. note hvrsted haus (p111to&) (x 100) (courtesy of C Hugnet)
Figure 16: 10 :Harr mrcroscopy noteflotrened, rotated harrs ( p h tortr) 1xlMJ)(courtesy of C Hugnet]
Figure I6 :11 :Hrstopatholagy nore harr dysplasra and aggregates of melanin wcthm harr shafts (ph torti) (sla~nedwith H and E, x 200) (courtesy of F Degorce)
Figure 16 :12 :Histopathology: nore dysplastic hair (hair rolled around itselJ) and aggregates of melanin within the hair shaft (pili tolti) (stained with H and E, x 400) (courtesy of F. Degorce)
Figure 16 :13 :A .... .Jat a n d . Waardenburg Syndrome
Figwe16:14:Depigmenfation of the nasalplanum and lips in a Siamese cross cat with vitiligo
hehlrochromfn in a ci.
&....-...-. -~mpleleach~orniain a young female cat with tyrosinasepositive oculo-cutaneous albinism
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common mutations lead to total loss of tyrosinase activity and are referred to as OCA tyrosinasenegative 14. OCA type 1 (Fig. 16 : 16) is characterised, clinically, by complete loss of pigmentation not only in the coat and skin (white coat) but also in retinal and choroidal epithelium in the eye, with associated abnormal optic visual fibres cross over and severe ocular abnormalities (e.g. reduced visual acuity, loss of binocular vision) li-".
Chediak-Higashi Syndrome Chediak-Higashi Syndrome (CHS) is a particular form of oculo-cutaneous albinism reported in the Persian la,involving an abnormality of melanocytes and other cells. As melanosomes, lysosomes and platelets have a common origin, any mutation which affects genes coding for melanosomal proteins, will affect the structure or function of these otber organelles. CHS results from a mutation of the beige gene which codes for a large protein called lysosomal traficking regulator (LYST). LYST has a pivotal role in the synthesis of cellular organelles 14. Clinical signs result from abuormalities in vesicular transport from lysosomes, associated with the presence of giant inhacytoplasmic inclusion bodies in leucocytes, melanocytes and many otber cells. These giant organelles interfere with the normal functioning of these cells, resulting in increasing sensitivity to infections and haemorrhage. CHS therefore involves hypopigmentation of the skin, coat and irides, immunodeficiency and primary clortihg disorders. The condition leads inexorably towards death by secondary infection or haemorrhage 'O.". There is no treatment.
Genetic hypermelanoses Lentigines are circumscribed hypermelanoses associated with an increased number of epidermal melanocytes. Clinically, a lentigime is a uniform brown or black macule, varying from 1-10 mm in diameter (Fig. 16 : 17). Ginger cats often have multiple lentigines around the mucocutaneous junctions of the face (lips, nose and eyelids), referred to collectively as lentigo simplex l 9 (Fig. 16 : 18). These lesions often appear at one year of age and progressively increase in sue and number, eventually coalescing.
Hereditary epidermolysis bullosa Hereditary epidermolysis bullosa refers to a heterogeneous group of genetic, mechanobullous diseases of the skin and mucous membranes. The diseases are characterised by spontaneous development of vesicles, erosions and ulcers, following minimal trauma, caused by excessive fragility of the demo-epidermal junction. In the cat only two forms are seen: junctional epidermolysis bullosa 20 (JEB) and dystrophic epidermolysis bullosa 2',z2 @EB).
Junctional epidermolysis bullosa JEB is caused by cleftiig in the lamina lucida of the demo-epidermal junction, associated with abnormalities of the hemidesmosome/anchoring filament complex. These abnormalities result from mutations of genes coding for various proteins in this complex. In cases reported in the cat, the protein abnormalities responsible have so far not been characterised. One particular form of JEB has been reported in a line of Siamese cats with onychomadesis and multiple onychodystrophy lo. Histopathological examination of skin biopsies reveals cleftimg within the basement membrane. These vast demo-epidermal clefts leave the epidermis intact. Various immunohistochemical techniques involving antibodies to hemidesmosome/anchoring filament complexes, are used to characterise these protein abnormalities. Electron microscopy can also demonshate precisely the site of the cleft within the demo-epidermal junction. Prognosis is guarded and there is no speciJic treatment. Only symptomatic treatment, the aim of which is to improve quality of life, is possible.
Dystrophic epidermolysis bullosa DEB is caused by intradermal clefting in the anchoring fibres of the dermal sub-lamina densa. It is caused by mutations of the gene coding for collagen VU of the anchoring fibres. Various forms of DEB have been described in the cat. &I early case was reported in a cat o i uncertain and onychomadcsis oiall the ieel (Figs 16 : breed : wh~chprescnted with pedal and ordl ~lrerdt~ons
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j
CCI'
'
>&,
figure 16 :17 :lsolaied ientigine on the medialpinna
Figure 16 :18 :Multiple lentigines on the lips of a ginger cat (lentigo simplex)
Figure 16 :19 :Ulceratrons on the gums and hardpalate of a cat wrth dystmphic ep~dermolystsbullosa (courtesy of S W Whifel*
Figure16 :20 :Same catas inFigure I 6 :19: note emsions and cfoliation of thefootpads (courtesy 0fS.W. White)*
Figure 1 6 : 21 :Hyperexfens~bilityof the skin in o 9-month old cat with Ehlers-Danlos Syndrome (EDS 1-111)
Figure 16 :22 :Hyperextensibility of the skin in two catsfmm the same litter, with Ehlers-Danlos Syndrome (EDS 1-111): slow growth was also seen
Figh., .23 :Skin tear following minor traumn in a cat withEhlersDonlos Syndrome (EDS 1-111)
Figure 16 :24 :Skin tear following minor trauma in L Danlos Syndrome (EDS 1-111)
8 White.
S. D.,D u r n , R.W & Oliwy. T Ve~Defmaot. 4.91-95 (1993).
th Ehlers-
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19,20). A more recent case was reported in a two and a half year old Persian cat 22, one of a litter of 8 kittens, two of which presented with skin and mucous membrane lesions from the age of 10 weeks. Both parents were normal. Skin lesions are characterised by footpad ulceration, multiple onychomadesis, and ulceration of the tongue, gums and palate. Skin fragility can easily be demonstrated in areas of mechanical trauma.
Histopathological examination of skin biopsies reveals demo-epidermal clefting beneath the dermoepidermal junction. Histochemical andlor immunohistochemical techniques (e.g. PAS staining), using for example, anti-collagen N antibodies, confirm cleftiig beneath the demo-epidermal junction l ' . In the Persian cat, reduced imunoreactivity of collagen VII in the basement membrane of the skin and mucous membranes is observed 12. Ultrastructural microscopy reveals hypoplasia or a reduction in the number of anchoring fibres. Hemidesmosomes and anchoring filaments are normal 2',". Prognosis is very guarded. There is no spec@c treatment. Only symptomatic treatment, the aim of which is to improve quality of life, is possible.
Hereditary cutaneous asthenia Hereditary cutaneous asthenia refers to a group of genetic abnormalities of collagen fibres (Ehlers-Danlos Syndrome (EDS) and elastin fibres (Cutis Laxa), characterised clinically by changes in the texture, elasticity and resistance of the skin These conditions are extremely rare in the cat.
Ehlers-Danlos Syndrome (EDS) Aetiopathogenesis Ehlers-Danlos Syndrome (EDS) is better known by the name dermatosparaxis (which means that skin can be tom), but this term actually designates one particular type of EDS, characterised by an abnormality of the enzyme system, procollagen aminopeptidase, and inherited as an autosomal recessive trait. In the cat, two types of EDS have been reported. The extremely rare form, inherited as a recessive trait x,s, has been described in the Himalayan breed and is similar to EDS VIIc in man and dermatosparaxis in calves and sheep. This form is caused by a defect in procollagen peptidase. The form inherited as a dominant trait " results from a biochemical defect referred to as type EDS 1-111 and has not yet been characterised. No breed predisposition has been observed. Clinicalfeatures Dermatological signs are the principal features of EDS in the cat 242'. They usually appear in young cats, less than one year old, and involve increased elasticity and extensibility of the skin (Figs 16 : 2422) and, in some cases, spontaneous skin tearing. These tears do not bleed much (Figs 16 : 23,24) but heal with scarring. Sometimes, the skin feels very thin. Non-dermatological signs observed in the dog, have, to date, not been described in the cat. Diagnosis Diagnosis is based on the history, clinical appearance of the lesions, measurement of the skin extensibility index, and skin biopsies taken for conventional histopathological and ultrastructural examination. Although clinical diagnosis is easy in severe cases, it can be much more difficult in milder cases. The difSerential diagnosis should include other causes of acquired cutaneous hyperfragility (e.g. hyperadrenocorticism, hepatic chlolangiocarcinoma, hepatic lipidosis, etc.. .) >. Histopathology of skin biopsies reveals qualitative and quantitative abnormalities of dermal collagen fibres: very thin dermis; implantation of hair follicles in the hypodermis; bundles of loose, sparse collagen fibres (Fig. 16 : 25); or compact, dense, diluted or smaller collagen fibres 242'. Although abnormal collagen fibres in the dog sometimes lose their affinity for trichrome stains (e.g. Masson's hichrome), this oddity has not been seen in the cat. Scanning electron microscopy reveals, in EDS 1-111, dense, sometimes angulated, clumps of collagen fibres. These fibres can be coarser, variable in size and organised in irregular, parallel bundles 2626. Transmission electron microscopy confms these abnormalities in transverse section (Figs 16 : 2628). The collagen fibres are irregular in shape and diameter. In type W c , they look l i e hieroglyphics ".
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Figure 16 :25 :Hrstopathology collngenfibres are loose and sparsely drshrbut~d(Ehlers-Danlos-. me, EDS 1-111)(stained wrth H and E, x lOq)
F@m 16: 26 :nansmission electmn micmscopy:collagenfibresresemble hieroglyphics (Ehlers-DanlosSyndrome,EDS VIIcJ
Figure 16 :27 :Transmisszon electron microscopy (transverse section) note rrregular appearance of transverse sectron of collagenfihres (+I (EDS 1-111) ( x 65500)
Figure I6 :28 :Transmission electron microscopy (transverse section): note regular appearance of transverse section of collagenfibres (control cat) ( x 65,500)
Figrae 16 :29 :Brown papular lesrons on the trunk of a Sphrnr car wlth urtrcarra prgmentosa
Figure16 :30 :Brownpapular lesions on theforelimb of a Sphinv cat with rrm'caria pigmentosa
Fipre 16 :31 :Histopathology: note epidermal hyperplasia and massbe mast cell infiltration of the dermis (urticaria pigmentosa) (stained with H and E, x 250)
Figure 16 :32 :Histopathology: massive mast cell infiltration of the dermis (urticaria pigmentosa) (stained with Toluidine blue, x 400)
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Measurement of the skin extensibility index (El) EI =
E x 100 L
E: Vertical skin extensibility (cm) at the dorsolumbar junction. L: distance (cm) between the occipital crest and the base of the tail. This index is not very reliable. In the cat, the maximum EI tolerated is 19%. The index depends on numerous factors: age, breed, general health, state of hydration, gastric retention, lactation, experience of the investigator and the degree of muscle relaxation in anaesthetised or non-anaesthetised animals. Prognosis and treatment Prognosis is always guarded since signs usually worsen with time 262'. Only certain forms are compatible with a subnormal life. Life expectancy of cats with EDS type VIIc seems better than in other species 'I. This could be linked to the relatively fewer abnormal collagen fibres resulting from a partial defect in procollagen peptidase =. There is no specific treatment, only hygienic measures aimed at avoid'mg or limiting mechanical stress 'I.
Cutis laxa Curis laxa is a rare disease characterised clinically by a flaccid, inelastic skin with excessive folding. It is associated with genetic abnormalities in elastin fibres, especially involving reduced synthesis or destruction of elastin fibres (elastolyse) Cutis laxa has not yet been reported in the cat.
Urticaria pigmentosa Chronic urticaria resembling urticaria pigmentosa in man has been described in the Sphinx " and Devon Rex jO. In the Sphinx, a familial predisposition is reported lo. Pathogenesis in the cat is unknown. In man, urticaria pigmentosa is associated with cutaneous mast cell turnours and could well be due to a cutaneous metabolic disorder of the mast cell differentiation and growth factor, stem cell factor (SCF), which causes mast cell proliferation.
Clinical signs are characterised by the appearance, from a very young age, of a generalised, macular and papular rash (Figs 16 :29,30) and intense chronic pnuitus. Darier's sign is positive. Some papules become progressively darker brown in colour. The rash sometimes develops in serious acute episodes. Histopathological examination of skin biopsies reveals a very acanthotic epidermis with discrete spongiosis in the deep layers, congestion in the superficial dermis, and large numbers of mast cells which can also be found in deeper parts around the blood vessels (Figs 16 : 31,32). Prognosis must be guarded given the chronic evolution of the dermatosis. Treatment with both oral antihistamines (e.g. hydroxyzine 2 m a g TID) and corticosteroids (e.g. prednisolone 0.5 m a g BID) given orally, gives inconsistent results lq. Recently, the use of cyclosporin (7.5 m a g SID) given orally, two hours either side of food, produced definite regression of signs within 3 weeks. The frequency of admi~~tIati0II was then altered to every 2 or 3 days, depending on the appearance of skin lesions. No side-effects were seen during this treatment (E. Guagukre, personal observations, 1999).
REFERENCES 1. Params, M.& ScoL D. W.Fane Prachce IS, 17-20 (1990).. 2. Scott, D. W.,MiUET, Jr, W. H.& Grif611,C . E. MuNer & Kirk's SSmnllAnirnal Dermafology,5th Ekhon (Saunders, W. B., Piuladelphu, 1995) 3 Bourdeau,P., Lwnem, D., Mamille, 1~-M.& Midot, M.Rec Med Vet 164, 17-24 (1988). 4. Robmsw, R . I Herd 64,47 (19731. 5. Scott, D. W.LeMidecin Vlt6r~wire& Quebec 28,1,38-44 (1998). 6. Willanson, G. T.& Knstensw, T. S. J. small Anrm Prncr 30,27-28 (1989). 7. Geary, M.R. & Bakw,K. P. J mllAnim.Pract 27,8546 (1986). 8. Heanng, V. 1.& Kmg, R. A. in Pigmemtioh aMPigmentq Abnormalrt~es.(edLevine,N.)3-32 (NewYork, CPR Press ,1993).
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. 16 : Genodermatoses 9. Alhaidari, Z., Olivry, T & Ortonne, 1.P , Vet Dermatol.lO, 3\16 (1999). 10. Guaguhre, E. & Alhaidari, Z, in Current Veterinary Therapy X (ed Kirk R.W.) 628-632 (Saunders, W. B., Philadelphia, 1989). 11. Strain, G. M. Comp. Cont. Educ. Pract. Vet.l3,245-253 (1991) 12. Delack, J. B. Comp. Cont. Educ. Pracr. Vet. 6,609-618 (1984). 13. Lopez, R., Ginel, P. 1.& Molleda, I. M. and others, Vet. Dermntol. 5,27-32 (1994). 14. Spitz, R. A. & Hearing, V 1.in Advances in Human Genetics (ed Hirschlhom K. and Harris, H.) 1-45 mew York, CRC Press,1994). 15. Creel, D. I. Nature 231,465-466 (1971). 16. Johnson, B. W. Comp. Cont. Educ. Pract. Vet. 13,374-379 (1991). 17. Giebel, L. B.,Tripati,R. K., King, R.A. & Spritz, R.A. J. Clin. Invest. 87, 1119-1122 (1991). 18. Earner, I. W , Davis, W. C., Prieur, D. J.,Baxter, I., Norsworthy, G. D. J.Amer: Vet. Med.Assn. 166, 1103-1104, (1975) 19. Scott, D. W. Comp.Anim. Pract. 1,23 (1987). 20. Johnstone, I. Mason, K. W. & Sutton, R. Proc 2nd World Congress of Veterinary Dermatology, Montral 111 (1992) 21. White.. S. D... Dunstan,R. W. & O ~ ~.V. T.N Vet. , Dermatol. 4.91-95 (1993). . . 22. Olivry, T. Dunston, S. M. & Marinkovich, M. P Vet. Patkol. 36,616-618 (1999). 23. Fontaine, 1. & Olivly T. in Encyclopidie Vltirinaire Dermatologie, Paris 2450, 11 (1995). 24. Collier, L. L., Leathers, C. W. Feline Practice 10,25-36 (1980). 25. Counts, D. F., Byers, B. F. & Holbrook, K. A. J. Invest. Dermatol. 74.96-99 (1980). 26. Holbrook, K. A,, Byers, P. H., Count, D. F. & Hegreberg, G. A. J. Invest. Dermatol. 74, 1W-104 (1980). 27. Fontaine, I., Charlier, G. & Henroteaux, M. Point Vit. 24,255-258 (1992). 28. Ultto, I,, Fazio, M J. & Qlristiano,A. M. in Connective Rssue anditsHeritableDisorders(ed,Royce P M., Steinmann BJ 409423 (Wdey - L i s NewYork 1993). 29. %tale, C. B., Ihrke, P. I., Olivry, T. & Stannard,A. A. Vet. Dermntol. 7,227-233 (1996). 30. Noli, C. & Scarampella, F.Proc. AAVD-ACVD,Maui, 65 (1999).
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I Skin conditions associated with behavioural disorders -
Skin conditions associated with behavioural problems are rarely described in the cat, even though Siamese and Burmese breeds seem to be predisposed '. Their incidence is probably underestimated because they are always last on the list of differentials. For a long time, the only skin condition for which a behavioural link was even considered was bilaterally symmetrical truncal alopecia, inappropriately classed as a "neurodermatosis" or "psychogenic alopecia" ','. Recent developments in veterinary psychiahy have now revealed a number of dermatoses with behavioural origins. Thanks to a better understanding of the behaviour of the domestic cat, advances in the study of animal behaviour, and the availability of new psychotropic drugs, pheromones and behavioural therapies, specific diagnosis and effective treatment are now possible4.
Neurophysiology The cenaal nervous system 1s responsible for organising and assirmlating, and adapting an individual to its surroundings. A continuous flow of information circulates along neurons in the form of electrical impulses, triggered by chemicals called neurotransmitters, released at the level of the synaptic cleft. The principal neuroUansmltters involved in displacement activltis and stereotypic behaviour ate: serotonin, dopamine, noradrenalin, peptides (such as endorphins) and the gamma amino butync acid complex (GABA) 6.
Dopamine regulates motor and muscular activity, arousal and aggression It is involved m anticipation (being in a state of readiness to act), collating information and "stop signals" 4'. Too much dopamine leads to stereotypic behaviour. Signs suggesting dopamine overactivity include ptyalism, large intestinal diarrhoea, anticipation and aggression. Those suggesting dopamie underactivity are Inhibition (mechanism withii nervous system which permits blocking of transmission of information or response, leading to inability of animal to reactj, reduced sleep, abnormal feeding habits and displacement activities. Noradrenalin and adrenalin are the modulators of vigdance (taking in information from the environment) and sensitivity of the organism to changes in the environment. Tachycardia, tachypnoea, emotional urination and hypervigilance (constantly responding to all information in the envuonment) are suggeshve of noradrenalin overactivity, which is often involved in early anxiety states. Serotonin affects hormonal equdibrium and, by reducing skin sensitivity, is involved in perception of pain and pruritus ' It plays avital role in social behaviour, the capacity to learn, concentration and memory. A reduction m the level of serotonin leads to a depressive state. Serotonin exerts an inhibitory action on dopaminergic neurones. Peptides are derivahves of pro-opiomelanocortin. They produce analgesia, are involved in pruritus and act as anxiolytic agents. They increase dopamine transmission and -play a role in the development of stereotypic behavioh and in maintaining displacement activities. The gamma aminobutyric acid (GABA) complex has an inhibitory action on all the other mowaminergic systems i'6. It is involved in "stop signals" and helps determine .~ motor, sensory and cognitive function. Other agents involved in the pathophysiology of pruritus interact with these substances and include histamine, proteases, substance P and leucotnenes 8
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Lickmg, nail chewing and scratch'mg can all be displacement activities. Like all types of behaviour, these displacement activities are arranged in a behavioural sequence starting with an initial preparatory phase (e.g. sniffing at a particular part of the body) followed by a second "active" phase (e.g. licking or scratching) which can sometimes be very long. Then, there is a phase of rest or satiety, during which the behaviour is unlikely to occur. These activities are performed out of context by an animal in a conflict situation. There is a definite sequence and a "stop signal". Displacement activities relieve the cat's emotional tension but prevent other adaptive responses from taking placeg. Bulimia (an increase in overall food intake in the absence of diabetes or parasitic infestation) is another very common displacement activity which can be associated with licking lo
Table 17 : 1 Aetiology of anxiety
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Anxiety illnesses of the cat are linked to either developmental disorders or the environment. Deprivation anxiety affects cats wich were kept in isolation (e.g. in a barn or cellar). Such cats are often considered to be fearful and will trv to avoid anxietv-inducing situations. for examole . bv. eoine - outside. However.. ohobias. anxietv and even depression frequently develop when the cat cannot escape. Developing an excessive attachment to a human may be one of the ways in which a cat chooses to react. 'Territorial" anxiety is higgered by upsets in the cat's Me (moving house, change of furniture, death of a person or another animal). Owners often seek advice early on because of frequent urine spraying. Cleaning up the spray and punishing the cat can often further alter the environment and affect the bond between cat and owners. Reactional, reversible spraying rapidly leads to anxiety. Enclosed environment anxiety develops in cats which are prevented from going outside and is caused by a profound lack of visual stimuli. The cat has regular bouts, notably in the evening, of hyperactivity, consisting of racing around in all directions, licking its body and predatory aggression towards its owners. Fear of these things happening leads to correction by the owners which can make the cat even more anxious.
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Stereotypic behaviour Stereotypic behaviour refers to an act or a small collection of acts, carried out in a regular, identical and unusual way, without obvious purpose. Here, there is no sequence, and outside intervention is needed, for example from the owners, to stop the behaviour. Tail-biting, licking and scratching can be examples of stereotypic behaviour.
Aggression During episodes of m i e t y and dysthymia, the cat can cause severe self-trauma through scratching and biting. In particular, it can attack its tail as if it were pouncing on a prey.
Pathogenesis
1 dermatitis in dogs 6 , " . 1 L ' 3 . The serotonin system could be the first to be upset in anxious individuals 'O. This could lead to dopamine and noradrenalin underactivity and behavioural problems preventing the animal from adapting and producing appropriate behavioural responses. The production of displacement activities (e.g. licking) is the only compatible behavioural response. Licking of the skin leads to serotonin release which reduces nociceptive perception. More intense licking provokes release of endorphiis which further upsets the serotonin and dopamine systems. This vicious circle, perpetuated by licking, nibbling and scratching, may lead to stereotypic behaviour '. In man, a link has been established between anxiety and atopy, with stress aggravating the clinical signs 14. It is possible that a similar l id exists in the cat. Signs might, therefore, reflect both a hypersensitivity and a behavioural problem. Severe, prolonged pruritus can induce a state of anxiety and behavioural problems: abrupt movements, racing, nibbling, dorso-lumbar hyperaesthesia ("rolling skin syndrome") and intolerance of stroking.
www.vet4arab.co.cc 17 : Skin condihons associated with behavioural disorders
Figure17: 1 :Marked inhibitionin the consulting room; cat burying itself in a bag (courtesy of E. Gaullier)
Figure 17 :2 :Symmetrical self-induced alopecia (courtesy ofE. Gaultier)
Figure 17 :3 :Partial alopecia of theflanks and lateral hindlimbs (permanent anxiety)
Figure 17 :4 :Self-induced abdominal alopecia (permanent alopecia)
Figwe 17 :5 :Symmetrical self-induced alopec,a (peratane,lf alopecia)
Figure 17 :6 :Self-induced alopecia of the medial and caudal thighs (permanent anxieiyj
Figure 17 :7 :Licking of the lower forelimb (permanent anxieiy); the cat is also bulimic
Figure 17 :8 :Close-up of the cat in Figure 17 :7
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Clinical features
~ associated with behavioural disorders are brought about by the cat itself, through licking, scratching or biting various parts of its body.
~ermatblo~ical signs Self-induced alooecia Self-induced alopecia is the dermatological sign most frequently associated with behavioural disorders 16,'8. Depending on the amount of damage to the hair follicle and skin, the coat in the affected region may be lost completely or hair loss may be diffuse but.quite mild. A hair can be broken at several points along its length ". Symmetrical alopecia Tlis is brought about by excessive grooming la. It can be very extensive, affecting the whole of the abdomen, flanks and back, or relatively localised, involving the caudal thighs and abdomen " (Figs : 17 : 1-6). The coat may he completely lost or may just appear sparse or thin. The back and flanks are generally affected. When licking is severe or long-standing, alopecia can be associated with erythema and cutaneous erosions. Focal alopecia When licking or sucking is confined to well-demarcated parts of the body, alopecia may be seen in various places. Preferred sites include the fore limbs (Figs 17 : 7-9), tail ', (Fig. 17 : lo), trunk.(Figs 17 : 11-12) and dorsally between the shoulder blades (Fig. 17 : 13). These lesions can assume the appearance of acral lick dermatitis, (Figs 17 : 14-16) sometimes just like that seen in dogs, with skin thickening and ulceration ' O (Fig. 17 : 17). These lesions do not seem to be restricted to one particular side Id. Stereotypic licking of the nose can produce erosions, sometimes triangular-shaped, on the nasal planum or on the undersurface of the upper lip (Figs 17 : 18-20). The lip lesions may develop' into indolent ulcers (Fig. 17 : 21). Excoriations Excoriations brought about by scratchiig and biting can look like real self-mutilation and the spectacular consequences (e.g. necrosis, ulceration and crusting) are often shocking to cat owners. Excoriations are localised to the face and neck (scratchiig) (Fig. 17 : 22), limbs (biting) and tail (scratching and biting) (Fig. 17 : 23) 'I. Nail chewing Nail chewing can be a cutaneous sign of a behavioural disorder in the cat. Nails are often broken and split (Fig. 17 : 24). These ungual lesions develop without paronychia 4. Nail chewing is often associated with self-induced alopecia.
Non dermatological signs Somatic manifestations Behavioural disorders have direct repercussions on other organs, in particular the vascular and digestive systems, causing tachycardia and tachypnoea, and ptyalism and diarrhoea respectively. Bulimia may be the cause of excessive weight gain. Behavioural manifestations Anxiety (Tables 17 : 1-2). Symptoms of intermittent anxiety are characterised by an increase in emotional reactions. The cat may have episodes of vigorous self-licking. It may bite and scratch particular parts of its body and scratch around its head. When anxiety is permanent and dominated by behavioural inhibition (Fig. 17 : I), prolonged bouts of localised licking predominate giving rise to focal or diffnse areas of alopecia, often associated with bulimia.
www.vet4arab.co.cc 17 : Skin conditions associated with behavioural disorders
Figure 17 :9 :Self-rnduced ctrcumscr~bedalopecia ofthe forelrmb (courtesy of J Dehasse)
Figure 17: 10 :Self-inducedolopeciaofthe tip ofthe toil (comes) of C. Lopez)
Figure 17 :11 :Unilateral, self-mduced, 1, uncal alopecra rn a Sramese cot (permanent nnnetyj
Figure 1 7 : 12 :Dorsal view of the cat infigure 17 :I1
F i g w 1 7 : 13: Se~mduceddopecraandaneroswn m the ~nterscapular regron @ermaneni amefy)
Figure 1 7 : 14 :Self-inducedalopecia anderosion on the lateral hindlimb of a Siamese cat (courtesy ofD. N. Carlotti)
Figure 17 :15 :Close-up of fhe cat rnfigure 17 14 (courtesy of D N Carlonr)
Figure 17 : 16 :Selfinduced alopecia and erosions on the flank (permanent anxiety)
A Pmhcal Guideto Pelme h t o l o g y
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Table 17 :2 : Symptoms of anxiety Anxiety is a reactional, pathological state characterised by an increased probability of emotional responses, akin to fear, following any variation in the external or internal environment. It results in a breakdownof self-control and a loss of adaptability. Anxiety can take on three distinct clinical forms. Paroxysmal anxiety. Attacks are short lasting and consist predominantly of neurovegetative signs: tachycardia and tachypnoea, ptyalism, diarrhoea, sweating, expression of anal sacs. Neither aggression nor displacement activities are seen. Intermittent anxiety leads to prolonged disorders and presents as neurovegetative signs, increased marking and aggression, dorsolumbar hyperaesthesia and "rolling skin syndrome" (violent waves running through the skin of the cat's back). Displacement activities (e.g. licking and scratching) may be seen and the cat may attack particular parts of its body. Sleep patterns may be disturbed. Permanent anxiety may ensue. Permanent anxiety reflects a severe loss of capacity for adaptation. Inhibition is predominant. Displacement activities, especially licking all bulimia, are always present.
