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Eric GUAGUERE
Pascal PRELAUD
A PRACTICAL GUIDE TO
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.
Area of initial presentation of notoedric
mange: base of the anterior concha1
cartilage. It is from here that samples
should be taken.
"Diagnosis is an art I pursue with passion
Treatment is a chore"
Distribution m a s of notoedric mange
Distribution areas of notoedric mange
Documents pour servir d l'~d@cation d'une Dermatologie Animale.
~d i t ions Vigot, 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 e en Dermatologie des Animaux de Compagnie (GEDAC),
for keeping us motivated
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Our thanks go particularly to :
- 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
- 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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acal Guide 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 the feline 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).
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A Practical Guide to Feline Dermatology 1
Blaise HUBERT
Clinique VCtCrinaire Foch
38, avenue du MarCchal Foch
34500 BCziers - France
Chapter : 24
Ken MASON
Albert Animal Hospital
333 1 Pacific Highway
Springwood 4127 -Australia
Chapter : 12
Catherine MEGE
Clinique V6t6rinaire des Grands Cms
60, avenue du 14 juilllet
21300 Chenove - France
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
Chapter : 4
Ralf S. MUELLER
Department of Clinical Sciences
Colorado State University VTH
Fort Collins - CO 80523 - USA
Chapter : 6
Chiara NOLI
Via Sismondi 62,
20133 - Milano - Italy
Chapter : 1
Translator
PIN Didier
Cabinet de Dermatologie VCt6rinaire
HCliopolis B3 -Avenue de Magudas
33700 Bordeaux-MCrignac - France
Chapter : 2
Pascal PRELAUD
2, me Gay Lussac
44300 Nantes - France
Chapters : 1 0 , 1 1 , 2 3 , 2 4 , 2 6
Maite VERDE
Servicio Dermatologia - Facultad de Veterinaria
C/Miguel Servet, 177
Zaragosa - Espana
Chapter : 25
Margreet VROOM
Veterinaire Specialisten Oisterwijk
Boxtelsebaan 6
5061 VD - Oisterwijk - The Netherlands
Chapter : 9
Ton WILLEMSE
Utrecht University
Faculty of Veterinary Medicine
Department of Clinical Sciences
of Companion Animals
Yalelaan 8
3584 CM - Utrecht - The Netherlands
Chapter : 13
Mark CRAIG
Re-Fur-All Referrals
3 1 Porchester Rd
Newbury, Berks
RG14 7QH
England
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-
SUMMARY OP CONTENTS
I
1 Structure and functions of skinand 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.
1 2 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.
01 3 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.
1 4 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 e ~ mycoses
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.
1 6 Bacterial dermatoses
R. 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.
1 7 Viral dermatoses
E. 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.
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, self-
induced 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), anti-
inflammatory 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
gastrointestinal problems.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~rm the 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 hypersensitivity and 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~oise Delisle - 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 l e i 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 dermo-
epidermal 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.
17 Skin conditions associated with behavioural disorders
Catherine Mege
Sldn conditions associated with behavioural disorders are probably rare hut remain under-
diagnosed 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 t i c approach 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, spontaneously-
appearing 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 '~ ia~nos t i c approach 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.
1 2 4 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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-l 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, the fact 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 a feline 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 in fehne
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~ncipal dermatoses, 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 CD~+. 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 pilo-
sebaceous 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 situatedmainly 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.
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1 : Strucw and functions of sldn and coat
Figure I : I : Normal cot epidermis: note thinness of the epidermis Figure 1 :2: Normalfoofpadepidermis: note thickness of the horny layer
(HE, x 402) (HE, x l w
Figure I : 3 : Intraepidermal mast cells, (+) (Tolu~dlne blue, x 100) Figure 1 : 4 : I n ~ u l w n of a normal hairfoNicle (HE, x 460)
Pigave 1 : 5 : Hairfoll~cle bulb in nnagenphose(HE,x400) Fkure I : 6 : Tr~ctwgmm of 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.
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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~nran corpuscle (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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Isthmus
Diagram 1 : 2 : Schematic diagram of a hair follicle
Cuticle
Medulla
Hair
Apocrine sweat gland \
Dermal papilla
Inner root sheath
Outer root sheath
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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1 : Structure and functions of skin and coat
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
numberof 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 convoluted secretory 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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~~ ~ 1 ~ ; ~.4hctical GuidetoFehe Dermatology I
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_particularly true 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 excessive heat 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 longOne, 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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1 : Structure and functions of skin and coat
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 : 1 l), 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
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).
I 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 Tierischen Haare (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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I F'
D. N. Carlotti - D. Pin
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 arisingfrom
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 1 to 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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1 A h r i c a l Gude to F h e Dermatology I
Persian Dematophytosis
Cheyletiellosis
Histoplasmosis
Lupus erythematosus
Idiopathic facial dermatitis '
Facial interhigo
Hereditary greasy seborrhoea
Congenital hypotrichosis
Chediak-Higashi syndrome '
Dystrophic epidemolysis bullosa '
Exotic Short Hair Hereditary greasy seborrhoea6
Siamese Demodicosis
Self-induced alopecia of behavioural origin
Food intolerance?
Sporotrichosis
Cryptococcosis
Lupus erythematosus
Vitiligo '
Junctional epidetmolysls bullosa
Periocular leucohichia
Histiocytic mastocytoma
Abysinnian Self-induced alopecia of behavioural origin
Blastomycosis
Cryptococcosis
Follicular dysplasia
Havana Blastomycosis
Sphinx Urticaria pigmentosa
Alopecia universalis
Birman Congenital hyponichosis 'I
Burmese Demodicosis
Self-induced alopecia of behavioural origin
Congenital hypotrichosis
Devon Rex Urticaria pigmentosa "
Himalayan 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 t ips 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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2 : Diagnostic approach
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
~~~~~~~~ ~ ~ -
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 scratchingand 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.
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cal Guide
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
superficial dermis '~'~"~''. Papules are classified according to their location: epidermal, follicular,
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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2 : Diagnostic approach
,.:..:
: t Figure 2 : I : Generalisedfacial erythema in a cat with food intolerance Figure 2 : 2 : Localisedpinnal eryihema in a cat with dermarophytosis
caused by Microspomm canis
Figure 2 : 4 :Multiple hypermelanotic macu ... ... - .. ..h pancr~
paraneoplastic alopecia
Figure3 : 6 ; Pal~~~~(Iarpurtoles und papules in a L, ,,,.,,.=, ,.!ergy
dermantb
Figure2 :8 :Dermalp~pu.,, ,., ,.u.iations in a cat with foodiiitolerance
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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, herpesvirus-
associated 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 ',I6 (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 elastinfibres) 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.
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7. . -
2 : Diagnostic approach
Figure 2 : 9 : Eosinophillc plaques lurresy of B. Hubertj
Figure 2 : 11 : Multrple dermal nodules in a cat w ~ t h cryptococcoszs Figure 2 : 12 :Dermal nodules, some of wl... .. ... .....-..., ... J cat
wrth mult~cenrric sebaceous adenocarc~noma
Figure 2 : 13 : Pytiriasiform scale and crust in a cat with Pea allera Figure2 :14: Psoriasiform scale in a cat with cutaneous epitheliorruprr
dermatitis and dermatophytosis caused by ~icrospomm canis 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).
