Bacillary hemoglobinuria is an acute, infectious, toxemic disease with high mortality caused by Clostridium haemolyticum. It affects primarily cattle but has also been found in sheep and rarely in dogs, horses, pigs, elk; and possibly camelids. It occurs in the western part of the US and Canada, along the Gulf of Mexico, in South America, Great Britain, Middle East, India, Japan, Australia, New Zealand, and other parts of the world.
C haemolyticum (also called C novyi Type D) is a soilborne organism found in poorly-drained pastures with alkaline pH and, rarely, as spores in liver tissue, bloodstream, bone marrow, kidneys, and the GI tract of healthy cattle. It can survive for long periods in contaminated soil or in bones from carcasses of infected animals. After ingestion, latent spores ultimately become embedded in the liver. The incubation period is extremely variable, and onset of clinical signs depends on the presence of a locus of anaerobiosis in the liver. Such a nidus for germination is most often caused by liver fluke (Fasciola hepatica) infection, rarely by high nitrate concentration in the diet, accidental liver puncture, liver biopsy, or any other cause of localized hepatic necrosis. When conditions for anaerobiosis are favorable, the spores germinate, and the resulting vegetative cells multiply and produce beta toxin (phospholipase C). This causes intravascular hemolysis, resulting in hemolytic anemia and hemoglobinuria.
Cattle may be found dead without premonitory clinical signs. Usually, there is a sudden onset of severe depression, fever, abdominal pain, dyspnea, severe diarrhea , and hemoglobinuria. Anemia and jaundice are present in varying degrees. Edema of the sternum may occur. Hgb and RBC levels are quite low. The duration of clinical signs varies from ~12 hours in pregnant cows to ~3–4 days in other cattle. Mortality in untreated animals is ~95%. Some cattle suffer from subclinical attacks of the disease and thereafter are immune carriers.
Dehydration, anemia, and sometimes subcutaneous edema may be seen. At necropsy there may be bloody fluid in the abdominal and thoracic cavities. The lungs are not grossly affected, and the trachea usually contains bloody froth with mucosal hemorrhages. The small intestine and occasionally the large intestine are hemorrhagic and sometimes have blood clots in the lumen. An ischemic infarct in the liver is characteristic of bacillary hemoglobinuria. Such lesions are slightly elevated, lighter in color than the surrounding tissue, and outlined by a bluish red zone of hepatic congestion. The bile ducts may be thickened, indicating possible fluke infestation. 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 clearest clinical 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 postmortem. The normal size and consistency of the spleen serve to exclude anthrax and anaplasmosis. Bracken fern poisoning and leptospirosis should also 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 confirming the presence of the organism in liver tissue samples by PCR assay, fluorescent antibody or immunohistochemical tests, or by demonstrating presence of toxin in peritoneal fluid or in a saline extract of the infarct. Recently, matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) has been used to diagnose disease due to C haemolyticum.
Early treatment with penicillin or tetracyclines at high doses is essential. Whole blood transfusions and fluid therapy also are helpful early in the disease; however, the prognosis is guarded. C haemolyticum bacterin prepared from whole cultures confers immunity for ~6 months. In areas where the disease is seasonal, one preseasonal dose followed by a second dose 4–6 weeks later 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, because the latter may be carriers.
Hussein HA, El-Amir YO, Aamer AA, et al. Bacillary hemoglobinuria in dairy cows: clinical, hematological, biochemical, and pathological alterations. Comp Clin Pathol. 2013; 22:1137.
Navarro M A, Dutra F, Briano C, Romero A, Persiani M, Freedman JC, Uzal FA. (2017). Pathology of Naturally Occurring Bacillary Hemoglobinuria in Cattle. Vet Pathol. 54(3): 457–466.