Depression (Table 17 : 3). In acute depression, characterised by anorexia and inhibition, scratching and licking can occur although grooming behaviour is generally absent ". In a long-standing depression (often harder to detect), scratching and licking can be seen.
Table 17 :3 : Different types of depression Depression is areactional state chacacterised by reduced receptivity to stimuli and spontaneous and irreversible inhibition. It may occur from the outset or arise out of untreated anxiety problems. Acute depression is reactional and characterised by excessive sleep, poor appetite and displacement activities. Chronic depression is characterised by disordered feeding, sleep problems, changes in cleaning and grooming habits, and displacement activities. Reactional depression in the adult occurs several days after a severe emotional shock. The cat is lethagic, anorexic itself even though frenzied licking follows any physical contact. Displacement activities are and no 10n~er~~roorns present, and excoriations can develop in the cervical region. This depression can, because of the associated anorexia, be fatal. Chronic deoression in the adult can develon from acute denression but also from untreated anxiew. It can also result from prolonged administration of syntheticprogestagens. The cat appears chronically withdrawn with bouts of agitation, snraving, . . "calling" and licking" fdesoite . . altered moomine habits). Involutive depression is associated with ageing of the brain and occurs in animals aged 10 years or over. It often has an organic cause like a brain tumour. Loss of grooming and cleaning habits, and sleep problems (with calling and aimless night-time walks) are suggestive signs. Displacement activities can be seen.
Dysthymia (Table 17 : 4). In dysthymia, cutaneous problems arise from an animal biting itself violently during episodes of varying duration. This biting is often confined to the tail and may lead to amputation of the tail and / or euthanasia of the animal.
Table 17 :4 : Dysthymia Dysthymia 1s an unpredictable, cyclic fluctuation in mood involving impulsive behaviour, stereotypic behaviour, loss of social inhibition, aggression, disturbed sleep and problems in feeding behaviour. It may be unipolar or bipolar, depending on whether the cat is normal or depressed in periods between activephases. It is strongly influencedby endogenous factors such as the sexual cycle. It is rare and can be disconcerting. It may manifest as self-mutilation, notably of the tail, which can lead to successive amputations and subsequently euthanasia. Affected cats can present with completely unpredictable and uncontrollable bouts of aggression and it must be pointed out that these cats are very dangerous.
www.vet4arab.co.cc 17 : Skin conditions associated with behavioural disorders
Figrrrel7 :1 7 : Severe dermatitis caused by licking of the lowerforelimb (reactional depression) (courtesy of i? Habran)
F i g m l 7 : 18 :Triangular-shapederosionr on the nasalplanurn(siereoiypic licking)
Figure 17 :19 :Erosion on the ~iusalpla,~eniniid ~iiiderljiiigirglo~ioil the upper lip (sfereotypic licking)
Figure 17 :20 :Erosions andpunched-out ulcers on the nasal planum (stereotypic licking)
Figure 17: 21 :Ulcer on the nasalplanurn and upper lip (indolent labial ulcer) (stereotypic licking) (courtesy of G. Muiler)
Figure17 :22 :Unilateralscratchwoundon the cheek(chmnic depression) (coufesyof?i Habran)
I Figure 17 :23 :Clawing and selfmrctilation of the rail (courtesy of C . Laubis)
Figure 17 :24 :Onychopagia (permanent ann'ely)
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Diagnosis History Getting a good history from the owners is critical. This should be as detached as possible and not be embroiled in the owners' own interpretations of events (e.g. "he knows he's doing wrong, he's bored, he's jealous, he's getting his own back etc ..."). Information on the type of dwelling (e.g. flat or house), number of animals and other species in the household, and the make up of the family may reveal if the animal's surroundings are conducive to having a healthy emotional state. The history should highlight all the environmental changes that occurred before the appearance of skin signs, as well as the pattern of the behavioural disorder itself. The behaviour of the cat within its environment should also be considered: behaviours which affect the cat itself (e.g. feeding and drinking hehaviour, touch, excretory behaviour and sleep) and those which affect the interaction of the cat with the environment (e.g. aggression, exploration and marking) '. Sometimes, owners do not see the animal licking. Carrying out a trichogram is the only way to prove that the alopecia is traumatic in origin 22. Lack of improvement in either cutaneous or hehavioural signs, after drug treatment of any sort, is of no diagnostic value. Equally, the efficacy of corticosteroids or synthetic progestagens cannot be used to conclude that a hypersensitivity skin disease is present. This is especially true with megoestrol acetate, which has marked neuroleptic activity. Nor is the efficacy of certain psychotropic drugs of any diagnostic value, as some of them have sedative or antihistamine action 13. Clinical examination Diagnosing cutaneous signs as manifestations of a behavioural disorder is often troublesome because these signs are mostly non-specific even though some, such as self-induced alopecia, nail chewing and tail mutilation are strongly suggestive. The presence of pruritus is very difficult to evaluate because an increase in grooming activity may be the only means by which the cat can get relief lo. A general examination will reveal concurrent diseases along with organic and dermatological manifestations of displacement activities. Organic manifestations may be direct (e.g. tachycardia, tachypnoea, ptyalism, diarrhoea and emotional urination) or indirect (e.g. obesity). Valuable information can be obtained from the demeanour of the cat during the consultation. Behavioural inhibition, the presence or absence of exploratory- behaviour, aggression or marking behaviour would suggest either "productive" conditions (e.g. intermittent anxiety and dysthymia) or "non-productive" conditions (e.g. permanent anxiety and depression). Differential diagnosis The differential diagnosis includes all the pruritic, parasitic and allergic dermatoses ""6. The diagnostic approach is complex in the cat because behavioural disorders can often be associated with chronic, pruritic skin conditions, especially hypersensitivity. Additional tests The purpose of carrying out additional tests (e.g. a trichogram) is two fold: 1) to demonstrate that the alopecia is traumatic in origin and 2) to eliminate ectoparasitism and allergy as differentials. Behavioural diagnosis The diagnosis of acute behavioural disorders poses few problems. The diagnosis of anxiety, on the other hand, is less straightforward (Table 17 : 1). Distinguishing a cat that is stressed and bothered by its chronic pruritus from an anxious cat that licks and has dorsolumbar hyperaesthesia is often difficult. Permanent anxiety is actually well-tolerated by owners, who find their cats very calm. Owners, here, cope well with the alopecia whicb they perceive only as being unattractive. Diagnosing cutaneous disease as a manifestation of a behavioural disorder is still too often a diagnosis of exclusion, indeed a "last chance" diagnosis after all tests and therapeutic trials have been carried out. In a good number of cases, after carrying out basic dermatological and behavioural investigations, a behavioural association should be suspected quite early on.
www.vet4arab.co.cc 17 : Skin conditions associated with behavioural disorders
Treatment Two types of therapy are used in the treatment of behavioural disorders: psychotropic drugs and "ecological" therapy. Physical devices such as Elizabethan collars and bandages produce only temporary remission and can aggravate an already strongly disordered emotional state 'O. They are, however, sometimes unavoidable at the start of treatment in the case of very severe skin lesions.
Psychotropic drugs Until recently, the choice of psychotropic agents was restricted to neuroleptics (dopamine antagonists) such as haloperidol or acepromazine, and anxiolytics (acting on GABA) such as diazepam. Recent advances in veterinary psychiatry have led to the development of effective, more convenient treatments with a minimum of undesirable side-effects (extra-pyramidal syndrome for neuroleptics; disinhibition, memory difficulties and developing a tendency to bite for the benzodiaze~ines) . . ''. Anxiolytic agents The drug used is trioxazine (where available) (20 mg/kg/day in two doses for 2-3 months). Trioxazine has a very rapid onset of action (3-5 days) and is nin-kdacng, but as its anxiolytic action is strongly associated with a disinhibitory effect, it must be used with great care. It should not, therefore, be given to cats with a history of aggression. It can be used right at the start or at the end of treatment as a change from other therapies. The treatment can be given over a long period but a rapid onset of action should be seen. A withdrawal period of one week for every 3 weeks of treatment is advised 2',28. Modulators of the noradrenalin system Modulators of the noradrenalin system can be prescribed in early anxiety problems with hyperaesthesia, tachycardia and tachypnoea (rare in the cat). Propranolol, a beta-blocker, can be used, at a dose of 5-10 mg/kg SID for one to two months. An examination of cardiac function is necessary before prescribing propran~lol"~~~. Modulators of the dopamine system Neuroleptics, although theoretically an option, are rarely prescribed for the treatment of skin disorders of behavioural origin. Only sulpiride at 200 mgimz SID (stimulating the dopamine system) can be used when inhibition is very marked. Monoamine oxidase B inhibitors (MAO-BI), on the other hand, are a treatment of choice for behavioural dematoses. The only drug available is selegiline chlorhydrate which acts on the three principal systems. It regulates the transmission of serotonin and noradrenalin and reactivates dopamine transmission (important in depression and anxiety). It also helps restore "stop signals" in behavioural sequences (important in stereotypic behaviour and dysthymia). No side-effects have been reported. Treatment can be continued for a very long time and no withdrawal period is needed before stopping. Results are seen rapidly, within a month of starting treatment. The dose is 1 mgkg SID given once in the morning on an empty stomach. The bitterness of the tablets may be an obstacle to treatment compliance Antidepressants Antidepressants, generally, are serotonin reuptake inhibitors 27. However, their mode of action is complex and not limited to just one mediator. Clomipramine, acting on the noradrenalin and serotonin systems, is a peripheral and central anticholinergic agent. It improves mood and sleep patterns and stimulates a retum to exploratory activity. It possesses anxiolytic and sedative properties. Clomipramine is indicated in problems of anxiety or depression, accompanied by displacement activity 16. The dose is 0.3-0.8 mg/kg SID given once or in two divided doses. Its beneficial action can be seen from the tenth day but this may be preceded by a deterioration. A reduction in licking occurs on average within 25 days ". Treatment can be continued for several months, but a withdrawal period is recommended before stopping. Overdosing can produce anticholinergic signs (e.g. constipation, dry mouth and urinary retention) and owners should he warned of this. It has arrhythmogenic properties so-cardiac function should be carefully monitored IP. Fluoxetine, a more specific serotonin re-uptake inhibitor, is anxiolytic and promotes good recovery of exploratory behaviour. Improvement may be detected only after about 3 weeks and may be preceded by increased licking and poor appetite. These side-effects are often poorly tolerated by owners. The dose of fluoxetine is 1-2 m a g SID. Treatment can he given for several months but a withdrawal period is needed before stopping.
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Morphine antagonists Morphine antagonists used are naloxone (injectable solution) and naltrexone lo. Their efficacy has been demonstrated but effects are short-lived. The dose of naltrexone is 2.2 mgkg SID. Despite their reasonable efficacy and absence of side-effects, their use is limited by their prohibitive cost.
"Ecological" therapies Pheromone therapy The aim of pheromone therapy is to make the cat's surroundings more soothing by applying familiarisation pheromones (active fraction F3) present on cats' faces ",32. These pheromones help to reassure and relax the cat. Their use ought to be routine in problems relating to anxiety or depression. Cessation of anxiety licking can be obtained by early treatment. The F4 fraction contains marking pheromones. It can be used in cases of anxiety associated with other individuals, either human or animal. Behavioural therapy The aim of behavioural therapy is to modify a patient's reactions, either by applying learning techniques or by structuring events in such a way as to m o w the cat's perception of the environment. Once obvious environmental causes have been identified, the initial approach should be to try to reestablish normality or to reinstate a range of activities appropriate for the cat ''. Play is the principal tool. As well as helping to reactivate and structure the animal's activity and combat certain phobias, play encourages new bonding with the owners. It can be used to stop a licking sequence right at the start (e.g. throwing a ball just when the cat is ready to begin its displacement activity). A return to play in an anxious or depressed cat is a good prognostic sign. To treat anxiety in a cat kept in enclosed surroundings, the environment should he enriched with movable objects. The cat should be allowed to help itself to food, with feeding points spread out in order to reduce aggressive behaviour. Often, just allowing the cat to go outside can resolve the problem. These simple methods must be used whenever possible. For some cats, stroking will be comforting and helpful, for others, it will only increase the stress.
REFERENCES 1. Mason, L & Moriello, K A. Small Animal Dermatology (Pergamon, Oxford. 1995). 2. Kummel, B. A. Color Arias of Small Animal Dermatology (Mosby Company, Saint Louis, 1990). 3. Shanley, K. & Overhall, K. in Current Veterinary Therapy X I (ed W, R.W.), 552-558 (Saunders, W.B., Philadelphia, 1991). 4. Meuniernier J. M. & Shvaloff, A. in Les neumfransmetteurs.Bases neumlogiques etpharmdcologiques (Masson, Paris, 1992). S;Shuster, L. & Dodman, N, H. Psychopharmacology ofAnimal Behavior Disorders 185-202 (1997). 6. Reynaud M. & Malmwicz, 1,k La s o u i n c e de I'homme (Albin Michel, Paris, 1996). 7. Shanley, K. J. Vet. Ciin.N.Amer. 18,971-982 (1988). 8. Luescher, U.A,, McKeown, D. N. &Halip, J. Vet. Clin. N. Amer 21,401-413 (1991). 9. Overhall, K. L. Canine Practice 17,40-44 (1992). 10. Goodma W. K., Mc Dougle, C. 1.&Price, C. H. Int. Clin. Psychopharmacol. 7S, 35-38 (1992). 11. Goldberger, E. & Rapoport, J. L J h e r . Anim. Hosp. Assn. 27, 179-182 (1991). 12. Dodman, N. H., Shuster, L., White, S. D.. Cow, M. H.,Parker, D. & Dixon,R. J,Amer. k t . Med,Assn. 193,815-819 (1988). 13. Page$, P. PathDlogie du camportement du chien &itions du PointV&t4rinaire,Paris, 1998). 14. Taieb, A. Prar. M4d. Chir.Anim. Comp. 33,295-303 (1998). 15. Sawyer,L, S. J. Amer. Vet.Med.ASs*. 214,71-74 (1999). 16. Swn, D. IT Millet Jr, W. H. & Griffin, C. & in Muller & KirKs Small AnimalDematology, 5th edition (Saunders, W.B., Philadelphia, 1995). 17. Bourdin, M.,& Pageat, P. in Encyclopddie Vdtblnaire 2550 (Elsevier, Paris, 19951. 18. Beaver, B. & Barton, C1. J.h e r . Vet. Med. Assn. 203,651-652 (1993). 19.O'Dair.H. A. & F~ster,A. P. k t . Clin.N.her. 25,851-870 (1995). 20. Dramard,V. &Hannie~;I, Point Vet. 27,8186 (1996). 21. Thoday, K. L, in Advances In VderinaryDermatology, vol. I (eds von Tschamer, C & Halliwell, R.E.W.) 47 (BaUi2reTmdal, London, 1990). 22. Hdripret, D. Prat. Mld. Chir. Anim. Comp. 28,73-80 (1993). 23. Gilbert, S., %laud, P. 8i Guagut-re, BE.Prat. Mdd. Chir. Anim. Comp. 3 4 , 5 3 1 (1999). 24. Guagkre, E. Prat. M6d. Chir.Anim. C o q . 28,451-460 (1993). 25. Overd, K. L. Canine PracIice 17,39-43 (1992). 26. Mertens, P. A. & Dudman, N. H. Psychopharmacology ofAnimd Behavior Disorders 122-140 (1997). 27. Pageat, in EncyclopPdie VMinaire 2150 elsev vie^, Pans, 1997). 28. Overall, K. L. CeninePructice 17,25-27 (1992).
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17 : Skin conditions associated with behavioural disorders 29. Willemse, T , Mudde, M., Josephy, M. & Spmijt, B. M. Europe~Neuropsychopharmacology4,39-45 (1994). 30, Dehasse, 1.& De Buyser, C. Prat. Mdd. Chir. Anim. Comp. 28,469-478 (1993). 31. Dehasse, 1.& De Buyser, C.L'iducation du chat (Les ~ditionsde I'Homme, Montdal, 1993). 32. Neville, P.In Practice 13,43-50 (1991).
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Z. Alhaidari
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Diagnostic approach to pruritic dermatoses The diagnosis of pruritic dermatoses in the cat is not always easy, partly because of variation in clinical presentation and partly because of the range of different aetiologies. The owner also faces considerable difficulty in even recognising pruritus, sometimes expressed only as excessive licking, and may find it difficult to distinguish from normal grooming behaviour I-'. Often, pnuitus is not the reason for consultation. Some owners may actually cite alopecia as the reason for presentation, assuming the hair loss to be spontaneous. Others may be mainly concerned about the presence of an eosinophilic plaque, which develops from repeated licking in one particular area. Owners do not suspect that such problems&e~elf-induced,particularly if the cat hides away when it licks. Signs of scratching, on the other hand, are more obvious, especially in pmritic dermatoses involving the face. The diagnostic approach to pruritus must, therefore, be particularly thorough and methodical, and should include certain fundamental diagnostic steps. The history and clinical examination allow formation of a differential diagnosis which can be narrowed down by carrying out appropriate diagnostic procedures (Table 18 : 1). Table 18 : 1 : Diagnostic approach to pruritic dermatoses
Ectoparasitic infestations
Kral dermatoses Tumours Auto-immune dermatoses
mange, notoedric mange)
folliculitis Allergic dermatitis Eosinophilic granuloma comple* Flea allergy dermatitis
Food intolerance
Aeroallergens hypersensivity
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A M c a l Guide to Feline ~ 0 1 o g y
History The histoly can identify various risk factors (.Table 18 : 2) and help steer the clinician towards a differential diagnosis. Important factors to address are :
Breed: generalised, often pnuitic, forms of dermatophytosis are particularly common in Persians (Fig. 18 : 1) ",'. Primary, generalised seborrhoea, a true hereditary disorder, has also been reported in Table 18 : 2 : Important historical factors and conditions they may indicate, SIGNALMENT Breed Persian, Sphinx, Devon Rex Age of onset of lesions Before 6 months
Between 8 months and 3 years
Older animal
Dermatophytosis Flea allergy dermatitis Urticaria pigmentosa Flea allergy dermatitis Dermatophytosis Ectoparasitism (cheyletiellosis, Otodectes infestation) Flea allergy dermatitis Food intolerance Atopic dermatitis Epitheliotropic T ceU lymphoma (mycosis fungoides)
LIFE STYLE Indoor/outdoor Free to roadaccess to outside
Catteriesishows Anxiety-inducing situation Moving house Death of an owner Anival of a child or new animal Management Absence of flea control Previous illness Conjunctivitis, rhinitis Asthmatic bronchitis Digestive disorders
Flea allergy dermatitis Dermatophytosis Ectoparasitism Mosquito bite hypersensitivity Poxvhs infection Dermatophytosis Cheyletiellosis Self-induced alopecia of behavioural origin
Flea allergy dermatitrs Herpesvirus infection Atopic dermatitis Food intolerance
EVOLUTION OF THE DERMATOSIS Circumstances surrounding development Catteriesishows Evolution of clinical signs Seasonality
Prior therapy Treatments and duration Time interval between stopping therapy and reappearance of cutaneous signs Response to prior therapy Corticosteroids effective Corticosteroids variably effective Contagion to in.contact.%wners
Flea allergy dermatitis Dermatophytosis Cheyletiellosis Flea allergy dermatitis Atopic dermatitis Tmmbiculiasis Mosquito bite hypersensitivity Cutaneous drug reaction
Flea allergy dermatitis Atopic dermatitis Food intolerance Dermatophytosis Cheyletiellosis Notoedric mange Otodectic mange
www.vet4arab.co.cc 18 : Diagnostic approach to pruritic dermakses
Figure 18 :1:Generalrseddemtophymsrr caused by ~ c m p o cams ~ m rn a Persian cat
Figure 18 :2 :Hered~taryprimaryseborrhoea in a Persian cat
Figure 18: 3 :Papular lesions on theface of a Sphinx cat with urticaria pigmentosa
Figure 18 :4 :Same cat as in Figure 18 :3, urticariapigmentosa in a Sphinr cat. Note papular, eryihematous and pigmented lesions on the elbow and trunk
Figure18 : 5 :Papules andalopecla on the venbum ofa cat infested with the louse, Fehcola subroshatus
Figure 18 . - . - orsolumbar crusting and scaling in a Persian cat with Cheyletiella blakei infestation
Figure 18 :7 :Generalised crusa., fungoides
- .-....... ...,---.andscaling associated with mycosisfungoides
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Persians (Fig. 18 : 2). Urticaria pigmentosa has to date only been reported in the Sphinx and Devon Rex ','O (Figs 18 : 3,4).
Age of onset of signs: the appearance of pruritus before the age of 6 months must lead to strong suspicion of flea allergy dermatitis, dermatophytosis, pediculosis (Fig. 18 : 5) or cheyletiellosis "5 (Fig. I8 : 6), whereas the development of pruritus in a young adult, aged between 8 months and 3 years, suggests an allergic dermatitis '"~'.".". In an older animal, pruritic exfoliative erythroderma would lead to mycosis fungoides being high on the list of differential diagnoses (Fig. 18 : 7,8). Lfe style and environment: cats that are free to roam, and therefore in contact with other cats, are at greater risk of having flea infestations, dermatophytosis and ectoparasitisms such as Otodectes infestation and trombiculiasis. Cutaneous lesions caused by larval ticks or mosquito bites (Fig. 18 : 9) are also seen. Contact with wild animals, notably small rodents, predisposes hunting cats to a rare dermatosis, poxvims infection i,' (Fig. 18 : 10). As for show cats, they are more likely to present with dermatophytosis or cheyletiellosis. Rapid screening measures, at the entrance to shows, are of little benefit. Knowledge of the diet allows the clinician to institute, if necessary, a suitable elimination diet. The presence of anxiety-inducing situations (e.g. moving house, death of an owner, amval of a new animal or child) should always be investigated. Intense pruritus may also generate severe behavioural disorders, with cats avoiding all contact, hiding away and not eating. These behavioural disorders stop once pruritus is under control and their reappearance indicates relapse. Presence of previous illness: digestive problems associated with facial pruritus strongly suggests food intolerance 4,s. The presence of respiratory signs before the development of severe, pruritic and painful lesions on the face and body suggests a dermatosis of viral origin (e.g. herpesvirus infection and herpesvirus-associated erythema multiforme) 'I. Circumstances surrounding development of the clinical signs: Iiving with other cats (e.g. in shows or catteries) favours emergence of dermatophytosis and infestation with fleas or other ectoparasites (e.g. Cheyletiella spp.). Evolution of signs and seasonality: regular scratching in particular places should raise suspicion of atopic dermatitis or flea allergy dermatitis. Pruritic dermatoses in summer or autumn suggest a parasitic cause (e.g. Trombicula) or allergy, especially flea allergy dermatitis or, more rarely, pollen allergy. Initial distribution of the dermatosis should be ascertained as many dermatoses have preferential distribution sites. Efficacy of prior therapy should be evaluated and dosages and duration of treatment checked. Response to corticosteroids is good in flea allergy dermatitis, atopic dermatitis and early food intolerance; it is partial or poor in cases of long-standing food intolerance. Flea control strategies must be critically and rigorously assessed. Transmission to in-contact animals or owners should lead to the investigation concentrating specifically on tests for dermatophytosis, cheyletiellosis, Otodectes infestation and notoedric mange. The possibility of massive environmental flea contamination should also be investigated.
Clinical examination The clinical examination is a pivotal step in the diagnostic approach to pnuitic dermatoses (Table 18 : 3). General clinical examination is concerned with signs associated with atopy (conjunctivitis, rhinitis, asthmatic bronchitis), food intolerance (vomiting, diarrhoea etc...) and behavioural disorders.
Dermatological examination enables lesions to be identified and their distribution noted. Four main types of lesion can he seen, either alone or combined, in pruritic cats 4,6. Self-induced symmetrical alopecia, characterised by diffuse hair loss and broken, jagged hairs. This is associated, in the vast majority of cases, with flea allergy dermatitis (Fig. 18 : l l ) , behavioural disorders, or more rarely, with another allergic dermatitis (Fig. 18 : 12). Miliary dermatitis, often generalised and presenting as many small crusted papules
www.vet4arab.co.cc 18 : Diagnostic approach to pruritic dermatoses
Figure 18 :9 :Ulcerated nodules on the face of a cat with mosquito bite hypersensitivity (courtesy of 0. CozetteJ
Figure 18 :10 :Confluent macular, erosive and ulcerative lesions on the abdomen of a cat with poxvirus infection (courtesy of J. Declerq)
Figure18 :I1 :Self-inducedsymmelricalalopecia in a cat withfleaallergy dermatitis
Figure 18 :12 :Self-induced symmetrical alopecia in a cat with food intolerance
F i g ... .. .'elf-induced alopecia and dorsolurnbar eosinophilic plaques in a cat withflea allergy dermatitis
F W e 1 8 :14 :Eosinophilicplaques in o cat with food intolerance (fish)
Figure 18 :15 :Erosive, crusting cervicofaciai dermoriiis in a car with atopic dermatitis
Figure 18 :16 :Severe miliaq dermoritis and eosinophilic plaques in a cat with food intolerance (beefl
A hoical Guide to Felinekmtology
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Table 18 : 3 :Important elements of the clinical examination and conditions they indicate LESION DISTRIBUTION Head and neck
-
Atopic dermatitis Food intolerance Hypersensitivity to tick bite lmae Mosquito bite hypersensitivity Otodectic mange Tmmbiculiasis Notoedric mange Poxvirus infection Helpesvims infection
Lumbosacral region
Flea allergy dermatitis
Dorsal midline
Cheyletiellosis
Nose
Mosquito bite hypersensitivity
Generalised
Dermatophytosis Epitheliotropic T cell lymphoma (mycosis fongoides) Cutaneous drug reaction
Lesions of the eosinoph~licgranuloma complex (EGC).These may be typical (indolent ulcer, eosinophilic plaque (Figs 18 : 13-15), and linear granuloma) or atypical (nodules on the chin, in the buccal cavity or between the footpads). Erosive and crusting dermatosis of theface and neck (Fig. 18 : 16). This tends to be very pruritic and, in most cases, very striking in appearance. The cat has violent bouts of itching, and inflicts severe and spectacular excoriations on itself. Noting the distribution of lesions is a critical element of the clinical examination, especially in the early stages of the dermatosis. Almost exclusive involvement of the head and neck would favour a diagnosis of atopic dermatitis, food allergy, mosquito bite hypersensitivity, trombiculiasis, Otodectes infestation or notoedric mange. Involvement of the lnmbosacral region suggests flea allergy dermatitis (Fig. 18 : 11). Scaling on the dorsum and lumbar region suggests cheyletiellosis (Fig. 18 : 6). In the snmmer, the presence of pruritic, erosive and crusting lesions on the nose of a cat living outdoors, points towards mosquito bite hypersensitivity. A generalised pnuitic, erythematous and exfoliative dematosis suggests an epitheliotropic T cell lymphoma (Figs 18 : 7,s) or a cutaneous drug reaction.
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Diagnostic tests T strip examinations and mycological procedures are the most appropriate diagnostic tests.