I 2.7
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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&s essential information as many conditions have specific distribution patterns (Table 2 : 4).
~ i w e v e r , these patterns may change as a dermatosis They maialso he modified by
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
Large lesions
nurnmular (coin-shaped)
a
indented
d
annular
0
part-bordered
-., *. C;
linear
1
Very large lesions
lenticular
0
indistinctly bordered
4-4.
& v*- J c'
map-shaped
s
arcifom (ring-shaped)
Q, : '
part-serpiginous
G/ !:-:.:>.: ,.---
rosette-shaped
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2 : Diagnostic app~oach
I
5 ~ - .
Hgure2 : 17 : S:l.ler,~~L( In a COI W I I ~ mbrpbro (cou~lery o fE Bemrgnor,'
I
Figure 2 : 18 : Alr'phy ill a cal hrld idrrqrnrc Oul~ing'r S)ndr~nrs
! . Figure2 : 19 : Erosionsandexcoriations on the pinna o f a cat wirh food Figure2 :20: Extensive ulceration in a cat with acquired hypefra&G,LJ
, intolerance syndrome
Figure2 :22 : Punctate c r m s in a cat wrth m ~ b a r y d e r m t r s associated
fohceus withflea allergy
Figure 2 ; 24 : Cmedonesnnd follicular casts on the chin of a cat with
laferal pinno of a cat with atopic dermatitis Malassezia dermatitis
: * ~msignor, E., Pm. D. BrCar1atti.D. N. I. s d A n i m . P r c t 39.538-54C (1998).
- - -. - I 2.9
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r~ght profile
ventral dorsal
left profile
nght profile left profile
face
nght foreleg nght hmdleg
left foreleg left hmdleg
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FACE
- Ponvirus infection - Indolent ulcer
- Herpesvirus infection - Eosinophilic granuloma
- Herpesvirus associated erythema multiforme
- Papillomavirus infection - Superficial pemphigus
- Pemphigus vulgaris
- Bacterial folliculitis - Bullous pemphigoid
-Bite abscess - Discoid lupus erythematosus, systemic lupus erythematosus
-Acne
- Lepmsy - Cutaneous drug reaction
-Atypical mycobacterial infection -Auricular polychondritis
- Nocardiosis - Pseudopelade
- Actinomycosis - Hereditary epidermolysis bullosa
- Botryomycosis - Vitiligo
- Dermatophytosis -Bums
- Malassezia dermatitis -Frostbite
- Candida albicans dermatosis -Actinic keratoses
- Subcutaneous mycoses -Irritant contact dermatitis
- Sporotrichosis
- Cryptococcosis - Squamous cell carcinoma
- Histoplasmosis - Multicentric squamous cell carcinoma in sifu
- Blastomycosis -Basal cell tumour
- Coccidioidomycosis - Eibrosarcoma complex
- Cutaneous epithelionopic T cell lymphoma
- Notoedric mange - "Mastocytic" mast cell tumour
- Otodectic mange - "Histiocytic" mast cell tumour
- Demodicosis
- Trombiculiasis - Pancreatic paraneoplastic alopecia
- Cheyletiellosis - Paraneoplastic enofoliative dermatitis
- Leishmaniasis - Degenerative mucinous lymphocytic mural folliculitis
- Atopic dermatitis - Skin conditions associated with behavioural disorders
-Food intolerance
- Mosquito bite hypersensitivity
-Allergic contact dermatitis
FOOT
- Ponvirus infection - - Eosinophilic plaque
-Herpesvirus infection - Eosinophilic granuloma
- Calicivirus infection - Pemphigus foliaceus
- Herpesvirus-associated erythema multiforme - Discoid lupus erythematosus, systemic lupus erythematosus
-Bite abscess -Cutaneous drug reaction
- Bacterial paronychia -Plasma cell pododermatitis
-Leprosy
-Atypical mycobacterial infection - Congenital hypotrichosis
- Nocardiosis - Pili torti
- Actinomycosis -Hereditary epidermolysis bullosa
- Botryomycosis - Vitiligo
- Dermatophytosis -Bums
- Malasseiia dermatitis -Frostbite
- Candida albicans dermatosis - Initant contact dermatitis
-Subcutaneous mycoses
- Sporotrichosis - Squamous cell carcinoma
- Cryptococcosis - Trichofolliculoma
- Histoplasmosis - Fibmsarcoma complex
- Blastomycosis -Cutaneous epitheliohopic T cell lymphoma
- Coccidioidomycosis - Digital metastasis of a pulmonary adenocarcinoma
- Trombiculiasis -Pancreatic paraneoplastic alopecia
- Demodicosis - Paraneoplastic exofoliative dermatitis
- Vasculitis - Notoedric mange
- Anahichosomiasis - Degenerative mucinous lymphocytic mural folliculitis
- Leishmaniasis - Xanthomatosis
- Atopic dermatitis
-Food intolerance
-Mosquito bite hypersensitivity
-Allergic contact dermatitis
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Table 2 : 4 : Examples of lesion distribution (continued from previous page)
i
TRUNK
- POXV~NS infection - Pseudopelade
- Herpesvirus-associated erythema multiforme -Cutaneous asthenia
- Dermatophytosis - Hereditary greasy seborrhoea
- Cheyletiellosis - Pancreatic paraneoplastic alopecia
- Otodectic mange - Paraneoplasticexofoliative dermatitis
- Notoedric mange - Hyperadrenocorticism
-Degenerative muchous lymphocytic mural folliculitis
-Flea allergy dermatitis
- Food intolerance - Cutaneous epitheliotropic T cell lymphoma
- Eosinophilic plaques - 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-mutilation of the tail associated with a behavioural disorder
REGION AROUND THE NIPPLES
- Pemphigus foliaceus
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 Figure2 :28 : Tape stnp~pressrng rrunsparent sficky lope onto the skrn
forej%gex The skin scraping should be t a k n m the same d~reetron i.e.
pi-pendwlar to the futd ofsEn
Figure2 :29 : Coat brushing: skin debris is collected onto a large piece Figure 2 : 30 : Coat br
of white paper 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.T Wilkinson)
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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; Allergic dermatitis
distal ends of hairs damaged 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 l a .
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 i.
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.
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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 theother hand, cytoplasmic structures and bacteria stain poorly with
these products 20. Special stains can be used to identify particular cellular structures or micro-
organisms. 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
detailed examination under high power (~1000) . Cytology is indicated in allergic dermatitis,
eosinophilic granuloma complex, pustular, erosive and crusting dermatoses (including auto-
immune 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 r e c t smear I Papules, pustules, vesicles, bullae, nodules and fistulae I
Impression smear Erosions, ulcers, undersurface of crusts
Scraping Erosions, ulcers, undersurface of crusts
Incision Nodules
Fine needle aspirate Nodules
I Swab I Fistulae, buccal lesions, otitis extema I
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
pers icolor . 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 j4.
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.
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.
