Atopic dermatitis is a common hypersensitivity reaction pattern that is associated with a typical history and characteristic clinical signs:
– Classic atopic dermatitis (AD) is associated with sensitisation to environmental allergens (pollens,dusts and/or moulds). The patient may or may not produce immunoglobulin E (IgE) antibodies to allergens.
– Food-induced atopic dermatitis (FIAD) is used to describe cases where food is one of the triggers for the skin condition. Dogs with FIAD may or may not have concurrent sensitisation to environmental allergens.
Aetiology and pathogenesis
The development of atopic dermatitis is a complex interaction between genetics and the environment involving poor skin barrier function, abnormal skin inﬂammation and sensitisation to environmental and/or food allergens. Subsequent self-trauma, altered cutaneous microﬂora populations and secondary staphylococcal and Malassezia skin and ear infections drive chronic inﬂammatory changes. Some dogs become sensitised to staphylococcal and Malassezia proteins and glycoproteins, which then act as endogenous allergens.
Most known allergens are proteins, but carbohydrates are likely also to play a role. There is evidence that constant exposure to certain allergens (such as ﬂea saliva) at a young age may impart tolerance, whereas intermittent exposure or exposure later in life often triggers an allergic response.
T lymphocytes are the main cells involved in atopic dermatitis. Exposure to allergens is by inhalation, ingestion or cutaneous penetration. These allergens are presented by Langerhans’ cells causing sensitisation of memory T cells. Subsequent allergen exposure and T-cell activation release inﬂammatory mediators that cause skin barrier dysfunction, skin inﬂammation and pruritus. Secondary yeast and bacterial infections greatly intensify the symptoms. The cascade of inﬂammatory mediators recruits and activates other cells (e.g. mast cells, eosinophils, neutrophils, macrophages and keratinocytes) that contribute further to the skin inﬂammation and skin barrier dysfunction.
The clinical features of canine atopic dermatitis are extremely variable, with no single physical or historical fnding that defnitively diagnoses the disease. The true incidence of canine atopic dermatitis is unknown and probably varies by geographical region, but it is thought to affect nearly 10% of all dogs (and more in predisposed breeds). There are well-recognised breed predispositions, although these vary regionally and any breed or cross can be affected.
Generally, clinical signs are frst seen when dogs are between 1 and 3 years of age, and at least some signs should be present before age 6 years. However, the disease has been noted in very young (3 months old) and older (7 years old) animals.
Seasonal disease or seasonal ﬂares are commonly associated with pollen allergies, and the clinical signs should match local pollen production (although seasonal parasites such as Neotrombicula autumnalis should be eliminated). Year-round clinical signs are associated with sensitivity to indoor allergens and/or foods.
About 7–25% of allergic dogs have a food allergy, alone or in combination with an environmental allergy. Clinical signs before 1 year of age, nonseasonal symptoms and concurrent gastrointestinal symptoms are often associated with allergy to foods. Dogs with food allergy tend to react to more than one food. Beef, lamb, chicken, dairy products,
maize, wheat, soy and eggs all seem to be common allergens in canine food allergy, although the data are poor and this may reﬂect feeding patterns. Food allergic dogs may have a higher incidence of gastrointestinal signs, although more subtle abnormalities (e.g. more than three bowel movements/day, borborygmi, ﬂatulence, variable faecal consistency, straining, blood and mucus) are more common than vomiting or diarrhoea.
Pruritus and erythema are the primary lesions in atopic dermatitis.
The degree of pruritus and erythema varies from very mild to intense and may be generalised or localised. Some animals, particularly with acute disease, have no primary lesions and show only pruritus. Erythema may be localised to ears, periocular skin, muzzle, ventral neck, axilla, groin, ﬂank, feet (especially the interdigital webs) and ﬂexor surfaces (under the tail, elbow, carpus and tarsus).
Secondary staphylococcal and Malassezia skin and ear infections are very common, and greatly intensify the pruritus and inﬂammation.