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Skin serapings demonstrate adult and immature mites. Cheyletiella blakei, Otodectes cynotis, Notoedres cati, Demodex cati and Demodex gatoi, Trombicula autumnalis larvae and the louse Felicola subrostratus may he seen. Tape strip examination (scotch test) can reveal mites living on the surface of the skin. Cheyletiella blakei adults and, in particular, eggs bound to the hair shaft may be found. The sensitivity of the test is quite poor but better results can be achieved if a coat brushing is also performed. Coat brushings, well performed, can be used to collect scale, eggs, parasite faeces and even adult parasites from the skin surface. They are useful in diagnosing cheyletiellosis and flea infestation. Testing for dermatophytosis should be routine in any cat with a pruritic dermatosis. Wood's lamp examination, carried out carefully, is the f i s t step. However, it is not very sensitive as 50% of Microsporum canis isolates fail to fluoresce. Direct microscopy of hair and scales reveals the type of hair invasion by dermatophyte hyphae and spores. Fungal culture is needed to identify the genus and species of the dermatophyte involved.
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www.vet4arab.co.cc 18 : Diagnostic approach to pruritic dennatoses
The skin smear is a routine, straightforward procedure which can aid the diagnosis of pruritic dermatoses by demonstrating bacteria, yeasts of the genus Malassez~a,and cells such as neutrophils and eosinophils present on the surface of eroded plaques or within crusts and pustules. Allergy testing (intradema1 and serological tests) is unreliable and hard to interpret in the cat When allergic dermatitis is suspected, the diagnosis should be based mainly on resoonse to avoidance measures (e.g. flea control andelimination diet) ". Skin biopsies are sometimes necessary if the history and clinical examination suggest an uncommon condition which requires histological diagnosis: bacterial folliculitis (rare in the cat), epitheliotropic T cell lymphoma (mycosis fungoides), poxvirus infection, urticaria pigmentosa, etc ....It should be remembered that in the diagnosis of pnuitus, the skin biopsy,if not directly indicated from the history and clinical examination, is a constant source of frustration for the clinician and may regularly lead to misdiagnosis. All it will show in the majority of these cases is a hyperplastic perivascular dermatitis, a reaction pattern of poor diagnostic value, commonly associated with any inflammatory dermatosis. whatever the cause.
REFERENCES 1. Ihrke, P. J. inFelineMedecine (ed Pratt, P.W.) 560-562 (Amencanveterinary Publications, Santa Barbara, 1983): 2. Fadok, V. Proc. ESVD Feline Dermatology Workshop, Oirecht 1-10 (1994). 3. Foil, C. S. Vet. Clin. N.Amer. 18,999-1011 (1988). 4. Alhaidari, Z. Proc. Congris Annuel CNVSPA 460-462 (1996). 5. Mason, I. in Handbook @Small Animal Dermatology (eds MorieUo, K . & Mason, I.) 153-162 (Pergamon Press, Oxford, 1995). 6. Kunkle, G. A, in Current Veterinary Therapy X(ed Kirk, R.W.), 583-586 (Saunders, W.B., Philadelphia, 1989). 7. Scott, D. W. Miller Jr, W, H. & Griftin, C. E. Muller & Kirk's Small Animal Dermatology, 5th edition (Saunders, W.B., Philadelphia, 1995). 8. Paradis, M. &Scott, D.W. Feline Practice 18, 17-21 (1990). 9. Vitale, C. B., Ihrke, P. J., Olivvry, T. & Stannard,A. A. Vet. Dermatol. 7,227-233 (1996). 10. Noli, C., Scarampella E Proc. AAVD-ACVD, Maui, 65 (1999). 11. Scott, D. W. J.Amer. Anim. Hosp. Assn. 23,255-274 (1987). 12. Gilbert, S., Pdlaud, P. & Guagukre, E. Prat. MPd. Chir. Anim. Comp. 3 4 , 5 3 1 (1999). 13. Hargis, A. M., Ginn, P. E.,Mansell, J. E. K. L. & Garber, R. L. Proc. AAVD-ACVD, San Antonio 11-12 (1998). ~ 2 (eds Ihrke, P.J., Mason, I. &White, S.D.).51-62 14. DeBoer, D. J., Saban, R., Schultz, K. T. & Bjoding, D. E,in Advances in Veterinary D e r m a f o l o vol. (Pergamon, Oxford, 1993). 15. Foster, A. P., Duffus,W. P H., Shaw, S. E. & Gmfydd-Jones, T. J. Res. Vet. Sci. 58,70-74 (1995). 16. Gilbert, S. & HalliweU, R. E, W. Vet. Immunol. Immunopafhol. 63,235-252 (1998). 17. Foster,A. P. & O'Dair, H. Vet.Dermatol.4,lll-115 (1993). 18. Prklaud, P. Prat. Mid. Chir Anim. Comp. 33,281-293 (1998).
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i d Guide m Feline t?qmaf0108y
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I Diagnostic approach to alopecia Alopecia is defined as a partial or generalised loss of hair and is the second most common reason for consultation (after pruritus) in the cat ". Self-induced alopecia is the direct consequence of licking, which may occur for many different reasons. The diagnostic approach to self-induced alopecia is the same as that of the pruritic dermatoses. This type of alopecia has often been thought of as an endocrine problem, partly because of its bilaterally symmetrical, and apparently non-inflammatory, appearance but also because of its favourable "response" to various hormonal therapies. However, skin problems due to endoc~opathyare very rare in cats The diagnostic approach to alopecia, therefore, must be particularly rigorous and methodical, and should involve certain fundamental steps (Table 19:l). The history and clinical examination allow formation of a diierential diagnosis which can be narrowed down by canying out appropriate diagnostic procedures.
Table 19 : 1 : Diagnostic approach to alopecia
Fungal investigation
ermatophytosis
8I
APPEARANCE OF THE SKIN
Non.lesional, seborrhoeic,
4--=T
Skin biop
Teiogen efiuvium, Alopecia areata, Pseudopelode Congenital hypotrichosis, Cutaneous epitheliotropic T ceii lymphoma,
Skin hyperfragility
Haematology
Hormonal testing Skin biopsies, ..,Diagnostic imaging
Gushing's syndrome, Hyperthyroidism Acouired cutaneous hvoerfro~iliivsvndrome
1c6calGuide to Ahe DnmatoIogy
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History The history can identify various risk factors (Table 19:2) and help steer the clinician towards a differential diagnosis. Important factors to address are :
Breed: Birman I,', Burmese, Devon Rex and Siamese breeds are predisposed to congenital hypotrichosis which is a localised or total loss of hair, sometimes associated with other ectodermal disorders affecting whiskers, claws and teeth. Generalised congenital hypotrichosis, referred to as alopecia universalis, has been described in the Sphinx (Fig. 19 : 1). Abyssinian cats sometimes present with congenital structural disorders of the hair shaft affecting the whiskers and primary hairs which fracture at the site of onion-shaped swellings 9. Genetic follicular dysplasia has been described in the Cornish Rex lo. Persians are particularly predisposed to dermatophytosis caused by Microsporum canis l4 (Fig. 19 : 2). Self-induced symmetrical alopecia of behavioural origin is more common in Siamese (Fig. 19 : 3), Abyssinian and Burmese breeds '. Age of onset of signs: alopecia present at birth or developing soon after suggests congenital hypotrichosis 14. Equally, pili torti is a congenital structural disorder of the hair shaft, reported in kittens. This syndrome, which affects secondary hairs only, is characterised by flattening and rotation of the hair shaft, excessive fragility and fracture. Affected kittens also present with pododermatitis and paronychia ". In any kitten with focal or multifocal alopecia, dermatophytosis should be suspected ". In a young adult, aged between 8 months and 3 years, alopecia can be self-inflicted and a direct consequence of pruritus associated with allergic dermatitis Turnours, paraneoplastic alopecia and endocrinopathies affect mostly older cats. Life style and environment: cats living together in groups, breeding colonies or rescue premises are predisposed to contagious dermatoses: dermatophytosis due to Microsporum canis and pnuitic ectoparasitic infestations which cause self-induced alopecia. These cats are also more exposed to flea infestations and therefore more inclined to develop symmetrical alopecia related to flea allergy dermatitis (Fig. 19 : 4). Flea allergy dermatitis is the most common dermatosis in the cat and must always be considered in the differential diagnosis not only of the pruritic dermatosis but also of alopecia Presence of anxiety-inducing situations (e.g. moving house, death of an owner, arrival of a new animal or child) should always be investigated, given their role in some cases of self-induced alopecia. Presence of previous illness: a progressive change in general condition associated with gastrointestinal signs (e.g. anorexia and vomiting) often precedes the appearance of skin lesions typical of paraneoplastic alopecia (Figs 19 : 5,6). Circumstances surrounding development of the clinical signs: living with other cats (e.g. in shows or catteries) favours development of dermatophytosis or pruritic ectoparasitic infestations which cause self-induced alopecia. Evolution of signs and seasonality: self-induced alopecia in summer or autumn suggests flea allergy dermatitis. Initial distribution of the dermatosis should be ascertained, as many types of alopecia have preferential distribution sites. The efficacy of prior therapy should be evaluated and dosages and duration of treatment checked. Response to corticosteroids is good for self-induced alopecia arising from flea allergy dermatitis, atopic dermatitis and early food intolerance; it is partial or poor in long-standing food intolerance and . behavioural disorders. In the cat, it is also important to check for possible development of atrophic, circumscribed alopecia at the site of injection of corticosteroid or synthetic progestagens (Fig. 19 :7) and also for extensive atrophic alopecia associated with iatrogenic Cushig's syndrome (Fig. 19 : 8). Flea control strategies must be critically and rigorously assessed.
www.vet4arab.co.cc 19 : Diagnostic approach to alopecia
Figure 19 :I :Alopec~auruversalis in an adult Sphrnr car. Note the presence of hair on the extremit~es
Figure 19 :2 : Diffuse generalised alopecia in a Persian cat with dermatophytosis caused by Microspomm canis
Figure 19 :3 :Self-rduced symmetrical alopeaa of behavloural origrn [permanent anrreiy) in a S~amesecat.
Figure 19 :4 :Self--mdun , hair cat withflea allergy d e m i t r s
Figure 19 :7 :Iatrogenic, at,. -.,...-,,-... ...., injection of medronyprogesterone in a female domestic short hair cat
syndrome) in a Persian car
alopecra in a domesa
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A W e a l Guide to F e h ~ 0 1 o g y
Transmissionto in-contact animals or owners should lead to the investigationconcentrating specifically on tests to demonstrate and identlfy a dermatophyte. If other animals or people are pruritic, self-induced alopecia may be associated with infestation of fleas or CheyletieJla blakei (Fig. 19 : 9). Table 19 : 2 : Important historical factors and conditions they indicate. SIGNALMENT Race Persian, Burmese, Devon Rex, Siamese, Sphinx
Age
Congenital hypohichosis
Abyssinian
Hair shaft dysplasia
Persian
Dermatophytosis
Siamese, Abyssinian, Burmese
Self-induced alopecia of behavioural origin
Cornish Rex
Follicular dysplasia
Birth
Congenital hypotrichosis
Kitten
Dermatophytosis
Young adult (aged between 8 months and 3 years)
Allergic dermatitis
Old cat
Epitheliotropic T cell lymphoma (mycosisfungoides) Paraneoplastic alopecia Cushing's syndrome Hyperthymidism
LIFE STYLE Living with other cats
Dermatophytosis Flea allergy dermatitis Ectoparasitic infestation (Cheyletiella,Otodectes)
Anxiety-inducing situation
Self-induced alopecia of behavioural origin
DEVELOPMENT OF THE DERMATOSIS Contagion
Dermatophytosis Ectoparasitic infestation (Cheyletiella, Otodectes)
PRIOR DISORDERS Episodes of anorexia or vomiting
Pancreatic panneoplastic alopecia
Polyuria-polydipsia,abdominal enlargement
Gushing's syndrome
Clinical examination I
. f alopecia which are in fact merely dermatological manifestations of systemic disease. Cushing's -~
~
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&
syndrome, in addition to the alopecic lesions sometimes observed, manifests as polyuria-polydipsia, polyphagia and abdominal enlargement '>-I6(associated with modification and redistribution of fat depots). A syndrome involving polyphagia, polydipsia and polyuria associated with weight loss, hyperactivity, vomiting or diarrhoea in an old cat also suggests hyperthyroidism, which can sometimes produce alopecia associated with atrophic, hypotonic skin ".". A change in general condition and various gastrointestinal signs are common in paraneoplastic alopecia relating to a pancreatic or biliaq neoplasia, whether or not there is metastasis 12. Finally, whenever self-induced symmetrical alopecia is present, evidence of behavioural disorders should always be looked for and investigated.
The dermatological examination demonstrates the distribution of hair loss , which can be focal, multifocal, or extensive and /or diffuse. Focal or multifocal lesions should set a l m hells ringing for dennatophytosis (Figs 19 : 2, 10). Examination of the coat will determine whether or not hair lesions are present. When hairs are broken and not easily plucked, alopecia is self-induced. The diagnostic approach to self-induced alopecia is
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19 : D~agnosticapproach to alopecia
Figure 19 :9 :Self-induced dorsolumhar alopecra in a Perstan cat wlth cheyletrellos~s
-
Figure 19 :10 : Multifocal alopecia and scaling in a cat with dermatophytosis caused by Microsporum canis
y dermatitis*
Figure 19 :12 :Close-up of the cat in Figure 19:Il. Note the whitish nodes along the hair shafts*
Figure 19 :13 :Microscopic view of hair (x 100): swellings along the hair shufl and alterations in cuticle lead to hairfractures, leaving the distal end with a characteristic brush-like appearance
Figure 19 :14 :Ultrastructural view of hair (x 1951: swellings along the hair shar and alterations in cuticle lead to hair fractures, leaving the distal end with a characteristic brush-like appearance
Figure 19 :15 :Pseudopelade iii a cat (courtesy ofH. Power]
Figure 19 :16 :Generalised alopecia with erythema and scaling in a Siamese cat with cutaneous epitheliompic T cell lymphoma
19 :11 :Trichorrhexis
secondary toflr
Alhaidan. 2. & Olivr/,n. Ortonne, J.P.Vet Domialol. 7,235-238 (1996).
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therefore the same as that of the pruritic dermatoses. Sometimes, other macroscopic hair defects, such as whitish nodes on the hair shaft, will be revealed. These are indicative of trichorrhexis nodosalg(Figs 19 : 11-14). When hair is completely absent or easily plucked, lesional analysis is paramount. Non-lesional disorders include telogen effluvium, in which a pathological or physiological stress factor triggers all the hair follicles to enter synchronously the telogen phase, and alopecia areata and pseudopelade (Fig. 19 : 15), which are auto-immune diseases characterised by lymphocytic attack, directed against the follicular bulb and isthmus respectively lo. The skin is often seborrhoeic in cats with congenital hypotrichosis "'. Erythema and scaling are common and can have a focal distribution in de&atophytosis, a dorsal distribution in cheyletiellosis (Fig. 19 : 9) and a rather generalised distribution in cutaneous T cell epitheliotropic lymphoma (Fig. 19 : 16). In this last case, the hair loss is due to the neoplastic infiltratiobliteratGg the $10-sebaceous adnexae. Paraneoplastic alopecia is characterised by a particularly shiny appearance to the skin, mainly affecting abdomen and limbs (Fig. 19 : 5). This alopecia is sometimes generalised (Fig. 19 : 6). Lastly, the skin may be severely atrophic and excessively fragile in iatrogenic or spontaneous Cushing's syndrome ',2,'3~162' (Figs 19 : 7,8). Hypothyroidism is very rare in the cat and, except in congenital cases '"",manifests as a dirty, seborrhoeic coat rather than alopecia. Paradoxically, it is actually hyperthyroidism which is accompanied by alopecia, and in chronic cases, skin atrophy ". To our knowledge, there are no reports of alopecia linked to sex hormone deficiency in the cat.
Diagnostic tests In cases of alopecia, the first diagnostic test to perform is a trichogram. This is especially useful in determining whether or not alopecia is self-induced. When alopecia is self-induced, the distal extremities of the hairs are broken and jagged. When alopecia is not self-induced, these are normal. Given the incidence of ectoparasitic infestation and dermatophytosis in the cat, skin scrapings, tape strip examinations and mycological procedures are the most appropriate diagnostic tests to consider. Skin scrapings demonstrate adult and immature mites: Cheyletiella blakei, Otodectes cynotis, Notoedres cati, Demodex cati and Demodex gatoi. The tape ship examination (scotch test) can reveal mites living on the surface of the skin. Cheyletiella blakei adults and, in particular, eggs stuck to the hair shaft may be found. The sensitivity of the test is quite poor but better results can be achieved if a coat brushing is also performed. Coat brushings, well performed, can be used to collect scale, eggs, parasite faeces and even adult parasites from the skin surface. They are useful in diagnosing cheyletiellosis and flea infestation. Testing for dermatophytosis should be routine in any cat with alopecia. Wood's lamp examination, carried out carefully, is the first step. However, it is not very sensitive as 50% of Microsporum canis isolates fail to fluoresce. Direct microscopy of hair and scale reveals the type of hair invasion (endoectrothix) by dermatophyte hyphae and spores. Fungal culture is needed to identify the genus and species of the dermatophyte involved. Microscopic hair examination, in some cases, reveals structural hair shaft abnormalities (e.g. hair shaft dysplasia '" pili torti " and trichorrhexis nodosa 19). In trichorrhexis nodosa, microscopic examination reveals swellings along the hair shaft and alterations in cuticle which lead to hair fractures, leaving the distal end with a characteristic brush-lie appearance " (Fig. 19 : 13). Ultrastructural examination with a scanning electron microscope also c o n h s these abnormalities of the hair (Fig. 19 : 14). Allergy testing (inhadermal and serological tests) is unreliable and hard to interpret in the cat. When allergic dermatitis is suspected, the diagnosis should be based mainly on response to avoidance measures (e.g. flea control and elimination diet). Intradermal and serological testing are used only as a last resort in order to select allergens for immunotherapy). Skin biopsies are sometimes necessary if the history and clinical examination suggest a condition which requires histological diagnosis: congenital hypotrichosis, hair shaft dysplasia (e.g. pili torti), alopecia areata, pseudopelade and epitheliotropic T cell lymphoma. Additional diagnostic procedures may be necessary. Haematology, biochemistry and endocrine profiles are indicated when Cushing's syndrome or hyperthyroidism are suspected. Imaging techniques (radiography, ultrasonography and CT scanning) are essential for diagnosing, pancreatic paraneoplastic alopecia.
www.vet4arab.co.cc 19 : Diagnostic approach to alopecia
REFERENCES 1. Mason, I. in Handbook of Small Animal Dermatology (eds Moriello, K. & Mason, I,) 136-138 (Pergamon Press, Oxford, 1995). 2. Scott, D. W. Miller Jr, W. H. & Griffin, C. E. Muller & Kirk's SmaN AnimalDermatology, 5th edition (Saunders, W.B., Philadelphia, 1995). 3. Scott, D. W. J. Amer. Anlm. Hosp. Assn. 23,255-274 (1987). 4. Scott, D. W 1. Amer Anim. Hosp. Assn. 26,515-537 (1990). 5. Henfrey, J, I, in Manunl of Small Animal Dermafology vol. 114-120 (eds Locke, P.H., Harvey, R.G. & Mason, 1.) British Small Animal Veterinary Association, Cheltenham 114-120 (1993). 6. Miller Jr, W. H. Comp. Conf.Educ. Pract. Vet. 12,461-471 (1990). 7. Bourdeau, P., Lwneni, D., Maroille, J:M. & Mialot, M, Rec. Med. Vlt. 164,17-24 (1988). 8. Robinson, R. J. Hered. 64,47 (1973). 9. Wilkiuson, G. T. & Kristensen, T. S. J small Anim. Pract. 30,27-28 (1989). 10. Scon, D.W. Le Mldecin Vltirinaire du Quebec 28,1,3844 (1998). 11. Geary, M. R. &Baker, K. P. J. smaNAnim. Pract. 27,85-88 (1986). 12. Pascal-Tenorio, A,, Oliny, 2,Gross, T. L., Atlee, B. A. & Ihrke, P.J Vet. Dermatol. 8,47-52 (1997). 13. Helton-Rhodes, K., Wallace, M. & Baer, K. in Advances in Veterinafy Dermatology vol. 2 (eds Ihrke, P.J., Mason, I. &White, S.D.) 391-396 (Pergamon Press, Oxford, 1993). 14. Nelson, R. W & Eeldman, E. C. in Consultations in Feline Internal Medicine (ed August, J.R.) 267-270 (Saunders,W.B., Philadelphia, 1991). 15. Peterson, M. E. & Steele, P. J. Amer Vet. Med. Assn. 189,680-683 (1986). 16. Watson, P. J. and others J. small Anim. Pract. 39, 175-184 (1998). 17. Graves, T. K. &Peterson, M. E. in Current VeterinaryTherapy XI (ed Kirk,R.W.) 334-337 (Saunders, W.B., Philadelphia, 1992). 18. Thoday,K. J. &Mooney, C.T. Vet.Rec. 131,257-264(1992). 19. Alhaidai, 2. Olivry, Th & Oflome, J.P. Vet. Dermatol. 7,235-238 (1996). 20. Power, H.T., Olivry, T., Woo, I. & Moore, P. E in Advances in Veterinafy Dermatology "01. 3 (eds Kwochka, K.W., Wdlemse, T. & von Tschamer, C.) 538 (Buttemod Heinemann, Oxford, 1998). 21. Scott, D. W. FelinePractice 12,30-34 (1982). 22. Jones, B. R. Vet. Rec. 131,145-148 (1992). 23. Rand, J. S., Levine, J., Best, S. J. &Parker, W. J. Vet. Int. Med. 7,272-276 (1993). 24. Peterson, M. E. in Current Veterina~Therapy X (ed Kirk, R.W.) 1000-1001 (Saunders, W.B., Philadelphia, 1989).
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E. Bensignor
Diagnostic approach to crusting dermatoses Crusting dermatoses are a common reason for consultation in feline dermatology I". Crusts can be defined as a mixture of blood, serum, exudate, and/or pus which has dried on the surface of the skin and to which scale and hairs have adhered. To make a specific diagnosis and institute effective treatment requires a good knowledge of the clinical aspects and causes of crusting dermatoses. Three types of crusts are seen in the cat: 1) large, spontaneously appearing crusts, generally coalescing, thick and commonly found on the face (Fig. 20 : 1) 2) crusts secondary to excoriation, variable in size and found in various locations (Fig. 20 : 2). This type of crust is seen with all the pruritic dermatoses, especially allergic dermatitis. 3) punctate crusts seen in miliary dermatitis (Fig. 20 : 3), a cutaneous reaction pattern with various causes. The diagnostic approach to a crusting dermatosis must be thorough and systematic. It should involve takmg a history, a general and dermatological clinical examination and appropriate diagnostic tests (Table 20 : 1)
Table 20 : 1 : Diagnostic approach to crusting dermatoses
--
Otodectic mange, Notoedric mange, Demodicosis, cheyle:iellosis, ~ombiculiosis,pediculosis Dermatophytosis
Cytological examination
Flea allergy dermatitis, Pyoderma, Malassezia
dermatitis
Allergic dermatitis Auto-immune skin disease
Elimination diet
Food intolerance
Mosauito bite hvoersensitiviN ,. Solar dermaritis
Aeroallergens
Viral dermatoses
allergie
Tumours
k
Deep mycoses
1
Mycobacterial infection
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History The history directs the clinician towards certain differential diagnoses and is a critical part of the diagnostic process '",'. Important points to consider are : Breed: dermatophytosis is particularly common in Persians and in long-haired cats generally. In these breeds, dermatophytosis should always be suspected when crusts are present (Fig. 20 : 4). Age of onset of clinical signs: kittens and young adults are predisposed to ectoparasitic infestations (e.g. cheyletiellosis, Otodectes infestation and demodicosis), dermatophytosis and allergic dermatitis whereas older animals are more susceptible to auto-immune dermatoses (Fig. 20 : 5) and tumours (e.g. mycosis fungoides) (Fig. 20 : 6). Animal's life style and environment: cats that are free to roam, and therefore in contact with other cats, often present with dermatophytosis and various ectoparasitic infestations. Cats kept together (e.g. in catteries or shows) are more susceptible to dermatophytosis and cheyletiellosis. Contact with wild rodents predisposes hunting cats to poxvhs infection. Possibility of transmission between cats and also between cats, dogs andpeople must be thoroughly investigated. Ectoparasitic infestation, particularly involving Cheyletiella blakei, Otodectes cynotis or fleas and dermatophyte infection with Microsporum canis should be suspected. Presence of pruritus prior to lesions points towards an allergic dermatosis or possibly an ectoparasitic infestation. Dermatophyte infections are not pruritic except for some inflammatory forms. Prior treatments should be itemised to establish or exclude the possibility of a cutaneous drug reaction. Response to prior therapy can be an important factor in the diagnosis, as the majority of inflammatory non-infectious dermatoses respond well to moderate doses of corticosteroids. However, lack of efficacy of such treatment has no diagnostic value, given the possibility of inadequate dosing and uncertain compliance.
Clinical examination General clinical examination is concerned particularly with systemic signs associated with certain crusting dermatoses which are merely dermatological manifestations of systemic illness. Such systemic problems include hypereosinophilic syndrome, respiratory signs associated with a thymona or herpesvirus infection, gastrointestinal signs relating to food intolerance, and immunodeficiencies, joint and kidney signs relating to systemic lupus erythematosus (Figs 20 : 7, 8). Dermatological examination allows the clinician to identify lesions and to establish their distribution and configuration. Identifcation of lesions is less important in the cat that in the dog. However, the presence of primary lesions such as erythema, papules and pustules, although rare, should be thoroughly investigated. The type of crust should be noted: large, spontaneously appearing crusts, suggesting an exudative or ulcerative process (Figs 20 : 1,2); crusts secondary to excoriation, requiring a search for the cause of pruritus; and punctate, papular crusts (feline miliary dermatitis) suggesting mainly an ectoparasitism or flea allergy dermatitis. (Fig. 20 : 3). The colour of the cmst is also significant: yellowish crusts are seen in superficial exudative conditions, with the deeper the erosive process, the darker the colour. Large, black, adherent crusts are seen with deep dermal lesions with haemorrhage. Configuration and the way they develop is helpful in making a diagnosis. For example, dermatophytosis lesions are extensive and expand peripherally, tending to heal from the centre even when there is inflammation at the peripheq. Lesion distribution is suggestive of one or a group of dermatoses. A cervico-facial distribution points towards food intolerance, atopic dermatitis, auto-immune skin disease or demodicosis. Dorsal involvement leads to suspicion of cheyletiellosis. A dorso-lumbar distribution is very suggestive of flea allergy dermatitis. If only the pinnae are affected, Otodectes infestation, solar dermatitis or dermatophytosis come to mind. Involvement of the extremities may be l i e d with an auto-immune dematosis or a contact dermatitis. Lesions at the mucocutaneous junctions or on the mucous membranes suggest an auto-immune skin disease, a cutaneous drug reaction, poxvitus infection or candidiasis.
www.vet4arab.co.cc 20 : D~agnosticapproach to crusting dermatoses
Figure 20 : I :Large, spontaneously appearing crusts, secondafy to an ulceratrveprocess in a cat wlth a mahgnant mast cell tumour
Figure20 :2 :Small crusts secondary lo excoriations ina cat with atopic dermatitis
Figure 20 :3 :Mil~aiydermahtis in a cat withflea allergy dermntit~s
Figure 20 :4 :Generalised miliary dermatitis and scaling associated with dermatophytosis caused by Microspomm canis in a long-haired cat
Figure 20 :5 :Pustular and crusting lesions in a cat with pemphigus foliaceus
Figure 20 : 6 : Crusting, scaling and erosive lesions in a cat with epitheliotropic T cell lymphoma
, !20 :7 : General~sedc (courtesy of T Olrviy)
Figi
.