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2 : Diagnostic approach
. . -.
a microscope slide for staining and microscopical eramination
Figure2 : 35 :Fungal culture using Dermarophyte Test Medium (DTMJ: Figure2 : 36: Sreme toothbrush used to collect skin debris andinocu
the growth offungal colonies is revealed by the change in colour of the sample onto the fungal culture medium
medium from yellow to red (lefr: sterile culture mediwn, centre:
Micmostmr is ill dnnr rolhrw rioht rnntnminnnrol
Figure2 : 5 ) : rungal culture: aplatinum loop is ued to inoculate k i r s Figure 2 : 38 : Roth'sflag method: apiece ofsticky tape is used to remove
at the periphery of the agar a sectionfrom the centre of a colony
Figure 2 : 40 : Skin biopsy using a 6 mm biopsy punch
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1% Practical Guide to Feline Demmlogy 1
REFERENCES
1. Griffin, C. E. in Contemporary Issues in Small Animal Practice (ed Nesbitt, G.H.) (Churchill Livingstone, New York, 1987).
2. Foumer, P. in Techniques diagnostiques ~ I I dermatologie des carnivores (ed Guagukre, BE.) 7-22 (PMCAC Editions, Paris, 1991).
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-Venancib E & 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~etopy Xi (ed Kirk, R.W.) 509512 (Saunders, W.B., Philadelphia, 1992).
24. Alhaidari, Z. in Techniques diagnosh'ques en dermatologie des carnivores (ed Guagukre, E.) 107-1 14 (PMCAC Editions, Paris, 1991).
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Ectoparasitic skin diseases
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 long-
lasting protection '.
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 .
* T?is pmiun is not iieensed for use in ule cat and isponribiiiq for is use falls on ule p-bing veminar, surgeon
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Pradcal Guide to Feline hnatology I
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%0 in 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 spot-
on 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.
r Thk pmdun is not l i d for ue in Ule cat and responsibility for its l l le falh an Ule p-bw v e k m s u 'g a .
rr ms pmdun is no! l i d far his indieation in the cat and m p m i w t j for its u e falls on Ule prertibbg veminq s q u ) ~ ) .
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3 : Ectoparasitic skin diseases
Figure 3 : 1 : Eryrhema and crusting on the face and pinnae of a kitten Figure 3 : 2 :Same cat as in figure 3:l: alopecia and erythema around
with notoedric mange (courteq of 0. Cozette) the elbow (courtesy of 0. CozetteJ
Figure 3 : 3 :Thick crusts on the face andpinnae of a cat with notoedric Figure 3 : 4 : Interdigital crusting in a cat with notoedric ma,
mange (courtesy of J P Pages) (courtesy o fB . Hubert) *
Figure 3 : 5 : Erythemato-ceruminous otitis with dry, blackish cerumen Figure 3 : 6 : Erythema and crusting on the medialpinna of a cat with
in a cat with otodectic mange otodectic mange: skin scrapings demonstrated aduh Otodectes in this
reaion
Figure 3 : 7 :Alopecia, erythema and erosionson the neck of a I F, ... . . . - . - - . . - . - . .- -. -. , ~ n s in a cat with otodectic
otodectic body mange body mnnge
O u a g u i ~ , E.. Hukrf 8. & Delabre, C. Vet Dematol. 3.1-12 (1992).
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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 '.
r mis ~roduci is notl ieend fa we in the car and respnsibfiw fa ia use falls on be ~~bing veteimy sqm.
rr mis pmdun is not licensed for^ indii~tim i n ihe cat a d mmibiIity for i b use falls on the @ b i i vettinary surgeon.
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3 : Ectoparasitic skin diseases
-F
Figure3 : 9 :Pruritus andscaling in a Persian kiifen with cheyletiellosis Figure 3 : 10 : Pruritus and scaling in a Persian cat with cheyleriellosis
(courtesy of Z. Alhaidaril
1
I
Figure 3 : I1 :Erosive, crusting lesions at the base of the pinna in a cat I Figure3 : 12 : Tmmbicula autumnalis larvae in Henry'spocket (courtesy
with hambiculiasis (courtesy of E. Bensignor) of D. Smal)
Figure 3 : 13 : Very pruritic erosive lesions on the neck of a cat with Figure 3 : 14 :Same cat as infgure 3:13: note crusting on the medial
trombiculiasis (courtesy of D. Smal) pinna (courtesy of D. Smnl)
. . .;.. .-
'P.;' Figure 3 : 1.5 : Tmbieula autumnalis lawae in fhe claw fold of a car Figure 3 : 16 : Trombicula autumnalis larvae in the interdigital space of
%. . a, . with trombiculiasis (courtesy ofD. Smd) a cat with trombiculiasis (courtesy of D. Smalj
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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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3 : Ectoparasitic skin diseases
~.
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 identification rests 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~tology Laboratory, Lyon)
Trombicula (Neolrombicula) autumnalis (parasitic larvae)
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
I 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)
-
Prosoma almost as long as Ule opisthosoma.
I Figure 3 : h : Demodex gatoi (~400) (courtesy of D.N. Carlotti)
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A Weal Guide m Feline kmat010gy I
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%0 solution) 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
3.8 I
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3 : Ectoparasitic skin diseases
Figure 3 : 17: C~rrular lesron of erythema and scalrng in a cat w ~ t k ' Figure 3 : 18 : Erythematous and erosrve blepkar rtrs in a cat wrth
dernadicosrs (caused by Demodex gator) 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 of DN. Carlonil
D.N..CarlottiJ
Figure 3 : 21 : Locahsed celluht~s in a wt w ~ t h demodlcosrs 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, eryfhemato- Figure 3 : 24 ; Scoliiig oii tile Iatnvl yi,ma of u cut a'ith pediculuris:
ceruminous otitis (coused by Demodex cati) (courtpsy of D.N. CarloftiJ 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 : i j).
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~des cartis, Puler irritans, Archaeopsylla erinacei (hedgehog flea), Sp~lopsyllus cuniculi
(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~la notlluns~d for use 1" thccatand~ns lb lhv far w falkoa thepnscnbmg vehloary jwgaon
** Thls pmduet a ncd hcensrd far r h miteation m the oat and respaosibd~y far as usc falls on be p-kng vctennar). mrgcon
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.-- 3 : Ectoparasihc skin diseases
Table 3 : 2 : Identification of the principalinsects involved in feline skin disease.
1c:hnlquta J~dgndslyucr zn d:rmaolog~c dcc :lmlvoro, BourJriu P
rrd~tur Guijuirc i: pp 43-Sh .PM(:A(: Edmnn\, Pv~s 1991)
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.
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).
Cfenocepholides felis
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 1 post-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% surface-
acting 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.
