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Characterization of protection against systemic infection and disease from experimental bovine viral diarrhea virus type 2 infection by use of a modified-live noncytopathic type 1 vaccine in calves

Clayton L. KellingDepartment of Veterinary and Biomedical Sciences, Institute of Agriculture and Natural Resources, University of Nebraska, Lincoln, NE 68583-0905

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Breck D. HunsakerSchering-Plough Animal Health, 1246 W 3200 S, Preston, ID 83263

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David J. SteffenDepartment of Veterinary and Biomedical Sciences, Institute of Agriculture and Natural Resources, University of Nebraska, Lincoln, NE 68583-0905

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Christina L. TopliffDepartment of Veterinary and Biomedical Sciences, Institute of Agriculture and Natural Resources, University of Nebraska, Lincoln, NE 68583-0905

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Kent M. EskridgeDepartment of Statistics, Institute of Agriculture and Natural Resources, University of Nebraska, Lincoln, NE 68583-0905

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Abstract

Objective—To evaluate protection resulting from use of a modified-live noncytopathic bovine viral diarrhea virus (BVDV) type 1 vaccine against systemic infection and clinical disease in calves challenged with type 2 BVDV.

Animals—10 calves, 5 to 7 months of age.

Procedures—Calves were allocated (n = 5/group) to be nonvaccinated or vaccinated SC on day 0 with BVDV 1 (WRL strain). Calves in both groups were challenged intranasally with BVDV type 2 isolate 890 on day 21. Rectal temperatures and clinical signs of disease were recorded daily, and total and differential WBC and platelet counts were performed. Histologic examinations and immunohistochemical analyses to detect lesions and distribution of viral antigens, respectively, were performed.

Results—After challenge exposure to BVDV type 2, nonvaccinated calves developed high rectal temperatures, increased respiratory rates, viremia, leukopenia, lymphopenia, and infection of the thymus. Vaccinated calves did not develop high rectal temperatures or clinical signs of respiratory tract disease. Vaccinated calves appeared to be protected against systemic replication of virus in that they did not develop leukopenia, lymphopenia, viremia, or infection of target organs, and infectious virus was not detected in peripheral blood mononuclear cells or the thymus.

Conclusions and Clinical Relevance—The modified-live BVDV type 1 vaccine protected against systemic infection and disease after experimental challenge exposure with BVDV type 2. The vaccine protected calves against infection and viremia and prevented infection of target lymphoid cells.

Abstract

Objective—To evaluate protection resulting from use of a modified-live noncytopathic bovine viral diarrhea virus (BVDV) type 1 vaccine against systemic infection and clinical disease in calves challenged with type 2 BVDV.

Animals—10 calves, 5 to 7 months of age.

Procedures—Calves were allocated (n = 5/group) to be nonvaccinated or vaccinated SC on day 0 with BVDV 1 (WRL strain). Calves in both groups were challenged intranasally with BVDV type 2 isolate 890 on day 21. Rectal temperatures and clinical signs of disease were recorded daily, and total and differential WBC and platelet counts were performed. Histologic examinations and immunohistochemical analyses to detect lesions and distribution of viral antigens, respectively, were performed.

Results—After challenge exposure to BVDV type 2, nonvaccinated calves developed high rectal temperatures, increased respiratory rates, viremia, leukopenia, lymphopenia, and infection of the thymus. Vaccinated calves did not develop high rectal temperatures or clinical signs of respiratory tract disease. Vaccinated calves appeared to be protected against systemic replication of virus in that they did not develop leukopenia, lymphopenia, viremia, or infection of target organs, and infectious virus was not detected in peripheral blood mononuclear cells or the thymus.

Conclusions and Clinical Relevance—The modified-live BVDV type 1 vaccine protected against systemic infection and disease after experimental challenge exposure with BVDV type 2. The vaccine protected calves against infection and viremia and prevented infection of target lymphoid cells.

Contributor Notes

Supported by Schering-Plough Animal Health and the University of Nebraska Agricultural Research Division, Lincoln, NE 68583 (journal series No. 15014).

Address correspondence to Dr. Kelling.