8 :Close-up of the cat in Figure 20 :7lcourtesy of T. Oliviy)
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Given the frequency of ectoparasitic infestation and dermatophytosis in the cat, skin scrapings, tape strip examinations and mycological tests are the initial diagnostic tests to consider
Skin scrapings demonstrate adult and immature mites. Cheyletiella blakei, Otodectes cynotis, Notoedres cati, Demodex cati and Demodex gatoi, Trombiculo autumnalis larvae and the louse Felicola subrostratus may be seen. Tape strip examination (scotch test) can reveal mites living on the surface of the skin. Cheyletiella blakei adults and, in particular, eggs bound to the hair shaft may be found. Testingfor dermatophytosis should be routine in any cat with a crusting dermatosis. Wood's lamp examination, carried out carefully, is the first step. However, it is not very sensitive as 50% of Microsporum canis isolates fail to fluoresce. Direct microscopy of hair and scale reveals the type of hair invasion by dermatopbyte hyphae and spores. Fungal culture is needed to identify the genus and species of the dermatophyte involved. Skin smears are often very useful. When crusting and pustular lesions are present, .sytological examination of these lesions can point towards a diagnosis of pemphigus foliaceus or c o n h a possible pyoderma. Impression smears are necessary where there is greasy scale and crust, accompanied by excoriations, that may be linked to Malassezia dermatitis. This test can be canied out by gently lifting a crust and pressing a microscope slide on the underlying skin surface, or conversely by repeatedly applying the undersurface of the crust to the slide. With dry lesions, the crusty surface can be scraped gently with a scalpel blade. The scraping is then spread out on a slide and stained rapidly. If atypical yeasts are demonstrated, a fungal culture, using special lipid-enriched media, is indicated because lipid-dependent species of Malassezia can be found on cats 6. In cases where allergic dermatitis is suspected, cytological examination has no diagnostic value. Allergy testing (inhadermal and serological tests) is universally unreliable and hard to interpret in the cat'. When allergic dermatitis is suspected, the diagnosis should be based principally on response to avoidance measures (e.g. flea control and elimination diet). Skin biopsies are necessaq for large crusting lesions on an adult or aged animal to confirm a diagnosis of auto-immune skin disease, cutaneous drug reaction, poxvirus infection or epitheliotropic T cell lymphoma. This test does not always produce a diagnosis, but it can point the clinician in the right direction and allow certain differentials to be eliminated. Samples must be taken with care. In particular, it is important to mention on the histopathologist's submission form that crusts have been sampled. Crusts have a tendency to separate from the rest of the biopsy when immersed in fixative solution and may be forgotten when the tissue is placed into paraffin blocks. Other diagnostic tests must be performed in l i e with the differential diagnosis. For example, testing for FeLV and F N infections is necessary if immunodeficiency is suspected; haematology and differential cell counts are useful if hypereosinophilic syndrome is suspected and an antinuclear antibody test is indicated for systemic lupus erythematosns.
REFERENCES 1. Carlotti, D. N. & Bensignor, E. Prat. Mid. Chir. Anim. Comp. 30,%9-261 (1995). 2. Scott, D. W. Miller Jr, W. H. & Griffm, C. E. Muller & Kirk's SmaNAnimal Dermntology, 5th edition (Saundws, W.B., Philadelphia, 1995). 3. Willemse, T.in Current Veterinary Therapy VII (ed Kirk,R.W.), 459-462 (Saunders, WB., Philadelphia, 1980). 4. Sousa, C.A. Vet. Clin. N.Amer 25,813-831 (1995). 5. Scott, D. W. J A m e r Anim. Hosp. Ann. 16,331-459 (1980). 6. Guillot, I., Gueho, E., Mialot, M. & Chermette, R. Point Vdt. 29,691-701 (1998). 7. Gilbert, S., Pdlaud, P. & Guagukre, E. Prat. Mid. Chir Anim. Comp. 34, 15-31 (1999).
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a1 Guide to Fehe Bmatology
I
E. Bensignor
1 Diagnostic approach -
-
to erosive and ulcerative dermatoses In the cat, erosive and ulcerative dermatoses make up a common reason for consultation, probably because of the thinness of the epidermis. An erosion is a superficial defect affecting the epidermis but not, strictly
speaking, the dermis ',' (Fig. 21 : 1). On the other hand, the deeper ulcer does affect the dermis and heals with a scar ',' (Fig. 21 : 2). Distinguishing these two secondary lesions clically is not always easy nor necessarily helpful diagnostically. However, erosions and ulcers linked to external factors (e.g. environmental trauma or self-excoriation) should be distinguished from those associated with an inflammatory process ' , I . In the fust case, the diagnostic approach is the same as for the pruritic dermatoses. It is also the same as that applied to some crusting dermatoses. This is because erosions and ulcers leak out bloodand 1 or serum, or pus, which, when dry, form crusts '". In the second case, the defect may be l i e d to direct epidermal destruction by the inflammatory process or it may be secondary to poor blood supply to the skin I.". The diagnostic approach should involve taking a careful history, conducting a general and dermatological clinical examination and performing appropriate diagnostic tests (Table 21 : 1).
Table 21 : 1 : Diagnostic approach to erosive and ulcerative dermatoses
Tests for demonstrating ectoparasites and dermatophytes FeLV and FIV testing
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History The history directs the clinician towards certain differential diagnoses and is a critical part of the diagnostic process. Important points to consider are :
Age of onset of clinical signs: kittens and young adults are predisposed to genodermatoses (e.g. junctional and dystrophic epidermolysis bullosa, and cutaneous asthenia). Older cats are more likely to present with auto-immune skm conditions or tumours. Animal's life style and environment: cats that are free to roam or live outdoors, are vulnerable to actinic dermatoses and, more generally, to environmental trauma (bums, frostbite, etc.) I,'. In some cases, owners report spontaneously a link between trauma and development of lesions. Aggressive l and hunt cats are more likely to have bites and fight wounds la. Cats that live in ~ r a surroundings wild rodents are predisposed to poxvirus infection I.'. Transmission between cats andalso between cats, dogs andpeople: repeated contact with other cats may allow transmission of some viral diseases such as FIV,FeLV and herpesvirus infection '"i,6 (Fig. 21 : 3), as well as some superficial and deep mycoses such as dermatophytosis and cryptococcosis respectively. Ectoparasitic infestations (e.g. notoedric mange, cheyletiellosis and Otodectes infestation) are often contagious and manifest as erosive or ulcerative lesions '. Pruritus and its association with the development of erosive or ulcerative lesions: severe pruritus is often the sole cause of such dermatological lesions in cats. Some very pruritic dermatoses (e.g. atopic dermatitis, food intolerance, notoedric mange and behavioural self mutilation) involve violent scratching and biting which can produce extremely severe erosive or ulcerative lesions (Fig. 21 : 4). Prior treatments should be itemised systematically to establish or exclude the possibility of a cutaneous drug reaction. In cats, extensive ulcers may be l i e d to skin fragility resulting from excessive treatment with corticosteroids (iatrogenic Cushing's syndrome) (Fig. 21 : 5) although this is uncommon. Response to prior therapy can be an important diagnostic criterion I,'.
Clinical examination General clinical examination is concerned particularly with signs associated with some erosive and ulcerative dermatoses, which are in fact merely dermatological manifestations of systemic disease. Careful examination of the respiratory and digestive tracts is necessary because some viruses, notably herpesvirus infections, can cause dermatological signs in the form of ulcerative lesions of the face and I or mucous membranes 'as,6. In FIV and FeLV infections, oral ulcerations are common and often associated with diff~cultiesin eating and swallowing, depression and weight loss 'a,i (Fig. 21 : 6). Feliie infectious peritonitis sometimes causes ulcers in thin-skinned areas (e.g. pinnal marg'is), due to vasculitis. In addition to the systemic signs seen in Cushing's syndrome (a rare disease in cats), the epidermis becomes extremely thin, leading sometimes to severe skin fragility. Ulcerative lesions on the face, limbs and perianal region have recently been reported in a cat with paraneoplastic syndrome linked to a pancreatic tumour '. Dermatological examination allows the clinician to identify lesions and to establish their distribution. Ident$cation of lesions is essential. The skin should be examined for primary lesions, in particular pustules, vesicles and bullae. These lesions are unfortunately fragile and very short-lived because the feline epidermis is so thin. Their rupture is responsible for the development of erosions and ulcers. Purpuric macules associated with punched-out cutaneous ulcers require investigation for feline infectious peritonitis-induced vasculitis Ulcerated nodules are commonly seen with tumours and infectious diseases (e.g. systemic mycoses and mycobacterial infections) I,". Where ulceration is considerable, it is helpful to have an idea of the resistance and elasticity of the skin. Measurement of the cutaneous extensibility index is then useful Cases of cutaneous asthenia linked to a collagen disorder have been reported in the feline species. Acquired cutaneous fragility has also been described following excessive treatment with either corticosteroids or megoestrol acetate and more rarely, in association with diabetes or hepatic lipidosis.
www.vet4arab.co.cc 21 : Diagnostic approach to erosive and ulcerative dennatosas
Figure 21 : 1 : Facial erosions and ulcerations in a cat with food intolerance
Figure 21 :2 :Truncal ulcerations in a cat with deep pyodema and FeLV infection
Figure 21 :3 :Generalised erosive and ulcerative dermatitis in a cat which presented with herpesvirus infection eight days previously (herpemirur-associated erythema multforme suspected)
Figure 21 :4 :Ulcerations on the neck of a cat with food intolerance
Figure 21 :5 : Cutaneous fragility and ulcerations in a car with iatrogenic Cushing's syndrome (courtesy of D. Hiripret)
Figure 21 :6 : Ulcerations on the hardpalate of a cat with FNinfection
Figure 21 :7 :Idiopathic u
...-.
.-.
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1~
Lesion distribution is suggestive of one or a group of dermatoses. Auto-immune dermatoser frequently affect the face, (nose, nasal planum and pinnae), mucocutaneous junctions, digits and thr region around the nipples. Actinic dermatoses affect mainly depigmented and sparsely-haired regions (e.g. eyelids, nose and pinnae). A seborrhoeic, ulcerative, facial dermatosis, with a poorly understood pathogenesis, has recently been reported in the cat (Fig. 21 : 7) 9. Examination of the buccal cavity is important when ulcerative dermatoses are present ',lo.Both dermatological lesions and an ulcerative stomatitis may be seen in some illnesses (e.g. FIV and FeLV infections) and dermatoses (e.g. bullous pemphigoid, pemphigus vulgaris and systemic mycoses) lo.Idiopathic ulcerative dermatosis of the interscapular region, also called granulomatous panniculitis, is another disease of unknown origin (behavioural? post-injection sensory neuropathy?) (Fig. 21 : 8) ". An erosive, ulcerative lesion localised to one digit might suggest trauma, a tumour or poxvims infection (during its incubation phase) Involvement of the footpads would mainly suggest a contact dermatitis, an auto-immune dermatitis, plasma cell pododematitis, a primary or secondary tumour (e.g. cutaneous metastasis of a bronchial adenocarcinoma) or calcification associated with renal disease 'L.'2,'3. If only the upper lip was involved, an indolent ulcer would be suspected but cryptococcosis, pyoderma or squamous cell carcinoma would also have to be considered 14.
~.
Given the kquency of ectoparasitic infestations anddermatophytosisin the cat, skin scrap'igs, tape sbip examinations and mycological tests are the diagnostic tests to consider initially '".
Skin scrapings should be carried out at the periphery of eroded lesions to demonstrate adult and immature mites: Cheyletiella blakei, Otodectes cynotis, Notoedres cati, Demodex cati and Demodex gatoi; and Trombicula autumnalis larvae. The tape strip examination (scotch test) can reveal mites living on the skin surface. Cheyletiella blakei adults and, in particular, eggs bound to the hair shaft may be found. Testing for dermatophytosis should be routine in any cat with an erosive or ulcerative dermatosis. Wood's lamp examination, carried out carefully, is the first step. However, it is not very sensitive as 50% of Microsporum canis isolates fail to fluoresce. Furthermore, erosive and ulcerative lesions often give a false fluorescence. Direct microscopy of hair and scale reveals the type of hair invasion by dermatophyte hyphae and spores. Fungal culture is needed to identify the genus and species of the dermatophyte involved. Allergy testing (intradermal and serological tests) is universally unreliable and hard to interpret in the cat. When allergic dermatitis is suspected, the diagnosis should be based mainly on response to avoidance measures (e.g. flea control and elimination diet). Smears of erosions and ulcers can often help orientate the clinician and may allow a diagnosis to be made. Impression smears can be carried out by gently applying a microscope slide on the lesion. With dry lesions, the surface of the ulcer can fust be freshened up with a scalpel blade. A careful search for the following should then be conducted: acantholytic keratinocytes, suggesting pemphigus; eosinophils suggesting a lesion of the feline eosinophilic granuloma complex; infectious agents (e.g. fungi, bacteria and mycobacteria), either free or phagocytosed by macrophages; plasma cells, found in stomatitis and plasma cell pododermatitis; and tumour cells. Cytology of eroded and ulcerated surfaces must, however, be interpreted with care. These lesions are exposed and therefore easily contaminated by bacteria from the environment or buccal cavity following licking. The presence of degenerate neutrophils, macrophages, and numerous bacteria, either extra- or intracellular does not necessarily indicate bacterial invasion and pyoderma. Skin biopsies are indicated for most erosive and ulcerative dennatoses and will often confirm a diagnosis. The sample should be taken from the margins of the ulcerated surface, and it is essential to include both lesional and healthy skin. It is actually the perilesional epidermis, site of the pathological process, which must be examined. An excisional biopsy is preferable to a punch biopsy for two reasons, firstly, it helps the histopathologist to orientate the sample when cutting it for inclusion in the paraffin block, and secondly, it inflicts less trauma on these fragile lesions. An exception to this rule is when tumours are suspected (e.g. squamous cell carcinoma), in which case biopsies should be taken from well within the ulcer. The histopathologist will look for epidermal or dermal anomalies to explain the ulceration: acantholytic keratinocytes for pemphigus, apoptosis or massive epidermal necrosis for cutaneous drug reaction, demo-epidermal clefting in some auto-immune dermatoses
,
www.vet4arab.co.cc 21 : Diagnostic approach to erosive and ulcerative dematoses
(bullous pemphigoid, epidmolysis bullosa....), vasculitis, etc ... In poxvirus infection, it is possible to see eosinophilic inclusion bodies in the cytoplasm. Observation of micro-organisms on histopathology will rarely produce an aetiological diagnosis. Bacterial or fungal culture is needed to determine precisely the causal organism. This can be conducted directly by taking a swab from the lesion or, ideally, by taking a skin biopsy under aseptic conditions and placing it in transport medium before sending it to the laboratory. The bacteria or fungi to be looked for, should always be specified on the laboratory submission form 12. Other diagnostic tests may be needed. For example, FIV serology and a search for FeLV antigens are necessary when oral ulceration, gingivitis or chronic ulcerative stomatitis are present. Fifty per cent of these cats are infected with one of these virusesi6. Virology testing is more difficult in the case of herpesvirus or calicivhs infection. Swabs from ulcers must be placed in special medium before being sent away. Serology is of little value for these viruses because antibody levels will be raised through vaccination 5. Amplification procedures (e.g. polymerase chain reaction) are only possible in specialist laboratories. An antinuclear antibody test must be carried out when systemic lupus erythematosus is suspectedI6.Haematology, biochemistry and endocrine profiles should be performed if Cushing's syndrome or other systemic diseases are suspected. Imaging techniques (e.g. radiography, ultrasonography and CT scanning).are indicated for ulcerative lesions associated with systemic disease (e.g. pancreatic tumour).
REFERENCES I. Scott, D. W. Miller Jr, W. H. &Griffin, C. E. Muller & Kirk's SmaN Animal Dermatology, 5th edition (Saunders,W.B., Philadelphia, 1995). 2. Walton Angarano, D. Vet.Clin. N. Amer. 25, 871-885 (1995). 3. Carlotti, D. N. & Bensignor, E. Prat. Mid. Chir Anim. Comp. 30,249-261 (1995). 4. Sousa, C. A. Vet. Clin.N.Amer 25, 813-828 (1995). 5. Merchant, S. R. & Taboada, J Vet. Clin N. Amei: 25,945-959 (1995). 6. Rojko, J. L. & Hardy, W D. in The Cat: Diseases and Clinical Management (ed Sherding, R.G.) 263-432 (Churchill-Livingstone, New-York, 1994). 7. Runge-Harms, U. and Ioblich Beardi, B. Proc. ESVD-ECVD, Maastricht 175 (1998). 8. Beale, K. M. Vet. Clin. N. Amer. 25,887-900 (1995). 9. Bond, R., Curtis, C. E, Ferguson, E. A. Mason, I. S., and others J VetDerm, 11.35-41 (2000). 10. Rosenkrantz, W. S, in Current Veterinary Dermatology (eds Griffin, C.E., Kwochka, K.W. & MacDonald, R.W.) 325 (Mosby Year Book, St Louis, 1993) 11. Scott, D. W. Felinepractice 18,s-11 (1990). 12. Guaguhre, E., Hubert, B. &Delabre, C. Vet. Dermatoi. 3, 1-12 (1992). 13. Jackson, H. A. &Barber, P J. J. smaNAnim. Pract. 39,495-497 (1998). 14. Power, H. T &Ihrke,P. I. Vet. Clin. N.Ame% 25,833-850 (1995). 15. Gross, T. L. Ihrke, P. J. & Walder, E. I. Veterinary Dermatopathology (Mosby Year Book, St-Louis, 1992). 16. Person, J. M.,Person, P & P e l l e ~I., L. Rec.Med. Vit. 149,1125-1130(1998).
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1 Diagnostic approach to otitis externa Otitis externa is an acute or chronic inflammation of the external auditory canal and tympanic membrane '". It is the reason for consultation in 25% of cats presented for a dermatological problem in first opinion practice and in 2% of cats referred to a dermatologist 16. Long thought of as a local phenomenon, otitis externa should he reclassified in a broader dermatological context, as it is usually just one local manifestation of an underlying dermatosis '. Its pathogenesis involves predisposing factors, primary factors, microbial amplifying factors, and aggravating factors which prevent healing (Table 22 : 1) '"."'. Table 22 : 1: Aetiology of otitis extema
I ---
--
Cunform~riond thc e s t'nv!ronmcnr hurn~dirvr Treatment or inappropriate cleaning
titopdra.;~reir O r o J ~ w ~)nur~r.DernoJt~ i run
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Auto-immune dermatoses Foreign bodies Tumours
. \
OTITIS EXTERNA
1 AMPLIFYING FACTORS
..
.
Lichenlfication Sebaceous hyperplasia
Malasseiia pachydermatis Staphylococcus spp., Pseudomonas spp., Prflteus spp.,...
Otitis media
[
~
~
When dealing with otitis externa in the cat, it is essential that all causes of inflammation of the external auditory canal are correctly identified and treated'. To achieve this, a thorough diagnostic approach is necessary, not forgetting however, the importance of parasites as a cause of feline otitis extema.
History The history directs the clinician towards certain differential diagnoses and is a mitical part of the diagnostic proces~~'~~". Important points to consider are :
Age of onset of clinical signs: otoacariasis, caused by Otodectes cynotis, is seen particularly in young cats aged less than a year (Fig. 22 : 1). On the other hand, an erythemato-ceruminous otitis externa in an adult cat is more suggestive of an allergic dermatitis (Fig. 22 : 2). A purulent otitis in an old cat strongly suggests an auto-immune dermatosis (Fig. 22 : 3) or a tumour of the external auditory canal (Fig. 22 : 4).
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Animal's way of life and environment: cats that live outdoors are more susceptible to Otodectes infestation or otitis extema caused by a foreign body. Excessive humidity can also lead to maceration in the ear. Transmission between cats and also between cats and dogs suggests Otodectes infestation. The presence of pruritic, papular or vesicular lesions on the owner's body and anns would also support this diagnosis". Presence of pruritusprior to lesions is suggestive of an allergic dermatitis or Otodectes infestation. Development of signs and seasonality: the sudden onset of an acute painful unilateral otitis suggests a foreign body. A history of successive or seasonal episodes points more towards an allergic dermatitis. Recent systemic illnesses should be noted. For example, herpesvirus infection may trigger generalised erythema multiforme, with frequent involvement of face and ears (Fig. 22 : 5). The efficacy of prior therapy should be evaluated along with the possibility that topical medications may be causing irritant or allergic reactions (Fig. 22 : 6). It is also important to find out how the owner is cleaning the ears and applying the topical medication, as repeated trauma is an aggravating factor.
Clinical examination Clinical signs of otitis extema are quite characteristic: face rubbing (caused by pruritus in the ear), scratching, head shaking or aggressive reactions, sharp pain and unpleasant smell I-'.
General clinical examination is concerned particularly with neurological consequences of otitis extema (e.g. vestibular or labyrinthine syndrome) (Fig. 22 : 7). In cases of chronic suppurative otitis, testing for retroviruses should be routine. Some systemic illnesses such as thymoma-associated paraneoplastic exfoliative dermatitis, may cause scaling on the pimae (Fig. 22 : 8). Erythematous, scaling lesions are not uncommonly seen on the ears of cats with epitheliotropic lymphoma (Fig. 22 : 9). Otitis extema may also be seen in feline pancreatic paraneoplastic alopecia (Fig. 22 : lo), or degenerative mucinous lymphocytic mural folliculitis. General dermatological examination is an essential step in the aetiological diagnosis of otitis extema. Listing the general dermatological lesions and noting their distribution will help to identify the underlying dermatosis. This can then he confnmed by appropriate diagnostic tests. Auricular examination involves the pinnae (medial and lateral surfaces), the area behind the ears (Fig. 22 : 11) where basic lesions (e.g. erythema, pustules, nodules, erosions, ulcers and crusts) can be identified, and the entrance to the ear canals. The healthier ear should be examined first, followed by the more painful ear. Sedation, or even a short-acting general anaesthetic, is sometimes necessary. The external auditory canals should be palpated carefully to appreciate the degree of pain, the severity of proliferative lesions (thickness, fnmness and flexibility) and the auriculo-pedal reflex "~"".The presence of abnormal quantities of secretion can be detected by close inspection. Auricular examination will allow an erythemato-ceruminous otitis (ECO) to be distinguished from a suppurative otitis (SO) I-'. ECO is much more common than SO in the cat '.
- Erythemato-ceruminous otitis: erythema is associated with excessive secretion of thick cerumen. The appearance of the secretion is variable. It can be brown, blackish and dry, or brown, light and thick (Figs 22 : 12-14), Pruritus is often marked. ECO is usually bilateral, Aetiologically, parasitic and non-parasitic causes of ECO should be distinguished.
-Suppurative otitis: this is rare in the cat. It is characterised by lots of pus, varying in colour and smell with the causal organism (Fig. 22 : 15). A squelching noise is often heard when the ear is palpated. Pnuitus and pain, in particular, can trigger scratching and abnormal head shaking, leading frequently to scaling and alopecic lesions on the pinnae, and sometimes an aural haematoma or pyotraumatic dermatosis (Fig. 22 : 16). The pinnae are often oedematous. SO is unilateral in 50% of cases '.
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Fignrd22 :1 :Pamsltlc erythemuM-cerminou oktls caused by Otodectes cynow note the d p , hown, blacktshc e m n
Figure22 :2 :Non-paras& qtfiemafo-cemminou otrbs in a Eufopem domesiic cat with afopic demmntrs. note the erythematous Md emsive l e s w y on themedial pinna
Figure22 :3 :Suppurmve otitis in a cat withpempbigiisfoliacer~s:note the severity of ulceralive crusting lesions (courtesy of DN.Carlotti)
pinna
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Figure22 :5 :Severe crusting on the medial pinna a n d a t t k ennance to the &r canal, in a cat suspected of having herpesvirus-associated
Egnrd22 :6 :Lichm$c~~tionofthe ear c m l i n c cat with allergic otitis (conhretaiiergy to neowycin)
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F i p n 22 :7 :Anisocoria in a Persian cat with suppurative otitis and a perforated tympanic membrane
ding and crusting on the medial pinna of a cat with paraneoplastic e$oliative dermatitis (courresy of T Oliviy)
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Diagnostic tests Once a diagnosis of ECO or SO has been made, it is essential to look for predisposing, primaty, amplifying and /or aggravating factors, involved in the development of cliical signs (Table 22 : 1) 1-8,". A diagnosis limited to "otitis"mere1~describes inflammation of the ear and does not &e any indication of prognosis, treatment or likely recurrence. Carrying out appropriate diagnostic tests will iptimise the chances o f m&ing an aetiological diagnosis ' (Table 22 : 2). Table 22 :2 : Diagnostic approach to otitis externa
An initial auroscopic examination should be routine in both ears. Small attachments, suited to the narrowness of the extemal ear canal, should be used. Sedation is sometunes necessary to examine the ear canals under optimal conditions. Auroscopic examination can reveal possible foreign bodies such as grass seeds (Hordeum spp., Avena spp.) '-'.'.".Inflammatoq changes and self-inflicted trauma should also be noted because they can alter the conformation of the ear and the cutaneous lining, making treatment difficult and perpetuating the otitis lo.Lichenification (Fig. 22 : 14), ulceration, oedema, dermal calcification, and sebaceous and ceruminous hyperplasia resulting from chronic inflammation must be identified. Turnours can be seen at this stage of the examination '*. Tumours of the extemal ear canal are uncommon in the cat 4 Benign (e.g. papilloma, sebaceous adenoma, ceruminous gland adenoma and fibroma) and malignant tumours (e.g. squamous cell carcinoma, sebaceous carcinoma, ceruminous gland carcinoma, fibrosarcoma and mast cell tumour) can be seen (Fig. 22 : 17). Ceruminous gland tumours are the most common tumours and can completely obstruct the extemal ear canal, provoking a suppurative otitis. This is paaicularly common in older cats '*(Fig. 22 : 18).
www.vet4arab.co.cc 22 : Diamotic annrnach to otitis externa
.
Figure22 : 9 :Erythematous, scaling lesions on the medialpinno, and at the entrance to the ear canal, in a cat with epitheliotropic T ceii lymphoma
Figure 22 :10 :Shiny, erosive and erythematous lesions on the face and ear of a cat wlth degenerative mucinous lymphocync mural foNiculitis
Figure 22 :I1 :Crusting lesions (self-inflicted)in the area behind the ears of a cat with Otodectes cynotis infestation
Figure22 :12 :Parasitic erythemnto-ceruminousotitis caused by Demcdex cati: note the greasy, brown, blackish cerumen
Figure 22 :13 :Non-parasitic erythemato-ceruminous otitis caused by Malassezia pachydermatis
Figure22 :I4:Non-parasitic erythemato-ceruminous otitis in a cat with atopic dermatitis: note lichenification of the ear canal
L
Figure 22 :I 6 :Suppurative otitis and aural haemtoma
Figure 22 :I 5 :Suppurative otitis
Y
/A Racdcal Guide to Feline Dermatology
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Microscopic examination of cerumen, collected with a curette or swab, can be used to look for ectoparasites such as Otodectes cynotis (Fig. 22 : 19), Demodex cati (Fig. 22 : 20), Demodex gatoi, Notoedres cati, Trombicula autumnalis larvae, and larvae of the tick Otobius megnini '~3~7,8~'*~18. It must be carried out very carefully, even if there is little cerumen present, because most cases of otitis externa in the cat are caused by parasites Microscopic examination in chloral lactophenol or liquid paraffin will usually reveal the mite, Otodectes cynotis, in various stages of its life cycle (adult, nymph, lama, egg). In some cases in which a hypersensitivity reaction is probably involved, demonstrating mites is not easy as it may only take a few parasites to initiate clinical signs '6,". It is also possible that when inflammation becomes too severe, the parasites leave the ear canal or get destroyed '. Cytological examination of cerumen is the next step 1 5 ~ 5 ~ ' ~ 8 ~ ." ~Cernmen '9 should be collected on a swab and placed carefully on a microscope slide. The slide is dried and stained with a rapid stain, ready for examination at a magnification of between 400 and 1000. Non-parasitic, erythemato-ceruminous otitis: cytology reveals an abnormally elevated number of yeasts of the genus Malassezia, and bacteria. Malassezia is a yeast found in small numbers in the ear canal of normal cats, especially in the presence of cerumenzo.When present in large numbers, it is pathological. Malassezia pachydermatis is easily recognised by its characteristic peanut shape (Fig. 22 : 21). Bacteria seen are usually cocci. Suppurative otitis: cytological examination of pus reveals round cocci of variable size and appearance, and 1 or elongated rods. These indicate bacterial colonisation, a common finding in the ear canal 19. On the other hand, the presence of degenerating neutrophils, with phagocytosis of bacteria, indicates that the body is respondmg to infection l9 (Fig. 22 : 22). More rarely, Candida albicans may also be isolated from the ear canal of a cat. Its presence there is always pathogenic. If atypical yeasts are seen on cytology, fungal culture should be performed to identify the organism 19. Bacteriology of exudate should be performed in all cases of chronic or recurrent suppurative otitis and in cases where cytology reveals the presence of rods. A sterile swab must be delicately inserted down to the horizontal ear canal. To avoid contamination, the swab should be inserted through the sterile cone of an auroscope attachment '. Bacteria most frequently isolated in feline otitis externa are Staphylococcus intermedius and Streptococcus spp. (gram + cocci) with Pseudomonas spp. and Proteus spp. (gram - rods) being found less commonly '.
