Tuesday, 2 April 2019

Clinical signs and diagnosis of Canine Atopic Dermatitis: An Update




INTRODUCTION
Atopic dermatitis in dogs is defined as: “A genetically-predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features”. It is associated most commonly with Ig E antibodies specific for environmental allergens such as house dust mites and grass pollen”
Canine Atopic Dermatitis (CAD) is a frequent disease of skin associated with release of inflammatory mediators with estimated prevalence of around 10% (Hillier et al., 2001). Though the exact cause is unknown, it is commonly associated with IgE antibodies to environmental allergens. The primary clinical signs, erythema and pruritus is associated with lesions at ear pinna, paws, ventral abdomen, inguinal and axillary regions (Herbert et al., 2006). Though the diagnosis of atopic dermatitis is based on ruling out other etiological causes, Intra dermal allergic skin test (IDST) is still the gold standard diagnostic procedure. Though the literature on canine atopy is available, reports on long term research particularly on diagnosis using Intra dermal allergic skin test (IDST) and therapy is dearth in India. Hence, the present paper puts on record for the first of its kind clinical study from India.
Cutaneous adverse food reaction (CAFR) and CAD have been historically considered as two different conditions. In fact, CAFR includes both immune mediated and non-immune-mediated food intolerances and may be associated with a wide range of clinical signs such as gastro-intestinal disturbances, urticaria, angioedema, and signs mimicking those of atopic dermatitis. The present article will consequently describe the clinical features and diagnostic methods of dogs affected by CAD from whatever cause. The clinical signs and diagnostic methods of food allergy are however beyond the scope of this article.

SIGNALMENT OF CAD DOGS

Some studies reported predisposition for male, female or for neither sex. However, some sex predispositions were detected in some breed such as golden or Labrador retrievers (more female) or Boxer (more male). The typical age at onset of CAD is reported to be between 6 months and 3 years. We have however recently shown that about 78% of CAD present with clinical signs before three years of age. It does mean that every fifth CAD dog develops the first clinical signs later in life.

HISTORY OF CAD DOGS

Information regarding the history of the affected dog should be recorded carefully. Some important questions have already been mentioned (age at onset, breed, familial predisposition) but some others such as seasonality, presence of “pruritus sine material” (pruritus with no skin changes) at onset, efficacy of previous treatment, should be asked before any clinical examination. Clinical signs of CAD may be seasonal or not but seasonality is often present at onset (42-75%).  Approximately 80% of dogs with seasonal signs are symptomatic in spring or summer while the others exhibit signs in winter or autumn. It should be mentioned that some dogs with non-seasonal disease do exhibit worsening of clinical signs during one specific season. Pruritus must be present and its absence rules out the diagnosis CAD.
In fact, some CAD dogs do exhibit initially pruritus. This feature was recorded in 61% of affected dogs in recent study. As well, 43% of CAD dogs presented first with an episode of otitis externa. In comparison, associated conjunctivitis blepharitis is very much rarer. CAD dogs are often treated with glucocorticoids and responses to such therapy should be evaluated carefully.
 It is also shown in the study that 78% of CAD dogs responded adequately to such treatment. In the first stages of the disease, the pruritus responds well and readily to the administration of reduced amount of glucocorticoid (i.e. 0.3-0.5mg/kg Prednisolone daily). In chronic cases however, the development of secondary bacterial or yeast infections usually corresponds with a poorer response to such treatment. Last but not least, we have also showed that 82% of atopic dogs spend most of their time indoor. This suggests that prolonged exposure to house dust mites may trigger or worsen CAD clinical signs.

CLINICAL SIGNS OF CAD

Although very frequent, CAD may be difficult to diagnose owing to the lack of pathognomonic signs and the protean clinical picture. Erythema and pruritus are however virtually always present and often represent the first clinical signs. However, mild pruritus may remain unrecognized by the owner and the veterinarian may sometimes rely on indirect proofs of pruritus such as the presence of excoriations or saliva-coloured hairs. Most of the signs are actually due to self-trauma and/or secondary infections. In fact, small erythematous papules, which are considered the primary lesion of CAD, are rarely observed in CAD dogs.
The practitioner will usually observe the consequences of the inflammation and pruritus, namely excoriations and self-induced alopecia and/or the signs of the secondary bacterial infection (papules, pustules, crusts, erosions) and/or the symptoms of secondary yeast dermatitis (epidermal hyperplasia, hyperpigmentation, lichenification).
 Recurrent or chronic skin or ear infections are very frequently observed in CAD Most of these signs are however not specific at all and the distribution of these lesions is consequently more helpful. The most often affected areas are the pinnae (58%), the axillae (62%), the abdomen (66%), the front (79%) and hind feet (75%), the lips (42%) and the perineal area (43%). Unfortunately, all these areas are rarely simultaneously affected in the same individual, except in chronic cases.  Dermatological (pyotraumatic dermatitis, interdigital fi stulae)  and non dermatological signs are sometimes associated with CAD and their presence should reinforce the suspicion. Spring/summer conjunctivitis, for example, is presented in approximatively 20% of CAD dogs while gastro-intestinal signs (soft stools, diarrhea, vomiting) are recognized in 26% of FIAD dogs.
Clinical signs of FIAD dogs differ very slightly from those of classical, environment-induced AD. In fact, in our study, statistically significant differences were only uncovered for gastro-intestinal signs, seasonality, cortico-sensible pruritus and pruritus sine material (less frequent in FIAD dogs). As well, more FIAD dogs show the fi rst clinical signs early in life (less than one year) or, on the contrary, rather late (more than 6 years of age).

