In-depth Information on Contact Dermatitis in Dogs
Contact allergy is an immunologic reaction called type IV hypersensitivity in which lymphocytes are the predominant cell type. Contact dermatitis can be either allergic or irritant. Irritant contact dermatitis is not immunologically mediated. Allergens called haptens, which are responsible for contact allergy, are small molecules that are usually lipid soluble and require binding to larger proteins to become allergenic.
In humans a genetic predisposition to contact allergy has been observed. The same may be true for dogs. Dogs with atopy (inhalant allergic dermatitis) also seem predisposed to contact allergy.
Contact allergy involves two different phases: a sensitization phase and an elicitation phase.
Irritant reactions are not immunologically mediated and do not require a sensitization phase. The occurrence of a reaction in a control animal can be used to differentiate between irritant and allergic contact reactions.
A sensitization phase is required before clinical signs develop. This phase seems to vary from six months to two years in dogs. During exposure to the hapten, the immune system becomes sensitized to the substance but an allergic reaction is not elicited.
The hapten is taken up by specialized skin cells called Langerhans cells, modified, and presented on the surface of the cell along with major histocompatibility complex (MHC) class II antigens for presentation to T-lymphocytes. The MHC antigens normally distinguish individuals from one another and are evaluated in procedures such as tissue typing. T-lymphocytes are cells that play a key role in the immunologic process.
Antigen presentation occurs in the local lymph nodes. The T-lymphocytes become activated and proliferate, producing 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 information helps differentiate allergic and irritant contact reactions because clinical signs and microscopic pathology can be similar in these two disorders.
When this hapten is encountered by Langerhans cells it is presented to memory T-cells. These cells secrete chemicals called interleukin-2 (IL-2) and gamma-interferon which stimulate T-cell proliferation and the expression of special adhesion molecules on the surface of skin cells called keratinocytes. These molecules are responsible for the accumulation of inflammatory cells called mononuclear cells in the epidermis.
Inflammatory mediators (eicosanoids, tumor necrosis factor, histamine, interleukins) released by stimulated skin cells (keratinocytes) and specialized inflammatory cells of the skin (mast cells and basophils) are responsible for the redness, dilation of blood vessels and itchiness that occur in allergic contact reactions. Recent studies have focused on the clinical relevance of tumor necrosis factor in natural and experimentally-induced contact allergy.
Contact allergy is uncommon in animals due to protection of the skin by the hair coat. Detergents, waxes, cleansing agents, dyes, deodorants, shampoos, dips, insecticides, corticosteroids, antibiotics, and plants can cause allergic contact dermatitis.
Several plants have been documented to cause contact allergy in dogs. These include dandelion leaves, cedar wood, Asian jasmine and wandering Jew. Plants of the Commelinceae family, such as doveweed, spreading dayflower and 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 reproduce by seed and have blue to purple flowers. They are found in moist habitats and in warm climates and are not usually responsible for contact hypersensitivity in people. Calcium oxalate crystals are hypothesized to be responsible for the allergy-producing effect of these plants.
Related Symptoms or Ailments in Clinical Presentation
The onset of clinical signs usually is rapid once sensitization has occurred. The problem may be seasonal when plants are the offending allergens. Clinical signs include a pruritic eruption characterized by papules, secondary superficial bacterial infection, increased pigmentation, crusting, and thickening of the skin. Sparsely haired areas are more commonly affected (groin, axilla, abdomen). Papules, pustules and pruritus persist after resolution of the secondary bacterial infection. The muzzle and paws also are commonly affected.
Pruritus varies in severity and may be very intense. It is usually responsive to cortisone-like medications (corticosteroids), at least initially.