Medical Article


Doc, Why Does My Dog Scratch? A review of the pathogenesis of canine atopic dermatitis


By Amy Van Gels, DVM


Imagine the following scenario. After working an emergency into an overbooked schedule, you take a deep breath as you examine the medical record for your next appointment. Mrs. Smith has returned with her 4-year-old, male-neutered Golden Retriever, Max. Your technician noted on the top of the chart that Mrs. Smith seems upset because this is his third recheck appointment since the beginning of the allergy season. As you enter the room, you see that her mood has not improved during the half hour that she had to wait while you started treating the unscheduled emergency.


Skipping any opening pleasantries, she immediately demands, “Why is Max still scratching?! I can’t understand why you can’t seem to get his allergies under control.” Staying professional, you try to diffuse her anger as you examine and treat Max.


Favrot’s Criteria


Although there are many possible etiologies, you diagnose Max with canine atopic dermatitis (AD) partially based on Favrot’s criteria. In 2010, Favrot et al.1


described the


clinical signs frequently associated with AD and developed a set of criteria for clinicians to use as a screening test to aid clinicians in its diagnosis. Dogs with AD typically display 5 or more of the characteristics provided. While the full list of criteria is presented in Table 1, examples include “affected front feet” and “corticosteroid-responsive pruritus.” Based on 85%


sensitivity and 79% specificity, the use of these guidelines will miss 15% of the dogs with AD (false negatives) and inaccurately diagnose 21% of dogs that do not in fact have AD (false positives). To minimize misdiagnosis, Favrot et al. and other dermatologists2


recommend pairing the criteria


with the physical exam findings, signalment, history, and a thorough exclusion of ectoparasites and fungal or bacterial infections.


Food-Induced Atopic Dermatitis


Some dogs with food allergies have clinical signs indistinguishable from those of AD. These dogs are referred to as having food-induced AD. Favrot et al. found that the clinical signs of food-induced AD do not differ significantly from non-food-induced AD;1


therefore, Favrot’s criteria


cannot rule out food allergies. A 6- to 8-week elimination diet is still necessary in all dogs with AD to determine if food allergens are contributing to the development of clinical signs. Food-induced AD is particularly important in dogs that suffer from AD throughout the year.3


pattersonvet.com Allergen-Specific IgE Reactions


After diagnosing Max with AD, you can finally start answering Mrs. Smith’s question. Although she may not realize it, Mrs. Smith is asking about the pathogenesis of atopic dermatitis when she asks why Max scratches.


Back in veterinary school you may have learned that atopy is a hypersensitivity mediated by immunoglobulin E (IgE). That is, predisposed dogs become sensitized to allergens in the environment and create allergen-specific IgE, which then binds to mast cells. Following subsequent exposure to the allergen, a type 1 hypersensitivity reaction triggers the release of histamine and other proallergenic mediators.4


Serology


and intradermal testing can detect the presence of allergen- specific IgE.2


However, some dogs and humans with AD do not have detectible levels of allergen-specific IgE. This condition – called atopic-like dermatitis – illustrates that the pathogenesis of AD extends beyond IgE sensitization alone. While the effects of IgE reactions certainly play an important role in the pathogenesis of AD, recent research indicates that other major factors exist, including skin barrier defects and cytokine dysregulation.


Skin Barrier Defects


The outermost layer of the epidermis – the stratum corneum (SC) – protects the body by creating a barrier against water loss and the penetration of foreign molecules, including allergens. The SC consists of 20-30 layers of flat corneocytes that are surrounded by lipids, such as ceramides, cholesterol, and free fatty acids. These lipids are arranged into lamellae in the intercellular spaces.5


Recent studies suggest that


dogs with AD have skin-barrier defects.6,2 following have been reported in dogs with AD:6


Reductions in the


• The percentage of ceramides as compared to other lipids • The total amount of ceramides present


• The amount and organization of the lipid lamellae in the SC


• Skin moisture (i.e., an increase in transepithelial water loss)


• In some dogs, filaggrin expression (a protein that creates the structure of keratin)


• The function of tight junctions and corneodesmosomes neocytes in the SC7


These dermatologic abnormalities have been seen in dogs with AD whose skin appears clinically normal (i.e., no signs of dermatitis). The presence of inflammation secondary to AD further exacerbates many of these defects. Researchers do not know whether the skin-barrier changes are due to a primary genetic defect or secondary to inflammation associated with the clinical signs of AD. However it occurs, skin-barrier defects allow increased numbers of allergens to enter the body through the skin.6


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