ACCREDITED CPD
ACCREDITED CPD
Shaping the future of animal health
Canine Atopic Dermatitis
A Practical Approach A to Z
Dr Heidi Schroeder, BVSc MMedVet(Med)
Small Animal Physician
Willow Park Small Animal
Medicine Specialist Hospital,
Willow Glen, Pretoria
Pretoria, (012) 813 8009
Pathophysiology
CAD is mainly caused by aeroallergens that gain access
to the body via the percutaneous route. Outbreaks of
atopy have also been linked to allergens presented via
other routes e.g. the digestive tract. Numerous allergens have been identified in the pathogenesis of CAD.
These include house dust and storage mite allergens,
pollens from grasses, trees and weeds, mould spores,
epidermal allergens, insect allergens and miscellaneous allergens such as kapok. The majority of cases
result from hypersensitivity to house dust and storage
mite allergens, leading to a non-seasonal dermatitis.
Pollens usually lead to a seasonal dermatitis.
Atopic dogs are predisposed to penetration of the allergens because they have an inherited dysfunction of
the immune system as well as a defective cutaneous
epidermal barrier function.
From a practical perspective this means that all of the
potential components that contribute to the pathogenesis (immune dysfunction, infection, and epidermal barrier defects) need to be identified and considered in the diagnosis and eventual treatment plan for
successful control.
There is increasing evidence that animals with canine atopic dermatitis (CAD have abnormalities in their skin barrier function and that these changes contribute significantly to the disease severity. It is not yet clear if this is innate
(genetic) or acquired. The stratum corneum plays a vital role in the barrier function of the skin in mammals. Some of
the abnormalities that have been identified include: abnormal intracellular lipid lamellae, abnormal stratum corneum
morphology and abnormal and reduced ceramide content.
Atopic dogs are predisposed to penetration of the allergens because they have an inherited dysfunction of the immune system as well as a defective cutaneous epidermal barrier function. Both lipid and protein skeleton (fillagrin)
abnormalities have been described which lead to a weakened stratum corneum - which allows both allergens and
pathogens (bacteria) access to the deeper layers
The epidermis is composed of 4 or 5 layers of cell types depending on the region. The superficial stratum corneum
layer of the skin is made up of 10 – 30 layers of cells (keratinocytes and corneocytes). The cells are flattened and fit together like bricks. They are each encapsulated by water-retaining keratin and ceramide proteins as well as cholesterol
and free fatty acids. The cells are held tightly together by a skeleton of protein junctions. In-between the cell layers are
multiple stacked lipid layers (lamellae).
[email protected]
Definition
Canine Atopic Dermatitis (CAD) is defined as an inflammatory and allergic skin disorder, affecting genetically predisposed dogs, with characteristic clinical
features. It is generally associated with IgE antibodies
most commonly directed against environmental allergies (Type 1 hypersensitivity). The patient becomes
sensitised to environmental antigens that cause no
reaction in non-atopic dogs. In addition, is now also
recognised that CAD is a complex and multifactorial
disease involving immune dysregulation, allergic sensitisation, skin barrier defects, microbial colonisation
and environmental factors. CAD affects 3 to 15% of
the canine population. In some studies up to 50% of
dermatology cases are CAD cases.
Epidermal barrier function:
The following steps are important in the pathogenesis:
1. Allergens access the body via the percutaneous
route. Alteration of the epidermal barrier function
facilitates penetration via this route.
2. Once the allergen enters the epidermis it binds to
the epidermal Langerhans cells where it undergoes internal processing and is presented to naïve
T cells in the draining lymph nodes.
3. In allergic individuals this leads to Th2 differentiation/polarisation and these Th2 lymphocytes
release cytokines including IL-4, IL-5, IL-13 that
stimulate IgE production by B cells that bind to
cutaneous mast cells.
4. Re-exposure to allergens causes mast cell degranulation, cytokine release along with homing
of T cells to the epidermis. This leads to cutaneous inflammation, erythema and pruritus.
5. A variety of inflammatory mediators are involved
including histamine, leukotrienes and proteases
from mast cells and interleukins from keratinocytes.
6. Atopic dogs have impaired cell-mediated immunity predisposing them to secondary bacterial
and yeast infections.
7. It has become clear that in addition to the complex immune response, both epidermal barrier
dysfunction and infection play an important and
interrelated role in the pathogenesis and severity
of disease.
Epidemiology
The peak age of onset is between one and three years
of age, with a range of 6 months to 6 years. It is relatively uncommon but not impossible to see the disease first appear in middle aged or older dogs.
It can affect any breed, but there is a greater incidence
in pure bred dogs such as Terriers, Golden and Labrador Retrievers, German Shepherd dogs, Dalmations,
English Bull dogs and Shar Pei dogs. There are sig-
The epidermis is [