II Congresso Internacional de Medicina Felina. Anais Palestrante: Dra. Carol S. Foil

Transcription

1 II Congresso Internacional de Medicina Felina Anais Palestrante: Dra. Carol S. Foil

2 Índice Advances in diagnosis and treatment of allergic dermatoses in cats Diagnosis And Treatment Of Feline Autoimmune Skin Disease 3 6 Feline dermatophytosis - recent advances and recommendations for treatment 7 2 Feline Eosinophilic Skin Diseases 10 New Skin Diseases In Cats Nodules, ulcers and draining tracts in the cat: differential diagnosis and clinical features of important causes 11 13

3 Advances in diagnosis and treatment of allergic dermatoses in cats Carol S Foil DVM Dipl ACVD., Professor, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State niversity, Baton Rouge, Louisiana, SA; cfoil@mail.vetmed.lsu.edu INTRODCTION Feline atopic dermatitis has been characterized by specialists since the 1980 s and now is estimated to cause up to 15% of cases of feline pruritic dermatitis. Other forms of cutaneous allergy that are often distinguished from atopy are food allergy and flea allergy. It is becoming more apparent that these are variations on a theme and some would classify all as atopic dermatitis. PATHOGENESIS Atopy could be defined as the tendency to develop excessive IgE antibodies to commonly encountered environmental allergens and the consequent development of hypersensitivity disease. IgE antibody contributes to skin inflammation by several mechanisms: mast cell release, IgE-dependent late phase skin reactions, facilitated allergen presentation by dendritic cells, and IgE auto-reactivity to normal skin proteins have all been described in human and some in canine atopic dermatitis. Even basic cutaneous physiology can be shown to be aberrant in human atopic dermatitis patients, with abnormal cutaneous nerve function and insufficient stratum corneum barrier function both demonstrated. The disease is hereditary in man and a family history of disease has been described in some cats. In man, there may be a personal history of respiratory allergies in patients. This has not been shown to be the case in the cat, although allergic asthma is described. Seldom do cats have both cutaneous and respiratory signs of allergy. The role of aeroallergens such as pollens and mold spores is a subject of debate amongst those who study human atopic dermatitis. The environmental allergens most widely accepted to be important are those elaborated by house dust mites. These and other environmental allergens are thought to penetrate the skin, which is facilitated by an inherently insufficient epidermal barrier. For cats, suspicion of environmental allergen involvement is based on the occurrence of positive intradermal skin test reactions, and the ability to measure allergen-specific antibodies in serum. The are also poorly controlled studies of successful hyposensitization of atopic cats to corroborate the theories on pathogenesis. Much more needs to be investigated! Food allergens play an important role in infants and children with atopic dermatitis. We do recognize food hypersensitivities in cats, mainly by the observation of improvement on novel protein-source diets and relapse upon challenge with original foodstuffs. The exact pathogenesis for diet-influenced skin disease is poorly understood in animals. Immunological studies of allergic cat skin have shown increased numbers of potential antigen-presenting dendritic cells in the dermis and epidermis. In lesional skin of atopic cats, there are more T- cells with both CD4 and CD8 cells demonstrated, and there are more IL-4 positive cells than in controls. There are several ways that feline IgE has been demonstrated to exist, but unfortunately, difficulties in its isolation have meant that widespread availability of anti-ige antibody reagents for in vitro allergy testing is not yet a reality. Now, however, there is a test that utilizes feline IgE receptor assay, allowing serologic allergen-specific IgE titers to be investigated. Also, some subsets of IgG may be important in allergic disease and this is being investigated in cats. The exact role of mast cells in human atopic dermatitis is controversial. Feline mast cells and their role in allergic skin disease have been investigated. Mast cells are the predominant inflammatory cells in the lesional skin of allergic cats. Skin of allergic cats contains increased numbers of mast cells and contains increased levels of histamine. Mast cells are demonstrated to degranulate at the sites of positive skin test reactions in cats skin. Injection of anti-ige antibodies can also be shown to cause wheal and flare and degranulation of mast cells in cats. Cats with allergic skin disease have prominent tissue and blood eosinophilia, which is not a feature of human atopic dermatitis, although eosinophil-derived factors are increased in the skin. The role of eosinophils in allergic dermatitis needs much further study. CLINICAL APPROACH TO FELINE PRRITS Clinical Signs Pruritus is the hallmark of feline allergy. It is recurrent. nlike in the dog, however, there is not a distinctive clinical distribution or lesion type in feline allergy. We speak instead of the feline cutaneous reaction patterns. These are miliary dermatitis (papular eczema), eosinophilic granuloma complex and feline self-inflicted alopecia. I would add feline head and neck pruritus to this list. Combinations of these patterns are possible. Signalment and History There is not a breed or sex predilection. The onset of symptoms is early in life 6 months to 2 years. There are seasonal and nonseasonal patterns. History about pruritus/self inflicted hair loss can be very misleading. Instead of is your cat itchy? one must also ask does your cat lick or groom excessively? Diagnosis Other causes for pruritic dermatitis in the cat must be considered. Parasitic infestations, including Otodectic mange and Demodex gatoi are important considerations. Dermatophytosis should always be considered in feline skin diseases. Mastocytosis and cutaneous lymphosarcoma can have very confusing presentations with pruritus and alopecia. The diagnostic tests proposed will help sort out these differential considerations in addition to helping define allergic dermatitis. Simple Diagnostic Tests Hair Examination (Trichogram) Examination of hairs from an alopecic area can be helpful in several ways. If excessive licking is suspected, the hair shafts are normal from the bulb until the broken end. No tapering is seen. A differential diagnostic consideration in 3

