Bacillary hemoglobinuria is an acute toxemia of cattle caused by Clostridium haemolyticum (also called C novyi type D), a soilborne organism. After ingestion, spores remain in the liver until stimulated to germinate by conditions of anaerobiosis. Many affected cattle are found dead, with no premonitory signs. Port wine–colored urine is the most prominent clinical sign. Diagnosis is often presumptive, based on history and signs; it can be confirmed by characteristic histopathological findings in the liver, coupled with culture, PCR assay, fluorescent antibody testing, or immunohistochemistry for detecting C haemolyticum. Early treatment with high-dose penicillin or tetracyclines is essential. Control measures include prevention of fluke infestation and vaccination with a C haemolyticum bacterin given once or twice yearly, depending on the endemicity of the disease.
Bacillary hemoglobinuria is an acute, infectious, toxemic disease with high mortality rates that is caused by Clostridium haemolyticum.
Etiology of Bacillary Hemoglobinuria
The agent that causes bacillary hemoglobinuria, 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 C haemolyticum is ingested, latent spores ultimately become embedded in the liver. The incubation period is extremely variable, and the onset of clinical signs depends on the presence of a locus of anaerobiosis in the liver. Such a nidus for germination is caused most often by liver flukes (mainly Fasciola hepatica or Fascioloides magna) infection, and rarely, by a 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, C haemolyticum spores germinate, and the resulting vegetative cells multiply and produce beta toxin (phospholipase C). Beta toxin causes intravascular hemolysis, resulting in hemolytic anemia and hemoglobinuria.
Epidemiology of Bacillary Hemoglobinuria
Bacillary hemoglobinuria affects primarily cattle but has also been found in sheep and, rarely, in dogs, horses, pigs, elk, and possibly camelids.
Bacillary hemoglobinuria most often occurs in marshy areas with surface water that contains the intermediate host for liver flukes. It occurs in the western part of the US and Canada, along the Gulf of Mexico, in South America, Great Britain, the Middle East, India, Japan, Australia, New Zealand, and other parts of the world.
Without treatment bacillary hemoglobinuria is nearly always fatal. Some cattle in endemic regions experience subclinical disease, thereby developing immunity.
Clinical Findings of Bacillary Hemoglobinuria
Cattle with bacillary hemoglobinuria usually show a sudden onset of severe depression, fever, abdominal pain, dyspnea, cessation of lactation, blood-stained diarrhea, and hemoglobinuria. Pale or icteric mucous membranes might be present, and affected pregnant cows might abort. Edema of the sternum can occur. Hemoglobin and RBC indices can be quite low.
Death from bacillary hemoglobinuria occurs within hours to days after the liver insult. Affected cattle can be found dead without premonitory clinical signs.
Lesions of Bacillary Hemoglobinuria
Bacillary hemoglobinuria lesions are best described in cattle and typically include sequelae secondary to dehydration and anemia, sometimes also with subcutaneous edema. At necropsy, there might be widespread hemorrhages with petechiation and ecchymoses on serosal surfaces and the endocardium, as well as bloody fluid in the abdominal and thoracic cavities.
There might be pulmonary edema and splenomegaly. 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. Locally extensive coagulative necrosis 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 might be thickened, and there might be black-pigmented migration tracts in the hepatic parenchyma, indicating probable fluke infestation. The kidneys are dark, friable, and usually studded with petechiae. The urinary bladder often shows hematuria (see and ).
Necropsy photograph showing hematuria in the bladder of a cow that underwent a liver biopsy procedure and then developed pyrexia and recumbency within 24 hours. Urinalysis before death revealed hemoglobinuria. Postmortem examination demonstrated massive hepatic necrosis of the caudate liver lobe. Together, these findings led to a presumptive diagnosis of bacillary hemoglobinuria.
Courtesy of Dr. Teresa Southard.
After death from bacillary hemoglobinuria, rigor mortis sets in quickly. Lesions in other affected species are thought to be similar, but they are poorly described.
Diagnosis of Bacillary Hemoglobinuria
Clinical findings
Postmortem examination
Culture, PCR assay, fluorescent antibody testing, or other laboratory testing
In areas where bacillary hemoglobinuria is endemic (eg, marshy areas with surface water that contains the intermediate host for liver flukes), 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.
Pearls & Pitfalls
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The presence of the typical focal hepatic necrosis is sufficient for a presumptive diagnosis of bacillary hemoglobinuria on postmortem examination. Anthrax, anaplasmosis, theileriosis, bracken fern poisoning, and leptospirosis should also be considered.
Diagnosis of bacillary hemoglobinuria can be confirmed by isolating C haemolyticum from the liver infarct; however, 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 testing, or immunohistochemistry.
Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) has also been used to identify culture isolates as C haemolyticum.
Treatment and Control of Bacillary Hemoglobinuria
Vaccination
Antimicrobials
Supportive care
Because of the rapid progression of bacillary hemoglobinuria, treatment with antimicrobials is typically not effective and therefore not recommended.
A case report of bacillary hemoglobinuria in a Holstein cow in Japan described the successful treatment of bacillary hemoglobinuria with IV ampicillin sodium salt and cloxacillin sodium salt for 5 days (1). This extralabel drug use of a cephalosporin is prohibited in the US in food-producing species. Also in the US, the ampicillin-cloxacillin combination is not available for IV administration in cattle.
Whole blood transfusions and fluid therapy are helpful early in the course of bacillary hemoglobinuria; however, the prognosis is guarded.
Preventing liver fluke infestation by limiting access to the intermediate snail host in wet, swampy areas, is one important aspect of controlling bacillary hemoglobinuria. Affected carcasses should be burned, buried, or removed from the premises to avoid further spore dispersal.
Commercial C haemolyticum bacterins, as either monovalent or polyvalent preparations, are available. Susceptible animals should be given two doses initially, 4–6 weeks apart, followed by annual or biannual boosters, depending on the incidence of bacillary hemoglobinuria in the area.
Key Points
Clostridium haemolyticum causes bacillary hemoglobinuria.
Bacillary hemoglobinuria affects primarily cattle, with high mortality rates.
Prevention involves vaccination of cattle and control of liver flukes.
For More Information
Uzal FA, McClane BA, Gohari IM, Navarro MA, Popoff MR, eds. Clostridial Diseases of Animals. 2nd ed. John Wiley & Sons; 2026.
Hussein HA, El-Amir YO, Aamer AA, et al. Bacillary hemoglobinuria in dairy cows: clinical, hematological, biochemical, and pathological alterations. Comp Clin Pathol. 2013;22:1137-1143.
Navarro MA, Dutra F, Briano C, et al. Pathology of naturally occurring bacillary hemoglobinuria in cattle. Vet Pathol. 2017;54(3):457-466.
Navarro MA, Uzal FA. Pathobiology and diagnosis of clostridial hepatitis in animals. J Vet Diagn Invest. 2020;32(2):192-202.
References
Takagi M, Kohyama M, Ono T, et al. Recovery with a regular dose of antibiotics from bacillary hemoglobinuria in a Holstein cow. J Vet Med Sci. 2016;78(11):1737-1740. doi:https://doi.org/10.1292/jvms.16-0296