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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~mple application 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 in-
contacts). 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 c l i ca l 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-acting products (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-acting products 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 c l i ca l 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 o fpeh 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 substantial zoonotic 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 Trichophyton spp, 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 observationthat long-haired cats aremore susceptible to dermatophytosis. It is obvi&ly more difiicult for a long-
haired 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 merat ion 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'resolve if 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 non-
inflammatory. 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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4 : n-..,.MO phytosis
Fig, I : Erythmatow blepharitis with comedones in a Persian cat Figure 4 : 2 :Peripherally expanding patchof eqthema, scaling and hair
with demtophytosis caused by Microsporum canis loss inn kitten wiik demtophyiosis cawed by Microsporn canis
Figure 4 : 3 : Erythema and alopecia o n the nose of a cat with Figure 4 : 4 :Peripherally expanding area of scaling and alopecia on the
dermatophytosis causedby Microsporum canis. Note that the nasalplanum distal limb of a cat with dermaiopkytosis caused by Minosporn canis
(which hasno hnirfollicl~s) is u&ected (courtesy ofDiV. CarlottiJ
Figure 4 : 5 : Multiple areus of peripherally erpanding hair loss on the Figure 4 : 6 : Localised keratinisation defect in a Persian cat with
distal limb of a cat with dermatophytosis caused by Micmsporn canis dermatopkytosis caused by Microsporn canis
Figure4: 7 : Keratinisationdefect on the tail ofa cat with demtophytosis Figurn 4 : 8 : Keratinisation defect on the tail of a Persian cat with
caused by Microsporn canis dermatophytosis caured by Micmspomm canis
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4 Practical Gude to Feline Drrmatalogy I
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 helpmonitor 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 sterile) is nassed over the cat's bodv andlor clinicallv susnicious lesions. The bristles , u * , , , .
we then stabbed in~o iungal cultuw nwdi3. There are now many comm&ialiy available brmds of fungal
culrurc media (e.g. Sabouraud's Medium 2nd Dermatophyte Test Medium) and $election should be based
on cost, shelf lieand ease of inoculation of the p la t e s~~oo thb~sh fungal cultures are almost impossible
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, 111 a P r ~ ~ l u n car t ~ i r h
d~rnrotophylo!~~ crrur?d by Naosponm c3na
Figure 4 : 10 : Same cat as m fgure 4 9 after cl~ppinping - note the
pny,he& erpanding q f ~ l ~ a h v e larons
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~s eausdby Micrasponwnc&
Figure4 : 15 ; Kerron m ocaf wl thdennato~~sucmrsed~ Minaspamm
canui lcounesy ofDN C@loniI
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 o id a snrwith demmphyrotts caused by
@re 4 : 16 :Nodule in a cat with a mycetomu mused by McmspoNm
OZOIS
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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~ical examination 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~ppmg the 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.
I
Systemic treamzenrls tbe treatment of choice ",".
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 F&E 4 : 18 :Fungal culture of Mi is on S
imr ion in one hair with another healthy hair (~250) (courtesy o f ENV medium. The top surface has a downy buflcoloured appearance
Parasitology Loborntop, Lyon)
F&R 4 : 19 : Fungal culture of Micmspo~m canis on Sabouraud's
medium. The undersurface has a yellow-orange appearance thick echinulate wolh undmade u p ~ f m o n y cells
Figrue 4 : 21 :His .,,.., logy : n,, :,,,;, L..mlint fhe hair ,,, ,,,i
presence of spores around the outside (stained wirh PAS, r250)
Fipre 4: 23 : Histdpafhology ofa kerion : notefunvlculosis with rupture
of the basement membrane of the hair follicle, around an infected hair
kemtrn of o cat w~rh d ~ o p h ~ t o s l s caused by M~cmspom canis,
ossonared with FlV~$echon (statndd wrfh PAS, ~2501
canis : nofe fungal granuloma amund colonies of Microspo~um canis
(stained wifh PRS, ~ 2 5 0 )
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d Guide to Fehe DematoIogy I
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 Hair invasion Microscopic culture morphology
I
MICROSPORUM
GYPSEUM
Ma Mi
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i 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 vey 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 ". Itraconazole appears 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 pel-
0-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 cleaninghas 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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-
c *. : Dermatophytosis
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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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.
L. Ferrer - A. Fondati
Deep mycoses
Subcutaneous mycoses
Aetiopathogenesis
/ Subcutaneous mycoses are rare opportunistic infections caused by the multiplication of ubiquitous
saprophytic soil fungi. They are charactensed by dermal or subcutaneous pyogranulomatous k ions
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 generaAlternana, 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
MucannycosismdhyaEohyphomycosis arerarely descnied in the cat TrEy involve sy~temic signs more
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-grain fungal 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 inf imatory 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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5 : Deep mycoses
Figure 5 : I : Ulcerated nodule on a metacarpal footpad ofa cat with
phueohyphmycos~~ (courfeq ofD 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 : Prgfnenfed fungal 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 Figure 5 : 6 : Ulcers nndcrusrin$ on the face of a cat with spmfr~chom
(courtcq ofGH MullernndD W ScoffJ (courfesy ofG H Muller a d D W S&*
Figure 5 : 7 :Deep ulcerations on the drstal , - ...... Figure 5 : 8 : Sporothnx schenckix urtrucelldnr and extracellukzr,
sporotnchosrs (courtesy 4D.W Scott) cigar-shaped yens& 1-4 pi long (Dg-Qwk siam, x 400) (courtesy of
D w Scott)*
% D W MlUerlr, W H & GnfiiN,C E Mdler & KuL's Smallh~nal DemloIsgy. W1 e&bon (s&rs, WE, Ph~ladolpbfa 1995)
I 5.3
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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 examirration of exudae and histopathological examination 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 k cell 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 side-
effects (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
'even by direct contact with infected tissues or body fluids. ~ G v e s should, therefore, always be wom if
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 s FigaYcS: 10 :Nasal ulcer ina ilomesl~c short hair cotwith crypfococcosis
(couflesy ofB. HuheY (connesy of .4 Hubert)
F
S~amese cat with ctpt~~occosis tr
...., ,;ts as in Figure , . .., @er two months-withb..
?sionsniiw involve the whole of the lateral sideoftheface
Figuw 5 : 13 :'Ulcer on the upper lip @a cat with cr)ptococcosh (couiesy
0fD.W Scott) crypfococcosis
Figure5 : 15 : Fineneedieaspiratefmma lymphnode oftbe! cGrn F~gugure Figure 5 : I6 : Cytology mm-bu.sedb&~ng o f ~ c u neofonnm,
3 14. wcuolatedmocwphages and numerow clusters ofcf)pfococcr (D@- note the th~ck capsule (Indun I& stam, x ION)
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A M c a l Guide to P&e Ihmto10gy I
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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5 : Deep mycoses
Figure 5 : 17 : Uemral gmnalomtuus mu 'rrun ~~lthcn w h ~ ~ h c m he seen Figurr 5 : 18 : Profire numbers uf cryptorocn I+, ~ilihin ihe dermis
. . hrrh no nwrled gramlonrrrulo reuriion m J L ~ I I! ~ i h c~pivcoccoris and
Flt'infeciiun, nore r h ~ rhirkness ofif12 ~-upsak of 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 (Mucicarmine stain, x25Oj (courtesy of J P Magnol)
Figurn 5 : 20 : C~yptococeus nwfonnans m culture -
white colonies (courtesy o fB Hubefl
.
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)
Fig 3 : Difisepyogranulomatous reaction in the dermis withfungal
elementspresent (+), inassociation with histoplarmosis(PASstoin,x100)
Figure 5 : 2 4 : Close-up view ofFigure 5 : 23. Spherules and enhspores
( + j are clearly visible when srained with PAS (PAS stain, x250j
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1 I! Fmobl Guide ro &line Demmlogy
I I
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 always justifies using specialist laboratories
in case of suspicion.
Anaemia and hypercakaemia are often seen in systemic forms.
