A couple of weeks after handling the clostridium problem in the cattle, you are called by a swine producer who has experienced a number of deaths among his month-old piglets. He tells you that, "The pigs seem to do fine for the first six weeks or so but then they just die all of a sudden. I've only had this problem for a few days but, but I'm worried that it may get worse."
He offers you the bodies of two pigs he has kept since yesterday in a freezer. While they thaw you turn your attention to the other pigs. There are 30 of them, all roughly a month and a half old. Most seem healthy, but five are unsteady on their feet, and when you approach them they become very agitated. One of them vomits and then falls while running away from you. The pig struggles vigorously when you grab it....and then dies.
A necropsy of this piglet shows a swollen and discolored liver, and a great deal of hemorrhage and necrosis grossly visible throughout. Examination of the carcass shows some muscle atrophy.
You ask the producer about vaccines and parasite prevention and he tells you everything you want to hear. You ask what the pigs are eating and he shows you a commercially prepared product that he combines with soybeans and peanuts to provide high energy.
Your diagnosis is hepatosis dietetica, based on your necropsies, the setting, and the nutritional history.
Hepatosis dietetica is a disease caused by a deficiency of dietary vitamin E or selenium, typically affecting young, rapidly growing swine such as those seen in commercial growing operations. It's a well-recognized consequence of poor nutrition management and can be easily avoided by careful maintenance of appropriate dietary vitamin and mineral levels during growth. The exact mechanism of this disorder is unknown, but deficiency of vitamin E and/or selenium is known to be the underlying cause. It's thought that vitamin E and selenium-containing compounds are powerful antioxidants, and the lack of these compounds may allow free radicals damage to the liver.There are really no singular clinical signs indicating hepatosis dietetica; affected piglets are found dead, occasionally with subcutaneous edema. The typical signalment is a rapidly-growing commercial piglet between the ages of two weeks and four months. Multiple piglets can be affected by the disease, but deaths are usually sporadic
The nutritional deficiency may be either a primary deficiency in the diet itself (unlikely in a commercial ration by a reputable producer) or more often a secondary deficiency. It can be caused by other components of the diet—intentional or contaminating—that reduce the availability of Vitamin E. Diets rich in polyunsaturated fats or vitamin A can bring it about. It could also be due to malabsorption in specific individual animals.
Affected piglets will have edematous, mottled livers with a mosaic pattern of necrosis. Fibrin and serous ascites may be found throughout the abdominal cavity. In addition to direct hepatic trauma, signs of muscle wasting and necrosis may be found on skeletal muscle, particularly in the heart. Some piglets will have ulcerative lesions of the esophageal and gastric mucosae. Clinical pathology of tissue samples may show low vitamin E and selenium concentrations as well as elevated creatine kinase (CK) levels in the serum. The elevated CK indicates trauma due to the skeletal muscle lesions.
This is a low magnification view of one of the pigs' livers. Multifocal zones of necrosis are seen as lightened regions around the portal veins, with interspersed regions of hepatocytes in various stages of injury. Multifocal regions of hemorrhage and edema are visible in the parenchyma. (Note the relatively thick fibrous structure of the liver, a normal finding in pigs.)
This is a closer view of a necrotic center. The typical pale, eosinophilic ghosts produced by coagulation necrosis are evident. There's hyperremia and hemorrhage evident in the necrotic area, and relatively normal cells outside the necrotic zone.
There are signs of damage to the living cells: lipid inclusions, vacuolation and cellular swelling. In the necrotic area, nuclear pyknosis and karyorhexis are evident, as well, these all more easily visible at the high magnification of the image below at left. This image shows off a necrotic center quite nicely, with hemorrhage, mixed inflammatory cells, eosinophilic necrotic hepatocytes, pyknosis, and nuclear debris.
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