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An Urban Experience
C. Sousa1
1None - Retired, None, El Dorado Hills, USA
The past decade has provided much new information
on the pathogenesis of allergic skin disease in animals. This has allowed veterinarians to develop more effective treatment protocols – and safer ways to treat it. Canine atopic dermatitis (AD) has served as the model for allergic skin disease. Much of that science can be applied to other allergies, such as flea allergy dermatitis; cutaneous adverse food reactions (CAFR); and the allergic reactions to parasites, such as Sarcoptes scabiei.
Key Facts
• The cycle of itch/scratch in allergic skin disease is mediated by lymphocytes and the cytokines that they produce.
• Cytokines that utilize Janus kinase (JAK)1 enzymes are primarily involved in the itch and inflammation of allergic skin disease.
• Interleukin (IL)-31 is a key cytokine in many cases of inflammation.
• Traditionally, veterinarians focused on treatment
of allergic skin disease with drugs, such as corticosteroids, that targeted controlling pruritus and deceasing inflammation. This was driven by the need to address the owner’s complaints that persistent itching and scratching in their dog was detrimental for their pet and disrupted the quality of life of the pet and the owner.
• Decreasing pruritus remains a key therapeutic objective for veterinarians treating allergic skin disease, and veterinarians understand that treatment typically requires several modes of therapy aimed at both the primary disease as well as the secondary complications.
• Current treatment regimens focus on:
– Identifying and treating infestations, such as fleas, Sarcoptes scabiei, Notoedres cati, Cheyletiella sp., lice, etc.
– Controlling concurrent infections or colonization with common pathogens, such as Staphylococcus pseudintermedius or Malassezia yeast.
– Preventing any allergic conditions that are possible, such as cutaneous adverse food reactions, contact allergies, etc.
– Modifying the immune responses to allergenic stimulation.
– Controlling and breaking the itch/scratch cycle.
• Contemporary, multimodal treatment protocols can include one or more of the following therapeutics based on individual patient needs:
– Topical therapies, such as shampoos, to remove pathogens and allergens and to improve the skin barrier.
– Moisturizers and restructurant agents to improve the skin barrier.
– Nutritional supplements to enhance the skin barrier function.
– Antiparasitic products to treat and prevent parasitic infestations.
– Anti-infective drugs to treat secondary bacterial and yeast infections.
– Hypoallergenic diets.
– Antipruritic therapy to control itch and scratching.
– Allergen-specific immune therapy (ASIT) to modify the patient’s immune response to specific allergens.
• Today, options for treating allergic skin disease, including AD, comprise drugs that are targeted at controlling recently described mechanisms of AD, such as specific cytokines.
Immunopathogenesis of Atopic Dermatitis
In dogs, the immunology of atopic dermatitis starts with a cutaneous Langerhans cell presenting an antigen to
a naive T lymphocyte, which it polarizes for the correct response. The immune dysregulation in allergy is a shift toward a T helper (Th) 2 response. The Th2 lymphocytes release cytokines that mediate neuronal itch (such
as interleukin [IL]-31) as well as other inflammatory mediators including, IL-2, IL-4, IL-5,
IL-6, and IL-13 (Figure 1).

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