Bacillary hemoglobinuria is an acute, infectious, toxemic disease caused by Clostridium haemolyticum. It affects primarily cattle but has also been found in sheep and rarely in dogs. It occurs in the western part of the USA, along the Gulf of Mexico, in South America, Great Britain, the Middle East, India, and other parts of the world.
C haemolyticum is a soilborne organism naturally found in the GI tract of some cattle. It can survive for long periods in contaminated soil or in bones from carcasses of infected animals. After ingestion, latent spores ultimately become lodged in the liver. The incubation period is extremely variable, and the onset depends on the presence of a locus of anaerobiosis in the liver. Such a nidus for germination is most often caused by liver fluke infection, much less often by high nitrate content of the diet, accidental liver puncture, liver biopsy, or any other cause of localized necrosis. When conditions for anaerobiosis are favorable, the spores germinate, and the resulting vegetative cells multiply and produce β toxin (phospholipase C). This causes intravascular hemolysis, resulting in hemolytic anemia and hemoglobinuria.
Cattle may be found dead without premonitory signs. Usually, there is a sudden onset of severe depression, fever, abdominal pain, dyspnea, dysentery, and hemoglobinuria. Anemia and jaundice are present in varying degrees. Edema of the brisket may occur. Hgb and RBC levels are quite low. The duration of clinical signs varies from ~12 hr in pregnant cows to ~3–4 days in other cattle. The mortality in untreated animals is ~95%. Some cattle suffer from subclinical attacks of the disease and thereafter act as immune carriers.
Dehydration, anemia, and sometimes subcutaneous edema are present. There is bloody fluid in the abdominal and thoracic cavities. The lungs are not grossly affected, and the trachea contains bloody froth with hemorrhages in the mucosa. The small intestine and occasionally the large intestine are hemorrhagic; their contents often contain free or clotted blood. An ischemic infarct in the liver is characteristic; it is slightly elevated, lighter in color than the surrounding tissue, and outlined by a bluish red zone of congestion. The kidneys are dark, friable, and usually studded with petechiae. The bladder contains purplish red urine. After death, rigor mortis sets in quickly.
The general clinical picture and postmortem findings usually permit a tentative diagnosis. The most striking sign is the typical port-wine-colored urine, which foams freely when voided or on agitation. The presence of the typical liver infarct is sufficient for a presumptive diagnosis. The normal size and consistency of the spleen serve to exclude anthrax and anaplasmosis. Bracken fern poisoning and leptospirosis also should be considered. Diagnosis can be confirmed by isolating C haemolyticum from the liver infarct, but the organism is difficult to culture. Rapid and accurate diagnosis can be made by demonstrating the organism in the liver tissue by a fluorescent antibody or immunohistochemical test or by demonstrating the toxin in the fluid in the peritoneal cavity or in a saline extract of the infarct.
Early treatment with penicillin or tetracyclines at high doses is essential. Whole blood transfusions and fluid therapy also are helpful early in the disease. C haemolyticum bacterin prepared from whole cultures confers immunity for ~6 mo. In areas where the disease is seasonal, one preseasonal dose is usually adequate; where the disease occurs throughout the year, semiannual vaccination is necessary. Cattle in contact with animals from areas where this disease is endemic should be vaccinated, as the latter may be carriers.
Last full review/revision March 2012 by Henry R. Stämpfli, DVM, DrMedVet, DACVIM