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5 : Deep mycoses
*
E 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, ~traconazole can inibally be grven in associahon with intravenous
I 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
5 fluconmle (2.5-5 mgkg SID or BID) is an alternative therapy when there is ocular and neurologcal
i mvolvement. Treatment must be contmued for at least two months beyond chnical resolution. Response ? to treatment is usually good when there are pulmonary signs. e
\ I Blastomycosis
rr
f Aetiopathogenesis
I; Blastomycosis is a systemic mycosis caused by the saprophytic dimorphic fungus, Blastomyces
T derma~idis. Tht infective mycelial form of Blastamyces dermatidis lives m sandy, acid soils clam to
E 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 Thedisease canthen be spreadvia thelymphatics and 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 nahd resistance to the disease.
Clinical features
SI@S v a q according to the organ affected. Systemit signs (depresfion, weight loss, respiratory,
neurological and ocular signs) are common ha to log ica l lesionspresent as mdhple ulcerated nodules.
D i o s i s
Diagnosis is based on the history, ptemic (respiratory, neurological and ocular) and sometimes
dermatological signs, cytology, histopathology and fungal dtw.
Cytological and hisfopathologicul examidon 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 amhat ion 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~irgces dermtidis 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 spechlist laboratories in oase
of suspicion.
Serology (ELIMI tasting is m n t l y being ednated and may m the&- be usefnl for c o ~ g the
diagnosis of blastomycosis in tb eat.
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, itraconazole can initially be given m association with intravenous
amphottricin B (0.25-0.5 m a g , three times weekly) unii a combi i~dose of 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 rn present.
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Ractical Guide @ FelineDMnatologyolcgy I
CoccidioidomycosisAetiopathogenesis
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).
www.vet4arab.co.cc
I 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).
www.vet4arab.co.cc
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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.
Bacterial dermatoses
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%;.grive bacilli &u6h a~ Pasteurditz
m~tt~tac&, Frrsabactmua spg,, spimehaetes and &cam-pmitive eoaf, in particular 8-haemolyfis
streprowmi ! Entire males are p & ~ b u m of their ggres%ive qaturs.
Clinical features
Der@a@log&al &s are dh@eteriO.ed by .yastly well+hm$~W ;Urd fluehunt, painful
milings whkh submqudy burst. Bita marks are s o b m visible. A h s ~ s e s do not lomlii in
any one particular pi% although lh@ face, neck $ad l h b s (Fig, 6 : 11 are mmx &ted in dwninant
cats and the tail is a typical skin submhive cats.
Sj&emic &h6su~ha fever? an~rexia~letkargy~ an(i r&onal I y m p W n ~ t h f are almoslinvari&ble.
Diaguasis
Rmmis is a s y and b& an the bistoiy and c h i a d &a$. Cyni1o@cal ex&atim df pup*
ba@&I c u k and antibide &tivity, and saeming Eor retrwiru8e.s an: necessrvy in reeurrent
w,
Treatment
surghl &&wge artdflushing w@ mm6e: s o ? ~ m such Mof6eKidine 10.5%1,
dilute povidoneio$ine a 3% kydr@gm p ~ r i d e , is necessary in the majodty of casm.
S@e& craffjniw~aial &abwH invoIves the use of bm;td m m .;mtibioties for about 10 days.
A6 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 c (libla 6 : 1).
Cmtdan d nmii@&r oftifi.&k, by keeping the cat indwns, may redm tha &eI lh~~d of
ll%lma* '.
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A Weal Guide to %line Dermatology I
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 im 100 000 U I kg SID, BID
Clavulanate-potentiated amoxycillin PO, SC 12.5 to 25 mg I kg BID
Oxacillin PO 11to35mglkgBID
Cephalexin PO 20 mg I kg BID
Cefadroxil Po 20 mg I kg BID
Enmfloxacin PO, SC 5 to 20 mg I kg SID
Marbofloxacin PO 2 t o 5 m g l k g S I D
Clindamycin PO 5.5 mg I kgBID
Lincomycin PO 20 mg / kg BID
Trimethoprim-sulphadiazine PO 15 to 20 mg I kg SID, BID
Trimethoprim-sulphamethoxazole Po 15 to 30 mg I kg SID, BID
Doxycycline PO 5 t o 11 mglkgSID,BID
Minocycline PO 5 to I1 mg I kg SID, BID
Tehacycline Po 10 to 30 mg I kg BID
Gentamicin iv 4 mg I kg SID
Rifampicin PO 10 to 20 mg I kg BID
Clofazimine Po 2-8 mg I kg SID
Dapsone Po 1 mg I kg SID
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. Trimethoprim-
potentiated 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 Racacal Guide to Feline ~ 0 1 0 g y I
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
''.I4. If comedones and follicular casts are present, acne should be considered, whereas if they are
absent, an eosinophilic granulomashould 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.
Muuirocin pel (2%) is effective in the treatment of feline acne ". This eel is used twice dailv for 3-6 -
weeks. ~beiesibns should 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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6 : Bacterial dennatoses
F i p 6 : 1 :Abscess on the distal limb, caused b~ Pastewella multocrda Figure 6 : 2 :Secondary p y o d e m in a cat with atopic d e m n n s
Figb., . , . ...... ~ .,6.. uu..., .-by-, -,.,....- ... - --. ....,. . -, .. .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 Figure 6 : 6 : Same cat ns in Fig. 6 : 5. Multiple draining tracts on fhe
mycobacterial infection caused by Mycobacterium formihim abdomen
Figure 6 : 8 :Atypical mycobacterial infection:pyogranulomn surrounding
composed mainly of neumphils, surmunding visually empry vacuoles (HES a vacuole containing acid-fist bacilli (Ziehl-Neelsen srain, x 1000)
stain: haemntarylin, eosin s o f m x 4W) ( c o w e v of M. Mialot) (courtev of M. Mialof)
8 Ouagu&re, E., Huben, 8. &=labre, C.Vet Dcrmatol. 3 , l - I2 (1992).
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Radical Guide to Feline kmatology I
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
1
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 j. 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 >.