4 pruritic cats is dermatophytosis, in which hair shafts may be distorted as a result of invasion by fungal hyphae and hyphae or spores may be seen within or on hair shafts. (KOH prep). Another is endocrine alopecia in which hairs are essentially normal on trichogram. Skin Scrapes/Scotch Tape Preps/Combing and Fecal Flotation examination Skin scrapings may be helpful in helping with the differntial consideration of parasitic infestation: Cheyletiella, Otodectes, Demodex or Notoedres. The scrapings may not always identify cases of Cheyletiella or Otodectes and scotch tape preps, flea combing and concentration with fecal flotation solutions may be useful. Response to therapy may also be utilized in this consideration (ivermectin, selamectin, lime sulfur rinses). Wood s lamp/fungal Culture Dermatophytosis should always be ruled out in feline skin disease. Examination of the hair with ultraviolet light from a Wood s lamp is easy and inexpensive ( at most 80% of M. canis infections glow positive). A DTM culture is needed todefinitively rule it out. Cytologic Evaluation Cytology of surface exudate and the content of papules or pustules may show the presence of bacteria and neutrophils, which supports a diagnosis of secondary pyoderma that needs to be treated. In other cases, only eosinophils may be seen, suggesting a parasitic or allergic etiology. Trial Therapy If there is purulent exudate, yellow crusting or pustule formation, then a trial of antibiotic therapy along with the protection of an Elizabethan collar should be applied for five to seven days. Trial therapy with modern flea control products is always warranted. Also to be considered is an ivermectin response trial. Ivermectin ug/kg will resolve mite infestations and intestinal parasite hypersensitivities. Some dermatologists will do a trial therapy with Lime sulfur dips to rule out D. gatoi. More Complex/expensive Diagnostic Tests: Allergy testing Intradermal skin testing may be performed to aide in diagnosing flea allergy or atopic disease, and to identify pertinent allergens for hyposensitization therapy. In vitro tests have become available, but accuracy is still questionable. For both types of tests, false positives are possible, as many normal cats have positive tests. The diagnosis of food allergy cannot be made with intradermal testing or in vitro laboratory tests. A hypoallergenic diet trial must be prescribed. In the nited States, commercial diets with potato and novel protein sources such as rabbit and duck or hydrolyzed diets such as feline Z/D from Hill s are most often recommended. If improvement is noted, provocative exposure to the previous diet is required for a definitive diagnosis of food allergy. Diet trials should last for up to ten weeks. If home-cooked diets are used, they should be balanced appropriately. Caution should be exercised, especially in obese cats that can develop hepatic lipidosis while refusing to eat the diet trial food. Skin Biopsy Sample only primary lesions papules, pustules or plaques, that have been protected from the patient s licking with an Elizabethan collar for a few days. Histopathology is essential for diagnosing eosinophilic granuloma and is useful to establish a diagnosis of pyoderma, some genetic causes of alopecia that might be confusing. It may even provide a definitive diagnosis (Demodex, dermatophyte) that has been missed with other methods of testing. The histopathologic findings in miliary dermatitis, eosinophilic plaque and head and neck pruritus cases are all similar with dermal infiltration of mast cells, eosinophils, macrophages and lymphocytes. In excoriated cases, neutrophils are also added to the mix. Flea allergy, food allergy and classical atopy cannot be distinguished histologically. This recommended work-up is extensive. nfortunately, even after a complete work-up, some cases remain undiagnosed. Idiopathic cases are exceedingly difficult to manage. SPECIFIC PRRITIC DERMATOSES OF THE CAT Feline Symmetric Alopecia Self-inflicted Psychogenic alopecia is seen when an initiating stimulus apparently causes excessive grooming and hair loss. Pruritic causes should always be investigated before turning to behavior modification. Flea Allergy The most common cause of miliary dermatitis. Animals only intermittently exposed or exposed later in life have a greater tendency to developing flea allergy. Clinical features: Classic distribution - dorsal lumbar and groin; Ring around the collar distribution; Can be generalized; other presentations include bald - belly syndrome, other symmetrical alopecia patterns; Lesions can be restricted to the signs and consequences of pruritus- erythema, excoriation, lichenification, scale and hair loss. Clinical signs tend to worsen from year to year. Symptoms may be seasonal or constant. Even with continuous exposure, symptoms may wax and wane. Diagnosis of Flea Allergy: Compatible clinical signs; Presence of fleas or flea dirt; Fleas may be few or even absent pruritic animals excessively groom and scratch and effectively remove fleas. Hypersensitive patients only require a few flea bites. Other household animals may be carriers. Recent bathing may have removed the evidence. se flea comb to look for flea dirt (flea feces consisting of dried blood) Intradermal. Response to trial of excellent flea control: imidacloprid q 2 weeks for a while. Flea control for the Cat: Fipronil, Imidacloprid, Lufenuron, nitempyram. Feline Atopy The primary clinical sign is pruritus. Catopy may take the form of symmetrical hair loss instead of obvious self induced trauma as in the dog. Caused by house dust mite, mold and pollen allergens as in the dog Clinical features: Symmetrical alopecia, Miliary Dermatitis, Eosinophilic lcers, Eosinophilic Plaques, Linear Granulomas, Head pruritus Diagnosis of Feline Atopy: Intradermal Skin Testing, IgE receptor testing. Therapy: Avoidance Hard to do!, corticosteroids, antihistamines, Hyposensitization very successful when based on skin testing Food Allergic Dermatitis Allergic responses to ingested allergens may affect the skin, GI tract or rarely the respiratory tract. Sensitization usually takes 2-3 months or