Abstract
Canine atopic dermatitis (CAD) is a very common and sometimes difficult to control inflammatory pruritic skin disorder. Although the pathogenesis of CAD is not well recognized, several factors, including dysregulation of immune function, skin barrier dysfunction, genetic abnormalities, and environmental factors, are considered to be involved.
Diagnosis of CAD
The diagnosis of CAD is essentially made on the basis of the exclusion of other major frequently encountered pruritic skin diseases and the agreement of the history and clinical signs with the characteristics of CAD. So far, there is no specific laboratory test that diagnoses CAD solely. One process of diagnosis is briefly described below.
1. Exclusion of Scabies
A diagnosis of scabies should be made upon the discovery of mites in scraping materials under the microscope. The clinical symptoms of canine scabies may appear similar to those of CAD. Common body areas affected include pinnae, elbows, and knees. Multiple superficial skin scrapings are mandatory to detect mites and their eggs. Subcutaneous weekly injection of 300 µg/kg ivermectin may produce some improvement within one or two weeks. The diagnosis of scabies is excluded if there is no improvement after two weeks.
2. Exclusion of Superficial Pyoderma
A diagnosis of superficial pyoderma is made on the basis of clinical signs and cytology. Clinical signs usually include follicular papules, pustules, and epidermal collarettes on the body surface with variable levels of pruritus. Veterinarians should perform skin cytology whenever they find such clinical signs. Samples are collected by direct impression smear or fine needle aspiration. The existence of cocci, phagocytotic, and degenerated neutrophils is highly suggestive of skin surface infection.
As most superficial pyoderma cases are caused by Staphylococcus pseudintermedius, it is mandatory to administer antimicrobials that are effective against gram-positive cocci. Those antimicrobials include cephalosporins, fluoroquinolones, trimethoprim-sulfate, or clindamycin. The appropriate dosage, frequency, and treatment period are critical to prevent the emergence of resistant strains of S. pseudintermedius.
Topical therapy using shampoos and/or disinfectants is very useful to manage dermal bacterial infection. Shampoos should contain 2% to 4% chlorhexidine, benzoyl peroxide, ethyl acetate, and acetic acid.
3. Exclusion of Malassezia Dermatitis
Malassezia dermatitis is usually caused by the proliferation of Malassezia pachydermatis. Clinical signs include intense erythema of skin on the face, axilla, chest, and inguinal and interdigital regions with greasy or scaly skin. Thickness and lichenification of skin are notable in chronic lesions of Malassezia dermatitis. Cytology specimens are obtained by impression smear and three to five yeasts may be found by high-power microscopy. The diagnosis is based on clinical signs and cytology.
Ketoconazole (5 mg/kg, q12 h, 3 weeks) and itraconazole (5 mg/kg, q24 h, 3 weeks) are used as systemic anti-mycotic agents. Shampoos that contain miconazole or ketoconazole should also be applied three days a week.
4. Exclusion of Food Allergy
The exclusion of food allergy can be made by elimination diet trials and/or provocation with suspected foods. However, in many CAD patients, cutaneous clinical signs of CAD and food allergy are not distinguishable.
In addition, attempts to determine IgE and/or IgG antibodies against food substances using laboratory methods have failed to detect a correlation between them.
5. Clinical Signs, History, and Distribution of Lesions in CAD Patients
After the exclusion of ectoparasites and concomitant infectious diseases, veterinarians should consider if the patients' history and clinical signs agree with those of CAD in the following points.
1. There is an increased prevalence of CAD in specific dog breeds, such as Shi-tzu, Jindo dog, West Highland white terrier, French bulldog, Golden and Labrador retrievers, Shiba-inu, and Wire haired fox terrier, but breed predilection may depend on the geographical region.
2. Pruritus on skin or ears often appears without any skin lesions before 3 years old. It is critical to assess if the symptoms started between 6 months old and 3 years old. A history of CAD usually reveals chronic pruritus with or without seasonal occurrence.
3. CAD should appear on the ears, face, axilla, and inguinal and interdigital regions.
Evaluation of Pruritus and Treatment/Management of CAD
1. Anti-inflammatory Drugs
Corticosteroids
Prednisolone and methyl prednisolones are recommended to alleviate the symptoms of CAD. In the acute phase of CAD, 0.5 to 1 mg/kg prednisolone is given for 3 to 5 consecutive days and then withdrawn. In the chronic phase of CAD, the starting dose of 0.5 mg/kg prednisolone could be prescribed and later tapered to the minimum dose and frequency to control pruritus and skin lesions.
Cyclosporins
Cyclosporins have been approved for use in 22 countries for the treatment of CAD. Oral daily cyclosporine (5 mg/kg) is recommended and the dose is tapered to a minimum to control clinical signs after clinical improvement is seen. Clinical efficacy should be determined after administration for four to six weeks.
2. Skin Care
Allergic and non-allergic irritants lower the threshold to pruritus in atopic lesions as the skin barrier function is thought to be impaired in CAD patients. Weekly use of non-irritant skin shampoos with warm water will wash out these irritants. Skin conditioners and treatments may also contribute to the recovery of impaired skin barrier function that is characterized by dryness. Ingredients that are effective against skin dryness include propylene glycol, ceramide, glycerine, and oatmeal. These ingredients are included in shampoos, sprays, and spot-ons.