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Dealing with feline allergic skin disease

Treatment options for the pruritic cat are discussed in the first of a two-part series on the disease

17 September 2018, at 10:28am

There are several problems in the approach to allergic skin diseases in cats. The first is that it is difficult to make an unequivocal diagnosis of allergy in this species, largely because allergies have not yet been well defined in cats. In dogs, atopic dermatitis has been recognised and well described both clinically and immunologically, whereas in cats, research is at a very early stage.

Clinical manifestations of allergy in cats are not as site-specific as in dogs; for example, a cat scratching the neck may have a flea allergy as well as food allergy, or a cat licking its belly may have a flea allergy, food allergy or atopic dermatitis. To make things even more complicated, in cats there are some clinical manifestations of allergy that may be due to other causes. For example, a “bald belly” may be due to flea allergy or to psychogenic causes, and a linear granuloma may be associated with food allergy or may be hereditary or idiopathic.

Clinical appearance of feline skin allergy

The most frequent clinical signs of allergy in cats are facial pruritus, self-inflicted alopecia, miliary dermatitis, eosinophilic plaque and eosinophilic granuloma.

The eosinophilic granuloma is a well circumscribed, raised, firm, yellow-pink, linear lesion usually located on the caudal thigh (Figure 1). It is generally asymptomatic but can occasionally ulcerate and show pinpoint white foci of necrosis and become pruritic. It may also be located on the chin (Figure 2), paws or oral cavity (Figure 3). The eosinophilic granuloma has been associated with flea-bite allergy, food hypersensitivity, atopic dermatitis, mosquito bites, insect hypersensitivity, genetic predisposition and bacterial and viral infections (calicivirus).

The eosinophilic plaque is a very pruritic, well circumscribed, round to oval, erythematous, oozing, ulcerated plaque, mostly located on the abdomen and medial thighs (Figure 4). It is found in cats of all ages and breeds, and is often associated with flea allergy, atopic dermatitis and food allergy. Occasionally, it occurs together with feline miliary dermatitis. The eosinophilic plaque probably develops due to chronic trauma caused by the cat’s tongue, when licking pruritic areas. A secondary bacterial infection is frequent.

The lip ulcer (former name: indolent ulcer) is a well circumscribed, necrotic ulcer with raised borders located unilaterally or bilaterally on the upper lip (Figure 5). It is usually not painful and has also been associated with allergies.

Miliary dermatitis is characterised by discrete light brown crusts, diffusely distributed on the trunk (Figure 6). The animals are often only mildly pruritic. Miliary dermatitis has been associated with any allergy, but may also, albeit rarely, be associated with a number of other causes, including bacterial infection, dermatophytosis, drug reactions, pemphigus foliaceus and ectoparasites.

Self-induced alopecia

Bilateral symmetric alopecia is almost always self-induced due to licking (less frequently plucking) in cats (Figure 7). The most frequently affected areas are the abdomen, groin and medial thighs. Less frequently, the alopecia can affect the lateral thighs, flanks or forearms. While hair plucking is more frequently associated with psychogenic causes, licking can be induced by pruritus as well as by pain or stress. It is worth remembering that itch is not only due to allergy but can be elicited, albeit less frequently, by parasites, fungi, bacteria and/or yeast, immune-mediated/autoimmune diseases and tumours.

Head and neck pruritus

Cats can cause severe excoriations in the pre- and/or post-auricular skin, face, chin and neck due to scratching with their hindpaws (Figures 8 and 9). Head and neck pruritus is considered a sign of feline allergy – particularly, but not exclusively, a food allergy. Other less frequent causes of head and neck pruritus and lesions are ear mites, demodicosis (particularly Demodex gatoi infestation), pemphigus foliaceus, dermatophytosis and herpes virus infection.

Approach to cats with pruritus and lesions compatible with allergic dermatitis

The approach to cats with signs of allergic disease is essentially based on:

  1. Elimination of parasitic or fungal causes of pruritus.
  2. Identification and treatment of secondary bacterial and/or yeast infections, if present.
  3. Differentiation between adverse reaction to food and environmental allergy, if, after having completed steps 1 and 2, the cat is still showing excessive licking or scratching and/or signs of allergic dermatitis.

Ectoparasites are currently best eliminated with broad spectrum parasiticides, able to kill both fleas and mites (including Notoedres cati, Otodectes cynotis and Cheyletiella spp.), such as selamectin, imidacloprid/moxidectin or fluralaner spot ons. At the same time, in case the lesions are compatible with a dermatophytosis, a fungal culture should be initiated with hairs collected from both the centre and periphery of the lesions.