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 examinationof 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 ~ e and 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 I
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 ~ i c a l examination 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 Figure6: 10 :Multiple nodules, becomrngulcerated m a cat with lepr~xy
P IhrkeJ (courtesy of 0. Cozette)
Figure 6 i I 1 :Leprosy. drf fus~, granulomatous dermatitis (many
macmpha$es and grant cells are present) nr a cat w ~ t h feiine 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~gure 6 : 14 : Mulnplefislulous sor es ~n a cat wrth actrnomycosls
Figure6: 15:Drgrtalulce1s wtthyellow grarorns (n a cat wrthbot~omycos~s Fi-6: 16: Botryomycosir:pyogranulomafaus dermatitis, wirhin which
are bacterial colonies surrounded by a Splendore-Hoeppli reaction
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A Pl;lctieal Guide to Felh ~ 1 o g y I
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
(Staphylococcus spp., 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, withinwhich 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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6 : Bacterial dematoses
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 ~ l Medicine 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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'7 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~us infection 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~n abont 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 development of 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 i~S'~". 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 catcolonies. 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, non-
pnuitic, 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~tochemical studies 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 : 3 : Ulcerative, circumscribed, confluent lesions on the
abdomen of a cat withpoxvirus infection
Figure 7 : 2 : Ulcerative lesions on the tip of the tongue of a cat with
~ ~ ~ ~
poxvirus infection
Photo 7 : 4 :Impression smear - note intracytopias :inophilic
inclusion bodies (-+) in the keratinocytes (poxvirus infection) (Dlq
Quik, x 1000)
Figure 7 :5 : Histopathology - note severe hydmpic degeneration of many
keratinacyfes, and introcytoplasmic eosinophilic inclusion bodies in the
keralinocytes (pm'm infection1 I fH&E.x2501 fcouffem of.? De~orcel
Pigure 7: 6 : Histopafhoiogy - note iwacytopiasmic e~sinoPhilic inclusion
baiies in the keratinoqtes (poxvirus infectio) ) (H & E, ~ 4 0 0 ) (courtesy of
F. Degorcel
Figure 7 : 7 . ......, athology - note lntracyfoplasrmc eosmophlhc rnclusron
bmiies m the cells of the fdlrcularouter mot sheath (poxv~rus mfaftronJ (H
& E, x 400) (courtesy of F. Degorce)
Figure 7 : 8 : Paralleleprpedic, mndndndged vlralpartrcles wnh helrcal
symmetq ~harocterrsh'c of 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 wifh feline Figure 7 : 10 : Same caf as infigure 7 : 9 - note skin necrosis around
infectiousperitonitis 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 the face of a cat wth a giant cell Figure 7 : 14 : Same cat as rnfgure 7 . 13 - nofe scalrng and crusting
demalos~s associafed wrth FeLV mnfectmn (courfesy of D.W Scoftj on the trunk (courtesy of D W Scott)
Figure 7 : 15 : H~stopathology - nofe many apoptotic kerafinocyfes
(+j (giant cell dermafosisj (H & E, x 250) (courfesy of D. W Scoff)
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. .
L Raaical Ouide to Feline Dermatology I
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 in the 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 j8. 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 ".
Multicentric bacterial paronychia is very common in retrovirus-positive cats, especially those
that are FIV-positive j'. Stained smears taken from the digital region show several species of
intracellular and extracellular bacteria (cocci and bacilli). The prognosis is often guarded.
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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7 : V I dennatoses
Pipure 7: 17: Ep~dermal horns on a metacarpal foolpad of a cat lnfected
with FeLV
Figure 7 : 18 : H~sfopathology - note e p ~ d m l hyperplasra andthzckness
of the horny lager o f n cut with epidermal horns assoc~ated wrth FeLV
rnfechon (H & E, x 100)
Figure 7 : 19 :Necrosis ~ t h m the 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 h FeLVassocmted
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~ I cat wrth plasma cell
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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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
- Rhodotorulainfection
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
investigate an association between 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~e the local immunodeficiency which allows Demodex cati to multiply locally within tumours lo.
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- 7 : Viral dermatoses
ue 7 :25: Ulcemtive facial lesions in a cat with herpesvim dermatitis Figure 7 : 26: Hisfapathology - note intronuclear inclusion bodies in the
(courtesy 0fD.W. Smtt) keratimytes (+) (herpesvirus dermatitis) (H & $ x 250)
Pigwe 7:27: Hisfdpathology - note inlranuclear inclusion bodies in the Figure 7 : 28 : Histopathology - note markedfollicular necmsis (herpesvirur
kerarinocyres (herpesvirus dermatitis) (H & E, x 250) dermatitis) (H & E, x 250)
Figure 7 : 29 :Erosive lesions of the tongue andpalate of a cat with Figure 7 : 30 : Erythematous, emsiue, facial lesions in a cat suspected
herpesvirus-associated erythema multiforme (courtesy of B.A. Atlee) of having herpesvirus-associated erythema multiforme
Figure 7 : 31 :Same cat as infigure 7 : 30 - e ind ulcerative Figure 7 : 32 :Same cat as in Figures 7 : 30,31 - erythematous, scaling
lesions of the face and neck of a cat with herpesvirus-associated and crusting lesions on the trunk of a cat suspected of having
erythema multiforme herpesvirus-associated erythema muitiforme
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I
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-associated erythema 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
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483 (Saunder;, W B., Philadelphia, 1995).
13. Carney, H. C. I. Vet.Diagn.1nvest. 2,299 (1990).
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18. MillerJr, W H.,Affolter,V., Scott, D. W. & Suter, S. Vet. Dermatol. 3, 177-182 (1992).
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21. Hartmann, K. & Knft, W Revue Mid. Vit. 145, 191-197 (1994).
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39. Mancianti, E, Gianelli, C., Bendinelli, M. & Poli, A. J Vet. Mud. Mycol. 30,257-259 (1992).
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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 thetransmission 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.
Ctenocephalides felis 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 self-
induced 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
Van'ous studies canied out in Europe
in cats.
in the United States are infested mainly
: also show Ctenocephalides felis to be the
with Ctenocephalides felis '".
species most frequently found
Reproduction and host associations
Adult Ctenocephalides felis 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 Ctenocephalides felis. 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. Substantial reduction 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
Ctenocephalides felis 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 : 3 :Several female Cknm
rite subsranrial aniourlt ojfaeces emitted
Figure 8 : 4 : Crenocephalides fells laying eggs on a cat: numerous eggs
are produced m 20 mulures
F~gure8 5 Ctenocephalld uu loid appear ance,pearly-white
and smooth
Figure 8 : 6 : Fii 11 r t q r lawn newly emerged from the egg
24 hours afer hatching) and third stag; larva-(w) (5 days after
hatching)
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 RHis 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 Ctenocephalides felis 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 1 8 . 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 Cterlocephalides felis 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 Ctenocephalides felis 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 l l°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. Ctenocephalides felis 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, Ctenocephalides felis 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.
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8 : The cat flea: applied biology
Search for a host by the adult
Adult Ctenocephalides felis 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. Ctenocephalides felis 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
Ctenocephalides felis 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 Ctenocephalides felis 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 Ctenocephalides felis
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 Ctenocephalides felis 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 Ctenoeephalides felis can survive for 10 days at 3 O C or for 5 days at -l°C.
h u a l recurrence may be connected with the large variety ofhose of Ctenacephalides felis. 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 Ctenocephnlides felis.
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 reproductivecapacity, 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. Hman , 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 Ctenocephalidesfelis felis (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, ~tenocephnlides felis 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 19,1126-1 129 (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).
16. Osbrink, W. L. A. & Rust, M. K. J.Med. Entomol. 21,727-731 (1984). 1
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 Crenocephalides felis felis (Bouchi) in the domiciliary
environment (Ph. D. Dissertation, V i a Polytechnic InstiNte and State University, Blacksburg, Virginia, 1987).
19. S i l ve rn , 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 ve rn , 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 I
I
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 Ctenocephalides felis felis contains numer-
ous allergenic proteins, one of which, a high molecular weight protein, d e s i p a t e d ~ f e l 1, could be a major
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 mecha-
nisms 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 popu-
lation. 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 environ-
mental conditions. Peaks may occur between March and October. However, increased pruritus in win-
ter 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 own-
ers 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 respon-
sive 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 i16.
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 infesta-
tion by Ctenocephalides felis felis ',".
