Canine atopic dermatitis is a common, chronic disease which affects the quality of life for many dogs and their owners.
The various factors that influence the pruritus threshold should be addressed simultaneously in order to achieve successful treatment, especially when flares are present.
Symptomatic immunosuppressive treatment and allergen-specific immunotherapy both play an important role in controlling canine atopic dermatitis, and may be used simultaneously.
Treatment should always be individualized and adjusted for flares, seasonality and the general health of the patient.
Canine atopic dermatitis (CAD) is a common allergic skin disorder that develops from predominantly environmental allergens, such as house dust mites and pollens of grasses, trees and weeds. The etiology is considered multifactorial, whereby an epidermal barrier dysfunction, combined with dysregulation of the immune system, leads to the development of clinical disease in dogs with a suggested genetic background of CAD. In most cases the problem starts at a young age, but causes discomfort by dermatitis and pruritus throughout life.
Several therapies have been developed for CAD, but each has its pros and cons regarding effectiveness and health interference. This article offers a logical approach to the daunting question “where do we start?” The challenge is not only to treat the patient successfully, but also to avoid severe flares. For this reason, the treatment of CAD requires multifaceted management (Figure 1). Successful remission can only be achieved with a combination of approaches in order to control the clinical signs and prevent flares, and the options will depend on a patient’s individual needs and the severity of disease over time.
Avoidance of allergens
Since the most common causal allergens are house dust mite glycoproteins and aeroallergens, such as pollens, prevention of allergen contact is difficult or impossible to achieve. An uncontrolled study that used an environmental benzyl benzoate acaricide spray in an attempt to reduce the amount of dust mite allergens reported some clinical improvement in atopic dogs 1. Other environmental sprays currently also marketed for the human field contain probiotics which produce enzymes for isolating house dust mites' fecal proteins. Further controlled studies are needed to clarify the correlation of clinical improvement in atopic dogs and the reduction in dust mites allergens with these sprays. Likewise, the use of dust mite-free mattresses, regular vacuuming, and washing blankets at 60°C is also likely reduce the canine skin's exposure to house dust mites allergens.
Rarely, an atopic dog may be responsive to epithelia of other pets in the household (e.g., parrot or guinea pig). In this situation it is advisable to relocate either the causal pet or the patient to another household.
When food-induced atopic dermatitis is present, both food allergens and environmental allergens play a causal role 2. Food allergens may especially be significant when flares occur, and determining the role of food with an elimination diet trial and provocation is always essential for the atopic dog; if proven, prevention of exposure to causal food allergens is often relatively easy to establish.
Repairing the skin barrier
It is well known that atopic dogs suffer from an impaired epidermal barrier, which results in an increased transepidermal water loss (TEWL). Dry and scaly skin (xerosis) may be seen in some breeds. Supporting the epidermal barrier with topical moisturizers such as glycerol, glycerin, propylene glycol, panthenol and urea will increase the water-binding capacity of the epidermis, especially when used after bathing. This has been recently demonstrated in a chronically disrupted canine epidermal barrier model 3. Products containing phytosphingosine and ophytrium, a natural ingredient extracted from the root of the Japanese mondo grass plant, may also help improve the skin barrier and reduce pruritus and colonization of microbes at the epidermis 4.
Atopic dogs also have disrupted intercellular lipid lamellae of their stratum corneum. To restore this, oral essential fatty acids (EFAs), either as supplements or incorporated in the diet, have been deployed with varying results. Of interest is one good quality study which showed a significant reduction in the required prednisolone dosage in atopic dogs when oral EFAs were administered for 12 weeks 5. Alternatively, it is possible to use a complete diet containing compounds that offer skin barrier support. Topical EFAs in a spot-on formulation have also been proven to be effective 6, although this option may be less cost-effective if long-term application is required. Other topical formulations including shampoo, sprays, and lotions containing fatty acids and ceramides have been introduced for CAD. Unfortunately, there is still some inconsistency in the effectiveness of these products, but the clinician should bear in mind that by restoring the epidermal barrier, skin penetration by environmental allergens is probably reduced.
Controlling secondary skin infections
Most atopic dogs are prone to recurrent superficial pyoderma, and papules, pustules, collarettes, squames, and seborrhea are commonly seen (Figure 2). Colonization of the atopic skin by pathogenic Staphylococci spp. (usually S. pseudintermedius) is increased compared to healthy skin, which may be partly explained by lower antimicrobial activity of the cutaneous antimicrobial peptides of the innate immune system. During flares, dysbiosis of the atopic skin microbiota develops, with a relative increase in Staphylococci levels. This dysbiosis is restored with antimicrobial therapy and the remission of lesions 7.
About 40% of atopic dogs have recurrent skin infections with the yeast Malassezia pachydermatis, with a strong odor, greasiness, honeycomb crusts, squames, and paronychia with brown staining of the nails often noticed (Figure 3). A type I hypersensitivity reaction to Malassezia can also occur, leading to severe pruritus 8. Secondary skin infections by bacteria and yeasts must therefore always be controlled, and is achieved by regular use of topical antimicrobial therapy (shampoos, mousses, sprays, wipes and gels). Shampooing with 3% chlorhexidine has been shown to be clinically as effective against bacteria and yeasts as a 2% chlorhexidine solution and miconazole combination 9. Twice weekly washes are generally efficacious, but (depending on the severity of the infection) topical therapy should be administered more frequently initially. The author then uses daily washings for a week, followed by a week of every other day, and then twice a week. Protocols that include twice weekly application of a mousse, gel, or spray on the lesions, in addition to weekly shampooing, seem to work equally well.
Systemic antibiotics should only be used initially when the pyoderma is deep (e.g., with furunculosis (Figure 4), very generalized, or when the owner cannot treat the dog topically. When selecting an appropriate drug, this may either be done after culture and susceptibility testing, or following the basic principles of antibiotic therapy; options include clindamycin (10 mg/kg q12H), cephalosporins (cephalexin 10-30 mg/kg q8-12H), or clavulanic acid-potentiated amoxicillin (12.5 mg/kg q12H). Always treat until both clinical signs and cytological findings of pyoderma have resolved. Recurrent use of antibiotics should be avoided because of the risk of inducing bacterial resistance. Likewise, oral treatment with ketoconazole (10 mg/kg q24H or 5 mg/kg q12H) or itraconazole (5 mg/kg q24H) for yeasts should only be used in very severe cases, as yeasts can (rarely) become resistant to azole derivatives 10. However, remember that (especially with ketoconazole) various undesirable drug interactions are possible.