Bacterial skin infection is not considered to be as frequent in cats as in dogs. Recently, a report of 52 cases of feline superficial bacterial skin infections was published (Yu and Vogelnest, 2012). Interestingly, skin lesions affected the face and the neck in 62 and 37 percent of the cases, respectively, with 92 percent of the animals being pruritic. The authors concluded that in most cases, pyoderma was associated with an underlying allergic disease. This observation underlines the importance of looking for and treating a complicating pyoderma in cases of excoriations due to allergy, as well as looking for and controlling an underlying allergy in cases of feline pyoderma.

Every exudative lesion, particularly if subject to licking by the cat, should be sampled cytologically for the presence of bacteria (and/or Malassezia spp. yeasts).

Neutrophils containing bacteria indicate a real bacterial infection (Figure 10), while absence of neutrophils with large amounts of microorganisms is defined as a “bacterial overgrowth” (Figure 11). Antibiotics can be indicated in cases of eosinophilic plaque, severe excoriations and ulcers (neck lesion), only if cytological examination reveals the presence of intracellular bacteria.

In cases of first occurrence superficial pyoderma caused by cocci (Figure 10), an empiric treatment with amoxicillin/clavulanate 12.5-25 mg/kg q12h or cephalexin 15-30 mg/kg q12h or clindamicin 5-10 mg/kg q12h can be given for two to four weeks, or until one week after complete healing of the lesions. In cases of the presence of rods in the cytological preparation (Figure 12), a bacterial culture and susceptibility test should be performed for the choice of a suitable antibiotic. In cases of bacterial overgrowth or presence of Malassezia spp. yeasts (Figure 13), a topical disinfecting treatment (eg chlorhexidine foam, gel or spray) is usually sufficient. In cases of severe generalised yeast infection, systemic itraconazole (5 mg/kg PO q24h for two weeks) can also be administered. Antimicrobial therapy can be administered concurrently with the previously mentioned antiparasitic therapy.

TABLE 1 Criteria developed by Favrot et al. (2012) for the diagnosis of nonflea-induced hypersensitivity dermatitis: presence of five of the eight criteria gives a 75 percent sensitivity and 76 percent specificity for this diagnosis
TABLE 1 Criteria developed by Favrot et al. (2012) for the diagnosis of nonflea-induced hypersensitivity dermatitis: presence of five of the eight criteria gives a 75 percent sensitivity and 76 percent specificity for this diagnosis

If thanks to antiparasitic (with or without antimicrobial) therapy, pruritus has disappeared, the owner should be advised to continue rigorous flea control permanently. Should pruritus persist after the elimination of skin parasites and pathologic microorganisms, the cat probably suffers from a non-flea-induced hypersensitivity, either due to food or environmental allergens. The recently published criteria for the diagnosis of feline non-flea-induced hypersensitivity dermatitis may aid in the diagnosis of this condition (Table 1) (Favrot et al., 2012).

To differentiate adverse reaction to food from environmental allergy (equivalent to canine atopic dermatitis), an eight-week long dietary elimination trial should be started. This should be rigidly enforced by means of a home cooked or a commercial limited antigen diet containing protein and carbohydrate sources unknown to the pet, or with a hydrolysed food. Care should be taken that the cat does not scavenge scraps from other animals. It may be necessary to stop the cat leaving the house. If the cat is not cured but has improved after eight weeks, continue the food trial for a further two to six weeks to see if resolution occurs. If the food trial is negative or if the cat or owner refuse to participate, the clinician must proceed with the hypothesis that the cat may be suffering from atopic dermatitis.

Intradermal skin testing or serum IgE testing may indicate the allergens responsible for the reaction, but should not be used to diagnose atopic dermatitis, as many healthy cats show positive results (Diesel and DeBoer, 2011). If the test results are positive, allergen-specific immunotherapy (ASIT) can be undertaken with the appropriate allergens, with reported efficacy similar to that of atopic dogs.

In dermatology, as in other disciplines, cats cannot be considered “small dogs”. Cats have specific clinical manifestations, such as the eosinophilic granuloma complex, differential diagnoses and diagnostic and treatment modalities. The latter will be described in a future article dedicated to therapy of feline allergic dermatitis.

Vice-President at The European College of Veterinary Dermatology (ECVD)

Chiara Noli, DVM, Dip ECVD, is a dermatology specialist working in a referral practice in Italy. She lectures around the world, is author of several articles and three textbooks, and is co-editor of Veterinary Allergy. Chiara is currently Vice-President of the ECVD.

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