The abstract is reprinted from JAVMA Feb. 15, 1990, pg. 590.  The most frequently en­countered infectious agents isolated from cases of hemor-rhagic syndrome at ADDL are bovine virus diarrhea, Pasteurell a haemo1ytica.Escherichia coli.and Salmonella sp.  Furazolidone,neomycin,mycotox-ins, and polyunsaturated fatty acids have also been suggested as toxic agents that this syndrome.  None have been documented date.

The abstracted research observations provide stronger evidence that BVD may be the primary factor involved in hem-orrhagic syndrome.  In cases fully investigated by ADDL, BVD has been identified most often of any infectious agent.  However, P. haemolytia and/or one of the other gram negative agents is usually isolated a1 so.

THROMBOCYTOPEN1 A AND HEMORRHAGES IN VEAL CALVES INFECTED WITH BOVINE VIRAL DIARRHEA VIRUS.

Wayne V. Corapi,DVM,PhD;R. Dean Elliott, DVM; TracyW. French, DVM; Donald G. Arthur, BVSc; David M.Bezek, DVM; Ed­ward J.Dubovi, PhD.

SUMMARY: The relationship between bovine viral diarrhea virus (BVDV) infection and thrombocytopenia was studied in 18 veal calves experimentally infected with BVDV.  All calves were free of BVDV, and 13 calves were free of serum neu­tralizing antibodies to BVDV before virus inoculation.

Calves were inoculated at ap­proximately 10 days of age, and platelet counts were monitored over a period of several weeks. Ten additional calves housed "in close proximity were kept as umnoculated controls.  A pro­found decrease in platelet counts by 3 to 11 days after inoculation was seen in all calves that had neutralizing antibody titers <1:32 before infection.  Severe thrombocyto-penia (<5,000 p1atelets/ul) was seen in 12 calves, 11 of which also developed hemorrhages, Necropsy findings in 3 severely thrombocytopenic calves that died included multiple hemor­rhages throughout the body. Calves that recovered had in­creased platelet counts, and in most instances, a corresponding increase in neutralizing anti­body titers to BVDV.  At 11 days after inoculation, BVDV was detected on platelets by use of immunofluorescence, but evidence of surface-bound immu-noglobulin was not found.  The results suggest that a non-im-munoglobu1in-mediated method of platelet destruction or seques­tration develops as a sequel to BVOV infection.

Drs.T.L.Bowersock, Chief of Microbiology, and M.R White, Veterinary Pathologist