Differential diagnosis
The differential diagnosis of FAD includes all pruritic dermatoses: allergic skin disorders (food intoler-
ance, atovic dermatitis), infestation with Otodectes cynotis, Chqletiella blakei or lice, Felicola subros-
fratus a n d ~ino~nathus'setosus, and also pruritus associated with behavioural disorders. Sometimes, diag-
nosis 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 aller-
gy 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 composi-
tion of whole body extracts, and therefore antigenicity, is variable which poses problems of repro-
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9 : Flea allergy dermatitis
R i p 9 : 1 : Self-induceddDrsolumbar alopecia in a Persian cat with FAD Figure9 :2 :Self-induced dorsolwnbar alopecia i l iaii i papules arepresent
Figure9 : 3: Self-induced alopecia invoivingflonks, abdomen and iater- igure 9 croscoplc examination
oi rliiglis broken hairs (x 100)
Figure 9 : . ~ollm~bar- miliary der-maritis Figure 9 : 6 :Same cat as in figure 9 : 5 - lots of crusts ondj
are present
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 Ctenocephalides felis 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, intra-
dermal 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 need-
ed 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-inflam-
matory 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 adminis-
tration, 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: pyome-
tra, diabetes mellitus, gynecomastia, mammary hyperplasia or adenocarcinoma, polyuria and polydipsia, ohe-
sity, 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~ed fractions or recombinant anti-
gens could, in future, offer new treatment opportunities.
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i 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)
PigtueB :13: Hypersens~. ..., .,the bites of Ctenocephalides fehs fells Figure 9 : 14 :Flea faeces on a PeAra.. .-. ..rth FAD
on the nrms of a child- marry papule ate present (courtesy of R
Rrezruk)
Figure 9 : 15 : Mrcrarcoplc appearance offleo faeces (1 F ..-.. ) : 16 : I n t r a ~ -...... reactions to whole body extracts ,
~ ~ n o c e ~ h a l i d e s felis felis. Note the similar sire of thepositive reaction at20
minutes (erythemafour papule, P) and the positive conml (hismine, Hi
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i Raaid Guide to Peline Dermamlogy I
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 CwrentVeterinary TherapyXII, 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 n , S. 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 Veterinary Dermatology, 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).
l..,
25. Bevier, D., Rose, B. I., Kunkle, G. A. & Mondesire, R. Comp. Cont. Educ. Pract. Vet. 19s. 17-23 (1997). c
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).
www.vet4arab.co.cc
P. Prklaud - 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,
especially Demtophagoides farinae Allergies to human scale, pollens and moulds are muchless
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~y cells 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
Dermatoplragoides farinae - specific IgE do not correlate with results of either intrademal or passive
cutaneous anaphylaxis tests, 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 EVIDENCE AGAINST
EPIDEMIOLOGY
None 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 Similar incidence to that of normal animals livino
in the same surroundings
Incidence of food intolerance Impossible to demonstrate me allergy;
results of challenge often unconvincing.
Inflammatory infiltrate composed of CD4t -
cells producing IL 4 in lesional skin.
THERAPY
Favourable response to immunotherapy Only open studies performed, with variable group sizes;
efficacy not proven to date.
Control of experimentally induced -
asthma with cyclosporin A.
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, accompaniedby 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 U1.
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 ~ e s inn catallergicro home
dust mties
Figure 10 : 5 :Excoriations second zciaiprurirus in an atopic cat
Figare 10 : 4 : Eosinophilic plaques in the axilia in a car allergic to
house dust mites
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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/!I I A M e a l Gude m F h e Dermatology I
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 ~ l regions and
extremities in a cat allergic to house dust mites i
Figure 10 : 13 : Erythematousplaques in the aillae of an atopic cat
Figure 10 : 15 : Uninterpretable innadermal test
Figure 10 : 14 : Malassezia dermatitis secondary to atopic dermatitis
Figure 10 : 16: Positive intradermal test reactions (+) to house dust
mite extracts.
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APDctieal Guide to Feline Lkmatalogy I
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 andthe 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 intramuscular injection 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 anti-
inflammatory 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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c 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~v of choice for lone-term treatment of feline atow 6,m,". The m t ~ l is identical 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 j3. 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.
REFERENCES
1. Rcedy, L. M. MiU4, W. H. & W i s e , T. A l l q i c Skin Disemes ofDogsandCnrs &a, Phiaddphi& 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 (Sanndersz WB.,Phil&elphh 19951.
3. GilW S. &HdheU, B. E W. Vet. I m n ~ L . I m m m o p ~ f h o t 63,235-252 (1998).
4. Giin , S.,Maud, P. & GuaguS~ E. Prd. Mid. Ckk A m Camp 94,15-31(1999).
9, PrQau4 F',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&!unre d~ 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 o & ~ vd. 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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A PracM Guide m Feline tol logy I
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 foodmtolerance have 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 ~ngredients are 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~ommon allergens 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.
A Prackal Gui& lo Feline Demto1ogy I
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
-
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 erythemato-
ceruminous 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 theanimals. Most cases of recurrent
lymphoplasmacytic colitis, c'ommon in cats, seem to be related to food intolerance in this specie^'^.
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Figure 11 : 1 : Faciaiprur
cat with food allergy
11 : Food Intolerance
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 the face
I 113
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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 non-
diagnostic 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 wrrh food allergy (be@
Figure 11 : 10 : Same cat as in Figure 11 : 9 , erythematous
~ o d o d e r m a f i f i s
Figure 11 : I1 :Same cat us in Ft~ures 11 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 wrth foodallergy
Figwe 11 : 15 :Some cat as rnfgure I1 14, eruslons and ulrerafmons
on upper and lower Ips
Figure 11 : 14 :indolent ulcer on the upper lip of a domestic short hair
cat with food allergy (milk)
Fii zme cat as in Figures I1 : 14-l5,3 weeks afer starting
an elimination diet.
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A Practical Guide to Feline Dematology I
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 derived from 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 puttogether 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. Anti-
histamines 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 bi the aggravation of gastrointestinal lesions leading
to exacerbated dermatological signs.
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11 : Food Intolerance
5
i
g REFERENCES
1
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, auto-
immune 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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A Practical Guide to Feline Dermatology I
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 Foreign body reactions
Aeroallergens mite or insect particles
Flea bites Bacterial infections (secondary to allergy)
Mosquito bites Genetic background
Food Parasites
Intestinal parasites Cheyletiella spp.
Otodectes cynotis
Chemicals Notoedres cati
Irritant substances (contact) 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 o fD 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 P ~ e.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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A Pramid Guide to Feline DemtoIogy I
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 mosquito-
free 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.
