ISSN 2398-2977      

Skin: atopy

pequis

Synonym(s): Atopic dermatitis, Allergic inhalant dermatitis


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 localized or generalized pruritus. Recurrent, pruritic or non-pruritic urticaria. Respiratory disease, eg severe equine asthma Severe equine asthma and headshaking  Behavior: headshaking may also be manifestations of atopy.
  • Diagnosis: history, clinical examination, intradermal testing and/or serology to define which allergens are involved.
  • 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 epithelial and others.

Predisposing factors

General

  • Genetic predisposition.
  • 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. IL31 can bind neuronal receptors and induce pruritus.
  • 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.

  • Impaired barrier function is usually a feature of atopic skin.
  • Studies have shown that horses affected with severe equine asthma Severe equine asthma 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.
  • Van Damme C M M, van den Broek & Sloet van oldruitenborgh-Oosterbaan (2020) Discrepancies in the bilateral intradermal test and serum tests in atopic horses. Vet Dermatol 31 (5), 390-e104 PubMed.
  • Wilkołek P, Szczepanik M et al (2020) A comparison of multiple allergen simultaneous tests using allergen-specific IgE concentration and intradermal skin tests in atopic horses with pollen allergy. J Equine Vet Sci 90, 102992 PubMed.
  • Radwanski N E, Morris D O et al (2019) Longitudinal evaluation of immunological responses to allergen-specific immunotherapy in horses with IgE associated dermatological disease, a pilot study. Vet Dermatol 30 (3), 255-e78 PubMed.
  • Wilkołek P, Szczepanik M et al (2019) Evaluation of multiple allergen simultaneous (sIgE) testing compared to intradermal testing in the etiological diagnosis of atopic dermatitis in horses. J Vet Sci 20 (6), e60 PubMed.
  • Loeffler A, Herrick D, Allen S & Littlewood J D (2018) Long-term management of horses with atopic dermatitis in southern England: a retrospective questionnaire study of owners’ perceptions. Vet Dermatol 29 (6), 526-e176 PubMed.
  • Hallamaa R & Batchu K (2016) Phospholipid analysis in sera of horses with allergic dermatitis and in matched healthy controls. Lipids Health Dis 15, 45 PubMed.
  • Mueller R S, Janda J et al (2016) Allergens in veterinary medicine. Allergy 71 (1), 27-35 PubMed.
  • Fadok V A (2013) Update on equine allergies. Vet Clin Equine 29 (3), 541-550 PubMed.
  • Marsella R (2013) Equine allergy therapy update on the treatment of environmental, insect bite hypersensitivity, and food allergies. Vet Clin Equine 29 (3), 551-557 PubMed.
  • Stepnik C T, Outerbridge A, White S D & Kass P H (2011) Equine atopic skin diseases and response to allergen-specific immunotherapy: a retrospective study at the University of California Davis (1991-2008). Vet Dermatol 23 (1), 29-e7 PubMed.
  • 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 Educ 22 (12), 616-622 VetMedResource.
  • Rees C A (2001) Response to immunotherapy in six related horses with urticaria secondary to atopy. JAVMA 218 (5), 753-755 PubMed.
  • Fadok V A (1997) Update on equine allergies. Vet Allergy Clin Immunol (2), 68-76 PubMed.
  • Fadok V A (1995) Overview of equine pruritus. Vet Clin North Am Equine Pract 11 (1), 1-10 PubMed.
  • Halliwell R E W et al (1993) Local and systemic antibody production in horses affected with chronic obstructive pulmonary disease. Vet Immunol Immunopathol 38 (3-4), 201-215 PubMed.

Other sources of information

  • Noli C, Foster A & Rosenkrantz W (2014) Veterinary Allergy. Wiley-Blackwell, USA.
  • Scott D W & Miller W H (2011) Equine Dermatology 2nd edn. Saunders, USA.
  • Knottenbelt D C (2009) Pascoe’s Principles and Practice of Equine Dermatology. 2nd edn. Saunders, USA.
  • Scott D W (1988) Large Animal Dermatology. W B Saunders, USA.

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