longer, so its not a new food. Allergen is usually a protein substance in the diet. Many foods have been implicated, including, beef, milk proteins, fish, poultry and corn. Clinical features: No breed association. Always seen in adult cats. Onset is usually sudden. Cutaneous features are varied. Face and head pruritus is the classic distribution pattern of food allergy. Other manifestations include: miliary dermatitis, eosinophilic plaques or ulcers, symmetrical alopecia. Pruritus and secondary lesions may be generalized. Can mimic any other allergic disease in pattern of pruritus. Pruritus is only partially responsive to corticosteroids. Diagnosis of Feline Food Allergy: Intradermal skin testing not helpful. In Vitro Testing not helpful. One must use a Food allergy elimination diet, composed of ingredients that animal has never ingested. It must be given for a minimum of 8 weeks. If a positive response is seen at the end of the test period, then this should be confirmed with a challenge using the old diet. Symptoms should reappear in 24 hours to 7 days. Feline Demodicosis This is an uncommon, but not rare disease in the cat. Two species 4

5 of mites may cause demodicosis. Demodex cati - follicular mite (deep skin scrapings) and D. gatoi- broad blunted abdomen (superficial skin scrape) found in stratum corneum. The latter is more pruritic and harder to demonstrate on skin scrapings. Clinical features: Localized or generalized disease as in the dog. Alopecia, scaling, macules, erythema, hyperpigmentation. Some cats will have a sparse hair coat, and greasy skin. Can have ceruminous demodectic otitis externa - pruritic. Diagnosis: Skin scrapings - superficial and deep; Multiple sites to differentiate localized from generalized. If generalized D. cati then search for underlying disease (routine blood work +/-FeLV, FIP, FIV, Diabetes etc...) Therapy of Feline Demodicosis Superficial mites seems to be more easily treated. LymDyp -2% lime sulfur - weekly dips. ½ strength Amitraz - monitor for side effects (Anorexia, depression, diarrhea) if cure not achieved and no side effects seen - go to full strength; daily 300 mcg/kg. This perhaps not always successful in D. gatoi. THERAPY OF FELINE PRRITS Fatty Acids Many report that fatty acid therapy is more rewarding in feline allergy than it is in the dog, although no controlled trials have supported these observations. Dose recommendations for GLA/EPA are 500 mg daily. Antihistamines There are no well-controlled trials. Again, more reported efficacy for the cat than the dog is the rule. Most consider chlorpheniramine (2-4 mg QD or BID) to be most effective. Others prefer clemastine, mg daily. Cyproheptadine, 2 mg daily or BID, and hydroxyzine, 0.5 mg/kg BID are recommended, but are less satisfactory owing to behavior changes and excitability being frequent side effects. Behavior Modification Amitriptyline, 5-10 mg daily, fluoexetine 1 mg/kg QD, haloperdol, 1-2 mg daily are used to control symptoms, especially in self-inflicted alopecia.. Glucocorticoids Cats suffer fewer apparent side effects from chronic glucocorticoid usage and these drugs are used more commonly as the total management program in feline allergy. Methylprednisolone acetate is given 4-5 mg/ kg IM. This is used in cats with 1-2 episodes of pruritus yearly or those that cannot be pilled. Prednisolone and prednisone are given 2-4 mg/kg BID then tapered to 5 mg q 48 hrs.. Methylprednisolone oral is used at 80%of this dosage. Triamcinolone tablets are given.3.75 mg /kg QD., tapered to q hrs. Dexamethasone phosphate IV injectable can be given orally at mg.kg QD, tapered to mg q hours.. Side effects of chronic glucocorticoid usage in the cat include, obesity, diabetes mellitus, alopecia, skin fragility and predisposition to infection. Cause Notoedric mange Otodectes infestation Chiggers Demodicosis Lice Spilopsyllus cuniculi Intestinal Parasite allergy Dermatophytosis Bacteria infection Otitis externa Feline acne Food allergy Atopy Flea allergy Arthropod hypersensitivity Drug eruption Contact dermatitis Autoimmune skin disease Eosinophilic plaque Sterile granuloma /pyogranuloma Mast cell tumor Differential Diagnosis for Feline Pruritus Relative Importance R C R R R R C C C R R Comments Scrape Treat (ivermectin) to dx Dx by Hx, Scraping Scrape Scrape, treat to dx Observe the parasite Fecal, treat to dx DTM, Wood s lamp examination Often secondary, cytology, Tx Ear exam., Cytology, Tx If pruritic, consider other cause Trial diet Skin test Response to control, Skin test Skin test, Response to protection History, response to withdrawal Medication may cause Biopsy Biopsy, sually insect allergy Biopsy Biopsy 5

6 Diagnosis And Treatment Of Feline Autoimmune Skin Disease Carol S. Foil DVM Dipl ACVD., Professor, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State niversity, Baton Rouge, Louisiana, SA; All of the autoimmune dermatoses are rare in the cat; pemphigus foliaceous is the most common of them. Other autoimmune skin diseases in the cat are pemphigus vulgaris, pemphigus erythematosus, bullous pemphigoid, cutaneous and systemic lupus erythematosus and vasculitis. Also to be considered as autoimmune dermatoses are alopecia areata and pseudopelade. Most of these are caused by autoantibodies directed against various antigens within the epidermis. In the case of cutaneous lupus and vasculitis, immune-complex disease is involved. In pseudopelade and alopecia areata, there is a lymphocyte attack on the hair follicle. Pemphigus Pemphigus is caused by autoimmune dissolution of the intercellular connections that leads to intraepidermal vesiculation and loss of the epidermis. Various inflammatory events may accompany this, all focused on the epidermis. In some cases, pemphigus can be a form of drug eruption as either drugs or sunlight may trigger the auto-immune events. Some of the specific antigens that are targeted by auto-antibodies in various forms of pemphigus have been identified. These are various desmosomal glucoproteins that serve as intercellular adhesion molecules.. In PF the antigen is desmoglein 1.In PV it is desmoglein 3. These have not been specifically identified in feline cases however. Antibody binding is seen throughout the epidermis in all forms of pemphigus, but intercellular dissolution (acantholysis) occurs in the level of the epidermis where the