Hypersensitivity pneumonitis is a condition that appears to be similar to farmer’s lung disease in people and occurs in both acute and chronic forms in adult cattle. The human and bovine forms of the disease may coexist on problem farms because of common exposure to dust from moldy hay.
The disease occurs when sensitized individuals inhale antigens from thermophilic actinomycetes, commonly the spores of Micropolyspora faeni. The actinomycetes proliferate in vast numbers in hay, grain, or other vegetable material that has overheated to ~150°F (65°C) after damp storage (30%–40% moisture content). Dust that contains large numbers of spores is released when this moldy hay is shaken. The small size (1 μm) of the spores allows them to reach the smallest airways and alveoli to provoke a reaction that has been termed a “hypersensitivity pneumonitis”; this is considered to be predominantly a Type III hypersensitivity reaction, although a Type IV hypersensitivity component is suspected (see The Biology of the Immune System et seq).
Affected herds are found in areas where rainfall is usually significant during the haymaking season, suggesting that a clinical problem may arise only after repeated sensitization and challenge from the spores. Clinical disease tends to arise during the latter half of the winter feeding period and usually only when moldy hay is fed indoors. Under such circumstances, serum antibodies (usually detected by immunodiffusion) to M faeni are widespread among adult cattle by the end of each winter feeding period, and many apparently healthy cattle are seropositive. By contrast, few adult cattle are seropositive on other farms on which “good” hay or grass silage is fed.
Cattle may succumb to the acute form of the disease over a period of weeks. Usually, only severe acute cases are noticed. There is respiratory distress, anorexia, and agalactia in animals ≥5 yr old; coughing and pyrexia also occur, and adventitious sounds are occasionally heard on auscultation. Death is rare.
The chronic disease usually has a higher morbidity; in most instances, the signs are weight loss, poor production, and persistent coughing. Affected cattle are fairly bright and eat reasonably well, but tachypnea, hyperpnea, and coughing are widespread. Auscultation may reveal cranioventral crackles and sometimes, in more severe cases, scattered rhonchi. Exercise intolerance may be seen, and congestive cardiac failure can develop if pulmonary fibrosis is widespread.
The macroscopic lesions are often unremarkable; usually, there is mild peripheral lobular overinflation with diffusely scattered, small, gray, subpleural spots. Although transient pulmonary edema may be a feature of severe acute cases, the histologic lesions consistently found are interalveolar cellular infiltration, epithelioid granulomata, and bronchiolitis obliterans. In some chronic cases, small foci of alveolar epithelial hyperplasia and metaplasia with interstitial fibrosis are found. These areas may extend to include most, if not all, of the lung substance to produce cases clinically indistinguishable from diffuse fibrosing alveolitis (see Diffuse Fibrosing Alveolitis in Cattle). Circumstantial evidence suggests that some cases of diffuse fibrosing alveolitis are the end stage of hypersensitivity pneumonitis.
Because it is often impossible to completely shield cattle from further challenge, most recover only partially after dexamethasone treatment (1 mg/5–10 kg body wt). However, improvement is usually marked when cattle are turned out in the spring. Prevention is difficult in areas where hay is likely to be wet during the curing process and it is not possible to alter the feeding regimen.