Feline atopy is the most common hypersensitivity disorder seen in the cat, after flea bite hypersensitivity. Feline atopy has not been as intensely researched as in the canine, but several similarities exist. Feline IgE has been characterized and is now used in various monoclonal and polyclonal detection systems. Significantly higher levels of IgE specific for D. Farinae has been noted in atopic cats compared to age matched normals.¹ The skin of atopic cats appears to have changes similar to those seen in the skin of atopic dogs and humans: increased numbers of CD1a Langerhans cells, increased numbers of CD4⁺ T and CD8⁺ cells, and higher numbers of IL-4 producing cells.² To date, there are no studies on cutaneous barrier function of atopic cats. The importance of transcutaneous absorption versus inhalation of allergen has not been elucidated. Feline asthma has also been linked to atopy. An association with IgE has been shown and some individuals with experimentally induced disease have also been noted to develop skin disease.³ Affected cats had significantly more individual positive allergen reactions on both IDT and serum IgE testing than did unaffected cats.⁴ The efficacy of rush immunotherapy in an asthma experimental model has been noted.⁵ Responses to immunotherapy in naturally occurring cases have been variable.^6,7

There are many clinical manifestations of atopy in the cat. They include alopecia with or without dermatitis due to self trauma, pruritus directed at and restricted to the head and/or neck, pruritic military dermatitis, eosinophilic plaque, indolent ulcer, eosinophilic granuloma, otitis externa, chin dermatitis, rhinitis, conjunctivitis and asthma. Affected patients may manifest only one or many of these signs.

Secondary bacterial and/or Malassezia infections may contribute significantly to pruritus. In one study, Malassezia was most commonly noted on the face, ventral neck, abdomen and ear canals (in decreasing order of frequency).⁸ The Malassezia-affected lesions were characterized by some degree of alopecia, erythema, greasy adherent brownish scales, increased cerumen, hyperpigmentation, easily plucked hair and follicular casts. A reduction in pruritus was noted in 5 of 7 affected cats, with only azole therapy.⁸

Affected cats commonly have a peripheral eosinophilia and/or basophilia. The histologic examination of pruritus induced and surrounding areas commonly show increased numbers of eosinophils and mast cells. However, these changes are not unique to atopic skin (i.e., similar changes with food sensitivity, flea bite hypersensitivity, mosquito bite hypersensitivity).

Atopy is largely a diagnosis by rule out.

The therapy of feline atopy should always include the documentation and treatment of secondary bacterial or Malassezia infections and concurrent flea infestations. Of note are eosinophilic plaques that may dramatically respond to antibiotic therapy alone. These infections are best defined by cytologic examination.

Because glucocorticoids are generally well tolerated in the cat, they tend to be a cornerstone of therapy for both acute flares of disease and chronic maintenance therapy. However, as the disease becomes more chronic and severe, or the patient has been on glucocorticoids for longer periods of time, it is not uncommon to see a requirement for higher dosages and/or more frequent dosage administration to maintain comfort. Prednisolone is usually started at 1–2 mg/kg/day. Alternatively, methylprednisolone (same dosages as prednisolone), can be used to potentially reduce the incidence and severity of PU/PD. 'Depo' steroids (e.g., methylprednisolone acetate at 4–5 mg/kg or 20 mg/cat) are acceptable for periodic administration (ideally keeping the frequency of administration to less than once every 6–8 weeks). For very severe disease or patients refractory to prednisolone, longer acting, more potent oral dexamethasone (starting at 0.3–0.6 mg/kg/day) or oral triamcinolone acetonide (0.5–0.7 mg/kg/day)may be very beneficial. Emphasis should always be placed on reducing dosages to the least frequent administration possible for longer term maintenance therapy (i.e., every other or every third day). Glucocorticoids are diabetogenic in cats (more problematic with longer acting glucocorticoids) and have been noted to exacerbate congestive heart failure due to associated fluid retention in patients with pre-existing cardiac disease.

Omega three fatty acids benefit approximately 20–30% of cases (some quote 30–50%). Many cats, however, refuse to eat the fatty acids. The trial period is 3 months.

Antihistamines that have been of most benefit are chlorpheniramine (2–4 mg/cat q 12 hrs) or amitriptyline (2.5–5.0 mg/cat q 12–24 hrs). Amitriptyline may cause significant sedation, ataxia and hypersalivation and for this reason, we gradually work up on the dosage (e.g., starting at 2.5 mg once daily) to establish tolerance. Problems with palatability can be addressed by using amitriptyline powder mixed in fish/cod liver oil. Other antihistamines of potential benefit include cetirizine (0.5–1.0 mg/kg or 5 mg/cat), clemastine fumarate (0.34–0.68 mg/cat BID) or cyproheptadine (2 mg/cat BID; commonly causes polyphagia and behavioral effects). The trial period for each antihistamine is 3 weeks.