target antigen predominates as the major adhesion molecule. Thus, PF acantholysis occurs in the upper epidermis and PV at the basal cell layer. There is more dependence on Desmoglein 3 in the mucous membranes, accounting for different distribution of lesions in the two forms, as well. What does it look like? In pemphigus foliaceus, lesions are confined to the skin. Initial localization is often on the dorsum of the nose and the pinnae, or, less commonly, lesions may begin with onychomadesis, paronychia and footpad hyperkeratosis and erosion. There may be creamy exudate in the ungual folds that forms thick crusts. Primary lesions are vesicles and pustules, but these quickly progress to greyish crusts with erosion and collarette formation. Crusts and erosions form around the teats. Lesions may collect into circinate and serpiginous formations on the abdomen. Cats are often febrile and anorexic and pruritus may be pronounced. In pemphigus vulgaris, vesicles and bullae giving way to erosions, ulcers, collarettes and crusts. They develop in the oral cavity and at mucocutaneous junctions. Cats are depressed, anorexic and febrile. In pemphigus erythematosus, lesions resemble those in PF but are confined to sun-exposed skin on the head, and the planum nasale is markedly affected with erosions, ulcers and depigmentation. In PF and PE, sunlight exposure can exacerbate the disease. What is the differential diagnosis? One must consider dermatophytosis and ectoparasite infestation in crusting and scaling feline dermatoses. Notoedric mange can be quite similar. Miliary dermatitis with secondary impetigo may also be similar. How is the diagnosis established? Initial evaluation of cytology of pustule contents may demonstrate characteristic acantholytic cells in a sterile neutrophilic exudate. The ultimate diagnosis depends on histopathologic evaluation. Ideally intact pustules or vesicles should be sampled. Look for a bright erythematous base under crusts where new lesions often develop. The pathologist may choose to evaluate specimens immunohistochemically. CBC often demonstrates a marked mature neutrophilia. How is it treated or managed? In PV, the prognosis is poor, but it is fair for PF and PE. Corticosteroids are the initial treatment of choice. Oral prednisone or prednisolone at 2-4 mg/kg QD will normally induce remission. After remission, tapering to every other day doses at the lowest possible dose should be done slowly. Side effects include induction of diabetes mellitus and cutaneous skin fragility. Alternative or steroid-sparing agents include chlorambucil (0.1 mg/kg QD) with monitoring of CBC; may allow further tapering of prednisone. Chrysotherapy can be used instead of corticosteroids. A test dose of 1 mg/kg IM is given and if there are no side effects noted, then 2 mg/kg weekly IM. In remission, intervals are gradually extended. In PE and PF, sunlight avoidance is necessary. Bullous pemphigoid Antibodies are directed against collagen XVII, which is a major constituent of hemidesmosomes responsible for basal epidermal cell binding to the basement membrane. Loss of this molecule leads to subepidermal clefting. What does it look like? Vesicles, erosions and crusts in the oral cavity, perioral skin and on the pinnae. What is the differential diagnosis? PV, drug eruption, herpes dermatitis, other viral mucositis, plasmalymphocytic gingivitis. How is the diagnosis established? Histopathologic evaluation of primary lesions or edges of fresh erosions. The pathologist may rely on immunhistochemistry in this rare disease as well. How is it treated or managed? Prognosis is difficult to give owing to rarity of the disease in cats. Treatment with prednisone at 2-4 mg/kg daily is reported to be successful in a few cases. Cutaneous Lupus Skin damage in CL results from deposition of immune complexes in the epidermal basement membrane. V light, viral vaccines and genetic factors may be triggering factors. There is also some contribution from damage to vascular basement membrane in CL. What does it look like? In Discoid LE, there is crusting, erosion, erythema and depigmentation affecting the sun-exposed skin of the face and occasionally the footpads. Cats are not systemically ill. In Systemic LE, the clinical presentation is varied. There are systemic symptoms, including fever, anemia, glomerulonephritis, 6

7 polyarthritis, and ulcerative stomatitis, with attendant physical signs. Cats with skin lesions (20%) may have erythema, alopecia, erosions, crusts on the face and feet. Paronychia and onychomadesis may develop. Some will develop vasculitis with acrocyanosis and infarction. What is the differential diagnosis? All facial, pedal, erosive, ulcerative and crusting dermatoses with systemic signs in the case of SLE! For DLE, consider dermatophytosis, herpes dermatitis, mosquito hypersensitivity, pemphigus erythematosus and mycosis fungoides. How is the diagnosis established? Histopathologic evaluation of skin biopsies is very useful.pathologists may utilize immunohistochemical stains. In SLE, ANA may be positive. Also, evaluation of other systemic signs may be useful in both establishing the diagnosis and formulating a prognosis and treatment plan. How is it treated or managed? For DLE, topical corticosteroids and sun avoidance may be sufficient. Doxyclycline, 25 mg per cat once or twice daily may be useful. The treatment should not be worse than the disease, so be cautious with oral corticosteroids. Doses of 2 mg/kg are usually required. For SLE, the various clinical manifestations are managed individually. Prognosis is guarded, in general. Systemic immunosuppressive therapy will control the skin signs but other systemic signs may be difficult to manage. predominate in recovered sites. Pseudopelade has been described as a symmetric alopecia that begins on the face then becomes widespread. Onychomadesis is a consistent finding. What is the differential diagnosis? Dermatophytosis is the major consideration in any alopecic disease of the cat. Also to be considered are demodicosis, geno-alopecias, such as seen in Rex cats, reactions to injectable steroids or vaccine-induced alopecia, self-inflicted alopecias, telogen defluxion and paraneoplastic alopecia. How is the diagnosis established? For both, diagnosis is established by histopathological examination. It is important ot obtain