Acute Bovine Pulmonary Emphysema and Edema
(Fog fever, Bovine atypical interstitial pneumonia)
Acute bovine pulmonary emphysema and edema (ABPEE) is one of the more common causes of acute respiratory distress in cattle, particularly adult beef cattle, and is characterized by sudden onset, minimal coughing, and a course that ends fatally or improves dramatically within a few days. It is a disease involving groups of cattle; morbidity may be >50%, although usually only a small minority develops severe respiratory distress. Typically, ABPEE occurs in the fall, 5–10 days after change to a better, often lush, pasture. A similar condition has been reported when cattle are fed on a wide variety of grasses, alfalfa, rape, kale, and turnip tops.
Metabolites of the naturally occurring amino acid l-tryptophan probably are responsible for many outbreaks. In the rumen, l-tryptophan is degraded to indoleacetic acid, which can be converted to 3-methylindole by some ruminal microorganisms. 3-Methylindole is absorbed into the bloodstream and is the source of the pneumotoxicity after metabolism by the mixed function oxidase system, which is very active in the lungs. Apparently, the level of l-tryptophan in crops is most likely to be high in lush, rapidly growing pastures, particularly (but not exclusively) in the fall.
ABPEE is most common in adult beef cows but may occur in either sex and in dairy or beef cattle under similar management conditions. Nursing calves are unaffected. Outbreaks usually develop within 5–10 days of a change to better grazing and rarely occur in animals that have been on a field >3 wk.
Mild cases may go unnoticed. Cattle are subdued but still alert; there is tachypnea and hyperpnea, but auscultation is usually unrewarding. Such cattle usually recover spontaneously within days. Severely affected cattle show extensive respiratory distress with mouth breathing, extension of the tongue, and drooling. A loud expiratory grunt is common, but coughing is unusual. In the early stages, auscultation reveals surprisingly soft respiratory sounds. Mild exercise increases dyspnea and may precipitate death. If death does not occur, the animals improve dramatically and resume eating by the third day. At this stage, auscultation reveals harsh respiratory sounds and, in some animals, dorsal (emphysematous) crackles. Some cattle have subcutaneous emphysema extending along the back from the withers. Full clinical recovery may require 3 wk.
In affected cattle that have died or been slaughtered in extremis, the lungs are heavy and do not collapse normally. They are widely affected, with various degrees of firmness; there is extensive edema and emphysema, often with the formation of large, air-filled bullae in interlobular and subpleural regions. Submucosal hemorrhages are often present on the larynx and in the trachea and larger bronchi. Histologically, the lesion is characterized by congestion, alveolar edema, hyaline membrane formation, and areas of early alveolar epithelial hyperplasia of type II pneumocytes; occasionally, areas of bronchiolar necrosis may be found. The emphysema is often dramatic and is limited to interstitial fascia, where it is accompanied by edema.
In animals slaughtered after 3 days of illness, the lungs are still heavy and do not collapse normally. They are pinkish gray and of increased firmness; edema and emphysema are inconspicuous or absent. Histologically, widespread alveolar epithelial hyperplasia characteristic of a diffuse, acute, proliferative alveolitis is seen.
Severely affected animals have so little pulmonary reserve that any driving or handling must be done with caution to prevent immediate death. Removal of cattle from the offending pastures may not prevent the development of new cases for the next 4–7 days. No treatment has been identified that will reverse the fully developed lesions of ABPEE.
One approach to control is dietary management, including the following options: 1) avoiding pastures likely to induce ABPEE, 2) feeding hay before turn out on pasture and limiting exposure time on suspect pastures, 3) limiting grazing time and gradually increasing exposure to the pasture over time, 4) using pastures before they become lush, 5) delaying use of lush pastures until after a hard frost, 6) initially grazing pastures with less susceptible stock (cattle <15 mo old or sheep), or 7) using strip grazing.
A medical approach to control involves feeding monensin or lasalocid, which inhibit the bacteria that convert l-tryptophan to 3-methylindole. Treatment with monensin can be started 1 day before introduction to pasture, whereas lasalocid requires a 6-day pretreatment period. These drugs are of no benefit after onset of clinical signs.