A secondauroscopic examination should be camed out at this stage of the diagnostic process. If the ear canal is cluttered with inflammatory debris, cerumen and 1 or pus, it should be cleaned out, at the surgery, to allow further auroscopic examination I. Cleaning should involve cleansing, non-irritant substances, the selection of which depends on the type of secretion and lesions present. The ingredients should be diluted in tepid water and flushed into the ear canal, using an adapted enema bag. Synhges attached to flushing and suction devices can also be used ". Cleaning should be continued until the ear canal is relatively clear and free of debris. Once the ear canal has been dried (e.g. with absorbent paper), the second auroscopic examination can be carried out. This allows evaluation of the ear canal wall, further inspection for foreign bodies or tumours, and assessment of the patency and transparency of the tympanic membrane. A normal tympanic membrane is made up of two parts ": the parsflacida is dorsal, white, quite thick, and well-vascularised; the pars tensa is ventral, bigger, semi-transparent and shiny ' .
Radiography and CT scanning of the tympanic bullae are useful in chronic otitis extema and for invasive tumours of the ear canal (Figs 22 : 23,24). Recent studies in the dog suggest that otitis media should be looked for routinely in cases of chronic otitis, even if no rupture of the tympanic membrane can be seen ". The presence of pus in the tympanic bulla can be the source of chronic infections because topical antibiotics do not penetrate deeply enough into the ear canal ',2,2'. The tympanic membrane could heal rapidly and mask the development of this deep infection ". Radiography can also be performed after injection of radio-opaque, liquid contrast media into the ear canal 22. Paracentesb followed by cytology and bacteriology will probably be a diagnostic test of the future2'. Biopsies of nodules and ulcers may be necessag. Nodules may indicate tumours (e.g. squamous cell carcinoma, ceruminous gland tumour, mast cell tumour) or opportunistic infections (e.g. mycobacterial infections, cryptococcosis) in immunodeficient cats. Ulcerated lesions may be the lirst signs of an auto-immune dermatosis (e.g. pemphigus foliaceus) '".'.
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Figure 22 :17 :Invasive mast cell tumour in the ear canal
Figure 22 :18 :Ceruminous gland carcinoma in a catpresenting with chronic suppurative ofitis
Figure 22 :19 :Otodectes cynotis (microscopy of sampleprepared in chloral lactophenol, X 100)
Figure22 :21 :Malassezia pachydematis (microscopyofcerumen, stained with Diff-Quik, X 1000)
Figure 22 :22 :Cocci and neutrophils with many examples ofphagocytosis (microscopyofpus, smined with Dif-Quik, X 10WJ(counesy ofD. Pin)
.,-.- -. ... ,. .can
ofa cat with an invasive auricular tumour: note invasion of the brain by the rumour (courtesy o f F Delisle)
A Prsctieal Guide mFeline Dumato101
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REFERENCES 1. Scott, D. W. Miller 11, W H. & Griffin, C. E. Muller & Kirk's SmaNAnimal Dermatology,5th edition (Saunders, W.B., Philadelphia, 1995). 2. Gnffn, C. E, in Current Veterinary Dermatology, (eds Griftin, C.E., Kwochka, K.W. & MacDonald, R.W.) 245-264 (MosbyYear Book, Saint Louis 3. Carlotti, D. N. in Encyclopidie Vitirinaire 3300 (Elsevier, Paris, 1994). 4. Bourdeau, P. Rec. Med. Vit. 166,665-697 (1990). 5, GrEn, C. E. Comp. Cont.Educ, Pract. Vet. 3,741-750 (1981), 6. Scott, D. W. J. Amei: Anim. Hosp. Assn. 16,426-433 (1980). 7. Guagnkre, E. Proc. CNVSPA Sud-Ouest, La Mongie (1991). 8. August, J. R. Vet. Clin. N. Amer. 18,731-742 (1988). 9. Bradley, R. L. Vet. Clin. N.Amer 18,813-819 (1988). 10. Roth, L. Vet. Clin.N.Amer. 18,755-764(1988). 11. Rosser, E. I. Vet, Clin. N.Amer. 18,765-772 (1988). 12. Herwick, R. P. Arch. Dermatol. 114, 130 (1978). 13. Mansfield, P D. Vet. Clin. N. Arne,: 18, 845-858 (1988). 14. Rogers, K. S. Vet. Clin.N.Amer 18, 859-868 (1988). 15. Guaguh, E. Prat. Mid. Chir Anim. Comp. 28,211-223 (1993). 16. Powell, M. B., Weisbroth, S. H., Roth, L. & Wilhelmsen, C. Am, J Vet. Res. 41, 877-882 (1980). 17. Weisbroth, S. H., Powell, B.,Roth,L. &Sher, S. J.Amer Vet.Med.Assn. 165, 1088-1093 (1974). 18. Desch, C. E. & Stewart,T B. J.Med. Entomoi. 36,167-170 (1999). 19. Chickekg, W. R. Vet. Clin.N,Amer. 18,773-782 (1988). 20. Guillot, I., Gu&ho,E.,Mialot,M. & Chennette,R. PointVit. 29,691-701 (1998). 21. Bond, R.,Anthony, R. M., Dodd, M. &Lloyd, D. H. J.Med. Vet. Mycol. 34,145-147 (1996). 22. Bond, R., Howell, S.A., Haywwod, P. 1.&Lloyd, D. H. Vet.Rec. 141,2W-201 (1997). 23. Cole, L. K., Kwochka, K. W , Kpwalski, 1.1. &Hillier, A. J, Amer. Anim. Hosp. Assn. 212,534-538 (1998).
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1 Diagnostic approach to facial dermatoses Facial dermatoses are a very important and diverse group of diseases. In some cases, the face is affected directly whereas in others, facial involvement is a consequence of systemic disease. One reason why the face is frequently involved is that it is a very exposed part of the body, not easy to groom, and with sparse hair covering offering scant protection. Mucocutaneous junctions (e.g. lips, nose and eyelids) are predisposed to infectious, parasitic and immune-mediated dermatoses. There is such a plethora of potential causes of facial dermatoses (Table 23 : 1) that a very rigorous and methodical diagnostic approach is essential. The history and clinical examination (general and dermatological) are used to formulate a differential diagnosis, which can be narrowed down by performing well-chosen diagnostic tests. That said, the main facial dermatoses (excluding those of the external ear) are dermatophytosis. allergic dermatoses, superficial pemphigus conditions and squamous cell carcinoma.
History The history helps to steer the climclan towards particular differentials. It is a vital step in the diagnostic process. Important points to consider are :
Breed: Persians are predisposed to dermatophytosis and also, because of their nose and lacrimal duct conformation, to superficial bacterial (e.g. Staphylococcus spp.) and fungal (e.g. Malassezia spp.) skin infections IZ. A cond~tioncalled idiopathic facial dermatitis has also recently been described in this breed '. The Slamese is predisposed to vitiligo4(Fig. 23 : 1) and to "histiocytic" mast cell tumour '. Urticaria pigmentosa has, to date, only been observed in Sphinx and Devon Rex cats6. Age of onset: development of a facial dermatosis in a cat under 6 months would suggest congenital hypotrichosis, dermatophytosis @g. 23 : 2), a parasitic dermatosis ' (e.g. notoedric mange and demodicosis (Fig. 23 : 3)) or an allergic dermatitis (e.g. atopic dermatitis (Fig. 23 : 4) and food intolerance (Fig, 23 : 5)). On the other hand, facial lesions (especially when pruritic) in a young adult would inihaJly suggest an allergic dermatitis 83 or a viral or post-viral condition (e.g, poxvirus '@(Fig.23 :6),herpesvirus (Fig. 23 : 7) or herpesvirus-associatederythemamultiforme (Fig. 23 :8)). In an older, adult animal, auto-immune dermatoses " (e.g. superficial pemphigus figs 23 : 9,10)), dmatoses associated with systemic disease l2 (Figs 23 : 11,12) or skin tumours '' (e.g, squamous cell carcinoma, mast cell tumour and cutaneous epitheliotropicT cell lymphoma) (Fig. 23 : 13) would be more likely. Sex: entire male cats, being more aggressive and likely to come into dm1contact with lots of other cats, are more prone to dermatophytosis, abscesses and "opportunistic" skin infections associated with retrovirus infection. Life stystyle and environment: feral cats are more prone to dematophytosis l , parasitic dermatoses ' (e.g. notoedric mange, otodectic mange (Fig. 23 : 14) and trombiculiasis), and lesions associatedwith tick and mosquito bites ' (Figs 23 : 15,16). Contact with wild rodents predisposes hunting cats to poxvirus infection 'O. As for show cats, they are more prone to dermatophytosis 14. In very sunny regions, solardermatoses(e.g. actinic keratoses and squamous cell carcinoma) are especially common in white cats 4. Visits to certain countries: a hlstory of foreign travel might suggest notoedric mange or deep mycoses ". Diat: knowing the cat's diet will allow construction of a suitable elimination diet, where appropnate 9.
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A Practical Guide to Febc Dematology
Table 23 : 1 : Aetiology of facial detmatoses INFECTIOUS DERMATOSES Poxvhs infection Herpesvirus infection Herpesvirus-associated erythema multiforme Pap~llomavirusinfection Bacterial folliculitis Bite abscess Acne Leprosy Atypical mycobacterial infection Nocardiosis Actinomycosis Bohyomycosis
FUNGAL DERMATOSES Dermatophytosis Malassezia dermatitis Candidiasis Subcutaneous mycoses
~trichosis ~ptoCoCCoSIS
fistoplasmosis Blastomycosis
Pemphigus vulgaris Bullous pemphiioid Discoid lupus erythematosus, Systemic lupus erythematosus
OTHER IMMUNE MEDIATED DERMATOSES Cutaneous drug reactions Auricular polychondritis Pseudopelade HEREDITARY DERMATOSES Hereditary epidermolysis bullosa Vitiligo TRAUMATIC DERMATOSES Bums Frostbite Actinic keratoses Initant contact dermatitis
Coccidioidomycosis TUMOURS
PARASITIC DERMATOSES Notoedric mange Otodectic mange Demodicosis Trombiculiasis Cheyletiellosis Leishmaniasis
Squamous cell carcinoma Multicentric squamous cell carcinoma in sifu (Bowen's disease) Basal cell tumour Fibrosarcoma complex Cutaneous epitheliotropicT cell lymphoma "Mastocytic" mast cell tumour "Histiocytic" ma$ cell tumour
ALLERGIC DERMATOSES Atopic dermatitis Food intolerance Mosquito bite hypersensitivity Allergic contact dermatitis
DERMATOSES ASSOCIATED WITH A SYSTEMIC ILLNESS Pancreatic paraneoplastic alopecia Paraneoplastic exfoliative dermat~ns Degenerative mucinous lymphocytic mural folliculitis
EOSINOPHILIC GRANULOMA COMPLEX Indolent ulcer Eosinophilic granuloma
SKIN CONDITIONS ASSOCIATED WITH BEHAVIOURAL DISORDERS
AUTO-IMMUNE DERMATOSES Pemphigus foliaceus Pemphigus erythematosus
Previous illness: an association between gastrointestinal problems and facial pmritus strongly suggests a food intolerance If the cat has gastrointestinal problems and is in poor general health (e.g. with weight loss and dehydration), pancreatic paraneoplastic alopecia should be suspected ' I . If there is a history of respiratory infection prior to ulcerative facial lesions, consider a viral dermatosis (e.g. herpesvirus infection) or herpesvirus-associated erythema multiforme. Onset of clinical signs: the appearance of lesions some days after a change of environment (e.g. arrival of a new animal or change in living quarters) suggests a contagious condition such as a fungal infection (e.g. dermatophytosis), parasitic infestation or viral infection (e.g. poxvirus), or an allergic dermatitis (e.g. atopic dermatitis or food intolerance). If facial or generalised pruritus precedes the lesions, an allergic dermatitis, ectoparasitic infestation (e.g. trombiculiasis) or even a skin condition associated with a behavioural disorder (e.g. anxiety following a change in environment) should be suspected. Progression of signs and seasonality: if signs worsen when the cat is in particular locations, atopic dermatitis should be suspected. Pruritic facial dermatoses that are more prevalent in summer and
www.vet4arab.co.cc 23 : Diagnostic approach to facial dermatoses
Figure 23 :1 :Deprgmentatlon of the nasal planum andperrocular leucotr~chlain a S~amesecar wrrh vltrllgo
F i g m 23 :2 :Circular patches of hair loss on the face of a cat with dermatophytosis caused by Microspomm canis
Figure 23 :3 : Crusting and erosions on the face of a cat with demodicosis (courtesy of J . Poirson)
Figure 23 :4 :Erythema, erosions and crusts on the face of a cat with atopic dermatitis
Ficure 23 : 6 :Eiytiieniatoi~s,emsire ierioiis on thc nose and lips of a cot with poivirus infection
Fignre 23 : 7 :Erosive, crusting lesions on'fhe face of a car with herpesvirus infection (courtesy of D.W. Scott)
_urn23 : 8 : Scaling and crusting on the face of a cat with herpesvirusassociated erythema multiforme
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autumn, point towards parasitic dermatoses ' such as trombiculiasis, or allergic dermatoses such as mosquito bite hypersensitivity or pollen allergy.
bitial type and distribution of lesion: many dermatoses have particular distribution patterns. Response to prior therapy: this will allow the effect of particular treatments to he appreciated. Dosage and duration of treatment should he established. Response to corticosteroids is normally good in atopic dermatitis or early food intolerance and poor in dermatophytosis and ectoparasitic infestation such as demodicosis. Frequent application of topical ear and eye medications may promote a contact dermatitis l5. If signs are suggestive of a cutaneous drug reaction, a comprehensive list of all recent medications should he constructed with a view to identifying the drug responsible. Transmissionto other animals and people: this would indicate the need to test for dermatophytosis Id or more rarely, otodectic or notoedric mange '.
Clinical examination The clinical examination is the central part of tbe diagnostic approach to facial dermatoses
The general clinical examination is concerned, for example, with signs associated with atopy (e.g. conjunctivitis, rhinitis and asthmatic bronchitis), and physical signs of a behavioural disorder (e.g. tachycardia, polyphagia, obesity, excess salivation, diarrhoea and poor grooming). If the cat is in poor general health and also has a high temperature, the following conditions should be suspected: a viral or post-viral dermatosis (e.g. h&pesvi&s, poxvirus or herpesvirus-associated erythema multiforme); a systemic auto-immune disease (e.g. systemic lupus erythematosus); an oppomistic infection associated with retroviral infections; pancreatic paraneoplastic alopecia; or degenerative mucinous lymphocytic mural folliculitis. Cats with long-standmg facial pruritus are often off colour and this is of no diagnostic significance unless the temperature is raised. The dermatological examination is concerned with the presence of pruritus, identification of cutaneous, mucocutaneous and mucous lesions and the distribution of other non-facial lesions. Pruritic facial dermatoses are initially suggestive of an allergic dermatitis (e.g. atopic dermatitis, food intolerance or mosquito bite hypersensitivity), a parasitic dermatosis (e.g. notoedric mange, trombiculiasis or pediculosis), a viral or post-viral dermatosis (e.g. herpesvirus, poxvhs or herpesvirus-associated erythema multiforme), a deep bacterial or fungal infection (e.g. cryptococcosis or sporotrichosis) or a skin condition associated with a behavioural disorder. Non-pruritic facial dermatoses would initially suggest dermatophytosis, demodicosis, or, depending on location ( e . ~ears . and nose) an actinic keratosis or certain tumours (e.g. cutaneous epitheliotropic lymphoma).'~~te that this distinction between pruritic and non-pruritic isquite arbitrary and that condition that is initially non-pnuitic can become pruritic. Erythema and scaling, without pruritus, would initially suggest dermatophytosis, demodicosis, more rarely paraneoplastic exfoliative dermatitis, degenerative, mucinous, lymphocytic, mural folliculitis, or, depending on the distribution, actinic keratosis (m white cats). When pruritus is present, erythema and scaling can rapidly develop into erosive and ulcerative lesions. Erosive and ulcerative lesions suggest, when pruritus is severe, an allergic dermatitis or sometimes a behavioural disorder (especially when lesions are unilateral) or parasitic dermatosis (e.g, otodectic mange, notoedric mange or trombiculiasis). When pruritus is less severe or absent, dermatophytosis, a deep bacterial or fungal infection or an auto-immune dermatosis should he suspected. When skin and mucocutaneousjunctions are affected, the possibility of an auto-immune dermatitis, drug reaction or viral or post-viral dermatosis (e.g. herpesvirus, poxvirus or herpesvirus-associated erythema multiforme) should be investigated. Involvement of the lips suggests an indolent ulcer, squamous cell carcinoma or cryptococcosis. Crusting is common and usually characterised by spontaneously appearing, thick, coalescing crusts. When nose and ears are affected, it suggests dermatophytosis, an auto-immune dermatitis, mosquito bite hypersensitivity or notoedric mange; with generalised facial involvement, the differential diagnosis should include paraneoplastic exfoliative dermatosis, degenerative mucinous lymphocytic mural folliculitis and cutaneous epitheliotropic T cell lymphoma, especially if similar lesions are
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23 D~agnostlcapproach to fac~aldermatoses
Figure23 :9 :Erythema, erosions and crusi the face of a Siamese cat with pemphigus foliaceus (courtesy 0 f 6 a nrreej
Figure 23 :I 0 :Erosions and crusts on the face of a Siamese cat with pemphigus erythematosus (courtesy of T Olivry)
F@23 :11 :Aiopeciaandscalingon theface ofa cat with degenerative, mudnous, lymphocyfic,muralfolliculitis (courtesy of D. Hiripretj
F i g m 2 3 :12 :Erythematous, erosive, shiny lesions on the face of a cat withpancreaticparaneoplasric alopecia (courtesy of E. Bensignorj
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if'
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Figure 23 :13 :Exfoiiative erythroderma in a cat with cutaneous epitheliotropic T cell lymphoma (courtesy of E. Bensignorj
Figure23 : I 4 :Erosions and crusts in a Siamese cat with otodectic body mange and concomitant FeLV infection
Figure23 :15 :Erosions and crusts on the nose andeyelids of a cat with mosquito bite hypersensitivity
F i g m 23 :16 :Ulcers and crusting on the face of a cat with mosquito bite hypersensitivity. Squamous cell carcinoma would be a differential here (courtesy of E. Bensignorj
A Practical Guide to Feline Dermatology
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observed on the whole body.
Nodular lesions primarily suggest a specific deep bacterial infection (e.g. mycobacterial infection, nocardiosis, actinomycosis or botryomycosis), a deep fungal infection (e.g. cryptococcosis, sporotrichosis or histoplasmosis) or tumour (e.g. mast cell tumour or squamous cell carcinoma). Lesion identification in other parts of the body will help the clinician to strengthen hisiher clinical suspicions.
Given the incidence of dermatophytosis and ectoparasitic infestations in the cat, skin scrapings, tape strips and mycological procedures should be conducted routinely.
Skin scrapings demonstrate adult and immature mites (eggs, larvae and nymphs). Cheyletiella blakei, Otodectes cynotis, Notoedres cati, Demodex cati and Demodex gatoi, Trombicula autumnalis larvae and the louse Felicola subrostratus may be seen. The tape strip examination (scotch test) can reveal mites living on the surface of the skin. Cheyletiella blakei adults and, in particular, eggs stuck to the hair shaft may be found. The sensitivity of this test is quite poor but greater success may be achieved when combined with coat brushings. Coat brushings, well performed, can be used to collect scale, eggs, parasite faeces and even adult parasites from the skin surface. They are useful in diagnosing cheyletiellosis or pediculosis. Testing for dermatophytosis should be routine in any cat with a facial dermatosis. Wood's lamp examination, carried out carefully, is the fust step. However, it is not very sensitive as 50% of Microsporum canis isolates fail to fluoresce. Direct microscopy of hair and scale reveals the type of hair invasion by dermatophyte hyphae and spores. Fungal culture is needed to identify the genus and species of the dermatophyte involved. Cytology is a simple routine examination. It can be used in the diagnosis of facial dermatoses to demonstrate bacteria, yeasts of the genus Malassezia, and eosinophils (e.g. in eosinophilic plaques, allergic dermatoses and mosquito bite hypersensitivity). In pemphigus foliaceus, a smear, performed by pressing a microscope slide onto a crust or ulcer, will reveal acantholytic keratinocytes, noudegenerate neutrophils and sometimes eosinophils. Allergy testing (intradermal and serological testing) is universally unreliable and bard to interpret in the cat. When allergic dermatitis is suspected, the diagnosis should be based principally on response to avoidance measures (e.g. flea control and elimination diet). Skin biopsies are necessary for nodular, scaling (exfoliative), crusting and ulcerative, or alopecic lesions. Biopsies do not always produce a diagnosis, hut they can point the clinician in the right direction and allow certain differentials to be eliminated. Histopathology of biopsies may reveal diagnostic pathology or changes that are consistent with, for example, a specific deep bacterial infection (e.g. mycohacterial infection or nocardiosis), a subcutaneous mycosis, a systemic mycosis (e.g. cryptococcosis), pancreatic paraneoplastic alopecia, or degenerative, rnucinous, lymphocytic, mural folliculitis. Specijie bacterial and fungal culture should be performed in certain cases from biopsies taken aseptically. Biopsy samples should be placed in isotonic sodium chloride solution prior to inoculation onto specific media. Other diagnostic tests must be performed in line with the differential diagnosis: testing for FeLV and FIV infections, determination of the antinuclear antibody titre for systemic lupus erythematosus, abdominal ultrasonography for pancreatic paraneoplastic alopecia, and thoracic radiography for paraneoplastic exfoliative dermatitis.
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I. Guillot, J., Gukho, E., Mialot, M. & Chermette, R. Point Vit. 29,691-701 (1998). 2. Foil, C., S. Vet. Clin. N. Amer: 25,923-944 (1995). 3. Bond, R., Curtis, C. F,, Ferguson, E. A,, Mason, I. S., and Rest, J. VeiDerm., 11,3541 (2000). 4. Scott, D. W., Miller, Jr, W H. & Grifh C. E. Muller & Kirk's Small AnimalDermatology. 5th edilion (Saunders, WB., Philadelphia, 1995). 5. Vitale, C. B., Ihrke, J., Olivry, T & Stannard,A. A. Vet. Dermatol. 7,227-233 (1996). 6. Noli, C. & Scarampella, E Proc. AND-ACVD, Maui 65 (1999). 7. Guagubre, E. Prat M M Chir Anim. Comp. 28, 211-223 (1993). 8. Gilbert, S., Pdlaud, P. & Guaguhre, E. Pmt. Mid. Chir Anim. Comp. 34, 15-31 (1999). 9. Guagubre, E. & Prklaud, P. Praf. Mdd. Chir Anim. Comp. 33, 389-407 (1998). 10. Thomsett, L. R. J . small Animal Pracl. 30,236-241 (1989). 11. Olivry, Alhaidari, Z. & Hubert, B. in Encyclopidie Vdtdrinaire 1600 (Elsevier, Paris, 1992). 12. Merchant, S. R. &Taboada, J . Ver. Clin. N.Amer 25,945-959 (1995). 13. Magnol, I. P, Rec. Med. Vdt. 166, 1061-1074(1990). 14. Foil, C. S, in Current Veterinary Therapy (eds Griffin, C. E., Kwochka, K. W. & MacDonald, R. W.) 22-23 (Mosby,YearBook, St-Louis, 1993). 15. Gaafar, S. M. &Krawiec, D. R. J.Amer~Anim.Hosp.hsn. 10, 133-138 (1974). 2. Foil, C., S. Vet. Clin. N.Amer. 25,923-944 (1995).
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EpmcticalGuide to Feline IhnatoIogy
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to feline pododermatoses Pododermatoses are a very important and diverse group of diseases. In some cases, feet are affected directly whereas in others, pedal involvement is a consequence of systemic disease. Although pododermatoses are a less frequent reason for consultation than in the dog, the foot can be targeted directly in various specific conditions: bacterial paronychia, plasma cell pododermatitis and cutaneous metastasis of a pulmonary adenocarcinoma. Pedal involvement may also be part of a more generalised dermatological condition ". Periungual diseases are common, especially relating to a well-developed structure of mesodermal origin called the fibro-myxoid tissue. located between the nail and the third phalanx (Fig. 24 : 1).
Figure 24 : 1 : Topographical anatomy of the feline digit (longitudinal section, Goldner stain, x6) (courtesy of C. Delabre)
8 -Flexor tendon 15 - Sole of the claw
16 -Deep, non-kerathised epidermis
There is such a plethora of potential causes of pododermatoses (Table 24 : 'i')that a very rigorous and methodical diagnostic approach is essential. The history and clinical examination (general and dermatological) are used to formulate a differential diagnosis, which can be narrowed down by performing well-chosen diagnostic tests. Used alongside routine diagnostic tests (e.g. Wood's lamp examination, direct examination of hairs and scale, skin scrapings, fungal culture and cytology), the skin biopsy is often the key to diagnosis '.
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Table 24 :1 : Aetiology of pododermatoses INFECTIOUS DERMATOSES Poxvirus infection Herpesvirus infection Herpesvirus-associated erythema multiforme Calicivims infection Bite abscess Bacterial paronychia Leprosy Atypical mycobacterial infection Nocardiosis Actinomycosis Botryomycosis
OTHER IMMUNE MEDIATED DERMATOSES Cutaneous dmg reactions Plasma cell pododermatitis
HEREDITARY DERMATOSES Congenital hypotrichosis Pili forfi Hereditary epidennolysis bullosa Vltiligo
FUNGAL DERMATOSES
ENVIRONMENTAL DERMATOSES
Dermatophytosis Malasseiia dermatitis Candidiasis Subcutaneous mycoses Sporouichosis Cryptococcosis Histoplasmosis Blastomycosis Coccidioidomycosis
Bums Frostbite Irritant contact dermatitis
PARASITIC DERMATOSES Trombiculiasis Demodicosis Notoedric mange Anavichosomiasis Leishmaniasis
ALLERGIC DERMATOSES Atopic dermatitis Food intolerance Mosquito bite hypersensitivity Allergic contact dermatitis
EOSINOPHILIC GRANULOMA COMPLEX Eosinophilic plaques Eosinophilic granuloma
TUMOURS Squamous cell carcinoma Trichofolliculoma Fibrosarcoma complex Cutaneous epitheliotropicT cell lymphoma Digital metastasis of a pulmonary adenocarcinoma
DERMATOSES ASSOCIATED WITH A SYSTEMIC ILLNESS Pancreatic paraneoplastic alopecia, Paraneoplastic exfoliative dermautis Supelficial necmlytic dermatitis Vasculitis Degenerative, mucinous lymphocytic mural folliculitis Xanthomatosis
SKIN CONDITIONS ASSOCIATED WITH BEHAVIOURAL DISORDERS Nail chewing
AUTO-IMMUNE DERMATOSES Pemphigus foliaceus Discoid lupus erythematosus Systemic lupus erythematosus
History The history helps to steer the clinician towards particular differentials. It is a vital step in the diagnostic process. Important points to consider are :
Breed: Persians are predisposed to dermatophytosis. In the Birman, claws are absent or rudimentary in congenital hypotrichosis (Fig. 24 : 2). The Siamese breed is predisposed to vitiligo which will often affect the feet (depigmentation of the footpads (Fig. 24 : 3)), and more rarely junctional epidermolysis bullosa '. Age of onset: development of pedal lesions in a cat under 6 months would suggest dermatophytosis, a parasitic dermatosis (e.g. notoedric mange and demodicosis), a viral dermatosis (e.g. herpesvirus or calicivirus), or a genodermatosis (e.g. junctional7 and dystrophic epidermolysis bullosa 8", congenital hypotrichosis and pili torti). Pedal lesions in a young adult would initially suggest dermatophytosis or an allergic dermatitis (e.g. atopic dermatitis or food intolerance) (Figs 24 : 4-7). In an older, adult animal, auto-immune dermatoses Id (e.g. pemphigus foliaceus (Figs 24 : 8,9) or systemic lupus erythematosus (Fig. 24 : lo)), dermatoses associated with systemic disease'.' (e.g. superficial
www.vet4arab.co.cc 24 : Diagnostic approach to feline pododennatoses
Figure 24 :2 :Alopecia and rudimentary claws in a Bir-man cat with hereditary hypotrichosis (courtesy of P. BourdeauJ*
Figure 24 :3 :Depigmentation of the footpads in a Siamese cat with vitiligo
Figure 24 :4 :Venhnlpedal erythema in a cat with food intolera
FIgwe24: 5 :E~themtousparonychiawith scaling in a cat with atopic dermatitis
F i p 24 :6 :Erosivepododermatitis in a car with atopic dermritis
Figure 24 : 7 :Eosinophilicplaque on the ventral surface of the foot of a cat with food intolerance
....... ....... Figure24: 8 :Paron; foliaceus (courtesy of DN. CarlottiJ
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.:n a cat withpen,
Figure24: 9 :Scaling on thefootpads in a cat withpemphigusfoliaceus (courtesy of T. OlivryJ
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necrolytic dermatitis (Figs 24 : 11) and uraemia-associated vasculitis (Fig. 24 : 12)), or skin tumours '" (e.g. squamous cell carcinoma and digital . metastasis of a pulmonw adenocarcinoma) . (Fig. . - 24 : 13) would be more likely.