multiple biopsy specimens from advancing edges of newish lesion. The pathologist can then see a peribulbar accumulation of mononuclear inflammatory cells in AA. Chronic lesions are much less diagnostic and may show only an absence of hair follicles. In Pseudopelade, the histopathology is a lymphocytic mural follicluitis with monomuclear cells surrounding the isthmus region of the follicles, with eosinophils and neutrophils admixed. In late lesions, there is atrophic folliculopathy with absence of sebacesou glands. The trichogram can be suggestive in AA, but not pseudopelade, with hairs plucked from the margin of enlarging lesions. One may identify dysplastic and truncated (exclamation point) hairs mixed in with normal telogen hairs. Alopecia areata / psuedopelade Alopecia areata is caused by autoimmune tageting of anagen hair follicles. The disease is both antibody-mediated and directed by lymphocytic attack, at least in dogs and humans. Pseudopelade differs from AA in that the immune attack is directed at the isthmus of the follicle unit rather than at the bulb matrix as in AA. Both are rare diseases in the cat that cause alopecia. What does it look like? AA is characterized by focal or multifocal patches of asymptomatic, non-inflammatory alopecia. Head lesions often predominate In multi-colored animals, dark hair follicles may be preferentially affected, giving a color pattern distribution that mimics color dilution alopecia in dogs. Claws may be affected with brittleness or sloughing. As lesions regress, white hairs often How is it treated or managed? For AA, the prognosis for eventual recovery is fair without treatment. Anecdotally, topical or intralesional corticosteroids (triamcinolone up to 0.6 mg/site; 4 mg maximum dose) or topical tacrolimus (PROTOPIC 0.1% ointment; 30gm = $60) may be effective. In humans with AA, contact sensitizers and V therapy are also used in some cases. In very extensively distributed cases, the prognosis is more guarded. For pseudopelade, no spontaneous remission is reported and all cases have failed to respond to corticosteroids and chlorambucil. There are anecdotal reports of cyclosporine being beneficial and topical tacrolimus may be also, especially if treatment is initiated early in the course of the disease. Feline dermatophytosis - recent advances and recommendations for treatment Carol S. Foil DVM Dipl ACVD., Professor, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State niversity, Baton Rouge, Louisiana, SA; cfoil@mail.vetmed.lsu.edu 7 FIRST RLE: Suspect Dermatophytosis in virtually every cat with skin disease! SECOND RLE: Clinical signs are HIGHLY VARIABLE. Common presentations: Alopecia patchy / focal or generalized; Scale / hyperkeratosis / crusting patchy / focal or generalized ncommon presentations: Miliary dermatitis / pruritus (especially likely after corticosteroid therapy, paradoxically); Granulomatous dermatitis / pseudomycetoma; Onychomycosis Asymptomatic carriers; suspect when: Long-haired breeds come from catteries; Clients (or other cats) have lesions. GRANLOMATOS RINGWORM This problem is seen only in Persians and Himalayans with generalized M. canis dermatophytosis. It is usually one or two subcutaneous masses that often ulcerate or abscess. It can often be treated with excision, but if the ringworm is not cleared, the cats get new lesions. In some cases, owing to multiple lesions or

8 expanding abscessed lesions these have been very resistant to treatment and have proved fatal to affected cats. They will not resolve without excision or debridement. DIAGNOSTIC PROCEDRES: Wood s Lamp: - ltraviolet light filtered through nickel oxide (100- watt lamp is recommended) will cause a tryptophan metabolite of some fungi to emit fluorescent light. M. canis is the only common animal dermatophyte which will produce fluorescence on infected hairs. - Only about half of culture-proven M. canis infections cause fluorescence; thus a negative exam proves nothing. This percentage can be improved if the lamp is warmed properly prior to use, and the lamp is held over the lesion for several minutes. - False positive exams may be made with build-up of medication or sebum on hair shafts. Fungal fluorescence is bright and applegreen. Direct exam of hairs and scales (KOH Trichogram): - examination of carefully plucked hair and scale from suspect lesions for the presence of fungal hyphae and arthrospores. - requires clearing of keratin % KOH, KOH in DMSO, - Negative direct exams are inconclusive. - Technique for direct hair examination: 1. Choose hairs that appear damaged or dirty from the periphery of lesion. Scrape or pluck so as to collect the intrafollicular portion of suspect hairs. 2. Place sample into a large drop of clearing agent and coverslip. 3. Examine on low power for fractured hair shafts with clinging debris and disrupted cuticle. 4. Examine these hairs on high power for hyphae and masses of arthrospores. 5. False positive exams result from confusing melanin granules for spores or from the presence of saprophytic fungi on hairs. Dermatophyte elements are never pigmented. THIRD RLE: Fungal culture IS THE ONLY Definitive Rule-in or Rule-out -This is the diagnostic procedure of choice. Many veterinary dermatologists include fungal culture in their work-up of every inflammatory skin disease of dogs and cats. -Media - Sabouraud s dextrose agar (SDA) is the basic medium. It is modified for more ready distinction between dermatophytes and common saprophytes. - Dermatophyte Test Medium (DTM) is the most commonly used modification of SDA. DTM contains: 1. an antibiotic to inhibit bacterial contamination 2. cycloheximide to inhibit many saprophytic fungi 3. phenol red, a ph indicator. Turns red in alkaline ph. This will allow one to distinguish between a dermatophytic type of metabolism (alkaline by-products) and a saprophytic metabolism (acidic by-products). NOTE: Saprophytes utilize carbohydrates preferentially. However, when these are exhausted in the medium, they will shift to metabolizing nitrogenous substances. At this point, a red color change will occur, giving false + DTM results. Dermatophytes will produce the red color change on the DTM simultaneously with observable growth. Check the DTM for color change daily! -Once positive growth is observed, the fungus should be identified. This is based on fungal morphology - as below -Microsporum canis and M. gypseum are easy to identify. Trichophyton spp. on the other hand are easily confused with non-significant saprophytic species. Technique for stained slide preparations: a.se scotch tape, sticky side out to lift mycelia and spores from the colony. A light touch only is necessary. b.place the tape sticky side down into a drop of Lactophenol Cotton Blue stain on a microscope slide. Coverslip. c.examine spores on high power (400x). d.colonies which are not yet producing spores cannot be identified. Allow to mature (7-14 days) or subculture onto SDA. DTM culture - asymptomatic cat Technique: New toothbrush; brush patient all over for 1 minute. Make toothbrush impression marks all over the surface of the medium - gently. -Any positive culture from a single cat household patient is significant. In a multi-cat household, there can be false positives: The haircoat can be contaminated from infective debris from within the household or from exposure to a truly infected cat. To avoid mis-interpretation, separate all cats to be brush-cultured and bathe each in chlorhexidine shampoo the day before obtaining the brush culture. TREATMENT OF FELINE DERMATOPHYTOSIS Management of the Individual Infected Cat. Topical therapy See Table 1 for Recent Information. -Individual / localized lesions: Choices for therapy: miconazole, clotrimazole, human-use topicals (. ketoconazole, many others); all equally effective. FORTH RLE: Whole body treatments Should be used in all cases. To reduce environmental contamination and human exposure. 8

9 Enilconazole rinses (where available, not labeled for use in cats) has been shown to be the most effective. Miconazole or ketoconazole shampoo, lime sulfur (2 4%), Na hypochlorite (household bleach) 1:20. Miconazole shampoo, in combination with systemic therapy has been shown to hasten resolution. Lime sulfur rinses - every 5 days or so for 4 weeks. About Clipping: We no longer recommend clipping affected cats, unless you are having trouble getting it cleared up. Another argument for clipping is when the cat is newly acquired in the household and there are children at risk who have not yet gotten ringworm from the cat. Then the cat can be clipped all off and bathed immediately and confined IN YOR HOSPITAL for the first few days of therapy, while clean-up is done at home. Clipping can make the cat worse, at first, and also you have to take great precautions when handling the clipped hair (burn it!, or soak in straight bleach overnight.) FIFTH RLE: Systemic therapy is always recommended. Griseofulvin Therapy Microsized tablet size 250 mg; dose range mg/kg divided or given daily; to be given with a fatty meal to enhance and stabilize absorption to be given until brush culture negative twice 2 weeks apart, usually 6 8 weeks Side effects: GI upset, bone marrow suppression (dose-related or idiosyncratic; caution in FIV + animals) Monitor: CBC weekly or q 2 weeks; check immediately if anorexic or depressed or febrile Microsized elixer Grifulvin V 125 mg/5 ml ; dose the same ltramicrosized in PEG Gris-PEG 125, 250; dose range 5 15 mg/ kg; no need to use fatty meal; other usages the same Treatment should be continued until two successive brush cultures are negative, separated by two weeks. The first culture can be taken after 4 6 weeks of therapy. Itraconazole Therapy Sporonox 100 mg capsules; 10 mg/ml oral elixer (cherry flavored) dose range for this usage 5 mg/kg bid 10 mg/kg qd with food Give until culture negative 2 times at 2 week intervals, generally 3 5 weeks Side effects: anorexia, occasionally vomiting; rare liver enzyme elevation Administration of capsules: open capsule and measure out calculated proportion; give in butter or A/D. Can be stored in freezer in butter; no need to monitor liver enzymes routinely, check if anorexia a problem. Each 100 mg capsule costs about $7.00. Treatment should be continued until 2 successive brush cultures are negative, separated by 2 weeks. The first culture can be taken after 3 weeks of itraconazole tx. Pulse Therapy: To reduce expense and inconveninece, has been investigated empirically. se 5 mg/kg daily for 7 days, pause 7 days, treatment 7 days, pause 7 days, treatment 7 days, etc. At the beginning of the last treatment period examine with woods light, and culture (brush culture on DTM). If negative the treatment stops here, if positive continues with new Woods light/culture following two treatment periods. Terbinafine Therapy Manciati M et al Efficacy of oral terbinafine in feline dermatophytosis due to M. canis- J of Feline Medicine and Surgery (1999) 1, Given 30 mg/kg once daily over 2 week period: 92% success. Other use a lower dose and only increase if the case does not resolve.you can also pulse this drug:. After two to four weeks of treatment the frequency of dosing may be reduced to every other day because of the good persistence of the drug in hair and skin. Lufenruon Yair Ben-Ziony & Boaz Arzi. se of Lufenuron for Treating Fungal Infection of Dogs and Cats: 297 Cases ( ) J Am Vet Med Assoc 217[10]: , Nov 15, Lufenuron = PROGRAM; 75mg/kg; for cattery cats: 100mg/kg repeat in 2 weeks; treat all cats. Then go to normal 30mg/kg monthly. Some recommend a lower dose (50 mg/kg) but starting with itraconazole or terbinafine for the first 2 weeks. ENVIRONMENTAL CONTROL For each case, there is an environmental cleanup problem. Recent investigations have shown that many of our previously recommended environmental decontamination recommendations are ineffective and none are effective in an environment heavily contaminated with hair. Current recommendations: 1) very thorough vacumming and cleaning so that no visible hair contamination is present. 2) Then, triple cleansing and disinfecting with stabilized chlorine dioxide or 1:10 household bleach solutions. 3) Discard any fomites that cannot be thoroughly treated. Enilconazole in the form of a spray (Clinafarm Spray, Janssen Pharmaceuticals, Belgium) or fogger (Clinafarm Smoke ) are available in some countries and some data is available to indicate decent efficacy in a M. canis contaminated environment. AGENT Captan powder, shampoo Na hyposulfite (bleach) Lime-Sulfur dips Chlorhexidine shampoo; rinse Povidone Iodine Miconazole Miconazole Clotrimazole Enilconazole Table I. Frequently Recommended Topical Therapy in Dermatophytosis. FORMLATION NOT NOW RECOMMENDED 1:10 in water 2-4% in water NOT NOW RECOMMENDED NOT NOW RECOMMENDED Conofite lotion; cream Dermazol shampoo; Micatin products Lotrim,Veltrim creams Clinafarm, Imaverol FREQENCY 2x/wk 2x/wk 2x/wk 1/wk 1/wk as directed 2x/wk as directed 0.02% as a rinse COMMENTS top. sensitizer, ineffective not on black animals! not on white animals; TOC shown ineffective can be irritating; not in cats; not very effective small lesions newest product; efficacy of shampoo unknown small lesions not approved in the S for use on cat; very effective 9