Hyposensitization has been reported to benefit 60 to 78% of cases.⁹ Testing to determine allergens for inclusion in hyposensitization protocols may either be with intradermal testing or in vitro serology or both. Data from both appear to be associated with relatively similar success rates of hyposensitization.⁹ 'Rush' immunotherapy ('induction phase' of hyposensitization all given in one day; hyposensitization shot given every 30 minutes) has been conducted successfully in cats but, until there has been more experience with this protocol, it should be used with great caution.⁹ Hyposensitization for asthma, when it is the only manifestation of atopy, has shown variable results.^5-7

Oral cyclosporine has been noted to work well in the management of feline atopic dermatitis, benefiting about 70% of patients. Cats are generally treated with 5.0–7 1/2 mg/kg/day. Gastrointestinal absorption of cyclosporine is highly variable in the cat. With daily therapy at these dosages, some cats will achieve trough cyclosporine concentrations that will be immunosuppressive (e.g., > 1000 ng/ml) and, with long term daily therapy, this could predispose to opportunist infections. Measuring trough concentrations should be considered in those individuals who are on long term daily therapy to potentially circumvent this problem. Gastrointestinal upsets (nausea, vomition, inappetence, anorexia, diarrhea) are the most common problems associated with cyclosporine. The upper GI problems may be minimized by slowly working up to the target dose over several days, by giving the cyclosporine with a small amount of food, by stopping cyclosporine until the signs abate, then re-instituting therapy, by freezing the capsule a few hours prior to administration or by administering an anti-emetic (metoclopramide or maropitant). Once it is clear that the cyclosporine is tolerated well (i.e., after 10 or so days), it is given without food to enhance absorption (at least 2 hours before or after feeding). Time to the onset of benefit of cyclosporine therapy is usually 2–4 weeks. It may take 2–3 months to see the maximal benefit. Many patients can be maintained on every other day or twice weekly therapy. Some clinical manifestations of atopy may not respond as well as others (e.g., indolent ulcers being less responsive).¹⁰ In cats seropositive for toxoplasmosis, oocyst shedding is not reactivated by cyclosporine and cats infected with T. gondii prior to CsA administration failed to develop clinical signs after the administration of CsA.¹¹ However, cats without titers (not previously exposed to toxoplasmosis) and with high cyclosporine concentrations may develop fatal infections after exposure. Cats on cyclosporine should not be allowed to hunt and should be fed cooked or processed food. If they do hunt, cyclosporine concentrations should be monitored (e.g., goal for trough concentration < 250 ng/ml). Minimizing therapeutic dosages will hopefully reduce the risk associated with Toxoplasma exposure.

Chlorambucil (usually along with glucocorticoids) has also been shown to be an effective therapy for atopy. The recommended dose is 0.1–0.2 mg/kg q 24 hrs until 75% improvement in clinical signs is noted, then this dose is given every other day. Potential adverse effects include anorexia, vomition, diarrhea, bone marrow suppression and hepatotoxicity (check liver enzymes 2–3 weeks and 4–6 weeks in to therapy; CBC and platelet count every three weeks while on daily therapy; gradually taper off frequency of CBC and platelet rechecks during every other day therapy).

References

1.  Bexley J, et al. Vet Dermatol 2009;20:562–568.

2.  Roosje PJ, et al. Vet Immunol Immunopathol 2004;101:143–151.

3.  Norris Reinero CR, et al. Int Arch Allergy Immunol 2004;35:117–131.

4.  Moriello KA, et al. Vet Dermatol 2007;18,94–100.

5.  Lee-Fowler TM, et al. Vet Immunol Immunopathol 2009;129:49–56.

6.  Prost C. Revue Française d'Allergologie et d'Immunologie Clinique 2008;48:409–413.

7.  Trimmer AM, et al. 20th Proceedings NAVDF. 2006.

8.  Ordeix L, et al. Vet Dermatol 2007;18(5):316–323.

9.  Trimmer AM, et al. Vet Dermatol 2005 16:324–329.

10. Vercelli A, et al. Vet Dermatol 2006;17:201–206

11. Lappin MR. Proceedings NAVDF 2011:14–17.