Sex: entire male cats, being more aggressive and likely to come into direct contact with lots of other cats, are more prone to dermatophytosis 'O (Fig. 24 : 14,15) abscesses, deep bacterial infections (e.g. nocardiosis, actinomycosis and bohyomycosis (Fig. 24 : 16)), deep mycoses " (e.g. sporotrichosis), and "oppomnistic" skin infections associated with retrovirus infection (Fig. 24 : 17). Life style and environment: feral cats are more prone to dermatophytosis and parasitic dermatoses " (e.g. notoedric mange and trombiculiasis). Contact with wild rodents predisposes hunting cats to poxvirus infection " (Fig. 24 : 18). Show cats are more prone to dermatophytosis. Visits to certain countries: a history of foreign travel might suggest a deep mycosis such as blastomycosis. Diet: knowing the cat's diet will allow construction of a suitable elimination diet, where appropriate. Previous illness: if the cat has gastrointestinal problems and has pedal pruritus, a food intolerance should be suspected. If there is a history of respiratory infection prior to painful footpad lesions, a herpesvirus infection l4 or herpesvirus-associated erythema multiforme '* should be suspected (Fig. 24 : 19). Onset of clinical signs: the sudden onset of painful, swollen lesions, within minutes or hours, should lead to suspicion of external factors: wasp or bee sting (Fig. 24 : 20), bum, or irritant contact dermatitis '" (Fig. 24 : 21). If lesions develop within days of introducing a new animal, a contagious dermatosis (e.g. dermatophytosis or more rarely notoedric mange) should initially be considered. If lesions appear after a change in living quarters, atopic dermatitis l6 is quite possible. Necrosis of a digit or foot, a few days after a road traffic accident should arouse suspicion of an arteriovenous fistula ". If pedal pruritus precedes development of skin lesions, an allergic dermatitis, ectoparasitic infestation ' l (e.g. trombiculiasis) or even a skin condition associated with a behavioural disorder ' (e.g. separation anxiety) should be suspected, especially if lesions are restricted to one foot and involve only the nails (onychophagia (Fig. 24 : 22)). Progression of signs and seasonality: if signs worsen when the cat is in particular locations, atopic dermatitis should be suspected. Pruritic pododermatoses that are more prevalent in summer and autumn, point towards parasitic dermatoses such as trombiculiasis 12, or allergic dermatoses l6such as mosquito bite hypersensitivity or pollen allergy. Initial type and distribution of lesion: many dermatoses have particular distribution patterns. Response to prior therapy: this will allow the effect of particular treatments to be appreciated. Dosage and duration of treatment should be established. Response to corticosteroids is generally good in atopic dermatitis or early food intolerance and poor in dermatophytosis and ectoparasitic infestations such as demodicosis. If signs are suggestive of a cutaneous drug reaction '",(Fig. 24 : 23) a comprehensive list of all recent medications should be constructed with a view to identifying the drug responsible. Transmission to other animals and people: this would indicate the need for testing for dermatophytosis or more rarely, notoedric mange.
Clinical examination The clinical examination is the central part of the diagnostic approach to pododermatoses
The general clinical examination is concerned principally with signs associated with atopy (e.g. conjunctivitis, rhinitis and asthmatic bronchitis), signs of general ill-health associated with a high temperature suggesting a viral infection, auto-immune disease or opportunistic infection associated with retroviral infection. The cat may have a cough relating to digital metastasis of a pulmonary adenocarcinoma. If the cat has xanthomatosis or lesions compatible with superficial necrolytic dermatitis, tests for diabetes mellitus should be camed out.
www.vet4arab.co.cc 24 : Diagnostic approach to feline pododennatoses
Figure 24 :10 :Multiple paronychia with crusting and scaling in a cat with systemic lupus erythematosus
F@re 24 :11 :Scaling and crusting on the footpads of a cat with suspected superficial necrolytic dermatitis associated with a glucagonoma
Figure 24 :12 :Footpad necrosis in a cat with uraemia-associated vasculitis *
he distal extremities oj Figure 24 :13 :Ulcerated nodul digits in a cat with digital metastasis of a pulmonary adenocarcinoma (courte~yof T Olivry)
Figure 24 :14 :Erythematousparonychia in a cat with dermatophytosis caused by Miuospomm canis
Figure24: 15:Footpadscaling in a cot with dermatophytosis caused by
Microsporum canis
-
Figure 24 :16 : d ......., botryomycosis
,
".... ,
,-.. ...- --
'Guagulre. E..Hukn. 8. & Delabrc, C.Vet. D~rmofoi.3. 1-12 (1992).
Figure 24 :17 : , ulcerated nodule in a cat wlth rhodotorula rnfect~on*
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The dennatological examination is concerned with whether one or both feet are affected, the presence of pruritus, identification of lesions and their distribution on the feet and elsewhere. If only one foot is involved, microbial agents (e.g. dermatophytes, Trombicula autumnalis larvae, Demodex spp., or yeasts), physical factors '" (e.g. a bum or trauma), or chemical agents (e.g. caustic substances) should be suspected. Tumonrs such as squamous cell carcinoma, fibrosarcoma (Fig. 24 : 24) and digital metastasis of a pulmonary adeno~arcinoma'~, and in rarer cases, behavioural causes (e.g. anxiety), should also be considered. If more than one foot (or even all the feet) is involved, the above dermatoses should not be excluded but the possibility of a bacterial cause (multiple paronychia, linked to retroviral infection I.'" (Fig. 24 : 25,26)), allergy (e.g. atopic dermatitis, food intolerance or mosquito bite hypersensitivity), auto-immune dermatosis (e.g. pemphigus foliaceus), or even a tumour (e.g. trichofolliculoma) (Fig. 24 : 27) should also be investigated.
The presence or absence of pruritus is an important part of the clinical examination. Pruritic pododermatoses are initially suggestive of an allergic dermatosis (e.g. atopic dermatitis, food intolerance or mosquito bite hypersensitivity), one of the clinical forms of the eosinophilic granuloma complex (e.g. eosinophilic plaques or granulomas), a parasitic dermatosis (e.g. trombiculiasis), a viral or post-viral dermatosis (e.g. herpesvirus Id, poxvirus '' or herpesvirus-associated erythema multiforme 'I),a specific bacterial infection (e.g. nocardiosis, actinomycosis or botryomycosis), deep fungal infection " (e.g. histoplasmosis or sporotrichosis) or even a skin condition associated with a behavioural disorder '". Non-pruritic pododermatoses would suggest dermatophytosis, demodicosis, a tumour or even congenital hypotrichosis Identification ofpedal lesions, although not all of equal diagnostic significance, can often steer the clinician towards a group of dermatoses. Erythema and scaling are frequently observed in dermatophytosis, trombiculiasis, allergic dermatitis (e.g. atopic dermatitis or food intolerance), or demodicosis. Erosive lesions suggest an allergic dermatosis, trombiculiasis (even if Trombicula autumnalis larvae cannot be identified) or an initant contact dermatitis. Ulcerative lesions suggest an auto-immune dermatosis, a specific bacterial infection (e.g. nocardiosis or actinomycosis), a deep mycosis, a cutaneous drug reaction, poxvirus infection, herpesvirus infection, junctional or dystrophic epidermolysis bullosa, or a tumour. Crusting is often seen in notoedric mange, auto-immune dermatoses such as pemphigus foliaceus and systemic lupus erythematosus, and herpesvirusassociated erythema multiforme. Nodular lesions might indicate eosinophilic granulomas (Figs 24 : 28,29), plasma cell pododermatitis (Figs 24 : 30-33), specific bacterial infections (e.g. atypical mycobacterial infection, leprosy, nocardiosis and actinomycosis) or deep mycosis. Assessing the pedal distribution of lesions involves a detailed examination of the digits, interdigital spaces, the ventral surface of the feet, the footpads, the ungual pads and the claws. Involvement of the digits and interdigital spaces would suggest dermatophytosis, trombiculiasis, demodicosis, an allergic dermatosis, a specific bacterial infection, a deep mycosis, or a tumour (e.g. squamous cell carcinoma, trichofolliculoma, fibrosarcoma or metastasis of a pulmonary adenocarcinoma). Involvement of the ventral surface of the feet, less common than in the dog, would suggest an allergic dermatosis, eosinophilic granuloma complex lesions (e.g. eosinophilic plaques), trombiculiasis or less commonly notoedric mange. If the footpads are affected, the following conditions should be suspected: an autoimmune dermatosis (e.g. pemphigus foliaceus), plasma cell pododermatitis, eosinophilic granuloma, irritant contact dermatitis, a deep bacterial or fungal infection, more rarely, dermatophytosis, herpesvirus-associated erythema multiforme or dystrophic epidennolysis bullosa. If the ungual pads are affected, bacterial paronychia linked to retroviral infection (especially when multiple), calicivirus infection, trombiculiasis, dermatophytosis, cryptococcosis, an allergic dermatosis, an auto-immune dermatosis (e.g. pemphigus foliaceus or systemic lupus erythematosus), or more rarely a dermatosis linked to a behavioural disorder should be considered. Multiple claw involvement is rare and would suggest dermatophytosis (onychomycosis), or more rarely an auto-immune dermatosis (e.g. pemphigus foliaceus), or nail chewing linked to anxiety or depression. An extremely rare cause would be absence (or rudimentary presence) of claws in congenital hypotichosis (seen in Birmans) or junctional epidermolysis bullosa (seen in the Siamese) (onychomadesis). Lesion identification in otherparts of the body will help the clinician to strengthen hisher clinical suspicions.
www.vet4arab.co.cc 2P, : Diagnostic approach to feline pododermatoses
Figure 24 :18 :Crusting on the undersurface of a foot of a cat with poxvirus infection (courtesy of J. Declercqj
Figure 24 :19 :Crusting of the footpads of a cat suspected of havtng herpesvirus-associated efythema mulhforme
Figure24 :20 :Pa~nfulswellrng of the d~stalexiremrty of a foot of a cat bitten by an hymenopteran insect
Figure 24 :21 :Ulceration, scaling and crusting in a cat with irritant contact dermatitis caused by herbicides *
Figure 24 :22 :Nail chewing in a cat with separation anxiety
In on the metacarpal footpad Figure 24 :23 :Dermo-epidermal se of a cat with toxic epidermal necroiysis triggered by amoxycil1in *
--
Figure 24 :24 :Ulcerated nodule on the dlstal extremity of a foot of a cat withfbrosarcoma Guaguk, E.,Huben, B. 81 Delabre, C.Ht Demrol. 3,l-I2 (1992).
Figure 24 :25 :Digital horns andmultiple bacterialparonychia in a cat with FeLV infection
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A R a e M Guide to Feline DamabAogy
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Given the incidence of dermatophytosis and ectoparasitic infestations in the cat, skin scrapings, and mycological procedures should be conducted routinely.
Skin scrapings demonstrate adult and immature mites (eggs, larvae and nymphs). Notoedres cati, Demodex cati and Demodex gatoi, and Trombicula autumnalis larvae (which should be looked for at the base of the ungual pad) may be seen Testing for dermatophytosis should be routine in any cat with a pododermatosis. Wood's lamp examination, carried out carefully, is the first step. However, it is not very sensitive as 50% of Microsporum canis isolates fail to fluoresce. Direct microscopy of hair and scale reveals the type of hair invasion by dermatophyte hyphae and spores. Fungal culture is needed to identfy the genus and species of the dermatophyte involved. Cytology is a simple, routine examination, very useful in bacterial paronychia. Bacterial colonisation may often be demonstrated by the presence of extracellular cocci and bacilli (e.g. Pseudomonas spp. and Proteus spp.). In paronychia observed in pemphigns foliaceus, acantholytic keratinocytes may be seen, either alone or in rafts, associated with non-degenerate neutrophils and sometimes eosinophils. Smears taken from the encrusted footpads of cats with pemphigus foliaceus reveal an identical cytological picture. In cases of pododermatitis associated with an allergic dermatitis (e.g. atopic dermatitis or food intolerance), many eosinophils are observed. F i e needle aspirates are equally useful in the diagnosis of tumours, plasma cell pododermatitis and nodular bacterial infections. Allergy testing (intradermal and serological testing) is universally unreliable and hard to interpret in the cat. When allergic dermatitis is suspected, the diagnosis should be based principally on response to avoidance measures (e.g. flea control and elimination diet). Skin biopsies are necessary for nodular and ulcerative lesions (biopsies should include both normal and ulcerated skin) and when footpads are involved. Biopsies do not always produce a diagnosis, but they can point the clinician in the right direction and allow certain differentials to be eliminated. Histopathology of biopsies may reveal diagnostic pathology or changes that are consistent with, for example, a specific deep bacterial infection (e.g. mycobacterial infection or nocardiosis), a deep mycosis (e.g. cryptococcosis, sporotrichosis or histoplasmosis), superficial necrolytic dermatitis or digital metastases of a pulmonary adenocarcinoma Specifc bacterial and fungal cultures should be performed in certain cases from biopsies taken aseptically. Biopsy samples should be placed in isotonic sodium chloride solution prior to inoculation onto specific media. Other diagnostic tests must be performed in line with the differential diagnosis: for example, testing for FeLV and FIV infections in cases of multiple bacterial paronychia, plasma cell pododermatitis, and deep bacterial or fungal infections; determination of the antinuclear antibody titre if systemic lupus erythematosus is suspected; and pulmonary radiography to investigate the possibility of digital metastases of a pulmonary adenocarcinoma
REFERENCES 1. Guaguire, E., Hubert, B. & Delabre, C. Vet. Dermatol. 3, 1-12 (1992). 2. White, S. D. Vet.Dermoto1. 1, 1-18 (1989). 3. Scott, D. W. &Miller, W H. Comp. Conr. Educ. Pract. Vet. 14,449-457 (1992). 4. Guaguhre, E., Delabre, C. &Hubert, B. Prat. Mid. Chi%Anim. Comp. 30,219-234 (1995). 5. Bourdeau, P., Leonetti, D., Maroille, I. M. & Mialot, M. Rec. Med. Vit. 164, 17-24 (1988). 6. Lopez, R., Ginel, P. 1. & Molleda, J. M. Vet.Dermatol. 5,27-32 (1994). 7. Johnstone, I. Mason, K. W. 81 Sutton, R. Proc 2nd World Congress of Veterinary Dermatology, Monhbal 111 (1992). 8. White, S. D., Dunstan, R. W.& Olivry, T. and others Vet. Dermatol. 4,91-95 (1993). 9. Olivry, T. Dunston, S. M. & Marinkovich, M. P. Vet.Patho1. 36, 616-618 (1999). 10. Fod, C. S. in Current Veterinar) Dermtology (ed Griffin, C. E., Kwochka, K. W., MacDonald J. M., 22-23 (Mosby Year Book, Saint-Louis, 1993). l I. Rosser, E. 1. & Dunstan, R. W. in infectious Diseases of the Dog and Cat (ed Greene, C.E.) 399-402 (Saunders,\V. B., Philadelphia, 1998).
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, '.. .,
2.4 : Diagnostic appmach to feline pododemoses
Figure24 :26 :Multiple bacterialparonychia in a cat with FIVinfection
F i g m 2 4 : 27 :Muiiiple digital nodules, one of which is ulcerated, in a cat with multiple frichofolliculomata *
Figure 24 :28 :Footpad swelling in a cat with multiple eosinophilic granulomata
Figure 24 :29 :Close-up of the cat infigure 24 :28
Figure24: 30 :Soj?, scaly swellrngs of the footpads of a cat wrthplasma cellpododermatit~s
F!gm 24 :31 :Painful, ulcerated swelling of a footpad of a cat with plasma cellpododermafitis
Figure 24 :32 :Ulcerated nodule on a metacarpal footpad of a cat with plasma ceNpododermatifis
Figure 24 :33 :Histopathology: infiltration of the footpad by lots of plasma cells some of which are mature (Russell bodies) (+) ( (H& E stain, x 1000)
* Guagukre, E.. Huben, 8. & Delabre. C.Vet. Demarol.3.1-12 (1992).
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12. Guagubre, E. Prat. Mdd. Chir: Anim. Comp. 28,211-223 (1993). 13. Thomsett, L. R. in Current Veterina,)i Therapy IX (ed Kirk, R. W.) 605-608 (Saunders, W.B., Philadelphia, 1986). 14. Hargis, A, M., Ginn, P. E., Mansell, 1.E. K. & Garber, R. L. Ver. Dermatol. 10,267-274 (1999). 15. Olivry, T. Communication personnelle (1999). 16. Gilbert, S., Pklaud, P. & Guagdre, E. Prat M4d. Chii' Anim. Comp. 34, 15-31 (1999). , R. and others Comp. Cant. Educ. Pract. Vet. 10, 1044-1048 (1988). 17. Monroe, W. E., August, J. R., C h i c k e ~ gW. 18. May, C. & Newsholme, S. J. J small Anim. Ploct. 30, 302-310 (1989).
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I M. Verde
1 Zoonotic dermatoses Zoonoses are defined as diseases and infections that are transmitted naturally from vertebrate animals to man and vice versa (WHO definition, 1967). This definition is open to considerable criticism as it excludes parasitic infestations and assumes reciprocal transmission. Some diseases, however, cannot be transmitted in both directions. The term 'zoonotic dermatoses' refers to those zoonoses in which the causal agent causes skin lesions in man. In the cat, these represent a small fraction of the 200 zoonoses recognised today in this species '. Although signs are variable, the simultaneous appearance of lesions on the owner and his animal, or the presence on a person of lesions reshicted to areas of contact with the cat are strongly suggestive of a zoonotic dermatosis. Transmission in the house will not necessarily involve everyone because of variation in individual susceptibility. Occasionally, the owner makes the connection between his or her skin lesions and those of their cat and goes straight to the vet before consulting his doctor. Obtaining a precise diagnosis for the cat's skin condition can then help in diagnosing the owner's disease for which isolating an aetiological agent is often difficult.
Fungal dermatoses Dermatophytosis Dermatophytosis is a superficial mycosis caused by pathogenic, epidermotropic, keratinophilic and keratolytic funRi called dermatophytes. Tbe cat is, above all, the vector of Microsporum canis which is highiy contagious to man. ~r&mission is mainly by direct contact but can also occur by indirect contact via contaminated hair and scale deposited in the environment (e.g. grooming equipment and transport cages) '. Mechanical asymptomatic carriage is common and estimated to occur in 15-36% of animals depending on their life style I.'.
In man, exposed parts such as hair, face, beard and arms, and moist areas like the inguinal region, feet and axillae, are most often affected. Skin signs are extremely pleomorphic. Glabrous regions are most commonly involved, typically with annular, erythematous lesions (Figs 25 : 1-4). Here, the differential diagnosis must include other dermatoses l i e discoidal eczema (Fig. 25 :5), psoriasis (Fig. 25 : 6), pityriasis rosea and annular granuloma. Hair, eyelids and eyebrows are usually involved in children. This form of dermatophytosis involves erythematous, scaly plaques in which infected and healthy hairs can both be found (Fig. 25 : 7). Kerions are characterised by papulo-pustular lesions with deep folliculitis and perifolliculitis in a raised, semicircular lesion (Fig. 25 : 8). Pruritus, lymphadenopathy and sometimes pyrexia are seen. Diagnosis is based on Wood's lamp examination, microscopy of hair and scale, and fungal culture. Identifymg the species of dermatophyte gives important epidemiological information. Vets are often confronted with dermatophytosis in an owner whose cat is apparently unaffected but has been identified as the source of the infection by the owner's doctor. In such cases, submitting hair and scale for fungal culture, using the carpet square or toothbrush technique, should confirm or refute the doctor's diagnosis. Samples should also be taken from the owner to identify the causal dermatophyte. If the organism isolated is anything other than Microsporum canis, the cat is unlikely to be the source of the infection '.
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Sporotrichosis Sporotrichosis is a deep mycosis, highly contagious to man, caused by a dimorphic fungus, Sporothrix schenckii I. This infection should be suspected in cats with a non-healing wound or abscess following the use of appropriate antibiotics. Sporotrichosis is a serious zoonosis and individuals in diiect contact with soil and plants should be considered at risk 6. Infection in the cat usually results from wound contamination or penetration of a foreign body. More rarely, inhalation of spores can cause systemic illness. Man usually becomes infected directly following a bite or scratch but infection can also arise by diiect contact with infected tissues or fluids of affected cats. Signs are identical to those described in the cat '. The incubation period is variable (3 weeks to 3 months). The cutaneolymphatic form is the most common (seen in 80% of cases), characterised by a solitary nodule at the site of infection. The nodule, which eventually ulcerates, is typically seen on the back of the hand (Fig. 25 : 9), a fmger, a toe, or the face. Other nodules may appear along lymphatic vessels. The strictly cutaneous form is identical to the feline condition. The rare systemic form is probably caused by spread of infective Sporothrix schenckii spores via the blood. Usually, sporotricbosis can be treated successfully in immunocompetent people but it can be fatal in the immunosuppressed. Diagnosis is based on cytology, histopathology and fungal culture '. In man, diagnosing the condition on histopathology is difficult due to possible confusion with Cryptococcus neoformans and Histoplasma capsulatum.
In the cat, in addition to systemic antifungal treatment, hygienic measures must be carried out. Hands and arms must be thoroughly cleaned with antifungal agents l i e chlorhexidine and povidone-iodine. Wearing protective gloves is also recommended. Owners must be informed of the considerable zoonotic risk associated with this illness and euthanasia should be discussed for carrier cats because treatment is long and the risk of transmission is high '. Blastomycosis Blastomycosis is a systemic mycosis, caused by the fungus, Blastomyces dermatidis, reported mainly in North America, but also in Africa and central America, with well-defined endemic foci. Blastomycosis is a systemic illness seen in the dog and man, and rarely in the cat. To date, no case has been reported in Europe in the cat. Human infection can occur via wound contamination (bites from infected animals; knives or needles contaminated by autopsy or aspirate). In addition to characteristic pulmonary lesions following inhalation of spores from the soil, skin lesions can occur. These may take the form of papules and abscesses or sometimes proliferative, crusting nodules with a raised border. Diagnosis is based on fungal culture carried out by specialist laboratories '.
Histoplasmosis Histoplasmosis is a systemic mycosis, caused by a dimorphic fungus, Histoplasma capsulatum. There are two varieties of this fungus: var. capsulatum (American histoplasmosis) and var. duboisii (African histoplasmosis). The disease is endemic in the southern united States and also in many tropical countries. It is reported sporadically in other parts of the world, notably Europe lo.Histoplasmosis is a systemic disease seen in the dog, cat and man. The disease is contracted by inhalation of spores from contaminated soil, contact with contaminated bird or bat faeces or by contact with wounds contaminated by the fungus. In man, histoplasmosis is a marker for AIDS. American histoplasmosis is characterised by mucocutaneous lesions such as gingivitis and well-circumscribed ulceration of the palate and tongue. African histoplasmosis is characterised by cutaneous lesions: semicircular, lenticular papules, sometimes with a depressed centre, or nodules, indolent ulcers and fistulae '. Diagnosis is based on fungal culture canied out by specialist laboratories and histopathology of skin lesions I.
www.vet4arab.co.cc 25 : Zoonotic dematoses
Figure25 :1 :Circular, well-d@ned, erythematous,inflommaforylesions - derr . '.tosis caused by Micmspomm canis (courtesy ofR. Rzernik)
Pigun25 :2 :Annular erythematous lesron, wrth a scaly, very inflammaiory border. - dermntophytos~scaused by Wnospomm canis (courtesy o f M C Saem de Santa Marla)
Figure25 :3 :.Mulnple onnaldr, e g r h r ~ r o r alerio~n- dermardphjlusrs caused h! Mi;roapomm ciru, I ul4rles) 0IM.C. Saenl d? Sanla Mar 1 s
Figure 25: 4 :Well-circumscribed,elyrhematous macules - dermntophytosis caused by M i m p o m canis (courtes) ofR. Rzeznik)
Figure 25 :5 :A circular patch of erythema and scaling - discoidul eczema
Figure 25 :6 : A polycyclicpatch of erythema and scaling -psoriasis
Figure 25 :7 :Circular scaling lesion in the hair - dermatophytosir caused by Microsporum canis (courtesy ofR. Rzernik)
Figure25 :8 :Raised, very inflammatory lesion (kerionJ-dermatophytosis caused by Microspomm canis (courtesy of R. RzeznikJ
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.Practical Guide @Feline~ f 0 1 0 g y
Bacterial dermatoses Cutaneous tuberculosis Cutaneous tuberculosis (Mycobacterium tuberculosis, Mycobacterium bovis and Mycobacterium avium) is an infectious disease that is now rare in the cat. However, due to the resurgence of cases of human tuberculosis, especially in severely immunosuppressed people, it is essential to he familiar with the disease in this species ". Transmission is by direct contact with infected exudate (skin lesions, nasopharyngeal exudate) of affected animals or people and also via ingestion of contaminated meat or milk. Feline Mycobacterium tuberculosis infection is considered a 'reverse' zoonosis, transmission occurring from man to cat. In the cat, in addition to systemic signs (e.g. pyrexia, anorexia, weight loss, lymphadenopathy, cough and lameness) tuberculosis is characterised by indolent ulcers (single or multiple and often wellcircumscribed), abscesses, plaques or nodules which are sometimes very adherent to the subcutaneous tissues. The main areas affected are the head, neck and limbs.
In man, skin lesions of tuberculosis take various forms
12: tuberculous canker (an inflammatory, nodular lesion which can ulcerate with regional lymphangitis and lymphadenopathy) (Fig. 25 : 10); lupus vulgaris (small chronic papules and nodules which collect in plaques, and sometimes ulcerate, on the face, neck and arms; vemcous tuberculosis (thick, indurated, proliferative plaques restricted to the hands and knees; pen-orificial tuberculosis (ulcerative lesions of the mouth, anus, vagina or urethra); miliary tuberculosis (numerous papular lesions. associated with pulmonary miliary tuberculosis); and gomo tuberculoso (subcutaneous nodules which develop into ulcerated abscesses).
Diagnosis is based on clinical signs, cytology, histopathology and bacterial culture. Rapid acid-fast staining of needle aspirates and smears are the procedures used most frequently to confirm a diagnosis of tuberculosis. Findimg acid-fast bacilli confirms the presence of mycohacteria, but it is essential to follow this up with culture to determine the actual causal organism. Atypical mycobacterial infections are more common than tuberculosis in the cat j. Biopsy, culture and post-mortem examination are the preferred diagnostic procedures ". Cats with tuberculosis must be euthanased for public health reasons. This applies equally to cats carrying Mycobacterium tuberculosis and Mycobacterium bovis, which can be the source of infection for man and other animals ".