10 Feline Eosinophilic Skin Diseases Carol S Foil DVM Dipl ACVD., Professor, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State niversity, Baton Rouge, Louisiana, SA; cfoil@mail.vetmed.lsu.edu The eosinophilic skin diseases of the cat comprise a complex because each usually results in eosinophilic inflammation, is often idiopathic or associated with allergy and is initially responsive to corticosteroids. Also, many patients develop more than one of these syndromes either simultaneously or during their lifetime. There are four recognized members of the eosinophilic granuloma complex eosinophilic plaque, indolent ulcer, collagenolytic granuloma and mosquito-bite hypersensitivity syndrome. As more investigation of these entities is accomplished, we receive more evidence that each represents a variation in a spectrum of cutaneous reaction patterns in feline allergy and the most commonly defined etiologies are arthropod hypersensitivities. The eosinophilic plaque is closely related to miliary dermatitis - it might be called pregnant miliary dermatitis and is most often associated with flea allergy. The collagenolytic granuloma is the most well-organized histopathologically; it consists of one or more palisading granulomas organized around flame figures, which are foci of degenerating or necrobiotic collagen overlaid with eosinophilic debris. Atypical eosinophilic dermatitis is the best defined etiologically, being caused by insect hypersensitivity, but overlaps histopathologically with the other forms. The eosinophilic or indolent ulcer is the most non-nondescript histopathologically, but when it occurs in the classical lip location, is the most distinctive clinically. All forms of this syndrome are, at some time during development, eosinophilic and each can develop flame figures. Feline indolent ulcer What does it look like? Also called eosinophilic ulcer, lip ulcer, and rodent ulcer, FI is a common disease. In its typical location, the mucocutaneous junction of the upper lip opposite the upper canine tooth, and uncomplicated by infection, it is very distinctive clinically. The lesions are proliferative and in actuality represent ulcerated plaques, rather than true ulcers. Margins are wellcircumscribed and built up. The ulcer itself is shallow and dishshaped and the surface is covered with salmon-colored granulation tissue, or it may be necrotic and form a central eschar. There is little to no exudate. The lesion seems neither painful nor pruritic. Lesions may also develop elsewhere on the head (or body) especially within the lip margin and at the commissure of the mouth, and on the hard palate. In atypical locations, the syndrome cannot be diagnosed clinically. Lip ulcers may enlarge progressively, cross the mid-line and become quite destructive and disfiguring. How is the diagnosis established? The diagnosis is established by ruling out the possibility of other proliferative ulcerative diseases of this location, especially SCC and cryptococcosis. The diagnosis may be made presumptively or definitively on histopathologic examination by ruling out other possibilities or by the observation of eosinophilic dermatitis and/or flame figures. In some cases. How is it treated or managed? Treatment is straight forward, but may be frustrating. In its early manifestation, the lesions respond to corticosteroids (methylprednisolone acetate, SQ or IM, 20 mg every two weeks until healed) and puzzlingly, may respond to antibiotic therapy. The problem is recurrent however, and may become refractory to treatment, as is the case in other hypersensitivity syndromes. Other forms of treatment include doxycycline (25 mg/cat QD - BID), surgical excision, cryotherapy, laser excision or ablation, chlorambucil ( mg/kg), alphainterferon (300I daily), aurothioglucose (1-2 mg/kg weekly IM), and megestrol acetate (2.5-5 mg QD X 5, then 5 mg weekly). Here is a statement about surgical excision from Keith Thoday at Edinburgh, The technique is very simple. A small scalpel blade is used to produce an ellipse around the edge of the ulcer just into healthy tissue and wedged from either side medially so that all affected tissue is removed, in the same way that an ophthalmologist might treat a case of distichiasis. The edges are then simply sutured together using fine, non-absorbable, simple interrupted sutures close together. If the lesion is bilateral, the procedure is simply repeated on the other side. Amazingly, the sutures are ignored by the cat and I have, in about 10 cases, never had an animal remove one, all wounds healing by first intention and much more rapidly than with medical therapy. The best chance for successful outcome long-term is identification of the underlying etiology. This has proven to be more elusive in many cases of lip ulcer than in the other eosinophilic diseases. Some have been proved to be associated with Flea Allergy, with food allergy and even with atopy by virtue of responding to treatment for these diseases. Others have described these lesions in cats that are parasite free and apparently unaffected by identifiable allergies. It is possible that these and other indoor animals without fleas are exhibiting sensitivity responses to other indoor insect allergens such as cockroaches. Collagenolytic Granuloma Pharyngeal collagenolytic granulomas, like the other entities in the complex, may represent insect hypersensitivity, either as an id reaction or as a local reaction to ingested (and perhaps imbedded) insect parts. There is a young-onset idiopathic familial form as well, that usually shows as linear granulomas on the rear legs or else where on the trunk, and this form may prove to be self-limiting What does it look like? This lesion is variable. It most commonly appears as an eroded to ulcerated circumscribed plaque or nodule and can occur anywhere within the oral pharynx, as a linear plaque on the skin, especially over the popliteal fossa on the hind legs. It may appear as swelling without ulceration around the foot pads, on the chin, the lower lip or the nose. This form is sometimes called the fat lip, fat chin or fat nose syndrome. The collagenolytic granuloma is often seen in cats with other forms of the eosinophilic granuloma complex and responds to specific treatment for identified allergies. How is the diagnosis established? The collagenolytic granuloma is rather distinct clinically, but may be confused with eosinophlic plaque. Some forms of mast cell tumor in cats can be similar. On the chin, nose and feet, it is not clinically distinctive. The definitive 10