Chronic or recurrent yeast and/or bacterial otitis is seen in 80% of atopic dogs and may be the only or most prominent clinical sign in up to 20% of cases. Protracted inﬂammation leads to hyperplasia of the tissues on the inside of the pinnae and the ear canals. It also predisposes to sebaceous and ceruminous hyperplasia, resulting in excess wax accumulation and stenosis, which predisposes to further infection.
Periocular dermatitis results in varying degrees of erythema, alopecia, excoriation and lichenifcation about the eyes. Conjunctivitis is seen in about 80% of atopic dogs, and they may scratch at their eyes or rub them along furniture or the ﬂoor .
It may occur as the only sign ort ogether with other features of allergic dermatitis. Some dogs develop meibomian adenitis with granulomatous thickening of the eyelid margins, crusting nd draining tracts.
Acral lick dermatitis . Atopic dermatitis more commonly triggers acral lick dermatitis than anxiety, although concurrent psychogenic issues may make some atopic dogs more likely to develop acral lick lesions. These lesions almost always involve a secondary staphylococcal infection and sometimes become obsessive. These lesions are very diffcult to resolve without treatment of the underlying cause.
Interdigital furunculosis or cysts are a common and complex problem, and atopic dermatitis is the most common primary trigger. Inﬂammation in the interdigital skin results in the walls of the hair follicles becoming hyperplastic and hyperkeratotic. A follicle may become plugged and expand as sebaceous and apocrine gland secretions continue to be secreted into it. Finally, it ruptures into the dermis, resulting in a foreign body reaction
to sebum, keratin and hair. Bacteria in the hair follicles may lead to secondary infection.
The papules or nodules may break open and drain a serosanguineous ﬂuid. In many cases these lesions will develop
spontaneously and then disappear. Single or multiple feet may be affected.
Perianal dermatitis is often misdiagnosed as either intestinal parasitism or anal sacculitis . Lesions occur in the skin under the tail as well as in the skin of the perianal area. Erythema may be the only fnding in some cases, but in others the affected skin can become chronically inﬂamed and hyperplastic. Animals will lick excessively, drag their perineal areas across the ﬂoor or spin in circles while sitting to relieve the pruritus. Chronic changes and bacterial colonisation may predispose to anal sac impaction and infection.
Excoriations, hyperpigmentation, lichenifcation, seborrhoea, scaling, thinning hair and alopecia result from chronic skin inﬂammation, infections and self-trauma (licking, biting, chewing, rubbing and/or rolling).
However, these are non-specifc and can be associated with any chronic dermatitis.
• Parasites (ﬂeas, mites and lice).
• Yeast or bacterial infection caused by other disease.
• Dermatophytosis .
• Epitheliotrophic lymphoma .
• Pemphigus foliaceus .
• When affecting the ears only: ear mites, foreign body or middle-ear disease .
• When affecting periocular skin only: demodicosis, dermatophytosis, staphylococcal pyoderma, meibomian gland adenitis and other causes of conjunctivitis.
• For acral lick dermatitis lesions only.
• When symptoms affect the interdigital areas of feet only : hookworm dermatitis, interdigital cysts, demodicosis, contact dermatitis, necrolytic migratory erythema.
Atopic dermatitis is diagnosed by history, clinical fndings, ruling out other diseases and response to therapy. Hair plucks, tapestrips and skin scrapings should be taken from multiple affected locations to rule out demodicosis,
Cheyletiella and Neotrombicula spp. and lice, and possibly fnd sarcoptic mange. A fungal culture should be obtained if this is suspected, although it is rarely pruritic in dogs. Cytology for yeast and bacterial infections should be taken from several affected locations, especially the ears and feet (if affected). Infections should be treated and cleared, and an 8-week broad-spectrum treatment trial for ﬂeas, lice and mites should be performed. If the pruritus is year-round, an 8-week food trial should be started. If the pruritus persists then intradermal or serological allergen tests to identify allergens for allergen-specifc immunotherapy can be considered .
