Bacterial Disease - Bacillary Hemoglobinuria

Synonym: Red water disease


Bacillary Hemoglobinuria is an acute, infectious, toxemic disease caused by Clostridium hemolyticum (C.novyi type D). It affects primarily cattle but has also been found in sheep and rarely in dogs.


It occurs in the western part of the USA, also in the Gulf of Mexico, in Venezuela, Chile, Great Britain, the middle East, and other parts of the world.


Clostridium hemolyticum (C.novyi type D) is a soil-borne organism that may be found naturally in the GI tract of cattle. It can survive for long periods in contaminated soil or in bones from carcasses of animals that had been infected. 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 as 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. It produces β toxins (Phospholipase C), which causes intravascular hemolysis and its sequelae, including hemolytic anemia and hemoglobinuria.

Clinical findings

Cattle may be found dead without premonitory signs. Usually, there is 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.

Hb and RBC levels are quite low. The duration of clinical signs varies from approximately 12 hour in pregnant cow to 3 to 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 anemic infarct in the liver is virtually pathognomonic; 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 more rapidly than usual.


The general clinical picture usually permits a 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 clostridium hemolyticum (C.novyi type D) from the liver infarct, but the organism is difficult to culture.

v Rapid and accurate diagnosis can be made by demonstrating the organism in the liver tissue by a fluorescent antibody or immune histochemical 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 broad-spectrum anti-biotic is essential. Whole blood and fluid therapy also are helpful.

Clostridium hemolyticum bacterins prepared from whole cultures confers immunity for 6 months. In areas where the disease is seasonal, one pre-seasonal dose is usually adequate; where the disease occurs throughout the year, semiannual immunization is necessary.

Cattle that are in contact with animals from areas where this disease is endemic should be immunized because the latter may be carriers.

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