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Rational Therapy of Inflammatory Airway Disease in Equine Athletes
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1. Introduction
Inflammation is common in the lower respiratory tract of horses, due to their constant exposure to irritant material in the environment, the inhalation of cold dry air during intense exercise, and exposure to a variety of infectious diseases. The greatest challenge for the clinician lies in detecting this inflammation in horses that are not showing outward clinical signs of disease. We are usually comfortable identifying the horse affected with recurrent airway obstruction (RAO) because these horses by definition exhibit increased respiratory effort at rest, but it is much more challenging to assess the athletic horse that shows no evidence of resting pulmonary dysfunction. Typically, such an animal has been reported to suffer from exercise intolerance, poor performance, and/or coughing when worked. Horses exhibiting this pattern of abnormalities are often suffering from a condition termed inflammatory airway disease (IAD),1 and this condition is of increasing interest to owners, trainers, and veterinarians who want to ensure that these horses can achieve their full athletic potential.
Stabled horses live in environments containing extremely high amounts of particulates in the air caused by a combination of poor ventilation and dusty conditions.2 This exposure is exacerbated by the fact that they consume a diet primarily composed of hay, which inevitably contains dusts and mold spores that are potentially very irritating to the lower respiratory tract when inhaled. Human activity in the stable environment often leads to increased exposure to aerosolized antigenic material as well.3 Horses are also exposed to potentially noxious gases such as ammonia and irritant material such as endotoxin in organic dusts.4 Because horses are obligate nasal breathers, the upper respiratory tract is able to filter out much of the inhaled particulate material and minimize the exposure of the lungs to these materials. Unfortunately, this filtration system is not perfect, and very small particles (less than 5 to 10 microns in diameter) and gaseous materials are able to pass freely down the airways and reach the small airways and alveoli. These materials can initiate a nonspecific immune response that culminates with the movement of neutrophils, eosinophils, and/or mast cells into the alveolar and airway lumen and the increased production of mucus. This inflammatory response also results in activation of irritant receptors in the airway epithelium, triggering reflex bronchoconstriction and coughing. Although this is normally protective by limiting exposure of the alveoli to potentially noxious material, it results in impairment of pulmonary function. In addition, the presence of this active inflammatory response leads to tissue inflammation, with edema and exudation further decreasing the functional diameter of the airway. Over time, this lower respiratory tract inflammation may cause permanent tissue damage and permanent impairment of pulmonary function. Prolonged exposure to antigenic materials also may lead to the development of allergic airway disease, and, for this reason, one must consider that IAD may represent a preliminary stage in the development of RAO, although this relationship remains a matter of some debate.
Further complicating this situation is the fact that young horses being introduced to active training are fairly naïve to respiratory viral infections such as equine influenza, rhinovirus, and rhinopneumonitis. These young animals are introduced into environments containing large numbers of horses, many of which are frequently transported to other sites for competitions where they comingle with other groups of horses. The end result is that young horses may suffer from clinical viral respiratory infections, subclinical infections, or strong immune responses to viral agents. These conditions can result in lower respiratory inflammation that can impair clearance of antigenic and irritant material from the lower respiratory tract.5 At the same time, they are athletically active, which results in the inhalation of large volumes of air that exceed the ability of the upper respiratory tract to adequately warm and humidify the incoming air. This exposure of the lower respiratory tract to cold, dry air represents a strong proinflammatory stimulus and may be synergistic in the development of lower airway inflammation with the other risk factors previously discussed.6
The clinical presentation of the horse with IAD is typically that of a horse with a history of poor performance, exercise intolerance (fading) or coughing, with or without excess tracheal mucus.1 These horses do not exhibit increased respiratory effort at rest or any systemic evidence of infection, such as fever or an abnormal complete blood count. There is some evidence to suggest that coughing may be more common in older, nonracing athletic horses with IAD as compared with young racehorses.7 The most useful confirmatory diagnostic technique for evaluating these horses is bronchoalveolar lavage (BAL) because it gives insight into the character and degree of inflammation in the small airways and alveoli. There is some debate among the experts in this field because there is some evidence that endoscopic evaluation for tracheal mucus is also sensitive and specific for this condition, but BAL remains the gold standard. Endoscopy carries the advantage of being readily performed in the field, and often these horses are scoped to assess for exercise-induced pulmonary hemorrhage (EIPH). The limitation of endoscopy is primarily due to the somewhat subjective nature of this assessment, but horses with IAD will typically exhibit multiple specks of mucus along the trachea, a pool of mucus at the tracheal inlet, or a continuous stream of mucus of variable width.8
BAL cytology in horses with IAD demonstrates increased numbers of neutrophils (>5%), mast cells (>2%), or eosinophils (>1%) with increased mucus.9 If there is any suspicion of an infectious component, a tracheal aspirate should be performed prior to the bronchoalveolar lavage and the sample submitted for cytology, gram stain and bacterial culture, and sensitivity testing. Thoracic ultrasonography and radiography are of limited use in the diagnosis of IAD. Pulmonary function testing can provide additional information regarding the degree of pulmonary dysfunction and the presence of airway hyperreactivity, but this requires specialized equipment and is typically only performed in certain referral settings. A simple discriminatory test can be used to ascertain if a horse is affected by IAD versus RAO, and this is a hay challenge. Horses with IAD exposed to moldy hay may exhibit increased coughing and/or pulmonary neutrophilia on BAL, but they do not develop increased respiratory effort at rest, which would be consistent with RAO.10 EIPH can be difficult to differentiate from IAD and may represent a contributing factor to IAD in some horses. EIPH is identified by the detection of blood on tracheal endoscopy after exercise or the presence of large numbers of hemosiderin-containing alveolar macrophages on BAL.
The absence of fever or other systemic signs of infection can readily differentiate IAD from a number of other diseases, and these include respiratory viral infections, bacterial pneumonia, pleuropneumonia, and fungal pneumonia. More challenging differentials can include equine multinodular pulmonary fibrosis (EMPF), neoplasia, and lungworm (Dictyocaulus arnfieldi) infestation. Thoracic radiography is invaluable in identifying EMPF and pulmonary neoplasia, whereas direct examination of tracheal wash fluid represents the most reliable means of identifying lungworm infestations. [...]
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