Positive intradermal or serological tests for staphylococcal and/or Malassezia allergens should prompt rigorous topical antimicrobial therapy to reduce microbial burdens on the skin and in the ears.
Diagnosis of food allergy
The diagnosis of a food allergy is based on feeding a restricted diet composed of unique ingredients to which the animal has never, or only very rarely, been exposed. It is therefore critically important to obtain a full dietary history including data on commercial diets, scraps or leftovers, biscuits or chews, ﬂavoured medicines and any vitamin or mineral supplements. However, this may be diffcult where the owner cannot recall which foods have been fed or is unaware of the ingredients in commercial foods because overthe-counter and even prescription diets may contain
ingredients not on the label.
Serological food allergen tests are of limited value. Very few have been validated, and the positive predictive values are low (30–70%). However, the negative predictive values tend to be higher (approximately 80%), so they could be used to identify foods suitable for inclusion in a diet trial. Closed-cup patch tests with fresh foods are more accurate but are diffcult to perform outside specialist centres.
Diet trials are ideally performed using homecooked diets or commercially prepared hydrolysed or limited-ingredient prescription diets. Homecooked diets are in theory better because the foods can be very restricted, but they are not nutritionally balanced for very young animals, dogs with specifc nutritional needs and long-term use and are labour
intensive, and may (depending on the ingredients) be more expensive. Commercial single protein diets are easier to feed and should be nutritionally balanced, but it may be diffcult to fnd a diet with suitable ingredients. It is important not to confuse ‘novel’ with ‘exotic’, e.g. dogs sensitised to beef are likely to react to closely related species such as water buffalo, bison, antelope and sheep, but are unlikely to react to less closely related species such as horse and rabbit. Hydrolysed foods avoid some of these problems, but these diets must be completely hydrolysed to avoid
reactions, and a few dogs may still react to the highmolecular-weight maize-starch allergens present in these foods. These diets may also be more expensive and less palatable. In short, there is no single ideal approach to a food trial. The trial and the diet should be selected carefully, considering the owners’ wishes and abilities. Treat options (e.g. limited ingredient treats, shaped and cooked kibble or tinned food, and/or crisps, liver cake or jerky from novel sources) must be given where necessary to encourage compliance. Other problems can include scavenging, ﬂavoured
medications, dropped food, licking other animals’ ‘empty’ food bowls and coprophagia.
The length of a diet trial necessary to confrm an adverse reaction to food is controversial, but, for dogs, most authorities now recommend at least 8 weeks (and sometimes 10 weeks) for a good response.9 However, it is useful to follow cases carefully because gastrointestinal signs will improve more rapidly than acute dermatitis, which improves
quicker than chronic dermatitis. For example, if there are still gastrointestinal problems after two weeks, check compliance and/or consider changing the diet. In contrast, rapid resolution of the gastrointestinal signs should encourage persisting with the food trial.
As allergy symptoms commonly ﬂuctuate, an animal that improves with a restricted diet should be challenged with its original diet, which should include all treats, scraps, biscuits, chews and dietary supplements. If a food allergy is involved, there will be an increase in pruritus within 7 days of the dietary challenge (again gastrointestinal signs often relapse sooner). If there is no increase in pruritus after the dietary challenge, then a food allergy can be ruled
out and the apparent improvement was probably the result of some other effect. If there is recrudescence of pruritus with the dietary challenge, then the restricted diet should be reinstituted and there should once again be resolution of the pruritus. It is helpful to identify the specifc foods to which the animal is reacting using a series of sequential food challenges, with 2 weeks between each new food item.
Failure to recognise and treat secondary infections and ectoparasites during a dietary trial is a common cause of problems. Another major reason for poor compliance during a dietary trial is continued pruritus. One solution is to allow the use of short courses of glucocorticoids or oclacitinib for the frst 3–4 weeks of the trial and then taper to see if the improvement can be maintained. Alternatively, the owners can give 3- to 7-day courses of glucocorticoids
or oclacitinib at their discretion to manage unacceptable pruritus during the food trial.