In the beginning…
In 1906 a Viennese paediatrician named Clemens von Pirquet noted that some of his patients were hypersensitive to usually innocuous entities such as pollen, dust and certain foods. He called this phenomenon “allergy”, a word derived from the Ancient Greek words allos, meaning “other” and ergon, meaning “work” and historically all types of hypersensitivity were classified as allergies, thought to result from inappropriate activation of the immune system.
Allergic Disease
Canine allergic disease
Canine allergic disease manifests most frequently as skin disease or gastrointestinal disease. Some individuals will have clinical signs involving both systems.
Allergic skin disease
Canine pruritic dermatoses which are associated with hypersensitivity include:
- Flea allergic dermatitis (FAD)
- Atopic dermatitis (AD)
- Allergic and irritant contact dermatitis
Gastrointestinal disease
Adverse reactions to food may reflect food allergy or intolerance. Clinical signs include anorexia, weight loss, flatulence, vomiting, diarrhoea and borborygmus.
What is Canine Atopic Dermatitis?
The International Task Force on Canine Atopic Dermatitis definition is as follows: “A genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features associated with IgE antibodies most commonly directed against environmental allergens” (Halliwell 2006).
It is currently accepted, based on clinical experience, that dogs with AD may be hypersensitive to environmental allergens, food allergens (food induced AD) or both.
Certain breeds are recognised as being at increased risk of developing AD; these include the terriers (West Highland White, Cairn, Fox, Yorkshire), Chinese Shar Pei, Cocker Spaniel, Dalmatian, Bulldog, Boxer, Labrador and Golden Retriever.
The currently favoured route for allergen exposure is via percutaneous penetration, facilitated by a defective epidermal barrier and irregularities in cell mediated immunity.
The classical sign of AD is pruritus. The incidence of canine AD in the general population is unclear – studies quote between 3.3% – 30% – but this appears to be increasing, possibly due to the changing lifestyle of dogs; proposed risk factors include spending more time indoors, increased uptake of routine vaccination and ecto/endoparasite control (Hillier, Griffin 2001).
Clinical signs are rarely seen in dogs less than 6 months old, except perhaps in the Shar Pei. Most become symptomatic between the age of 6 months and 3 years. Late onset disease is less common and is rare in dogs over seven years of age.
Dogs may present with the “triad” of facial rubbing, axillary pruritus and paw-licking but lesions can be found anywhere on the body. Initially pruritus may be seasonal, depending on the inciting cause, but may become perennial as an increasingly wide range of allergens become problematic. Secondary (Staphylococcal) pyoderma and Malassezia dermatitis are common complications. Otitis externa may accompany generalised pruritus but can be the major, or only, presenting sign.
Feline Allergic Disease
Feline allergic disease may present as skin, respiratory, GI disease or a combination of these.
Feline pruritic dermatoses which are associated with hypersensitivity include:
- Flea allergic dermatitis (FAD)
- Atopic dermatitis
- Allergic and irritant contact dermatitis
- (Feline eosinophilic granuloma complex)
- (Feline psychogenic alopecia)
Feline atopic dermatitis is less well characterised than it’s canine counterpart. The pathogenesis of disease is unclear and there are no recognised breed associations.
Disease usually manifests between 6 months – 3 years of age as a chronic pruritic, usually corticosteroid responsive dermatosis.
Lesions include miliary dermatitis, over-grooming/barbering, non- lesional alopecia or eosinophilic granuloma complex. These are not pathognomonic for atopy; FAD, cutaneous adverse food reactions, neurological and behavioural problems may have a similar presentation.
Respiratory disease. Feline asthma is a chronic respiratory disease affecting the small airways. The aetiology is imperfectly understood however studies have demonstrated high levels of allergen specific IgE in cats diagnosed with asthma, suggesting the pathogenesis involves a hypersensitivity response (Halliwell 1993) (Caro, Rodriguez, Gonzalez 2002).
A study to investigate the efficacy of allergen specific immunotherapy (ASIT) in cats with eosinophilic bronchitis, diagnosed on clinical findings and tracheal wash cytology and utilising the allervet® serological assay for allergen identification, demonstrated an excellent clinical response in 62.5% of cats (became asymptomatic), with a good response in a 25% (significant clinical improvement but required sporadic supplementation with inhalation therapy). A further 12.5 % improved but required additional oral therapy (Caro Vadillo et al 2010).
The results provide strong support for a hypersensitivity disorder which includes a type 1 component, and demonstrate the potential of ASIT as a management tool for feline asthma.
Gastrointestinal disease. Feline eosinophilic enteritis is one example of an adverse food reaction; other histological patterns of inflammatory bowel disease may also represent adverse reactions to food. Clinical signs include anorexia, weight loss, chronic vomiting/diarrhoea and increased frequency of defecation.
Equine Allergic Disease
Equine allergic disease may present as skin or respiratory disease, headshaking or a combination of these.
Equine pruritic dermatoses which are associated with hypersensitivity include:
- Atopic dermatitis
- Insect bite hypersensitivity (Culicoides spp., Simulidae spp.)
