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Severe equine asthma


Synonym(s): Recurrent airway obstruction (RAO), Chronic obstructive pulmonary disease (COPD), Heaves, Broken wind, Summer pasture associated obstructive pulmonary disease (SPAOPD), Chronic hypersensitivity bronchitis, Chronic hypersensitivity bronchiolitis (CB), Chronic alveolar emphysema, Small airway disease (SAD), Allergic airway disease


  • Common, chronic, progressive lower respiratory disease syndrome of horses and ponies.
  • Severe equine asthma is a relatively new term for lower airway inflammation associated with dyspnea at rest and encompasses recurrent airway obstruction (RAO) and summer pasture associated obstructive pulmonary disease (SPAOPD), often applied to older horses with lower airway disease characterized by inflammation, bronchoconstriction and accumulation of mucus.
  • Cause: chronic exposure to inhaled dust particles containing allergens, eg moldy hay, thermo-actinomycetes, pollens.
  • Signs: range from poor performance, to chronic coughing and increased expiratory effort, and acute onset dyspnea.
  • Diagnosis: clinical signs and history; tracheal aspirate Trachea: transendoscopic aspiration / washing or bronchoalveolar lavage Lung: bronchoalveolar lavage.
  • Treatment: palliative only; change environment - remove allergens and improve management; control inflammation - corticosteroids; increase airway diameter - bronchodilators.
  • Prognosis: clinical signs reversible on removal of allergens; susceptible horses may develop hyper-reactivity.
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  • Exposure of susceptible horses to allergens, eg hay and dusts rich in organic material containing spores of fungi and thermophilic bacteria, pollens.
  • Over 50 species of molds have been identified in stable air.
  • Combination of genetic predisposition, environment and disease history.
  • May be a final common pathway for structural damage to the bronchopulmonary system.

Environmental factors

  • Poorly cured hay (high levels of thermo-actinomycetes - see below).
  • Dusty feeds.
  • Poor ventilation.
  • Prolonged stabling.
  • Endotoxins.
  • Animal debris - dander, hair, urine, feces.
  • Plant material.
  • Insect debris, eg forage mites Lepidoglyphus destructor.
  • Fungal debris, eg spores, hyphae, mycotoxins, sporangia.
  • Pollens.

Predisposing factors


  • Genetic susceptibility to inhaled allergens.
  • Poor stable management:
    • Inadequate clearance of wet bedding (humid environment).
    • Poor ventilation.
    • Poor quality bedding and hay.
  • Changes in bedding or hay.
  • Increased amount of certain plant pollens at a particular time of year.


  • Precise immunological mechanisms not yet determined.
  • Types 1 (immediate), 3 (arthus) and 4 (delayed) reactions implicated.
  • Repeated/chronic exposure to inhaled allergens → deposit on mucosa → primary irritation; inhaled endotoxin may also have a primary irritant effect or potentiate the effects of allergen inhalation.


  • Airway reactivity:
    • Susceptible horses develop severe airway obstruction in response to apparently minor stimuli → hyper-reactive airways.
    • Airway hyper-reactivity is non-specific - occurs in response to exposure to anything, including inflammatory mediators, that might cause bronchospasm.
    • Reactivity lessens when exposure to agents is avoided.
    • Exposure for 7 h to a dusty environment → hyper-reactivity persists for <72 h.
  • Inflammation →:
    • Neutrophils invade airways.
    • Release of proinflammatory mediators, eg histamine → smooth muscle contraction, increased airway sensitivity.
    • Leukotrienes → bronchospasm.
    • Reduced availability of inhibitory mediators, eg prostaglandin E2.
    • Inactivation of nitric oxide, a neurotransmitter in the NANC nervous system.
    • Increased mucous production and secretion + increased bronchial blood flow and vascular permeability → edema and plugging of airways with mucous.
  • Lung function → :
    • Airway obstruction → increased pulmonary resistance + decreased compliance → increased respiratory effort to achieve necessary tidal volume.
    • Ventilation-perfusion mismatching and hypoxemia.

    Although the horse must increase its respiratory effort there is no evidence of hypoventilation expressed as an increase in PaCO2.

    • Increased respiratory drive + airway obstruction → 'heaves' (double expiratory effort).
    • Despite airway narrowing → increased peak tidal flow rates.

Structural changes

  • Clara cells (non-ciliated bronchiolar epithelial cells) undergo ultrastructural alteration even in mild disease leading to degeneration and loss of differentiation.
  • Metaplasia of goblet cells.
  • Focal changes in peribronchiolar alveoli including necrosis of Type I cells, fibrosis, transformation of Type II cells, emphysema and increased numbers of Kohn's pores.
  • Conducting airways show secondary non-specific changes including focal loss of ciliated cells.
  • Chronic inflammation → mucosal and smooth muscle proliferate enhancing the ability of the airways to contract.
  • Although an immune-mediated basis has been supported by many studies, positive skin tests and serum precipitins to fungal and thermophilic actinomycete antigens probably reflect a history of exposure in normal and susceptible horses, rather than a specific susceptibility to severe equine asthma.


  • Chronic.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Couteil L et al (2020) Equine Asthma: Current Understanding and Future Directions. Front Vet Sci 7, 450 PubMed.

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