DIAGNOSIS OF CAD

The diagnosis of CAD is based on the history (age at onset, seasonality, pruritus sine material at onset, familial or breed predisposition, previous response to glucocorticoids), the development of the disease (seasonality, “wax and wane” character, development of secondary skin infections) and the lesional pattern.
A diagnosis of CAD should however never been made, as long as resembling diseases such as fleas, ectoparasites (sarcoptic mange) and primary skin infections have not been ruled out. Depending on the clinical presentation and the age of the affected dog, some other differentials, i.e.demodicosis, dermatophytosis, cheyletiellosis, cutaneous lymphoma should be properly ruled out. It should also be mentioned that the histological aspect of allergic skin is usually not specific and that his test is consequently not adequate to make the diagnosis.
It may be indicated, however, to perform skin biopsies in some instances, to rule out some differentials such as cutaneous lymphoma, for example. As well, allergy testing (serological evaluation of allergen-specific Ig E and intradermal skin testing) are not regarded as criteria for the diagnosis of CAD. This is because numerous healthy dogs are sensitized to environmental allergens and are consequently positive (poor specificity of this criterion) and ALD and some FIAD dogs are deemed negative. These tests should consequently be only carried out to identify the offending allergens (i.e. to choose the allergens for allergen specific immune therapy: desensitization). In the same way, in order to identify FIAD dogs, a 6-to 8-week elimination diet and a subsequent challenge with the previous food should be carried out in all dogs with clinical signs of CAD. Several sets of criteria have been proposed for the diagnosis of CAD.
CRITERIA FOR THE DIAGNOSIS OF CANINE ATOPIC DERMATITIS AND ASSOCIATED SENSITIVITY AND SPECIFICITY.
1. Age at onset < 3years
2. Mostly indoor
3. Corticosteroid-responsive pruritus
4. Chronic or recurrent yeast infections
5. Affected front feet
6. Affected ear pinnae
7. Non –affected ear margins
8. Non-affected dorso-lumbar area
Sensitivity when 5 criteria are fulfilled: 85%
Specificity when 5 criteria are fulfilled: 79%
Sensitivity when 6 criteria are fulfilled: 58%
Specificity when 6 criteria are fulfilled: 88 %

SUMMARY
Canine Atopic Dermatitis (CAD) is the most frequent canine dermatosis. It has been defined by the International Task Force on Canine Atopic Dermatitis (ITFCAD) as a “genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features associated with IgE antibodies most commonly directed against environmental allergens”.  ITFCAD-revised nomenclature for veterinary allergy also takes into account dogs with clinical signs of atopic dermatitis but no demonstrable allergen-specific IgE (Intradermal tests and/or serology).

REFERENCES
1. Favrot, C., Steffan, J., Seewald, W., & Picco, F. (2010). A prospective study on the clinical features of chronic canine atopic dermatitis and its diagnosis.Veterinary dermatology, 21(1), 23-31.
2. DeBoer, D. J., & Hillier, A. (2001). The ACVD task force on canine atopic dermatitis (XV): fundamental concepts in clinical diagnosis. Veterinary immunology and immunopathology, 81(3), 271-276
3. Nambi, A. P., & Kavitha, S. (2013). Canine atopic dermatitis. Intas Polivet,14(2), 236-24
4. Bensignor, E. (2010). [Canine atopic dermatitis]. Bulletin de l'Academie nationale de medecine, 194(7), 1357-1364.
5. Olivry, T., & Mueller, R. S. (2003). Evidencebased veterinary dermatology: a systematic review of the pharmacotherapy of canine atopic dermatitis.Veterinary dermatology, 14(3), 121-146.

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