Canine atopic dermatitis (CAD) is a disease that has been recognised by veterinary dermatologists for almost a century. The first paper to suggest that eczema in the dog was an allergy was published in 1933 (Schnelle, 1933). In their first edition of Veterinary Clinical Immunology in 1989, Gorman and Halliwell defined canine atopic dermatitis (referred to at the time as atopy) as an inherited predisposition to develop IgE antibodies to environmental allergens resulting in allergic disease (Gorman and Halliwell, 1989).
As our knowledge of the pathogenesis of the disease has increased since that time, the definition of CAD has evolved. A recent excellent review article by Marsella described CAD as a common genetically inherited clinical syndrome that encompasses a diversity of mechanisms and can have a variety of triggers. Development of clinical disease is the result of genetic factors and environmental conditions which shape the resulting immune response (Marsella, 2021).
The simplistic view of CAD which was held last century (type 1 hypersensitivity reaction to environmental allergens, which for a long time were thought to be inhaled, leading to pruritus) has now been superseded by the recognition of a much more complex disease process through the interaction of a range of factors (Figure 1). CAD is not just a hypersensitivity reaction to environmental allergens.
How can our knowledge of the pathogenesis of canine atopic dermatitis help us tailor therapy for our patients?
Many different factors need to be considered when choosing therapy for cases of CAD. All treatment will be needed on a lifetime basis, meaning that the ease of application of therapy for patient and owner, the safety of the regime (ie side effects versus benefits) and the ongoing expense all need to be discussed with the owner. There is little point putting together a complex combination of medications if the owner’s lifestyle, capabilities and finances do not allow its long-term use. In addition, the complexity of the pathogenesis of CAD, where the interaction of multiple factors undoubtedly plays different roles in individual dogs, means there can be no one therapy that is suitable for every dog with CAD. The most successful protocols are usually multimodal.
The complexity of the pathogenesis of CAD, where the interaction of multiple factors undoubtedly plays different roles in individual dogs, means there can be no one therapy that is suitable for every dog with CAD. The most successful protocols are usually multimodal
All dogs with atopic dermatitis benefit from ongoing ectoparasite control. It is well recognised that reactions to ectoparasites can lead to an increase in inflammation and pruritus and push atopic dogs over their pruritic threshold, so maintenance therapy is important.
As diet is known to be a trigger for CAD, many dogs also need some form of ongoing dietary management. Where the institution of a hypoallergenic diet has produced a complete or partial improvement in clinical signs, it is important to undertake dietary challenge to establish which specific ingredients of the dog’s diet induce clinical signs. This allows specific advice to be given for ongoing feeding regimes.
|Proactive therapy||Reactive therapy|
|Allergen-specific immunotherapy (ASIT)|
• Sublingual ASIT (SLIT)
• Subcutaneous ASIT (SCIT)
• JAK inhibitors
• Monoclonal antibodies to IL31
While the control of pruritus is important, it should form a part of a broader holistic approach. The most effective of the drugs, accepted on a sound evidence base, to control pruritus in CAD are often referred to as foundation drugs. These include allergen-specific immunotherapy, glucocorticoids, ciclosporin, JAK inhibitors and monoclonal antibodies to IL31. This group of foundation drugs can be subdivided into proactive and reactive regimes (Table 1). Reactive therapy is generally given to control clinical signs after they occur. Proactive therapy aims to control the disease rather than responding to it after it has happened.
While foundation drugs help control inflammation and modulate the aberrant immune response in dogs where it occurs, there is only minimal evidence to suggest they are able to improve skin barrier impairment which is known to promote cutaneous dysbiosis and increased allergen penetration (Marsella et al., 2020). There is no doubt that changes in the skin barrier, the immune response and the skin microbiome are interconnected meaning that any therapy must be directed at various areas concurrently to maximise the benefit (Marsella, 2021).
Skin barrier defects in CAD
Topically applied emollients and moisturisers in the form of shampoos, sprays and mousses, and oral essential fatty acid supplements should therefore play a part in a multimodal approach to the therapy of CAD.
It is widely accepted that skin barrier defects occur in CAD (Inman et al., 2001). Measurement of lipids in the skin of dogs with atopic dermatitis has shown a reduction in the levels of free fatty acids and ceramides (Chermprapai et al., 2018). Electron microscopy of the stratum corneum has shown disorganisation of the lamellar lipids within the skin (Inman et al., 2001; Popa et al., 2012) but it has also shown the potential to improve barrier function by the use of topically applied lipids (Popa et al., 2012) and orally administered essential fatty acids (Popa et al., 2011). Topically applied emollients and moisturisers in the form of shampoos, sprays and mousses, and oral essential fatty acid supplements should therefore play a part in a multimodal approach to the therapy of CAD.
Skin microbiome and CAD
Dogs with atopic dermatitis have been shown to have a reduction in the richness of their skin microbiome and an increased presence of Staphylococcus compared to normal dogs (Rodrigues Hoffmann et al., 2014). Allergen challenge is recognised as causing an exacerbation of that dysbiosis (Pierezan et al., 2016). However, the use of both antibiotics and topical antiseptics has shown that it is possible to increase the biodiversity in atopic dogs to more normal levels, therefore reducing the risk of the development of bacterial infection (Bradley et al., 2016). Topical antiseptics such as chlorhexidine, which has been shown to be useful to treat superficial pyoderma (Borio et al., 2015), also have a part to play prophylactically in atopic dogs prone to infection. Regular use of a chlorhexidine shampoo, mousse or spray has the potential to minimise the dysbiosis seen as allergen challenge occurs and acts to prevent the development of infection.