I had never heard of it before, but Googled, and found this from the
Merck Veterinary Manual:
Tyzzer’s disease is an acute bacterial infection of a wide range of animals (see also Intestinal Diseases and Gastrointestinal Diseases) that is seen worldwide. Sporadic fatal infection of foals is common, and acute fatal epidemics occur in laboratory animals. The disease is rare in dogs, cats, and calves. It primarily affects young, stressed animals; however, some species appear resistant unless stressed or immunosuppressed, while others are susceptible without immunosuppression. Immunosuppressive drugs and some antibacterials, especially sulfonamides, predispose animals to the disease.
Etiology and Pathogenesis:
The cause is Clostridium piliforme (previously Bacillus piliformis ), a motile, filamentous, gram-negative, sporeforming, obligate, intracellular bacterium. It does not grow in cell-free media but can be cultured in the yolk sac of chick embryos or tissue culture cells. The vegetative phase is very labile; spores may survive in soiled bedding at room temperature for 1 yr and can also survive at ~133°F (60°C) for 1 hr.
The pathogenesis is poorly understood. Infection most likely results from oral exposure. Possible sources include infective spores from the environment, contact with carrier animals, and in foals, ingestion of horse feces. The primary site of infection is the lower intestinal tract with subsequent dissemination via the blood or lymphatics. The bacterium has an affinity for the intestine (epithelial and smooth muscle cells), hepatocytes, and cardiac myocytes. Stress factors such as capture, overcrowding, shipping, and poor sanitation appear to be predisposing. Sulfonamide administration predisposes rabbits to the disease. Mortality is highest at weaning age except in foals, in which the disease is seen between 1 and 6 wk of age, with most cases between 1 and 2 wk. In some species, the disease has been identified concurrently with other diseases, eg, feline infectious peritonitis in cats, distemper and mycotic pneumonia in dogs, and cryptosporidial and coronaviral enteritis in calves.
The disease most often affects well-nourished animals during periods of stress. Under laboratory conditions, stress is created by immunosuppressive drugs or other factors that can be easily identified. With many experiments, stress may be involved as part of the protocol, and when the disease develops, it is devastating.
Clinical Findings:
After experimental infection, the incubation period in foals is 3-7 days; under natural conditions, the period is unknown. Most foals are found in a coma or dead. Clinical signs, if seen, are of short duration (a few hours to 2 days). Signs are variable, but may include depression, anorexia, pyrexia, jaundice, diarrhea, and recumbency. Terminally, there are convulsions and coma. Signs vary slightly between species. Laboratory animals may show depression, ruffled coat, and varying degrees of watery diarrhea; at the start of an outbreak, they often are found dead.
Clinicopathologic tests are of little value in laboratory animals because they die so rapidly. In foals, the serum enzymes sorbitol dehydrogenase, AST, alkaline phosphatase, lactate dehydrogenase, and γ-glutamyltransferase are increased. There is also hyperbilirubinemia, leukopenia, hemoconcentration, and terminally profound hypoglycemia.
Lesions:
Characteristic lesions are seen in the liver, myocardium, and intestinal tract. In the liver, white, gray, or yellowish foci of necrosis, 2 mm in diameter, are few to disseminated. The hepatic necrosis is most marked and disseminated in foals in which the multiple necrotic foci with slightly depressed hemorrhagic centers appear to infect almost every hepatic lobule. In addition, there is marked hepatomegaly, and the hepatic lymph nodes are hyperplastic. In rabbits, severe lesions develop in the intestines and heart. The terminal ileum, cecum, and proximal colon are diffusely reddened. Diffuse (“paint-brush”) hemorrhage is frequently seen on the serosa of the cecum. Patchy areas of mucosal necrosis are present in the cecum and colon, together with marked edema of the wall of the cecum. Mesenteric lymph nodes may be enlarged and edematous. White streaks in the myocardium may be present, especially near the apex. Intestinal and heart lesions are generally milder or absent in other animals.
Microscopically, randomly distributed and coalescing foci of necrosis in the liver are associated with scant to moderate infiltration of neutrophils and macrophages. The causative bacteria are found in a crisscross pattern in viable hepatocytes at the periphery of the necrotic foci. In the cecum and colon of rabbits, patchy areas of necrosis extend as deep as the muscularis externa with associated mucosal and submucosal infiltrates of neutrophils. Organisms may be found in the epithelium, muscularis mucosa, and muscularis externa of the affected intestine. When cardiac lesions are present, they consist of foci of fiber fragmentation, vacuolation, loss of cross-striations, and minimal inflammatory cell infiltration.
Treatment and Control:
Little is known about the effectiveness of antibiotics for treatment; some antibiotics are known to aggravate the disease. C piliforme is sensitive to tetracycline and partially sensitive to streptomycin, erythromycin, penicillin, and chlortetracycline; it is resistant to sulfonamides and chloramphenicol. In foals, the disease seems to be nearly 100% fatal, although it is likely that some foals survive. A definitive clinical diagnosis is not possible due to the lack of a definitive diagnostic test. Once the disease is present on a farm, it may be seen sporadically year after year. Animals suspected of being infected may be treated IV initially with 50% dextrose, followed by 10% dextrose (slowly), other fluid therapy, and antibiotics. Most foals respond dramatically to the dextrose therapy but relapse into a coma and die in a few hours. Rarely, an occasional foal appears to survive the disease after prolonged treatment with dextrose given slowly IV with antibiotics.
Because the disease in foals is sporadic and not highly contagious, specific preventive measures are usually not indicated. Reducing factors that cause stress and immunosuppression lessens the incidence. When the disease is seen in a colony, treatment is not recommended because it prolongs the disease and possibly produces carrier animals. It is best to destroy all animals in the colony and attempt to restock with disease-free animals.
I also found another link, its REALLY technical, way over my head, but some folks might be interested...
History and Technical Info
