Page 1477 - Clinical Small Animal Internal Medicine

160 Allergic Skin Diseases 1415

in allergic contact dermatitis, which may represent dif- areas if the sensitizer is in liquid, powder or aerosol form.
VetBooks.ir ferences in regulatory mechanisms. The skin lesions are characterized by macules, papules,
and erythema which may progress in chronic cases and
become lichenified, hyperpigmented, and alopecic.
Epidemiology
Secondary bacterial and yeast infections are commonly
A wide range of allergens, such as various plants (e.g., present. Excoriations may also occur due to the associ-
dandelion, Asian jasmine, cedar mulch), cement, plastic ated pruritus. As with other hypersensitivity reactions,
toys and bowls, household cleaners, and topical drugs previous allergen exposure is necessary for the develop-
(e.g., neomycin, propylene glycol), have the potential to ment of sensitization and resultant clinical signs.
trigger contact hypersensitivity. An overlap of contact
hypersensitivity with atopic dermatitis (AD) may also Diagnosis
exist, since it is suspected that about 20% of dogs with
contact hypersensitivity also suffer from AD. Allergic contact hypersensitivity is diagnosed based on the
patient’s history, physical examination findings, resolution
Signalment of clinical signs after elimination of the offending allergen,
provocation of skin lesions with reexposure, and patch
Allergic contact dermatitis is considered to be a rare pru- testing. The most common differential diagnoses associ-
ritic condition and has no age or gender predisposition. ated with contact hypersensitivity are cutaneous adverse
However, some short‐haired breeds such as the boxer, pit food reaction, atopic dermatitis, scabies, pyoderma,
bull, dachshund, and Boston terrier appear to be affected Malassezia dermatitis, and insect bite hypersensitivity.
more frequently.
Therapy
History and Clinical Signs
The primary goal should be to prevent further exposure
Skin lesions typically occur on sites which are sparsely to the offending allergen. Symptomatic therapy with glu-
haired and directly exposed to allergens such as the ven- cocorticoids (e.g., prednisone/prednisolone at 0.5–1 mg/
tral aspects of the neck, chest, abdomen, tail, digital kg PO daily) may be attempted where elimination is not
spaces, muzzle, concave aspects of the pinnae, and scro- feasible; however, response to glucocorticoids occasion-
tum (Figure 160.3). Lesions may also develop in haired ally fails. Pentoxifylline (10–30 mg/kg PO 2–3 times
daily) has shown some beneficial effect for long‐term
management and prophylaxis. Patients with a poor
response to glucocorticoids may benefit from treatment
with ciclosporin (5 mg/kg PO daily).

Prognosis
Prognosis is considered good if the allergen can be elimi-
nated from the patient’s environment and good clinical
response can be achieved with immunomodulating drugs.

Flea Allergy Dermatitis

Etiology/Pathophysiology
Several allergens responsible for flea allergy dermatitis
(FAD) in dogs and cats have been identified in flea saliva.
So far, one major allergen, a protein called Ctef1 from the
cat flea Ctenocephalides felis, has been associated with
flea allergy in dogs.

Figure 160.3 Severe contact dermatitis to a plant fertilizer in a 5‐
year‐old golden retriever. Erythema, edema, serosanguinous to Epidemiology
purulent exudate, and brownish crusts were present on the
ventral abdomen and inner thighs. Source: Courtesy of Sheila The prevalence of FAD varies greatly depending on the
Torres. climate and geographic location, but it is the most