- Urticaria
- Cutaneous adverse food reactions
Genetic influences are recognised as a strong predisposing factor in the development of equine allergic dermatoses. Pruritus is often the primary presenting sign – frequently involving the mane, withers or tail. Lesions include a papular rash, hair loss, urticaria and facial/periorbital oedema. A diagnosis may not be possible based on the clinical presentation alone – findings are rarely specific.
The pathogenesis of equine atopy is incompletely understood; as in other species it is thought to involve a predisposition to develop IgE antibodies against environmental allergens and may result in dematological or respiratory disease.
Age of onset of atopic dermatitis is variable, typically between 18 months and 6 years. Clinical signs commonly involve chronic relapsing pruritus and urticaria with scaling, hyperpigmentation, alopecia and secondary trauma. Lesions may develop anywhere on the body but frequently involve the head, mane and tail.
Insect bite hypersensitivity (sweet-itch) is an allergic reaction to the saliva of biting flies including midges, black flies, stable flies, horse flies and mosquitoes, thought to be mediated by both type 1 and type IV hypersensitivity reactions. Signs develop in young adults with a peak incidence around 3 years and are seasonal (during the fly season); the severity and duration of signs may intensify with time. Lesions usually affect the dorsal midline (mane, rump and tail) and predominantly reflect self-trauma (papular rash, scaling, alopecia, hyperpigmentation, urticaria). Sweet-itch is often a severely irritating and potentially debilitating disease; horses may show behavioural changes or loose weight due to constant discomfort.
Urticaria is a common condition in horses with no age, breed or sex predilection. Classical lesions are flat topped wheals with pitting oedema or angio-oedema. Lesions are transient, should pit under digital pressure and resolve in 24-48 hours although new lesions may develop close by. It may be useful to demarcate lesions in waterproof marker to monitor their progress.
Urticaria describes a clinical manifestation and is not a diagnosis. It has been associated with drug eruptions (penicillin, tetracycline, sulphonamide, PBZ, flunixin, phenothiazine, ivermectin, moxidectin, vaccines), foods, topically applied products (shampoos, ectoparasiticides, rugs, tack), allergic disease (atopy, sweet-itch, contact or irritant dermatitis), systemic disease, stress/excitement and mechanical effects (cold, heat or pressure). In approximately half of all cases there is no identifiable cause.
Cutaneous adverse food reactions have been reported anecdotally in horses. It is a relatively common belief that high protein foods can cause papular eruptions, so called “protein bumps”. Whilst this cannot be explained by our current understanding of hypersensitivity reactions it is possible that plane of nutrition and level of training may modify immune responses and unmask sub-clinical atopy. As with many diseases stress can play a significant role. Horses suspected of suffering from “food allergy” may subsequently be diagnosed with atopy (Littlewood 2001); could this be the equine equivalent of food-induced atopic dermatitis?
Respiratory disease. Recurrent airway obstruction (RAO)/Chronic obstructive pulmonary disease or “heaves” is a chronic condition of horses involving an allergic bronchitis characterised by wheezing, coughing and laboured breathing. Affected horses show a marked increase in respiratory effort and may become increasingly dyspnoeic in response to exercise. A productive soft cough may be induced by feeding and exercise. With long standing disease there may be hypertrophy of the extrinsic respiratory muscles causing the classic “heave line”. Horses with RAO may present in acute respiratory failure as a veterinary emergency.
Allergens precipitating bouts of RAO include mould spores, mites, pollens, hay and grain mill dust.
In a 2006 study (Monreal et al) serum samples from 23 horses with confirmed RAO, 11 horses with non-allergic airway disease and 23 control horses were blindly tested for IgE against various environmental allergens using the allervet® equine serological assay and a serological test performed by a major commercial competitor.
Results from the allervet® test demonstrated excellent sensitivity and negative predictive values (95.7% and 96.0% respectively), with acceptable specificity and positive predictive values (72.7% and 71.0% respectively). The main allergen detected was grain mill dust, followed by mites, grass pollens and moulds.
In comparison the results from the competitor’s test showed lower sensitivity and negative predictive values (69.6% and 66.7% respectively), with poor specificity and positive predictive values (42.4% and 45.7% respectively). Mites were the major allergens detected, followed by tree and weed pollens.
Differences in test performance may be explained in part by the type of allergens included in the panels; the allervet® panel includes grain mill dust, the competitor’s panel does not. allervet® results in clinically confirmed cases of RAO suggest that for some horses grain mill dust is a significant allergen.
These findings support a Type 1 hypersensitivity component in the development of RAO (although the pathogenesis also involves neutrophil mediated inflammation) and indicate that serum IgE evaluation can be a useful tool when investigating the inciting cause of allergic respiratory disease.
Studies are ongoing to evaluate concentrations of allergen specific IgE in bronchoalveolar lavage fluids from horses with respiratory disease.
Headshaking and other head vices are thought to be manifestations of hypersensitivity in some horses. In an allervet® study from 2009 we found that 30% of horses undergoing serological evaluation for allergic disease presented with a combination of respiratory signs and head shaking.
