You are working at a mixed animal practice in Suffolk County when you get a call from a local resident that two of his cows are dead. The caller says he hadn't really checked on his small herd for a few days and that he found the dead cows this morning. The property is located on flat land at the edge of the Great Dismal Swamp, a nice place with a few hills, a lot of forest, and a couple of creeks flowing through. The field in which the dead cows are lying is rather swampy. Both are quite ripe and are their undersides have turned a dark blackish color.

You ask to look at the rest of the herd. Four cows are standing in the shade of a small patch of trees. Three of them seem just fine; the fourth is running a fever and you can't auscult any rumen sounds. When you move your stethoscope around to listen to the bowels, you find your patient to be rather painful on the right hand side. You also notice that she seems jaundiced and is reluctant to move. You take a blood and urine sample and chat about vaccinations. It appears that the owner is not really sure just what vaccinations were given and fudges his answer when you ask about parasite control. You decide to pick up a fecal sample for good measure and you notice a number of snails crawling around the feces.


When half of a herd of animals dies without warning, and there are some others obviously need to be thinking about some sort of infection. The jaundiced appearance of the cattle indicates that there's liver involvement somewhere. You're not the least bit surprised when your cultures come back positive for Clostridium novyi, A spore-forming anaerobic bacterium commonly present in the environment or on the body surface. C. novyi , is found in the ruminant intestinal tract and is often detected on the skin; it's a common cause of skin infection from superficial wounds. The snails and the wet condition of the ground contribute to the likelihood of these animals having been infested by liver flukes, as the snails are vector. In the presence of liver damage from flukes, C. novyi opportunistically invades the liver. The diagnosis is infectious necrotic hepatitis.


This disease typically affects sheep and cattle. The infection is always fatal as hepatic necrosis is swift and severe. Affected animals will demonstrate nervous, respiratory, and vascular signs, and will die quickly: sheep within 24 hours of onset and cattle within two days.

Infestation by immature liver flukes precipitates the events. They cause areas of inflammation and necrosis, fertile breeding grounds for clostridial spores that reach the liver through portal circulation. Grossly the hepatic parenchyma (left) appears irregular and patchy. This appearance comes from the tracks left by the migrating juvenile flukes. Adult flukes are rarely found since the damage associated with this disease is caused by migration of immature flukes.

The bacterial organisms (right, in a microscopic preparation) produce a powerful necrotizing toxin that further destroys the liver parenchyma. This in turn provides a hospitable environment, resulting in more growth and continued hepatic necrosis. This cycle eventually builds to a point where the liver fails acutely and the animal dies.

In sheep most victims are found dead: in cattle, the process lasts longer and most will show signs of depression, lethargy, rumen atony, muffled heart sounds, and hypothermia. Palpation of the right flank can elicit a sharp pain response. In both a common finding is one that's typical of many clostridial diseases: the nectrotizing toxin can cause massive rupture of the subcutaneous capillaries, giving the skin a dark blue-black hue (hence the name 'Black Disease'). Definitive diagnosis is established by successfully culturing C. novyi from the liver or spleen or by isolating the toxin.

The liver in this animal has undergone coagulative necrosis. This pattern of necrosis leaves the architecture of the tissue temporarily intact and recognizable, even though the cells are dead. Coagulative necrosis is seen in some tissues and not in others. Typically ischemia will produce it in the liver and in muscle, and it's also associated with the sort of rapid bacterial invasion discussed here.

In these images you can see this preservation of architecture: this is quite recognizably liver, despite the absence of nuclei in the hepatocytes in the affected area. Notice the thread-like bacteria present in the sinusoids: these are the organism causing the lesion! Darker staining viable hepatocytes are visible around the portal regions (right) and pale, necrotic hepatocytes are visible in the central lobular zones. Hepatocytes near the blood supply have more physiologic reserve and will be more able to fend off the infection than those in the oxygen and nutrient-poor central region: but in this case the "advantage" is moot.

This is a higher magnification view of the area of necrosis. Pyknosis, karyorrhexis, and karyolysis are all on display. Pyknosis is the shrinkage and increased density of nuclei, which will be followed by karyrrhexis, their breakup into fragments; or karyolysis, their complete dissolution with no remnant left behind.

These cells are also strongly eosinophilic, a characteristic of coagulation. Their borders are indistinct and they seem to run together; hence the term, "coagulative" necrosis.


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