Literature DB >> 11042409

Morphologic lesions in type 2 BVDV infections experimentally induced by strain BVDV2-1373 recovered from a field case.

B Stoffregen1, S R Bolin, J F Ridpath, J Pohlenz.   

Abstract

Widespread outbreaks of severe acute BVDV, some associated with hemorrhagic syndrome (HS), were reported in Quebec and Ontario in 1993. These outbreaks caused significant economic hardship in infected herds. In the Ontario outbreak 150 dairy, 600 beef and 100 milk and grain fed veal herds were affected with losses estimated at $40000-$10000 per herd in lost animals, milk production, abortions and genetics. Fever, pneumonia, diarrhea, and sudden death occurred in all age groups of cattle. Abortions were frequently observed in pregnant cattle. The viruses associated with this outbreak were determined to be noncytopathic BVDV from the type 2 genotype. All BVDV2 associated with these outbreaks were noncytopathic. One of the viruses isolated from the Ontario outbreak, BVDV2-1373, was used to experimentally induce HS in 5-6 weeks old colostrum deprived, seronegative calves. All animals developed leukopenia and thrombocytopenia within 6-10 days with some developing bloody diarrhea and becoming moribund. Animals were killed for necropsy between 6 and 11 days postinfection. Histopathologically lesions were similar, but more severe, to those seen early on (within first 9 days after superinfection) in animals with experimentally induced mucosal disease (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 resulting in crypthyperplasia. Apoptotic cells were present in crypts and areas of lymph follicles where viral antigen was detected. Out of the six animals, VA was present in four animals in the pancreas, three animals in the pituitary and in two animals in the adrenal glands. The results suggest that the pathology resulting from acute infection with a highly virulent noncytopathic BVDV2 differs from the pathology observed in classic mucosal disease.

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Year:  2000        PMID: 11042409     DOI: 10.1016/s0378-1135(00)00272-8

Source DB:  PubMed          Journal:  Vet Microbiol        ISSN: 0378-1135            Impact factor:   3.293


  8 in total

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2.  Platelet aggregation responses and virus isolation from platelets in calves experimentally infected with type I or type II bovine viral diarrhea virus.

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3.  Phylogenetic analysis of bovine pestiviruses: testing the evolution of clinical symptoms.

Authors:  L R Jones; M M Cigliano; R O Zandomeni; E L Weber
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6.  Experimental infection of mice with noncytopathic bovine viral diarrhea virus 2 increases the number of megakaryocytes in bone marrow.

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7.  Bovine viral diarrhea virus: An updated American College of Veterinary Internal Medicine consensus statement with focus on virus biology, hosts, immunosuppression, and vaccination.

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8.  BVD-2 outbreak leads to high losses in cattle farms in Western Germany.

Authors:  Jörn Gethmann; Timo Homeier; Mark Holsteg; Horst Schirrmeier; Michael Saßerath; Bernd Hoffmann; Martin Beer; Franz J Conraths
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  8 in total

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