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12 : Eosinophilic granuloma complex
Figure 12 : 9 : Ulceraied eosinophilic plaques in a cat wlrh a fwd
allergy to lmnb
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 : 11 : Eosinophilic granu ,.....-., -.. -.,..
and thorax (courtesy o f Z Alkaidari)
Figure 12 : 12 : Eosinophilic granuloma (linear) on the lateral forelimb
(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 nosefineluding 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
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12 : Eos~noplul~c granuloma complex
i , figure 12 : 17 : H)pe~rrnririvrg ro mosqu~fo bites: ulcerario~rc on rhe
r no,r (inrl~tding r ~ n i ~ l plankm,, larer~lpitmde and jorelimk
Figure 12 : 19 : Same cat as m figures 12 : 17,18~ m a r k d swellmng @
the fompads
Figrrre 12 : 21 : Hypeisens~f~v~ty io mosquito htes oral eostnoph~lrc
granulomas
FigunM :23 : Histopafholog~cal section ofan eosrrwphrlic granuloma'
note central collagenolys~s flanked mmocMphages artaged in a
pdrsade (pal~sad~ng granuloma) (stainedwlth H a n d E , x 2 0 (covrfesy
o f J P Magml)
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 Hypersensirivitg to mosquifo bites: indolent ulcer and
lingual eosinophilic granulomas
Figure 12 : 22 : Cytolog~nrl smear of an aosimph~lic plaque note that
only arsrnopluls are present (stonred wrth RAL, x 1MO) (courtesy of
DN Carf~flr)
Figure 12 : 24 : Hrslopatholog~cal sectton of a lmgual eosinoph~ltc
granuloma w ~ t h a fragment of rnsect leg (starned w ~ t h H and E, x 200)
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mMh 1 A W e a l Guide to kh DamarmOgy I
-
Tableau 12 : 2 : Differential diagnosis of the different forms of the EGC
Indolent ulcer Oral granulomaslulcers
Squamous cell carcinoma Squamous cell carcinoma
Mast cell tumour Fibrosarcoma
Excessive grooming in lactating queen Lymphosarcoma
Herpesvirus or calicivirus infection Pemphigus vulgaris
Cryptococcosis Plasma cell stomatitis
Vial stomatitis (hevesvirus or calicivirus)
Eosinophilic plaques
Cutaneus epitheliotropic T cell lymphoma Plaques and granulomas of the digits
Mast cell tumor Plasma cell pododermatitis
Squamous cell carcinoma Bite abscess
Cutaneous metastasis of mammary carcinoma Tumours
Demodicosis Contact dermatitis
Poxvirus infection Herpesvirus or calicivirus infection
Subcutaneous mycoses Poxvirus infections
Systemic mycoses
Idiopathic ulcerative dermatosis Mosquito bite hypersensitivity
Mycobacterium infection Dermatophytosis
Chronic abscess Pemphigus foliaceus
Xanthoma 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 ulcerswhich 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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12 : Eosinophilic granuloma complex
t
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 side-
effects 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/Smali h1m1 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@50sbyYear Book, 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. l98.2086-2088 11991).
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 4 5 (1990)
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. Observnfionspersonnelles noapublides (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 auto-
antibodies 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~lection has 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
I
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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t 13 : Auto- i iune 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 - pustules on tke abdomen of a cat wrth
pernphrgus fohaceus
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 Figure 13 : 8 : Crusting on the face and neck m a cat wi . J I ~ lupus
pemphrgus erythemntosus erytkematosus*
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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 ~ustules in 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 generaliseddermatoses.
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Fig~igure 13 : 9 : $mail crusts on lhepinna ofa cat w ~ t h drsco~d 1quS
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~s and 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~s i n p cat wrthsysfem~c lupus eryfhen ......-
(courtesy of 6 Hubert)
* Wilki"s~;T BKueman,l P YILDammol 1,19-M(1989).
Figure 13 : 16 : Smear showing numerous acantholytic keratinocytes
(+j and neutrophils in a cat with pemphigus foliaceus (stained with
D@-Quik, x 250)
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A M c a l Guide m Feline tol logy I
Prognosis-Treatment
Pemphigus
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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i 13 : Auto -mune dermatoses
I El
1 1 :
1 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 in Advances 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-corticotropic hormone (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 dermo-
epidermal 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-specificdermal 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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lil/ 1 A h c t i d Guide to F h e Dmnatology I
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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14 : Dermatological manifestations of systemic diseases
Figure 14 : 1 :Pancreatic paraneoplastic alopecia: note shiny
app;.::..::::: of the skin
Figure 14 : 3 : Pancreatic paraneoplastic alopecia: note shiny Figure 14 : 4 : Pancreatic paraneoplastic alopecia. note almost
appearance of the skin and the presence of black pigmented macules on generalised shiny appearance of the skin
the abdomen
- -
Figure 14 : 5 : Pancreatic paraneoplastic alopecia, note epidermal, Figure 14 : 6 :Pancreatic paraneoplastic alopecia, note pancreatic
follicular and adnexal atrophy (H andE, x 100) (courtesy of T. Olivfyj tumour and hepatic metastases (courtesy of B. Atlee)
Figure 14: 7 :Acquired cutaneous hyperfragility syndrome in a cat with Figure 14 : 8 :Idiopathic acquired cutaneous hyperfragility syndrome,
hepatic lipidosis presentfor several months in a cat which has already had several suture
repairs.
i
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-md Guide rn Fe'ineDmatoIogy
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.
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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! .
L 14 : Dermatological manifestations of systemic diseases
i
Figure 14: 9 : Paran~opla~nc e ~ f ~ l t r r n e drtmanrir norr ayrhema and Figure I4 : 10 : Some i a f or rn Figure 11 9 n6te eqthzmo and rcalmg
nwrkrl i;rI!ng o!! fbefacr ( C O U ~ ~ P I ) . 0 f T Olivry, p,oriastjorm onrbe las~,alpl,lna (Coerfer) ,f 'I. Olllr?
Figwe 14: 11 :Same cat as in Figures 14 : 9 and 14 : 10: note alopecia
andpsoriasiform scaling on the neck (courtesy of T. OlivryJ kyperplasia, dermal lymphoplasmytic infiltration,
keratinocytes and absence of sebaceous glands (cou
Figure 14 : 13 : Paraneoplastic exfoliative dermatitis: thoracic
radiograph (lateral view): note region offluid density w) in front of surgery: note multiple cysts within the tumour (courtesy of T. Olivry and
the heart, suggest in^ a tumour (courtesy of T. Olivry and C. Rivierre) C. Rivierre)
Figure 14. ., . Jame cat as in Figure 14 : 15: resolution of skin lesion?
the face andears, and the v e v inflamedappearance of the skin (courtesy 5 months after surgery (courtesy of T Olivty and C. Rivierre)
of T. OIivq 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 ",I4
(Fig. 14 : 13).
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 l i , and my~glohiiuriae~~.
The differential diagnosis must include all exfoliative dermatoses (cheyletieUosis, dermatophytosis,
allergic dermatitis, cutaneous drug reaction, herpesvirus-associated erythema multifome, auto-
immune dermatoses, lymphocytic folliculitis and epitheliotropic T cell lymphoma).
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 self-
induced 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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14 : Dermatological d e s t a t i o n s of systemic diseases
E!
Figw nphocytic mucinous degenerative mural folliculitis:
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 di f ise 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
Figure 14 : 21 : . ..,..,.,~..,...~.... hyperadrenocorticism: note Figure 14 : 22 : Hyperadrenocorticism in a cat: note skin atrophy and
pendulous abdomen and fruncal alopecia prominent subcutaneous blood vessels (courtesy of D.W. Scott)
tears (acquired cutaneous hypeeagility syndrome) afier iwo days
hospitalisation
* Guagu&n, E., Hubcn. B. & Ihlabre. C. Vli Dermolol. 3. 1-12 (1992).
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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 1b18 and 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, auto-
immune 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'(80-
100%) 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 catz0 since 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
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