|Bolin, Steven - Steve|
Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/15/1999
Publication Date: N/A
Citation: Interpretive Summary: The most highly studied form of fatal bovine viral disease virus (BVDV) infections is mucosal disease (MD). This disease only occurs in animals that become infected with BVDV before birth and remain infected their entire lives. Recently, it has been shown that there is a type of BVDV virus that causes death when it infects healthy cattle of all ages. This form of BVDV infection is called hemorrhagic syndrome (HS). Because symptoms of HS do not look like those traditionally associated with BVDV infections of normal cattle, veterinarians were slow to associate HS with a BVDV infection. In this preliminary study we gave a virus that causes HS to calves and monitored them for signs of disease. It was found that while, in some ways, symptoms of HS looked similar to MD, there are important differences. Among these were differences in where the virus could be found in the body. We also saw differences in which virus was generated during infection and what type of damage the virus did. These results demonstrate that MD and HS are completely different diseases. This was only a preliminary study. More detailed studies of the effects on HS on cattle will need to be done to provide veterinarians with clear descriptions of HS to help in diagnosis. Information gained from this study will be of great benefit to dairy producers worldwide.
Technical Abstract: Widespread outbreaks of severe acute BVDV, termed hemorrhagic syndrome (HS), were reported in Quebec and Ontario in 1993. In the Ontario outbreak, 150 dairy, 600 beef and 100 veal herds were affected with losses estimated at $40,000 to $100,000/herd in lost animals, milk production, abortions and genetics. The viruses associated with this outbreak were determined to be noncytopathic BVDV from the type 2 genotype. One of the viruses isolated from the Ontario outbreak, BVDV2-1373, was used to experimentally induce HS in 5-6 wk old colostrum-deprived, sero-negative calves. All animals developed leukopenia and thrombocytopenia within 6-10 days with some developing bloody diarrhea. Animals were killed for necropsy between 6 and 11 days postinfection. Histopathologically, lesions were similar to, but more severe, than those seen early on in animals with experimentally induced mucosal disease (MD). Unlike MD, there were no erosions and ulcerations present in the upper digestive tract. In hemorrhages in the mucosa, virus antigen (VA) was present in macrophages of both the lamina propria and the submucosa and in basal epithelial cells. Cells containing VA were vacuolated and separated from each other. The most severe lesions observed in the digestive tract were in the Peyers patches and were characterized by depletion of lymphocytes and proliferation of crypt cells. Apoptotic cells were present in crypts and areas of lymph follicles where viral antigen was detected. Out of the 6 animals, VA was present in 4 animals in the pancreas, 3 animals in the pituitary, and 2 animals in the adrenal glands. The results suggest that the pathology resulting from acute infection with a virulent noncytopathic BVDV2 differs from the pathology observed in classic MD.