Canine atopic dermatitis: An evolving understanding

Canine atopic dermatitis (cAD), also known as atopy or allergic inhalant dermatitis, is one of the most common primary skin diseases leading to veterinary clinic visits. It is also a frequent cause of secondary otitis and skin infection, including pyoderma and/or Malassezia dermatitis.

Canine atopic dermatitis has long been recognized as a multifactorial disease resulting from a complex interaction between the host and the environment, and it is commonly encountered in general practice (1).

First recognized in 1941 as a “spontaneous allergy” (2), our understanding of the disease has evolved substantially over time and continues to progress.

Later, atopic dermatitis was described as a genetically programmed disease in dogs, in which the patient becomes sensitized to environmental antigens that, in non-atopic animals, do not cause disease (3). It has been classically defined as a “type I hypersensitivity toward environmental allergens” (3).

By 2001, the definition was updated by the ACVD Task Force (4) to: “A genetically predisposed, inflammatory and pruritic allergic skin disease with characteristic clinical features, most often associated with IgE antibodies to environmental allergens.”

The most recent revised definition (5), based on advances in knowledge and published studies, is from the 2023 International Committee on Allergic Diseases of Animals (ICADA) and states: “Canine atopic dermatitis is a hereditary, typically pruritic and predominantly T-cell driven inflammatory skin disease involving interplay between skin barrier abnormalities, allergen sensitization and microbial dysbiosis.”

This updated definition best reflects our current, broader understanding of the pathogenesis of the condition, highlighting factors beyond just allergies (5). It underscores the disease’s complexity, which makes it challenging and often frustrating for both pet owners and veterinarians. All veterinarians are encouraged to be aware of this updated definition, as it will aid in implementation of more individualized and multimodal treatment plans for atopic canine patients. Treatment options for canine atopic dermatitis will be reviewed in a future Dermatology Column of The Canadian Veterinary Journal.

HEREDITARY FACTORS

The genetic background of a dog, in combination with environmental factors, determines the risk of disease development and the clinical phenotype (1,6). Although many breeds are considered predisposed, the prevalence of the disease varies by geographic region. Five breeds that are considered predisposed to cAD irrespective of the region (i.e., breeds exhibiting worldwide predisposition) are: the boxer, bulldog, Labrador retriever, pug, and West Highland white terrier (1).

PRURITIC, INFLAMMATORY SKIN DISEASE

Pruritus is the primary clinical sign, although a manifestation of pruritus may not always be present. Various inflammatory mediators are involved, including gross inflammation (erythema, skin lesions, and skin changes) being evident in most patients (5,7). An imbalance of the immune system is present including up-regulation of T-helper cell cytokines. In the past decade, a consistently strong central role for interleukin-31 in pruritus has been shown, in line with successful therapies targeting this cytokine for relief of clinical signs of cAD (5).

SKIN BARRIER ABNORMALITIES

Skin barrier dysfunction is considered an important component of atopic disease; however, much remains to be learned about its significance as a primary contributor (8). Although primary skin barrier defects may contribute to cAD and its associated symptoms, many skin barrier alterations may be secondary results of cutaneous allergic inflammation (8).

ALLERGEN SENSITIZATION AND COMMON ALLERGENS IN ATOPIC DERMATITIS

Important, common allergens in cAD include house dust mites, environmental molds, weeds, grasses, and trees (7). Polysensitization, in which multiple allergens trigger reactions, is common in atopic individuals (7). House dust mites are the most common allergen in dogs, similar to humans, with Dermatophagoides farinae being the most prevalent house dust mite allergen involved in cAD (1).

Malassezia pachydermatis, part of the normal cutaneous microbiota in dogs, can trigger hypersensitivity reactions in atopic dogs (9).

MICROBIAL DYSBIOSIS

Cutaneous microorganisms, including bacteria, fungi, and parasites, have a crucial role in the local skin immune system. Cutaneous dysbiosis is defined as an imbalance in the composition of the microbial community, often characterized by a reduction in microbial diversity and a decrease in the number of beneficial bacteria (10).

In healthy dogs, the cutaneous microbiome is highly diverse. However, in cases of cAD, microbial diversity is significantly reduced, which promotes the overgrowth of Staphylococcus pseudintermedius, leading to an increased risk of secondary skin infections (8,11). There is a higher relative abundance of S. pseudintermedius and Malassezia pachydermatis on the skin of atopic dogs compared to healthy dogs (8,12). In addition, an increase in the relative abundance of Corynebacteriaceae and Staphylococcaceae has been observed in lesional skin, with this dysbiosis persisting for up to 2 wk after the remission of skin lesions (13).

Interestingly, skin microbiome diversity significantly increases immediately after the resolution of an allergic flare or bacterial infection, becoming more similar to that of healthy skin (14). However, 4 to 6 wk after treatment, microbial diversity gradually decreases, leading to a return to dysbiosis, with a subsequent rise in S. pseudintermedius abundance and an increase in the severity of clinical signs of cAD (14). Whether cutaneous microbial dysbiosis is a cause or consequence of cAD remains uncertain, and further studies are necessary to clarify this relationship (8).

CLINICAL FEATURES OF CANINE ATOPIC DERMATITIS

Canine atopic dermatitis is common in dogs, with an age of onset ranging from 6 mo to 7 y (3,7). Most often, symptoms first appear between 1 and 3 y of age (3,7). Some patients may present to the veterinarian much later in life with moderate to significant dermatological disease, although milder and/or waxing-waning symptoms of disease may have been present for many years prior. Canine atopic dermatitis patients typically exhibit characteristic clinical features, including lesions on the ventrum, pedal skin, flexural skin sites, muco-cutaneous junctions, and ears. Pruritus is the hallmark presenting sign, and gross cutaneous and/or otic inflammation is often present. Manifestations of pruritus include licking, chewing, scratching, rubbing, scooting, and head shaking. Some patients may be non-pruritic despite the visual presence of skin and/or ear disease.

Common primary lesions include erythema (Figure 1), and other findings may include papules, conjunctivitis, otitis, and chronic skin changes including secondary seborrhea, salivary staining, and lichenification, acral pruritic nodules, and acral lick granulomas (3,7). Pruritus and cutaneous inflammation often lead to secondary infections that result in pustular dermatitis, crusting, scaling, and hair loss (Figure 2). Secondary pyoderma, Malassezia dermatitis, and otitis externa are common. These cutaneous changes and secondary infections further complicate an already complex, multifactorial dermatological disease.

FIGURE 1.

Canine atopic dermatitis patient with facial erythema (Photograph supplied by Dr. Jangi Bajwa).

FIGURE 2.

Canine atopic dermatitis patient exhibiting ventral trunk inflammation with secondary pyoderma lesions (Photograph supplied by Dr. Jangi Bajwa).

Fortunately, a variety of treatments are available, and new options are being explored. This provides clinicians with opportunities to tailor treatment to each patient’s specific needs. As pets become more integrated into family life, pet owners are increasingly willing to pursue multimodal management. Understanding the complications of this incurable disease can lead to improved quality of life and better outcomes for both pets and their families.