Indice Autori

DERMATITI DA CONTATTO NEGLI ANIMALI

R. Marsella

DVM, DipACVD, Po Box 100126, Department of Small Animal Clinical Sciences,

College of Veterinary Medicine, University of Florida, Gainesville, FL 32610-0126

Pathophysiology

Contact allergy is a type IV hypersensitivity. Allergens responsible for contact allergy (haptens) have low molecular weight, are usually lipid soluble and require binding to proteins to become allergenic. In humans a genetic predisposition to develop contact allergy has been noted. The same may be true for dogs. Contact allergy involves two different phases: a sensitization phase and an elicitation phase.

a. Sensitization

A sensitization phase is required before clinical signs develop. This phase seems to vary from 6 months to two years in the canine species. During exposure to the hapten, the immune system becomes sensitized to the substance but an allergic reaction is not elicited. The hapten is pinocytosed by Langerhans cells, elaborated and re-exposed on the surface of the cell membrane together with major histocompatibility complex (MHC) class II for presentation to T cells. Antigen presentation occurs in the local lymph nodes.

The T cells become activated and proliferate, originating a clone of memory T cells. The existence of a lag phase before the development of clinical signs is an important piece of information for the clinician. This helps to differentiate between allergic and irritant contact reactions since clinical signs and histopathology can be similar. Irritant reactions, in fact, are not immunologically mediated and they do not require a sensitization phase. The presence of a reaction in a control individual can also be used to differentiate between irritant and allergic contact reactions.

b. Elicitation

Once sensitization has occurred, numerous memory T cells are present in the epidermis. When hapten is newly encountered by Langerhans cells, it will be presented to memory T cells. These cells readily secrete interleukin-2 (IL-2) and gamma-interferon (γ-IFN), stimulate T cell proliferation and the expression of adhesion molecules on the surface of keratinocytes. These molecules are responsible for the accumulation of mononuclear cells in the epidermis. Inflammatory mediators (e.g eicosanoids, TNF-α, IL-1, IL-3, IL-5) released by stimulated keratinocytes, mast cells and basophils are responsible for the erythema, vasodilation and pruritus that are clinically evident in allergic contact reactions. Recent studies documented the critical role of IL-1 and TNF-α in irritant and allergic contact reactions.

Incidence of contact allergy:

Uncommon in animals due to the protection of the haircoat.

Allergens: Detergents, waxes, cleansing agents, dyes, deodorants, shampoos, dips, insecticides, steroids, antibiotics, and plants can cause ACD. Several plants have been documented to cause contact allergy in dogs (e.g. dandelion leaves, cedar wood, Asian jasmine, wandering jew). Plants of the Commelinceae family (wandering jew) are frequently responsible for contact allergy in dogs in the southeastern United States. Common characteristics of these plants are lance-shaped fleshy leaves with closed sheaths and a few soft hairs on the upper margin. They are found in moist habitats and in warm climates. They reproduce by seed and have blue to purple flowers. These plants are not usually responsible for contact hypersensitivity in people and the only plant in this family that has been reported to be an irritant to humans is Rheo spathacea (commonly called Boat-lily, Moses-in-a-boat or oyster plant). This plant causes itching, burning rashes and respiratory difficulty. Calcium oxalate crystals are hypothesized to be responsible for the allergenicity of these plants.

Clinical presentation of Contact Allergy

History: a minimum of 6 months of age is required for appropriate sensitization. Onset of clinical signs is usually rapid once sensitization has occurred. Seasonality may be seen when plants are involved.

Clinical signs: primary maculo-papular eruption and pruritus, secondary superficial pyoderma, hyperpigmentation, lichenification and crusting. . Sparsely haired areas are more commonly affected (groin, axillae). Papules and pustules are seen even after resolution of the secondary bacterial infection. Face and feet are usually affected when the offending allergen is something that the animal walks on. Pruritus may be very intense but it is usually steroids-responsive, at least initially.

Diagnosis

It is based on clinical signs, distribution (variable depending on the type of substance involved), resolution of clinical signs with avoidance, relapse of clinical signs with re-exposure; patch testing (open or closed).

A. Boarding the animal at the hospital for 1-2 weeks to accomplish avoidance. Shampoo the animal before starting confinement to remove possible residual material from the skin.

B. Implicating a specific allergen is difficult and requires cooperation with the owner to identify possible sources.

C. Patch testing: difficult, time-consuming, potential allergens should be held in close contact with the skin for 48 hours. Skin should be shaved 1-2 days before the test. Usually a total body wrap is the best way to achieve the contact. Finn chambers may be used to apply the suspected allergen. A positive reaction is indicated by the appearance of a papular eruption 24-48 hours after the application of the allergen

Therapy

The treatment of allergic contact dermatitis remains a major challenge. Current management strategies consist of allergen avoidance and topical or systemic corticosteroids. Hyposensitization has been ineffective. Pentoxifylline, a trisubstituted xanthine derivative, has been recently used to inhibit allergic contact reactions in rodents, people and dogs (15-20mg/kg TID PO). It works by inhibition of tumor necrosis factor-α production, which is an important mediator of contact dermatitis.

Table 1. Comparison between irritant and allergic contact dermatitis.

Allergic contact dermatitis Irritant contact dermatitis
Pathogenesis	Type IV hypersensitivity	Non immunologically mediated
It requires prior sensitization (exposure without development of clinical signs)	It does not require sensitization Signs are evident at first exposure
Other animals are not affected	All animals are usually affected
Clinical signs are seen 24-48 hours after exposure	Clinical signs may be evident shortly after exposure depending on the nature of the offending substance
Lesions	Papules and pustules and pruritus	Vesicles, ulcerations Pain more than pruritus. Lesions are more exudative and severe than in contact allergy.

Table 2. Comparison between atopy and contact allergy

Atopy Contact allergy
Pathogenesis	Type I Immediate (15 minutes) IgE-mediated Excessive TH2 response	Type IV Delayed (24-48 hours) Cell-mediated Excessive TH1 response
Medium MW	Small MW, require protein to become allergenic (hapten)
Percutaneous absorption Inhalation	Percutaneous only
Genetics	Genetically inherited Familial history	? in animals
Onset of clinical signs	Slow and progressive 1-3 years of age	Sudden At least 6 months of age
Clinical signs	No primary eruption	Primary eruption; Papules and pustules
Distribution	Face, feet, ears	Depends on the offending allergen
Diagnosis	History, clinical signs R/O other diseases	Resolution with confinement Worsening with re-challenge
To determine responsible allergens	IDST and serology	Patch testing
Therapy Hyposensitization Glucocorticoids Antihistamines Fatty acids Pentoxifylline Cyclosporine	effective effective effective effective effective effective	ineffective effective ineffective ineffective effective effective