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Atopic Dermatitis

Alison Diesel, DVM, DACVD

College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX, USA

Etiology/Pathophysiology may also influence disease development. Abnormal
structure and composition of the stratum corneum inter-
In the dog, atopic dermatitis is defined as “a genetically cellular lipid lamellae, altered ceramide content, and
predisposed inflammatory and pruritic allergic skin dis- abnormal expression of filaggrin (the epidermal filament‐
ease with characteristic clinical features associated with associated protein responsible for binding keratin mole-
IgE antibodies most commonly directed against environ- cules) have been documented in many dogs with atopic
mental allergens.” Although the exact pathogenesis of dermatitis. Subsequent to these structural abnormali-
disease development is incompletely understood, cur- ties, increased transepidermal water loss is also noted.
rent theory supports a multifactorial involvement of The combination of these changes can increase inflam-
genetic predisposition, immunologic dysregulation, and mation and severity of disease. Whether these changes
epidermal barrier dysfunction. are seen in all dogs with atopic dermatitis or only a
During sensitization, it is suspected that epidermal percentage of patients is currently unknown. There is a
barrier defects allow enhanced contact of allergens with similar disease in dogs, termed “atopic‐like dermatitis,”
Langerhans cells in the epidermis. These cells capture which manifests with identical history and clinical signs
the allergens and migrate to regional lymph nodes, acting (see below), but in which documentation of IgE involve-
as antigen‐presenting cells. In the lymph nodes, ment cannot be confirmed. Epidermal barrier dysfunc-
Langerhans cells interact with T lymphocytes, creating a tion may be a more important contributing factor for
skewed distribution and formation of type 2 T helper disease development in these patients.
(Th2) cells. Upon repeated exposure to the allergen, the In the cat, the etiology and pathogenesis are even less
sensitized Th2 cells produce a variety of inflammatory well defined. Although many of the immunologic mech-
cytokines which promote production of IgE and infiltra- anisms appear to be similar to those seen in the dog,
tion of inflammatory cells into the skin. there is a question of the true implication of IgE involve-
Increased levels of interleukin (IL)‐4, IL‐5, and IL‐13 ment with disease development. Additionally, epidermal
are noted in dogs with atopic dermatitis, along with barrier function has not been evaluated in the cat as a
elevated levels of interferon (INF)‐gamma. Recent stud- contributing factor. For these and other reasons, many
ies have also documented elevated levels of IL‐31 in dogs prefer to use the term “nonflea nonfood hypersensitivity
with atopic dermatitis. This novel cytokine is also pro- dermatitis” when discussing atopic dermatitis in cats.
duced by Th2 cells and appears to be responsible for
much of the pruritus associated with clinical allergic skin
disease. In more chronic lesions, the response favors Th1 Epidemiology
cytokine production which will contribute to perpetua-
tion of the inflammatory process. Atopic dermatitis can present in dogs and cats world-
Historically, atopic dermatitis in dogs was believed to wide, though geographic differences may play a role in
be due primarily to immunologic dysregulation and the development of disease (e.g., clinical signs may mani-
genetic predisposition (as evidenced by the current defi- fest earlier in life in animals in warm weather climates
nition of the disease). However, more recent evidence where the level of allergen exposure is rather high), as
supports abnormalities in the epidermal barrier which well as prevalence in that region. A few older studies have

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical