Infectious necrotic hepatitis is a highly lethal, acute toxemia of sheep sometimes also affecting cattle and, rarely, pigs and horses.
The etiologic agent of infectious necrotic hepatitis, Clostridium novyi type B, is soilborne and part of the intestinal microbiota. It is also present in the liver 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 (alpha toxin). The disease is 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-concentration 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.
Typically, death is sudden, without clear clinical signs. Affected animals often are 2–4 years 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 highest. 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 with typical lesions found on a necropsy examination should arouse suspicion of infectious necrotic hepatitis.
The most characteristic gross lesions are grayish yellow, necrotic foci in liver tissue, caused by the migration of the young flukes. Histologically, 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 on microbial culture. 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).
Diagnosis of infectious necrotic hepatitis is based on history, clinical evaluation, and lesions found at necropsy; with use of similar criteria as for the diagnosis of bacillary hemoglobinuria.
Incidence of infectious necrotic hepatitis 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 achieved via 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 (via burning).