Viral dermatoses Poxvirus infection Poxvirus infection is a viral dermatosis caused by cowpox virus, an orthopoxvirus reported in various species, especially cats, cattle and man. The risk of transmission to man is reduced if simple hygiene precautions are taken ". However, there have been reports of transmission from cat to man '' and such cases carry a guarded prognosis in immunosuppressed or old people. The withdrawal of the smallpox vaccine has led to a reduction in protection of the whole population against pox viruses and left immunosuppressed, non-vaccinated people more susceptible to these infections.
In man, the incubation period is 2-6 days. Dermatological signs associated with cowpox are usually mild and characterised by lesions that are initially papular and then vesicular and vesiculopustular, with a central depression and a surrounding halo. Lesions are restricted to the face (Fig. 25 : 1I), hands and arms. More rarely, nodules with central ulceration can he seen (Fig. 25 : 12). Systemic signs, including pyrexia, peripheral lymphadenopathy and headache are sometimes encountered. In immunosuppressed patients, the signs are much more severe and characterised by a generalised pustular and haemorrhagic dermatosis which can sometimes be fatal. The differential diagnosis should include pseudo-cowpox and o d Diagnosis is based on initial clinical appearance and development of the lesions. Histopathology of skin biopsies is very. suggestive. The virus can be demonstrated by electron microscopy or by isolation . . on cell culture.
www.vet4arab.co.cc 25 : Zoonotic dermatoses
Figure 25 : 9 :Nodular, inflammatory lesion on the back of the hand, spomtrichosis (courtesy D.W. Scott)*
Figure 25 :10 : Cutaneous tuberculosrs A) Verrucous tuberculos~s B) Lupus vulgaris (courtesy oJP Thomas)
Figure 25 :11 :Vesicular lesions ofthe lips,poxuirus infection (courtesy of J. Dec1el.q)
Figure 25 :12 :Nodule wzth central ~lcer,poxvirus mfectlon (ceultesy oJD Groux)
F i g m 2 5 : 13 :Papulo-crustous lesions on the forearm, notoedric mange
Figure 25 :14 :PLF....
...."...,.,
Figure25 :15: Erythemarouspapul~. hypersensitivity
'Scon, D.W. Miller Jr, W H. & %fin,
...thfleo allergy
....-...
. ., ...,.,,.
J
on the abdomen, cheyletiellosis
Figure 25 . ,isease: A) annular papular lesions B) axillary lymphadenopathy (courtesy oJP Thomas) .A
C. E. Muller & Kirk's Small Animal Dermatology, 5th edition (Saundeo, W.B., Philadeiphia, 1995).
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Prophylactic measures should, therefore, be taken when dealing with poxvirus infection in the cat: wearing gloves and goggles when handling affected animals; preventing the cat coming into contact with old or immunosuppressed people or young children; and, given the highly resistant nature of the vims in the external environment, cleaning and disinfecting the environment.
Parasitic dermatoses Notoedric mange Notoedric mange is a parasitic dermatosis caused by the mite, Notoedres cati. It is contracted by direct contact or sometimes by indirect contact with contaminated objects. It is highly contagious between cats and to dogs and man. In man, notoedric mange causes transitory skin lesions characterised by vesicles, erythematous papules, urticarial plaques, cmsts and excoriations in areas of contact with the cat, especially arms (Fig. 25 : 13), legs, chest and abdomen. There is a sudden onset of severe pruritus. Lesions develop within 24 hours of contact with the affected cat and regress spontaneously within two weeks if infestation is slight and contact with the affected cat is avoided*. Otodectic mange Modectic mange is a parasitic dermatosis caused by the mite, Otodectes cynotis, and contracted by direct contact with an infested cat. It is highly contagious between cats, from cats to dogs and more rarely to man. In people, otodectic mange causes a transitory papular dermatitis on the body, characterised by vesicles, erythematous papules, urticaria2 plaques, crusts and excoriations on the arms and thorax. Pruritus is very marked. As the parasites can only survive for a few days off their host 16, skin lesions regress spontaneously within about two weeks. Cheyletiellosis Cheyletiellosis is a parasitic dermatosis caused by the mite, Cheyletielia blakei, and contracted mainly by direct contact with an infested cat. It is highly contagious between cats and from cat to man. In man, cheyletiellosis is characterised initially by erythematous, very pruritic macules, followed by papules on the trunk and forelimbs (Fig. 25 : 14). Urticarial plaques, vesicles or pustules can sometimes be seen. Generalised, non-lesional pruritus may also be observed5.As the life cycle is not completed on man, infestations with Cheyletiella blakei resolve spontaneously after affected cats have been treated.
Flea infestation The cat flea, Ctenocephalides felis felis, is the most common parasite of the cat. When young adults emerge from their pupae, they may bite people causing hypersensitivity reactions in some individuals. Lesions occur mostly on the distal limbs (ankles and wrists) and areas of constriction by clothes (socks, belt, bra). They are characterised by very pruritic papules, sometimes urticarial plaques, vesicles and secondary excoriations (Fig. 25 : 15). The cat flea is also the vector (for transmission between cats) of Bartonella henselae, the organism that causes cat scratch disease. The cat is therefore an asymptomatic carrier of this bacteria. Transmission to man occurs mostly via a bite or scratch, but sometimes indirectly via flea faeces. The typical form is characterised by the development,within 3-10 days, of a transient papular lesion at the site of the scratch. This is followed by marked regional lymphadenopathy within 2-3 weeks (Fig. 25 : 16). Cat scratch disease is non-febrile. In 5.15% of cases, it presents atypically: pyrexia, abdominal pain, headache, unilateral conjunctivitis, uveitis, hepatomegaly, splenomegaly and enoephalitis. One particular clinical form called bacillary angiomatosis is seen in severely immunosuppressed individuals and involves a vasoproliferative syndrome with purplish-blue, fragiie, haemorrhagic papules and nodules associated with severe systemic signs. Testing for antibodies against Bartonella henselae is the most common method of diagnosis. Culture is very rarely positive except perhaps in bacillary angiomatosis. The most sensitive and specific diagnostic test is in vitro gene amplification carried out on lymph node biopsies ". With cats also giving shelter to rodent fleas, cats can also be passive vectors of Yersinia pestis, the plague organism. Regular, rational flea control in cats is therefore necessary for both therapeutic and preventative purposes.
www.vet4arab.co.cc 25 : Zoonotic dermatoses
REFERENCES I. Lappin, M. R. in Current Veterinary Therapy XI (ed Kirk, R. W.) 284-291 (Saunders, W.B., Philadelphia, 1992). 2. Foil, C. S, in Current Veterinary Dermaiology (eds Griffin, C. E., Kwochka, K.W. & MacDonald, R.W.) 22-33 (Mosby Year Book, Saint-Louis, 1993). 3. Romano, C., Vdenti, L. &Barbara, R. Mycoses 40,471472 (1997). 4. DeBoer, D. 1.& Moriello, K. A. Comp. Cont. Educ. Pract. Vet. 17, 1197-1203 (1995). 5. Scott, D. W. Miller Jr, W.H. &Griffin, C. E. Muller & Kirk's SmnNAnimal Dermatology, 5th edition (Saunders, W.B., Philadelphia, 1995). 6. Rosser, E. I. in Current Veterinary Dermatology (eds Griffin, C. E., Kwochka, K.W. & MacDonald, R.W.) 49-53 (Mosby Year Book, Saint-Louis, 1993). 7. Shadomy, H. J. & Utz, J. P. in Dermatology in General Medecine (eds Pa@ick, T.B., Eizen, A. Z. & Wolff, K.) 2492-2494 (Mc Graw W, New-York, 1993). .. 8. Merchant, S. R. Comp. Cont. Educ. Pract. Vet. 12,515-522 (1990). 9. Werner, A. H. &Werner, B. E. Comp. Cant. Educ. Pract. Vet. 15, 1189-1197 (1993). 10. l egrndre A. M In Injer.trorr! Direores of llte Doq a ~ mCar cd (irecnc. C. E., 371-377 (Sunden, W B.. Phladclph~a,1498j. I I . Grcene, C E & Gum-\loure. D A. in 1 1 1 f i ; r r ~ uD~ l l e ~ s r 6i J r h ~D i g und C J I ed Grcene. C.C.)313-321 (Sdundrri. M:B Pluladelphld. 1998,. 12. G ~ ~ l l.cCn .. Rorclla. K & Sin Man~n.0.In ManaolofSkin Direores 407-421 !Jmln.
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II
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P. Prelaud E. Guaguere
1 Therapy in feline dermatology This chapter lists the principal medications used in feline dermatology. Dose, route of administration, indications a n d whether a product licence exists are outlined for each drug.
ANTIMICROBIAL Antifungal agents
L Ketoconazole Itraconazole Fluconazole Enilconazole Microsize griseofulvin Ulh.amicrosize gjiseofulvin
Route of administration PO PO PO TOP PO PO
Dose
Indications
10 mgikg SID 3-5 mglkg SID 10-15mgikg SID-BID 0,2%,sol., every 4days 25-50 mgjkg BID 5-10 mgkg BID
Dermamphytosis, Deep mycoses Dermamphytosis, Deep mycoses Deep mycoses Dermatophytosis Dermamphytosis Dermatophytosis
PO, SC PO PO PO PO PO PO
12.5-25 mgikg BID 15-20 m a g BID 20 mgkg BID 5.5 mglkg BID 2-8 mgkg SID 1 mg k g SID 5-11 mgkg BID
Bacterial infections
PO, SC
5-20 mgikg SID
IV PO PO PO PO PO IM
4 mgikg SID 20 mgkg BID 2-5 mgkg SID 10-20 mgkg BID 5-11 mgikg BID 11-35 mgkg BID 10000 Uikg SID-BID
PO PO PO
10-20 mg k g BID 10 mgikg SID 10-30 mg /kg BID
PO PO
15-20 mg /kg BID 15-30 mg k g BID
Chlorhexidine
TOP
Benzoyl peroxide
TOP
0,5% (lotion) 2 to 3 % (shampoo) 2%
Mupimcin
TOP
2%
Systemic antibiotics Clavulanic acid-potentiated amoxycillin Cephalexin Cefadroxil Clindamycin Clofazimine Dapsone Doxycycline Enrofloxacin Gentamicine Lincomycin Marbofloxacin Metronidazole Minocycline Oxacillin Penicillin G
. . •
• •
. . • •
.
Rifampicin Rifampicin Tetracycline Trimethoprim-sulphadiazine
Trimethoprim-sulphamethoxazole
-
Feline leprosy ,I ,, Bacterial infections, atypical mycobacterial infections
Atypical mycobacterial infections Bacterial infections
Nocardiosis, actinomycosis, bonyomycosis Feline leprosy Atypical mycobacterial infections Bacterial infections, atypical mycobacterial infections Bacterial infections
Topical antibacterial agents Bacterial infections Dennatophytosis Acne, Bacteiid infections Acne
Abbreviations:
L : licensed product available, PO : oral, IM: intamuscular, IV : intravenous, SC : subcutaneous, TOP : topical, SID :once daily, BID : twice daily
9 Fmd Guide m Elk Eematology
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ANTI-INFLAMMATORY AGENTS 1
Antihistamines
L Chlorpheniramine Clemastine Cyproheptadine Diphenhydramine Hydroxyzine Oxitimide Corticosteroids Dexamethasone
Dexamethasone Methylprednisolone
. .. . . . .
Route of administration
Dose
Indications
PO PO PO PO PO PO
2-4 mglcat SID-72D 0.5 mglcat BID 2 mgicat BID 0.5 mgicat BID
Allergic dermatoses
PO
0,25 mgicat SID, BID
SC, IM
0.24.4 mgicat SID, BID
PO
0.8-1.5 mgikg BID
Allergic dermatoses, eosinophilic granuloma complex auto-immune dermatoses
4-5m a g (long-acting)
Allergic dermatoses, eosinophilic granuloma complex
Methylprednisolone (acetate)
•
IM, SC
Prednisolone, prednisone
•
PO
Triamcinolone Triamcinolone acetonide
. •
5-10 mglcat BID 30 to 60 mgicat SID
Allergic dematoses, eosinophilic granuloma complex, auto-immune dermatoses Dexamethasone Allergic dermatoses, eosinophilic granuloma complex
eosinophilic granuloma complex, auto-immune dermatoses PO SC
0.25-0.5 mgicat SID eosinophilic granuloma complex
Synthetic progestagens Megeshol acetate
.
PO
2.5-5 mg SID
Allergic dermatoses
Ciclosporine A
PO
5-10 mgikg SID
Allergic dematoses, urticaria pigmentosa, eosinophilic granuloma complex
Aurothioglucose
IM
l mgikglweek
Chlorambucil
PO
0.1.0.2 mgikg BID
Auto-immune dermatoses, plasma cell stomatitis Allergic dematoses, eosinophilic granuloma complex, auto-immune dermatoses
Miscellaneous
Abbreviations: L :licensed pmduct aviulable,PO : oral, IM : inh'amuscular, N :inwvenous, SC :subeufaneous, SID :once daily, BID : twice daily, TID : 3 times daily
www.vet4arab.co.cc 26 : Therapy in feline dermatology ECTOPARASlTIC AGENTS I
L Carhamates Bendiocarb Propoxur Carbaryl
.. .
Route of administration
Dose
Indications
Collar Collar, powder Powder
Flea infestation
Formamidines Amitraz
-
Organophosphates Cythioate Fenthiou
..
Dichlo~os Fenitrothion
Lotion Ear preparation (diluted in pmpylene glycol)
0,25 & 0,5 &
Demodicosis, notoedric mange Dernodicosis, notoedric mange
Flea infestation
Drinkable solution Spot-on (systemic action) Spray Spray
Growth regulators Lufenuron Lufenuron Pyripmxifen
• •
Nitroguanidines
.
Imidacloprid
.
PO SC Spot-on (surface acting) Collar
monthly every 6 months 100 mg/ml
Flea iniestation
Spot-on (surface acting)
1070, monthly
Flea infestation
Spray Spray
0,25 % 025 %
Spot-on (surface acting)
10 %
Flea and tick infestation Pediculosis, cheyletiellosis, Otodectic mange Flea and tick infestation
sc
Pyrazolis Fipronil
Cheyletiellosis, Otodectic mange Neonicotinoids Nitempyram
•
PO
1 mgikg
Flea infestation
-
SC
0,2-0,4 mgikg
Spot-on with systemic action
6 rngikg
Otodectic mange, notoedric mange, Cheyletiellosis Flea infestation, Otodectic mange
PO
1-2 mgikg
Avermectins Ivennectin Selarnectin
Milbemycin
-
Abbreviations: L :licensed pmduct available, PO : oral, SC : sobcutaneous
.:.
Demodicosis
1Practical Guide to Feline Dermatology
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PSYCHOTROPIC AGENTS L Diazepam Fluoxitine Clomipramine Selegiline Naloxone Nalhexone Trioxazine Propranolol Sulpirih
Route of administration Collar Collar powder powder
1:
1
Dose
Indications
1-2 m& BID 1-2 m a g SID 0.3-0,Xmgikg SID-BID 1-2 mgkg SID 1 m& SID 2.2 m a g SID 10 m a g BID 8-10 m a g sm 200 mgim' S m
Behavioural disorders
I
ANTIMITOTIC AGENTS L
I
Route of administration
Dose
25 mglmi 5-8 times at 3 week intervals r pressure Reconstitule 50 mg of cisplatin powder in 6.5 ml of isotonic NaCI solution. Mix this solution in an equal volume of sesame oil. Inject, under pressure, 4 times at weekly intervals
Cisplastin
Indications Fibrosarcoma
Squamous cell carcinoma
SYNTHETIC RETINOIDS L
Route of administration
Tretinoyn Isotretinoin
TOP PO
Acitretin
PO
Dose 0,01% to 0,05% 2 - 5 m a g SID 10 mg S m - BID 1 mgikg SID
Indications Acne Acne, epitheliotropic T cell lymphoma T cell cutaneous lymphoma Cutaneous epitheliotropicT cell lymphoma,
DRUGS AVAILABLE FOR TREATING HYPERADRENOCORTICISM L Metyrapone Selegiline
Route of Administration
Dose
PO PO
65 m& BID-TID I to 2 mgkg SID
Indications Hyperadrenocorticism Hyperadrenocorticism
Abbreviations: L : licensed product available, PO :oral, IM :inhamuscular, IV : inuavenous, SC : subcutaneous,TOP :topical, IL : inhalesional, SID :once daily, BID :twice daily, TID: 3 times daily
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c d d Guide to Feline Dmna.toIogy
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r;/
Index A Abscess 6.1-2,6.6,6.10, 12.8 Abyssinian2.2,5.6,5.9, 16.2, 19.2 Acemannan 15.10 Acepromazine 17.9 Acitretin 15.2 Acne 2.8,6.4-6 ACTH 14.1, 14.8 Actinic keratosis 15.1, 20.4, 21.2, 21.4 Actinomyces spp. (see actinomycosis) Acrinomycosis 6.10, 7.8 Adenocatcinoma mammary 15.12 pancreatic 14.2 pulmonary 6.4, 15.12 Adrenal gland 14.8 Adriamycin 15.2, 15.10 Aggression 17.2 Agonti 1.7 Albinism 16.4 Allergens aeroallergens 10.1, 12.2 flea 9.4 food allergens 10.1, 11.1-2 mites 11.1 Allergy aeroallergens (see atopic dermatitis) food 12.8, 18.2, 11.1-7,20.2,21.2 aetiopathogenesis 11.1-2 features 11.2, 12.2 diagnosis 11.4-6 treatment 11.6-7 contact 12.2, 12.8, 20.4, 21.4 flea (see EA.D.) gastrointestinal parasites 12.2 mosquitoes 12.2, 12.4, 12.6, 18.4 Alopecia 16.2 atrophic 19.2 circumscribed 17.4, 19.2 dermatophytosis 4.2, 19.2,19.6 diagnosis 19.1-7 diffuse 14.6 genetic 19.2 paraneoplastic 14.1-2, 19.2 psychogenic (see behavioural) self-induced3.10,9.1,10.2,11.2, 14.2, 17.1, 17.4, 18.1, 18.6, 17.8 shiny 19.6 Alopecia ateata 19.6 Alopecia universalis 19.2
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maid Guide m WiDwnamlogy
Alternaria spp. 5.1,7.8 Aluminium hyroxide 15.6 Amelanoses 16.4-6 Amikacin 6.7 Amitraz3.1,3.2,3.4,3.8 Amoxycillin 6.2, 12.9, 13.1 Amphotericin B 5.2,5.8,5.9,5.10 Ampicillin 6.3 Antibiotic sensitivity 2.16,6.10,6.11 Antibiotic therapy 6.3,7.2,6.10,6.11, 12.9 Antibiotics 6.2 Antihistamines 9.6, 10.7, 11.6 Antinuclear antibody test 13.6, 21.5, 24.8 Anxiety 17.2, 17.6, 17.8-10 Anxiolytics 17.9 Archaeopsylla erinacei 3.10-11 Asthma 10.2 Ataxia 15.11 Ato~icdermatitis 10.1-8, 18.4, 20.2, 21.2 aetiopathogenesis 10.1 clinical features 10.2 diagnosis 10.4 treatment 10.6 Atopy (see allergy and atopic dermatitis) Atrophy 2.6, 14.8 Aural haematoma 3.2 Aurothioglucose 13.6 Auto-immune dermatoses 13.1-7, 14.6, 14.8,20.4,21.2,21.4 Auto-immunity (see auto-immune dermatoses)
B Bacillary angiomatosis 25.6 Bacterial culture 2.16 Bacteriology 22.8 Bartonella henselae (see cat scratch disease) Basal cell tumow 15.4 Basement membrane 1.2, 15.1 Basophils (in-vitro degranulation) 10.4 Beef meat 11.1 Behavioural disorders 17.1-11, 18.4 Behavioural therapy 17.10 Benzodiazepines 17.9 Benzoyl peroxide 6.6 Bipoloris spp. 5.1, 7.8 Biopsy 2.16 Birman 2.2, 16.2, 19.2,24.8 Bite 5.4, 6.1, 6.10, 17.2 Blastomyces dermatidis (see blastomycosis) Blastomycosis 5.9-10,25.2 Bleach 4.10 Blepharitis 11.2, 16.2 Botryomycosis 6.10-11 Bowen's disease (see squamous cell carcinoma in situ) Bulimia 17.4 Bulla 2.4 Bullous pemphigoid 13.1-2,21.4 aetiopathogenesis 13.1 -
~
-
-
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www.vet4arab.co.cc 27 :Index gknkal clinical features 2.4, 13.2 ' diagnosis 13.4 treatment 13.7 Burmese2.2,3.8, 16.2, 17.1, 19.2
C Cadherins 13.1 Calcification 21.4 Calcofluor 4.4 Calicivims infection 12.8, 21.5 Cancer (see skin tumours) Candida albicans (see candidiasis) Candidiasis 20.4 Carbamates 3.12 Carcinoma anaplastic 15.8 epidermoid (see squamous cell carcinoma) Cat scratch disease 25.6, 8.1 Cataract 16.2 Cefadroxil6.2,6.3 Cephalexin 6.2, 6.3, 12.9 Cerumen 3.2 Cemminoma 15.11,22.8 Cemminous glands 1.7, 15.11 Challenge test (food) 11.6 Chartreux 1.7 Chediak-Higashi syndrome 16.6 Cheilitis 11.2, 12.2 Chemotherapy 15.10 Cheyletiella blakei 3.7 (see also cheyletiellosis) Cheyletiellaparasitivorax (see cheyletiellosis) Cheyletiella yasguri (see cheyletiellosis) Cheyletiellosis 2.2, 3.4J2.2, 14.6, 14.8, 19.6, 18.2,20.2, 21.2, 25.6 Chicken (meat) 11.1 Chin 6.4, 12.2 Chitin 3.12 Chitin synthesis inhibitors 3.12 Chlorambucil 10.7, 13.6, 13.7 Chlorhexidine 6.3,6.6 Chlorinated hydrocarbons 3.1 Chlorine dioxide 4.10 Chlorpheniramine (see antihistamines) Cholangiocarcinoma 14.2 Chondritis (see plasma cell chondritis) Chondrosarcoma 15.8 Chrysotherapy (see aurothioglucose) Cimetidiie 13.1 Cisplatin 15.2 Cladosporium spp. 5.1,7.8 Clindamycin 6.2, 6.6 Clipping (in dermatophytosis) 4.6-9 Clofazimine 6.2, 6.8 Clomipramine 17.9 Coat brushing 2.14, 18.7, 19.6 Cobalt 15.9 Coccidioides immitis (see coccidioidomycosis) Coccidioidomycosis 5.10-11
I
A Radical Guide to Feline DermamIogy
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Colitis 11.2 Collagen 1.2, 2.6,12.1, 13.1, 14.4, 16.8, 16.10, 21.4 Collagen I Y 16.8 Collagen VII 16.8 Colour point 1.7 Comedone 2.8 Congenital hypotrichosis 16.2, 19.2J9.6, 24.8 Connective tissue (subcutaneous) 1.4 Contact allergy (see allergy) Coronavirus (see feline infectious peritonitis) Corticosteroids7.2,9.4, 10.6, 11.2, 11.6, 12.9, 13.6, 13.7, 14.2, 15.11, 15.12, 16.10, 17.8, 18.4, 19.2,20.2, LI
Cowpox (see poxvirus infection) Creatinine phosphokinase 14.6 Crust 2.6 Crusts diagnosis 20.1-4 Cryptococcosis 5.6-8,6.4,7.8, 12.8,21.2,21.4 ~r$tococcus neoformans 5.4,5.6-8 ~ ~ s c a n n 14.9 in~ Ctenoceohalides canis 3.1 1 (see also flea) ~tenocebhalidesfelis 3.1 1 (see also flea) Curvularia spp. 5.1,7.8 Gushing's syndrome 2.6, 14.2, 14.8-9, 19.2, 19.4,21.2,21.5 Cutaneous asthenia 14.4, 16.8-10,21.2,21.4 Cutaneous drug reaction 13.1, 14.6, 14.8,20.4 Cutis laxa 16.10 Cyclosporin 10.1, 10.7, 12.9, 16.10 Cyst 15.12 Cytokeratin 15.8 Cytokines 15.10 Cytology 2.14-15, 13.4, 14.6,22.8
D D.T.M. 2.15,4.6 Dapsone 6.2 Deafness 16.4 Deep mycosis 5.1-11,7.6,24.8 Deep pyoderma 24.8 Demodex felis 3.7 Demodex gatoi 3.7 Demoden spp. 2.8,3.8,6.4,7.8,7.10, 12.8, 13.4, 15.2, 20.2 Demodicosis (see Demodex) Depression 17.6, 17.9 Dermatophagoides farinae 10.1, 10.6 Dermatophytes 4.1 (see also dermatophytosis) Dermatophytosis 4.1-11, 6.4,7.6, 12.8, 13.4, 14.6, 14.8, 19.6, 20.2, 21.2, 21.4, 25.1 alopecia 4.2, 19.2,19.6 asymptomatic animals 4.4 biopsy 4.6 clinical features 4.2-4 contamination 4.1,ZS.l diagnosis 2.14-15,4.4 predisposing factors 4.1-2 prevention 4.11 pruritus 4.2, 18.2, 18.4 transmission to man 4.6, 4.11, 25.1 treatment (animals) 4.6-10
