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Infectious Necrotic Hepatitis

(Clostridium novyi infection, Black disease)


Henry R. Stämpfli

, DVM, DrMedVet, DACVIM, Large Animal Medicine, Department of Clinical Studies, Ontario Veterinary College, University of Guelph

Last full review/revision Mar 2014 | Content last modified Mar 2014

Infectious necrotic hepatitis is an acute toxemia of sheep that is sometimes seen in cattle and is rare in pigs and horses.

Etiology and Pathogenesis:

The etiologic agent, Clostridium novyi type B, is soilborne and present in the intestines and livers of herbivores; it may be present on skin surfaces and dormant in muscles and is a potential source of wound infections. Fecal contamination of pasture by carrier animals is the most important source of infection. The organism multiplies in areas of liver necrosis caused by migration of liver flukes and produces a powerful necrotizing toxin (α toxin). The disease is distributed worldwide, wherever sheep and liver flukes are both found, and is increasing in cattle where liver flukes are accidentally introduced.

C novyi has been suspected but not yet confirmed as a cause of sudden death in cattle and pigs fed high-level grain diets, and in which preexisting lesions of the liver were not detectable. The lethal and necrotizing toxins damage hepatic parenchyma, thereby permitting the bacteria to multiply and produce a lethal amount of toxin.

Clinical Findings:

Usually, death is sudden with no well-defined signs. Affected animals often are 2–4 yr old, tend to lag behind the flock, assume sternal recumbency, and die within a few hours. Most cases occur in the summer and early fall when liver fluke infection is at its peak. The disease is most prevalent in well-nourished adult sheep and seems to be limited to animals infected with liver flukes. Differentiation from acute fascioliasis may be difficult, but peracute deaths of animals that show typical lesions on necropsy should arouse suspicion of infectious necrotic hepatitis.


The most characteristic gross lesions are grayish yellow, necrotic foci in the liver along migratory tracks of the young flukes. Histologically, the liver lesions include central eosinophilic inflammation (fluke induced) surrounded by coagulation necrosis with an outer rim of neutrophils. The lesion is positive for gram-positive rods. Other common findings are an enlarged pericardial sac filled with straw-colored fluid and excess fluid in the peritoneal and thoracic cavities. Usually, there is extensive rupture of the capillaries in the subcutaneous tissue, which causes the adjacent skin to turn black (hence the common name, black disease).


The incidence may be lowered by reducing the numbers of Lymnaea spp snails, the intermediate hosts for the liver flukes, or by otherwise reducing the fluke infection of sheep. However, these procedures are not always practical, and active immunization with C novyi aluminum-precipitated toxoid seems more effective and can be also performed during outbreaks. Longterm immunity is produced by one vaccination. After this, only new introductions to the flock (lambs and sheep brought in from other areas) need to be vaccinated. This is best done in early summer. Pasture contamination can be minimized by proper disposal of carcasses (burning).

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