Inflammatory Airway Disease in Horses

Proposed etiologies of IAD include allergic airway disease, recurrent pulmonary stress, deep inhalation of dust, atmospheric pollutants, and/or persistent respiratory viral infections, most notably EHV-2. IAD often develops after an overt viral respiratory infection and may result from inability of the immune system to fully eliminate viruses or bacteria from small airways. Streptococcus pneumoniae has been isolated from horses with IAD; however, its role in the pathophysiology is unclear, because this population of horses is largely unresponsive (or transiently responsive) to antibiotic therapy.

The most common clinical signs are chronic cough and mucoid to mucopurulent nasal discharge. Fever and auscultable pulmonary abnormalities are rarely seen. Horses with IAD demonstrate poor exercise tolerance at maximal speed. Endoscopic examination reveals mucopurulent exudate in the pharynx, trachea, and bronchi.

Diagnosis of IAD is based on poor race performance and clinical signs. Bronchoalveolar lavage is performed to characterize the type of pulmonary inflammation. Cytologic evaluation of bronchoalveolar fluid will reveal one of the following inflammatory profiles: 1) mixed inflammation with high total nucleated cells, mild neutrophilia (15% of total cells), lymphocytosis, and monocytosis; 2) increased metachromatic cells (mast cells >2% of total cells); or 3) eosinophilic inflammation (5%–40% of total cells). The mixed inflammatory profile likely results from environmental irritation or the consequences of a previous infectious disease.

The type of inflammation in bronchoalveolar fluid will dictate the therapeutic plan. Regardless of the cytologic profile, all horses with IAD should receive aerosolized bronchodilator therapy before exercise to avert exercise- or irritant-induced bronchoconstriction. In horses with a mixed inflammatory cytologic profile, administration of low-dose interferon-α is recommended for immunomodulation and antiviral activity. Interferon-α reduces tracheal exudate and improves cytologic profiles in horses with mixed inflammatory IAD. Eosinophilic bronchoalveolar fluid likely represents a Type I hypersensitivity reaction. In addition to tracheal exudates, peripheral eosinophilia, miliary pulmonary opacities, and eosinophilic pulmonary granulomas may be seen in affected horses. If such fluid is identified, parasitic pulmonary disease should be considered in addition to hypersensitivity pneumonitis. Systemic corticosteroid therapy is recommended to reduce pulmonary inflammation in horses with eosinophilic IAD. Mast cell inflammation likely represents a local pulmonary hypersensitivity response and may represent an early form of recurrent airway obstruction (see Recurrent Airway Obstruction in Horses). In IAD-affected horses with increased mast cells in bronchoalveolar fluid, aerosol administration of an inhaled corticosteroid preparation (beclomethasone or fluticasone) improves clinical signs of respiratory disease.