Equis ISSN 2398-2977

Skin: atopy

Synonym(s): Atopic dermatitis, allergic inhalant dermatitis

Contributor(s): Timothy Nuttall, David Senter, Vetstream Ltd

Introduction

  • Cause: a hypersensitivity disorder in which the horse becomes sensitized to inhaled or percutaneously absorbed allergens such as pollens, molds, and dust.
  • Signs: seasonal or non-seasonal pruritus of the face, ears, ventrum, and legs. Recurrent, pruritic or non-pruritic urticaria. Respiratory disease, eg RAO   Lung: recurrent airway obstruction (RAO)  and headshaking   Behavior: headshaking  may also be manifestations of atopy.
  • Diagnosis: intradermal testing, serology, hematology.
  • Treatment: allergen avoidance, hyposensitization (immunotherapy), corticosteroids, antihistamines, fatty acids.
  • Prognosis: good.

Pathogenesis

Etiology

  • Environmental allergens such as pollens of grasses, weeds and trees, molds, dust, dust mites, storage mites, animal epithelials and others.

Predisposing factors

General
  • Genetic predispostion.
  • Dusty or moldy environment.
  • High levels of pollens.

Pathophysiology

  • An inherited predisposition to form sensitizing antibodies to environmental antigens resulting in mast cell degranulation and clinical signs such as pruritus and/or urticaria   Urticaria / angiedema  .
  • Atopy is classified as a type 1 hypersensitivity reaction.
  • Allergens enter the body from inhalation or percutaneous absorption and bind to allergen-specific IgE antibodies on the surface of mast cells in the skin. This results in mast cell degranulation and release of a wide variety of inflammatory mediators, eg histamine, heparin   Heparin  .
  • It is known in humans, dogs and rodents that atopic individuals tend to produce a T-helper-2 (TH2) lymphocyte response to allergens.
  • TH2 cells produce cytokines such as IL4, Il5, IL6, IL10 and IL13 which help to promote antibody production of B lymphocytes.
  • IL4 and IL13 are essential for the B cell immunoglobulin class switch to IgE.
  • In non-atopic animals, a TH1 response to environmental allergens is produced. Cytokines from TH1 cells can suppress the proliferation of TH2 cells and inhibit IgE production.

It now seems likely that TH1 cytokines participate in the development of chronic lesions and that tolerance is mediated by immunosuppressive cytokines such as TGFb and IL-10.

  • Studies have shown that horses affected with RAO   Lung: recurrent airway obstruction (RAO)   have significantly higher levels of allergen-specific IgE in their bronchoalveolar lavage fluid than normal horses.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Rendle D I, Durham A E, Wylie C E & Newton J R (2010)Results of intradermal testing for the investigation of atopic dermatitis and recurrent urticaria in 50 horses in the south of England.Equine Vet Educ22(12), 616-622 VetMedResource.
  • Rees C A (2001)Response to immunotherapy in six related horses with urticaria secondary to atopy.JAVMA218(5), 753-755 PubMed.
  • Fadok V A (1997)Update on equine allergies.Vet Allergy Clin Immunol5(2), 68-76.
  • Fadok V A (1995)Overview of equine pruritus.Vet Clin North Am Equine Pract 11(1), 1-10 PubMed.
  • Halliwell R E Wet al(1993)Local and systemic antibody production in horses affected with chronic obstructive pulmonary disease.Vet Immunol Immunopathol38(3-4), 201-215 PubMed.

Other sources of information

  • Scott D W (1988)Large Animal Dermatology.W B Saunders. Philadelphia.


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