11 diagnosis is easily established with skin biopsy. How is it treated or managed? In young cats, the disease is selflimiting, and as it is asymptomatic, it can be ignored. In more persistent or problematic cases it can be manged medically as the indolent ulcer is treated. Cyclosporine A may be useful for refractory or idiopathic cases(50 mg daily to remission then mg every 3 days or so). As in the latter, a work-up for underlying allergy is warranted. Eosinophilic Plaque What does it look like? This disease is best thought of as an exuberant form of miliary dermatitis. The lesions are alopecic, edematous or eroded and bright pink to salmon-colored papules and plaques. Older lesions may be crusted or scaly. Most often they are concentrated on the ventral abdomen, but can appear more widespread on the trunk. They are pruritic. How is the diagnosis established? The work-up is the same as one would do for miliary dermatitis. The most commonly recognized causes are insect hypersensitivities. EP seldom occurs in association with the other entities in the complex, but when it does, there is even greater reason to perform an allergy work-up in the patient. How is it treated or managed? Treatment is as for miliary dermatitis. The lesions respond to corticosteroid therapy (methylprednisolone acetate, SQ or IM, mg as needed or oral prednisone 2 mg/kg QD), but like most manifestations of allergy, are recurrent. Mosquito Hypersensitivity What does it look like? This is also called ears, nose and toes syndrome. This is a distinctive dermatosis and most often noticed because of lesions on the nose. It can develop suddenly and severely or it can be chronic. Primary lesions are papules and plaques or poorly defined swelling of the nose. These changes are associated with alopecia, crusting, erosion, excoriation, ulceration and macular depigmentation. Affected areas include the poorly haired sites on the dorsal muzzle, the pinnae, in front of the ears, around the eyes and the bases of the foot pads. On the ears, lesions are crusted or scaly erythematous papules. On the pads, there is swelling, depigmentation, crusting and scaling. How is the diagnosis established? Histopathologic evaluation helps rule out important differential diagnoses such as Cryptococcosis, squamous cell carcinoma and mast cell tumor. The finding of intense eosinophilic dermatitis in the affected areas is very suggestive of this diagnosis. How is it treated or managed? Mason and Evans have shown that lesions develop at the sites of mosquito bite and that the disease will resolve when the patient is protected from mosquito exposure It remains to be seen whether other biting flies will be implicated in some cases. If the animal cannot be protected from the insects, then the prognosis is guarded. Megestrol acetate or cyclosporine therapy could be tried. New Skin Diseases In Cats Carol S Foil DVM Dipl ACVD., Professor, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State niversity, Baton Rouge, Louisiana, SA; cfoil@mail.vetmed.lsu.edu 11 First the Feline Dermatologic Minimum Data Base Skin scrapes, DTM culture, thorough ear examination to look for ear mites, trial therapy with selamectin for ectoparasites. Mosquito Hypersensitivity This is an eosinophilic dermatitis with a distinctive distribution according to where mosquitoes have access to the skin surface (poorly haired areas). - When to suspect it: Erosive to ulcerative lesions with possible cellulitis on the nose. Papules and crusts on the ear tips and bases of footpads. ( Ears, Nose & Toes ). Cat goes outdoors or mosquitoes have access to the home. - How to begin: Surface cytology to look for complicating bacterial and look for Cryptococcosis. Treat with antibiotics. - How to confirm the dx: Punch biopsies to confirm eosinophilic dermatitis and rule out major ddx: SCC, Cryptococcosis. - How to treat it: Mosquito avoidance. Poor response to glucocorticoids. If cat cannot be confined, try megestrol acetate? Cyclosporine A? (3-5 mg/kg/day), tacrolimus ointment (Protopic)? Demodicosis There are two species of mites causing feline demodicosis, and one is recently named, although it is the more common of the two Demodex gatoi. The mite lives in the superficial layers of the epidermis and its life cycle is not well understood. - When to suspect it: Variable presentation... So, almost always! Alopecia, to pruritic dermatitis to Cutaneous Reaction Patterns. Otitis externa. In Persian cats, may be one cause of facial dermatitis (See below.) Way under-diagnosed, according to some of our Dermatology colleagues. - How to begin: S/S is part of the Derm MDB for this reason, mostly. - How to confirm the dx: Finding on S/S. Two species: D. cati (long, skinny), D. gatoi (short, fat). - How to treat it: Lime Sulfur dips weekly X 6; amitraz (0.25%) every 5 days for 4-6 weeks.daily ivermectin 300 ug/kg; selamectin?? Herpes Dermatitis Syndome that overlaps with classical mucous membrane herpes erosive disease. - When to suspect it: Pruritic ulcerative facial dermatitis concentrated around nose and mouth and poor response to standard TX. History of chronic herpes in cat or in household. - How to begin: Minimum Data Base to rule out other pruritic facial dermatoses. - How to confirm the dx: Skin Biopsies. However, it probably takes an experienced dermatopathologist to work it out and perhaps will require immunohistochemistry or PCR to find evidence of the virus. It is a tough diagnosis. - How to treat it: L-lysine. It comes as a 500 mg tablet; 1/2 tablet QD. Make certain that it is the form WITHOT propylene glycol.