www.vet4arab.co.cc 27 : Index g6n6ral
treatment (environment) 4.10-11 vaccination 4.9 Dematosparaxis 16.8 Dermis functions 1.8, 1.9 structure 1.2-3 Demo-epidermal junction 16.6-8 Desensitisation (see immunotherapy) Desmogleins 13.1, 13.4 Desmosome 13.1 Devon Rex (see Rex) Dexamethasone (see corticosteroids) Dexamethasone suppression test 14.9 Diabetes 2.6,3.8, 14.2, 14.9,21.4 Diagnostic tests 2.12-18 Diarrhoea 11.2, 17.4 Diazepam 17.9 Dipylzdium caninurn 8.1 Direct examination of skin and hair 2.14,4.4 Displacement activity 17.1, 17.2 DLE (see lupus) Dopamine 17.1 Doxycycline 6.2, 6.7, 12.9 D.T.M. 2.15 Dysmetaholic papule 2.6 Dysthymia 17.2, 17.6
E Ear canal 22.1 Ecchymosis 2.4 Echidnophaga gallinacea 3.1 1, 8.2 Ecological therapy 17.9, 17.10 Ecthyma 25.4 Elastin fibres 1.2,2.6, 16.10 Elimination (hypoallergenic) diet 10.4, 11.4, 12.8, 12.9, 19.4-5 Elizabethan collar 12.8, 17.9 Endorphins 17.1, 17.2 Enilconazole 4.9-10 Emofloxacin 6.2,6.3,6.4,6.7 Eosinophil 12.1 Eosinophilia 11.4 Eosinophilic granuloma complex 2.4,6.2, 10.4, 12.1-10, 19.1, 18.6 aetiopathogenesis 12.1 diagnosis 12.4-8 eosinophil 12.1 mast cell 12.1 features 12.2-4 treatment 12.8-9 Eosinophilic granuloma 6.4, 12.2, 12.4 Eosinophilicplaque 9.1, 10.2, 11.2, 12.2, 12.4, 15.12 Epidermal horn 2.6,7.4 Epidermis 1.1 functions 1.8, 1.9 structure 1.1-2 Epidermolysis bullosa 2.4, 16.6-8,21.2,24.8 dystrophic 16.8
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junctional 16.6-8 EpitheliotropicT cell lymphoma2.6, 12.8, 14.6, 14.8, 15.11, 18.2, 18.4, 19.6,20.2 Erosion 2.6,Zl.l-5 Erythema 2.4 Elythema multiforme 7.10, 14.6, 14.8 Escherichia coli 1.9 Essential fatty acids 10.7 Eumelanin 1.7 Evans blue 4.4 Exophiala spp. 5.1,7.8 Exotic Short Hair 2.2. 16.1 Extensibility index 16.10
F E.A.D. 8.1, 9.1-6, 10.4, 12.2, 18.2, 20.2 aetiopathogenesis 9.1 clinical features 9.1-4 diagnosis 9.1-2 man 8.1,25.6 pruritus 9.1 treatment (aetiological) 3.12-14,9.5-6 FAIDS 25.2 F3 (see pheromones) F4 (see pheromones) Facial paralysis 15.11 Familial eosinophilic granuloma complex 12.4 Felicola subrostratus (see pediculosis) Feline fibrosarcoma complex (see fibrosarcoma) Feline infectious peritonitis 7.2,21.2 FeLV2.3,2.6,3.8,6.10,7.4-10, 15.6,21.2,21.4,21.5,24.8 FeSV 15.6 Fibroblast 1.2 Fibromatose 15.8, 15.9 Fibrosarcoma 12.8, 15.2, 15.4-10 treatment 15.9-10 true 15.6, 15.8, 15.9 Filaments 4.8 F i e needle aspirate 2.16 Fi~ronil3.2.3.4.3.8.3.10.3.12.3.13-14 . . , ~ i a h(allergy) 11.1 Fistulae 6.6-11,7.6 FIV2.3, 3.8,6.10,7.1,7.2,7.4-10, 15.2,21.2,21.4,21.5,24.8 Flea allergy dermatitis (see F.A.D.) Flea infestation 25.6 Flea allergy 3.10, 10.1, 10.6 (see a1soF.A.D.) anaemia 8.1 biology 8.1-7 cocoon 8.4 control 3.12-14 egg laying 8.2 identification 3.1 1 larva 8.2-4 man 8.1,25.6 pruritus 3.10, 18.4 pupa 8.4 saliva 9.1. 10.1
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Fluconazole 5.8, 5.9, 5.11 Flufenoxuron 3.12,3.13 Fluoxetine 17.9 Follicular cast 2.8 Follicular dysplasia 16.2, 19.2 Food additives 11.1 Food intolerance 11 Footpads 12.4,21.4 Foreign body 6.6, 12.2 Fungal culture 2.15,4.6,4.8,4.10 Fungal mycetoma (dark grain) 5.2 Fusarium spp. 5.1,7.8 Fusobacterium spp. 6.1
G GABA 17.1 Gamma amino butyric system (see GABA) Genetic hypemelanoses 16.6 Genetics of coat 1.6-1.7 Genodematosis 16.1-11,21.2 Geutamycin 6.2, 6.7 Giant cells (dematosis) 7.4 Glomerulonephritis 13.2 Glucagon 14.1 Glutaraldehyde 4.10 Gluten 11.1 Granulomatous panniculitis 4.6, 6.6, 15.6, 15.8, 15.9, 21.4 Griseofulvin 4.9 Grooming 4.2 Ground substance 1.2
H Haemangiopericytoma 15.8 Haemangiosarcoma 15.8 Hair cycle 1.6 examination 19.4 functions 1.8 genetics 1.7 primary 1.4 secondary 1.4 structure 1.4 Hair dysplasia 16.2 Hair follicle 1.4-5, 14.8 Haloperidol 17.9 Havana 2.2,5.9 Hepatic lipidosis 14.2,21.4 Hepatoid glands 1.9 Herpesvirus infection 7.10, 12.8, 18.4,20.2,21.2,21.5 Himalayan2.2, 13.1, 16.1, 16.8 Histamine 17.1 Histiocytes 14.10 Histoplasma capsulatum (see histoplasmosis)
i &tical
Guide mFeline D a ~ t o l o g y
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Histoplasmosis 5.8,7.8,25.2 Homer's syndrome 15.11 House dust mites 10.1 Hyalohyphomycosis 5.1-2 Hydroxyzine (see antihistamines) Hypercalcaemia 15.2 Hyperchylomicronaemia 14.9 Hyperelasticity 16.8 Hyperextensibility 16.8 Hyperkeratosis 16.1 Hypersensitivity (see allergy) Hyperthyroidism 19.4, 19.6 Hypertriglyceridaemia 2.6 Hypoadrenocorticism 3.8, 14.9 Hypomelanoses 16.4-6 Hypopigmentation 16.4 Hyposensitisation (see imunotherapy) Hypothyroidism 9.4, 19.6
IgA 11.2 IgE (allergen specific) 9.4, 10.1, 10.4, 11.6, 18.7, 19.6, 20.4, 21.4 IGR (see insect growth regulators) IL-2 15.10 Imidacloprid 3.12,3.14 Immune complexes 13.2 Immunodeficiency 16.6, 20.2 Immunogenotherapy 15.10 Immunomarking 15.8 Immunomodulators 15.10 Inmunotherapy 9.6, 10.7, 12.9 Insect growth regulators 3.12,3.13 Insulin 14.1 Interferon 15.10 Interleukin (see U 2) Internal ear 16.4 Intradermalskin testing2.16, 9.4, 10.4, 11.6, 12.8, 18.7, 19.6,20.4,21.4 Inverse allergy work-up 12.8 Iridium 15.9 Isotretinoin (see retinoids) Itraconazole4.9-10,5.2,5.4,5.8,5.9,5.10,5.11 Ivermectin 3.1,3.2,3.4,3.8,3.10
J u v ~ hormone N ~ ~ 3.12 Juvenile pustular dermatitis 6.3
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. ,. 27 : Index g6n6ral
K Kanamycin 6.7 Keratinocyte 1.l, 4.2,13.2 Kerion 25.1 Ketoconazole 4.9,5.11, 14.9
L Lamb 11.1 Langerhans' cells 1.2 L-deprenyl 14.9 Lentigines 16.6 Lentigo 2.4 Lentigo simplex 16.6 Leprosy 6.7-8 Lesion distribution 2.3,2.9-12 Lesions 2.3-8 Leucotrichia 16.4 Leucotrienes 17.1 Lice (see pediculosis) Lichenification 2.6 ' Licking 17.2 Lime sulphur 4.9 Licomycin 6.2 Lipid 14.9 Liver 14.1 Lufenuron 3.12 Lupus, discoid (DLE) aetiopathogenesis 13.2 and demodicosis 3.8 clinical features 13.2 diagnosis 13.4 treatment 13.6 Lupus, systemic (SLE) 20.2 aetiopathogenesis 13.2 clinical featuresl3.2 diagnosis 13.6 treatment 13.7 Lymphocyte atopy 10.1 CD4t 10.1, 15.12 CD8t 14.4 Th2 10.1 Lymphocytic mural folliculitis 2.6, 14.6-8 Lymphosarcoma 12.8 LYST 16.6
Macroconidia 4.8 Macule 2.4 Maculera spp. 5.1 Maine Coon 1.6 Malassezia spp. 1.9,2.8,6.4, 14.4,23.1
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Malignant fibrous bistiocytoma 15.6, 15.8, 15.9 Mange (see Notoedres cati and Sarcoptes scabiei) MAO-B 17.9 Marbofloxacin 6.2,6.3,6.4 Mast cells 12.1, 15.10, 16.10 Mast cell tumour 12.8, 15.10-11,22.8,23.1 Mechanoreceptors 1.9 Medlar bodies 5.2 Meeestrol acetate 9.6, 10.7, 12.9, 14.2, 14.9, 17.8,21.4 Meianin 1.7, 16.2, 16.4 Melanocytes 1.2, 16.4 Melanoma 15.12 Melanosomes 16.2, 16.6 Merkel cells 1.2, 1.9 Metastasis 6.4, 12.8, 15.12,21.4 Methoprene 3.12,3.13 Methylprednisolone (see corticosteroids) Metronidazole 11.6 Metyrapone 14.9 Miconazole 4.10 Micrococcus spp. 1.9 Microconidia 4.8 Microsporum canis4.1-11, 1.9,7.8, 19.2,25.1 Microsporum gypseum 4.1,4.8 Microsporum persicolor 4.8 Milbemycin 3.8 Miliarv dermatitis 2.4, 3.2, 3.4, 3.10,6.2,9.1, 11.2, 18.6 Milk (intolerance, allergy) 11.1 Minocycline 6.2 Mites (house dust) 10.1 Mites (storage) 11.1 Mitoxantrone 15.2 Moniliella spp. 5.1,7.8 Monoamine oxidase inhibitor (see MAO-B) Morpbea 2.6 Morphine antagonist 17.10 Mortierella spp. 5.1,7.8 Mosquitoes (see allergy) Mucormycosis 5.1-2 Mupirocin 6.6 Mvcobacterial infection 6.6-7, 7.8, 12.8, 21.2, 22.8, 25.4 Mycobacterium (see mycobacterial infection) Mycosis fungoides (see epitheliotropic T cell lymphoma) Myoglobinuria 14.6
N Nails 17.2, 17.4, 24.6-8 Neotrombicula (see Trombicula) Neurodermatosis (see behavioural disorders) Neurofibrosarcoma 15.8 Neuroleptics 17.8, 17.9 Neuromediators 17.1 Nitenpyram 3.12 Nits (see pediculosis) Nocardia asteroides (nocardiosis)
www.vet4arab.co.cc 27 : Index g6n61al
Nocardiosis 6.8, 7.8 Noradrenalin 17.1 Norwegian Forest 1.6, 1.8 Notoedrescati2.2,3.1,3.6,7.8,12.2, 12.8, 13.4,21.2,25.6
0p'-DDD 14.9 Obesity 17.4, 17.8 Odontoclastic resorption 7.6 Onychomadesis 16.8,24.8 Onychomycosis 24.8 Onychophagia 17.2, 17.4,24.8 Opportunistic infections 22.8 Organophosphates 3.1,3.12 Osteoporosis 16.2 Osteosarcoma 15.8 Otitis 3.2,3.8, 10.2, 11.2, 14.6, 15.11, 16.1,22.1-8 Otodectes cynotis 3.6, 10.1 (see also Otodectes infestation) Otodectes infestation 2.2, 3.2, 12.2, 18.2, 18.4, 19.6,20.2,20.4,21.2,25.6 Oxacillin, 6.2
Pacinian corpuscle 1.9 Paecilomyces spp. 5.1,7.8 Palate 12.2 Palissading granuloma 12.6 Papilloma 7.2 Papillomatosis 16.1 Papillomavirus infection 7.2-3, 15.2 papule 2.4 Paraneoplastic exfoliative dermatitis 2.6, 14.4-6 ~aron~chia6.3-4,7.6,7.8, 16.2, 17.4,24.8 Pasteurella spp. 6.1, 6.3 Pediculosis 3.10, 18.4 Pemphigus erythematosus aetiopathogenesis 13.1 clinical features 13.2 diagnosis 13.4,24.8 treatment 13.6 Pemphigus foliaceus 6.4, 12.8,22.8 aetiopathogenesis 13.1 clinical features 13.2 diagnosis 13.4, 24.8 treatment 13.6 Pemphigus vulgaris 2.4, 12.8,21.4 aetiopathogenesis 13.2 clinical features 13.2 diagnosis 13.4 Penicillim 6.2,6.10 Peptides 17.1
A Weal Guide m Feli11eh a t o l o g y
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Perianal glands 1.7 permet& 3.12,3.13 Persian 1.6.. 2.2,. 3.4.. 3.8.4.4,4.10,5.8,7.2, 16.1, 16.8, 18.2, 18.4, 20.2,23.1 pH 1.10 Phaeohyphomycosis 5.1-2 Phaeomelanin 1.7 Pheromone therapy 17.10 Pheromones 17.10 Phialophora spp. 5.1,7.8 Phototherapy 15.2 Piebaldism 16.4 Pigmentation 1.7, 16.4 Pili torti 16.2, 19.2 Piproxifen 3.12,3.13 Plakoglobin 13.1 Plaque 2.8 Plasma cell chondritis 7.6 Plasma cell pododermatitis 7.6,21.4,24.8 Plasma cell stomatitis 7.6, 12.8 Pododematitis 10.2, 11.2, 16.2,24.1-8 Polyarthritis 13.2 Polyphagia 19.4 Polyuria-polydipsia 14.8, 19.4 Porphyromonas spp. 7.6 Potassium hydroxide 4.4 Potassium iodide 5.4 Potassium monoperoxysulphate 4.10 Potentiated sulphonamides 6.3,6.7, 13.1 Poxvirus infection 7.1-2, 12.8, 18.4,20.4,21.2,21.4,25.4 Prednisolone (see corticosteroids) Profiles for dermatological examination 2.10 Progestagens 17.8 Pro-opiomelanocortin 17.1 Propranolol 17.9 Proteases 17.1 Proteus spp. 1.9,6.10,7.8 Proton therapy 15.2 Pruritus 4.2, 9.1, 10.2, 11.2, 17.1, 20.2 hehavioural disorders 17.1 diagnosis 2.3, 18.1-7 face(andneck)3.1,3.2,3.4, 18.6, 17.4, 11.2,23.1-6 paraneoplastic 14.6 Pseudomonas spp. 1.9,6.10,7.8 Pseudopelade 19.6 Psychiatric (see behavioural disorders) Psoriasiform (scale) 2.6 Ptyalism 17.4 Pulex irritans 3.10-11,8.2 Putpura 2.4 Pus 6.1, 6.4, 6.10 Pustule 13.4 Pyodema 6.2-7,7.8,21.4 Pvothorax 6.8 &exia 12.4 Pythiosis (see Pythium insidiosum) Pythium insidiosum 5.1,7.8 F$iriasifom (scale) 2.6
www.vet4arab.co.cc 27 : Index g6neral
Radiography of the lungs 14.2, 14.6 Radiotherapy 15.2, 15.9-10, 15.11 Resistance (antimicrobial) 6.3 Reticulin fibres 1.2 Retinoids6.6, 15.2, 15.12, 16.1 Retrovirus 15.2. 15.6 Retrovirus infection (see FeLV and FIV) Rex 2.2, 18.2, 19.2, 16.2, 16.10 Rhabdomyosarcoma 15.8 Rhizomucor spp. 5.1,7.8 Rhodotorula spp. 7.8 Rifampicin 6.2 Rotb's flag method 2.15
S Sabouraud's medium 2.15,4.6 Sarcoma myofibroblastic 15.8 undifferentiated 15.8, 15.9 Sarcoptes scabiei 3.2,3.6 Scale 2.6 Sclerosis 2.6 Scolecobasidium spp. 5.1,7.8 Scotch test (see tape strip) Scratch 5.4, 6.1 Sebaceous pseudo-adenitis 14.6 Sebaceous glands 1.7,6.4, 14.8, 16.2 Seborrhoea 3.8, 16.1 Sebum 1.7 Selamectin 3.2 Selegiline 17.9 Self-mutilation 17.4, 17.6, 21.2 Serotonin 17.1, 17.2, 17.9 Shampoo 6.3,6.6 Siamese2.2,3.8,5.4,5.6, 19.2, 11.2, 15.10, 16.2, 16.4, 17.1,23.1,24.8 Skin biopsy 2.16 Skin hyperfragility 14.2-4, 14.8 Skin scraping 2.14 Skin smears 2.16 Skin test (see intradermal testing) Smallpox 25.4 Sodium polyborate 3.13 Solar dermatosis 15.1, 20.4, 21.2, 21.4 Somatostatin 14.1 Sphinx 2.2, 16.10, 18.2,23.1 Spilopsyllus cuniculi 3.10-11 Splendore-Hoeppli reaction 6.10,6.11 Spores 4.1 Sporothrix schenckii (see sporotrichosis) Sporotrichosis 5.4,7.8,25.2 Squamous cell carcinoma 7.10, 12.8, 15.1-3,21.4,22.8 Squamous cell carcinoma in situ 7.10, 15.2 Staining techniques 2.15,4.6 Staphylococcus spp. 1.9,6.2,6.3,6.10,7.8,23.1
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Weal Guide to RhDamatology
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Stemphyllium spp. 5.1,7.8 Stereotypic behaviour 17.1, 17.2 Stomatitis 12.2 Streptococcus spp. 1.9,6.3,6.10,7.8 Subcutaneous mycosis 5.1-2,7.6, 12.8 Substance P 17.1 Sulphadiazine 6.2,6.3, 12.9 Sulphamethoxazole, 6.3,6.2 Sulpiride 17.9 Sun 4.2 Superficial uecrolytic dermatitis 14.2 Supracaudal organ 1.7 Surface hydrolipid film 1.7, 1.9 Sweat glands 1.7, 15.11, 16.2 Systemic disease (dermatological manifestations of) 2.3, 14.1-10 Systemicmycosis5.4-11,7.6, 12.8,21.2,21.4,22.8
T I
Tabby 1.7 Tachycardia 17.4 Tachypnoea 17.4 Tape strip 2.14 Telogen effluvium 14.2, 19.6 Tetracycline 6.2, 6.7 Thrombocytopenia 2.4 Thymoma 14.4,20.2 Tongue 12.2 Topical corticosteroids 13.1 Toxocara cati 10.2 Transferrin 1.9 Transmission2.2, 3.4,4.6,4.11, 19.2, 18.4,20.2,25.1-7 Tretinoin 6.6 Triamcinolone 10.6 Trichorrexis nodosa 19.6 Trichogram 2.12-14J7.8 Trichophyton spp. 4.1,4.8 Trimethoprim 6.2, 12.9 Trioxazine 17.9 Trombicula autumnalis 3.7 (see also trombiculiasis) Trombiculiasis 3.4-8, 18.2 Tuberculosis 25.4 Tumou cutaneous 15.1-14,21.2,21.4 internal 14.1, 14.4 pancreatic 14.2 Turkish Van 1.8 Tympanic membrane 22.1,22.8 Typhus 8.1 Tyrosinase 16.5
www.vet4arab.co.cc 27 : Index gCn6ral
UCCR 14.8 Ulcer 2.6 diagnostic approach 21.1-5 eosinophilic (see indolent) indolent 11.2, 12.2, 12.4, 12.6,21.4 Ultrasound scanning 14.6 Ultraviolet rays 1.8, 13.2 Ungual pads 24.6-8 Urticaria pigmentosa 16.10-11 Urticaria 11.2, 18.2,23.1
Vaccination 10.2, 15.6 Vasculitis 2.4, 7.2, 7.4 Vegetations 2.6 Vermcosities 2.6 Vesicle 2.4 Rmentin 15.8 Vicristine 15.11 Vitiligo 2.4, 16.4,23.1 Vomiting 11.2
Waardenburg Syndrome 2.4, 16.4 Whiskers 1.9 Wood's Lamp 2.14,4.4,4.10,25.1
Xanthoma 2.6, 12.8, 14.9
Ziehl-Neelsen stain 6.6 Zoonotic dermatoses 25.1-7
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placncal Gude m k h e Dmaology
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Index of illustrations
A
Abscess 6.5 Acne 6.5 Actinic keratosis 15.3 Actinomycosis 6.9 Adenocarcinoma multicentric sebaceous 2.7 pulmonary 15.13,24.5 Albinism 16.5 Allergy aeroallergens 10.3, 12.3 food2.5, 2.9, 11.3, 11.5, 12.5, 18.5, 21.3, 23.3, 24.3 mosquito bite 12.5, 12.7,18.5, 23.5 Alopecia atrophic 19.3 behavioural disorder 19.3 bilaterally symmetrical 19.3 circumscribed 19.3, 17.5 degenerative mucinous lymphocytic mural folliculitis 23.5 dermatophytosis 2.5,4.3,4.5, 19.3, 19.5, 23.3 generalised 19.3 genetic 16.3, 19.3, 24.3 paraneoplastic 2.5, 14.3, 19.3, 23.5 pediculosis 18.3 psychogenic (see self-induced alopecia) self-induced9.3, 10.3, 10.5, 11.5, 17.3, 17.5, 18.5, 19.3, 19.5 Anxiety 17.3, 17.5,24.7 Atopic dermatitis 2.9,6.5, 10.3, 10.5, 18.5,20.3,23.3,24.3 Atopy (see allergy or atopic dermatitis) Atypical mycobacterial infection 6.5,6.5 Auricular chondritis 7.7
Bartonella 25.5 Behavioural disorders 17.1-1 1 Biopsy (see skin biopsy) Birman 24.3 Blepharitis 3.9,4.3 Botryomycosis 6.9,24.5 Bowen's disease 7.5, 15.5 Brushing 2.13
\
I I I
I
APracticai Guide to Fehw De~i~~&atalogy
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I
C Cancer (see skin tumour) Cat scratch disease 25.5 Cellulitis 3.9 Cerumen 3.3 Cemminoma 15.13 Cheilitis 11.5 Cheyletiella blakei 3.7 Cheyletiellosis (man) 25.5 Cheyletiellosis 3.5, 18.3, 19.5 Chondritis (see auricular chondritis) Coccidioidomycosis 5.7 Collagen 16.9 Comedoues 2.9,6.5 Conjunctivitis 11.3 Contact dermatitis 24.7 Crusts 2.9,20.3 Cryptococcosis 5.5 Ctenocephalides felis felis 8.3,9.5,25.5 Cushine's Syndrome 2.9, 14.7, 19.3,21.3 cutaneous horns 2.7,7.7,24.7 Cyclophosphamide 12.9 Cytology (procedure) 2.17 Cytology 13.5
D.T.M. 2.17 Demodex felis 3.7 Demodex gatoi 3.7 Demodex spp. 3.9, 15.5,23.3 Demodicosis (see Demodex spp.) Depression 17.7 Dermatophytosis (man) 25.5 Dermatophytosis 2.5,2.7,4.3,4.5,4.7, 18.3, 19.3, 19.5,20.3,23.3,24.5 Dermatosparaxis 16.7 Direct examination of ringworm hairs 4.7
Ehlers Danlos syndrome 16.7, 16.9 Elimination diet 11.5 Eosinophilic granuloma 12.5,24.9 Eosinophilic plaque 2.7, 9.3, 9.5, 10.3, 12.3, 18.5,24.3 Epidermal atrophy 2.9, 14.3 Enidermal cellarette 2.7 -rEpidermoid carcinoma (see squamous cell carcinoma) ~ ~ i d e r m o l ~bullosa s i s 16.7 Epitheliotropic lymphoma 2.7, 15.13, 18.3, 19.5, 20.3,23.5 ~iosionsand ul&s-2.9,21.3 Erythema 2.5,4.3 Erythema multiforme 7.9,23.3 --
www.vet4arab.co.cc 28 : Index iconogaphique
Excoriation 2.9
F' E.A.D. (man) 25.5 E.A.D. 2.5,2.9,9.3,9.5, 18.5, 19.3, 19.5, 18.5, 20.3 Face (head andneckpruritus) 3.3, 3.5, 6.5, 10.3, 11.3, 11.5, 17.7, 21.3, 23.3 Felicola subrostratus (see pediculosis) FeLV 6.5,7.5,7.7,21.3,23.5,24.7 Fibrohistiocytoma 15.7 Fibrosarcoma 15.7,24.7 Fistulae 6.5 F N 7.7,21.3,24.9 Flea (see Ctenocephalidesfelis) Follicular casts 2.9 Footpads 5.3, 12.7,24.3,24.7,24.9 Foreign body 12.7 Fungal culture 2.17,4.7
Genodennatoses alopecia universalis 19.3 primary seborrhoea 18.3 Giant cell dermatosis 7.5 Glucagonoma 24.5 Granulomatous panniculitis 21.3
H Hair self-induced alopecia 9.3 trichorrhexis nodosa 19.5 Hepatic lipidosis 14.3 Hereditary hypotrichosis 16.3,24.3 Herpesvirus infection 7.9,21.3,23.3 Histoplasmosis 5.7 Hyperextensibility 16.7 acquired 2.9 cutaneous 14.3 Hyperfragilitiy
A Practical G~lidelnpeline kmatoloev
I
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Idiopathic ulcerative dermatosis 21.3 Indolent ulcer 11.5, 12.3, 12.5, 17.7 Infectious peritonitis (see ELP.) Inhibition (behavioural) 17.3 Insect bite 24.7 Intolerance (see allergy) Inttadermal testing 9.5, 10.5 Iridium 15.7
Keratinocytes 13.5 Kerion 4.5, 25.5
L Laser therapy 12.9 Lentig'ine 16.7 Lentigo simplex 16.7 Leprosy 6.5,6.9 Lice (see pediculosis) Lichenificatiou 2.9 Licking 17.3, 17.7 Linear granuloma 9.5, 12.5 Lips 12.3, 12.7 Lupus erythematosus discoid 2.7, 13.3, 13.5 systemic 13.5 Lymphocytic mural folliculitis 14.7,23.5
Macroconidia 4.7 Macules 2.5 Malassezia 2.9, 10.5 Man (zoonotic lesions) 9.5 Mast cell tumour 15.7,20.3 Mast cells 16.9 Medroxyprogesterone 19.3 Melanin 16.5 Metastasis 24.5 Microsporum canis 2.5,2.7,4.3,4.5,4.7,20.3,23.3,24.5,25.5 ~iliG dermatitis 4.5,9.3, 11.3, 11.5, 18.5,20.3 Morphea 2.9 Mosquito bite hypersensitivity isee allergy) Mycobacterium spp. 6.5,6.5 Mycosis fungoides (see epitbeliotropic lymphoma) Mycosis, subcutaneous 5.3
www.vet4arab.co.cc . 28 : Index iconographique
Nail 17.7 Neotrombicula (see Trombicula) Neurodennatosis (see hehavioural) Nit (Felicola subrostratus) 3.11 Nocardiosis 6.9 Nodules 2.7,4.5,6.9 Notoedres cati 3.3,3.6,25.5 Notoedric mange
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Onychomadesis 13.3 Onychophagia 17.7,24.7 Otitis 3.3,3.9, 10.5, 15.13, 16.3 Otodectes cynotis 3.3,3.6,23.5
P
P.LE 7.5 Palate 12.3,21.3 Pancreatic tumour 14.3 Papillomavi~us7.5 Papules 2.5 Paraneoplastic exfoliative dermatitis 2.7, 14.5 Paronychia 10.5, 13.3,24.3,24.5,24.9 Pasteurella spp. 6.5 Pediculosis 3.9, 18.3 Pemphigus erythematosus 13.3,23.5 Pemphigus foliaceus 2.9, 13.3, 13.5,20.3,23.5,24.3 Perianal erythema 11.5 Persian 3.5,4.3,4.5, 10.5, 16.3, 18.3, 19.3, 19.5, 21.3 Phaeohyphomycosis (see mycosis) Pili torti 16.3-5 Plasma cell 24.9 Plasma cell pododermatitis 7.7, 24.9 Pododermatitis 3.3, 3.5, 5.3, 7.7, 10.5, 11.5, 12-3, 24.3 Poxvirus infection 7.3, 18.5,23.3,24.7,25.5 Pseudopelade 19.5 Purpura 2.5 Pustules 2.5 Pyoderma 6.5,21.3,23.3
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A Weal Guide m Feline kmatology
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R Radiotherapy 12.9, 15.5, 15.7 Rhodotorula infection 24.5
Sabouraud's medium 4.7 Sarcoptes scabiei 3.6 Scale 2.7,4.5 pytiriasiform 2.7 Sclerosis 2.9 Seborrhoea 3.9,4.3,16.3,18.3 Self-mutilation 17.7 Siamese 16.5, 19.3, 19.5,23.3,23.5,24.3 Skin biopsy 2.17 Skin fragility 21.3 Skin scraping 2.13 Skin tumours 15.3, 15.5, 15.7,15.13 Solar dermatosis 15.3, 15.5 Sphinx 16.9, 18.3,19.3 Splendore-Hoeppli reaction 6.9 Spores (Microsporum canis) 4.7 Sporotrichosis 5.3,25.5 Squamous cell carcinoma 15.3 Squamous cell carcinoma in situ 2.5,7.5, 15.5 Stereotypicbehaviour 17.7 Superficial necrolytic dermatitis 24.5
Tape strip 2.13 Thymoma 14.5,20.3 Toxic epidermal necrolysis 24.7 Trichogram 2.13 Trichorrhexis nodosa 19.5 Trombicula autumnalis 3.7 (see also trombiculiasis) Trombiculiasis 3.5
Ulcer 2.9 Urticaria pigmentosa 16.9 Urticaria 18.3
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Vasculitis 7.7,24.5 Vermcosities 2.7 Vitiligo 16.5,23.3,24.3
Waardenburg syndrome 16.5 Wood's Lamp 2.13
Xanthoma 14.7
Ziehl-Neelsen stain 6.5, 6.9
