Effect of experimentally induced type II bovine viral diarrhea virus infection on platelet function in calves

Paul H. Walz From the Department of Large Animal Clinical Sciences (Walz, Baker, Kaiser), the Animal Health Diagnostic Laboratory (Steficek, Bell), and the Department of Veterinary Pathology (Bell), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824-1314.

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 DVM, MS
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Barbara A. Steficek From the Department of Large Animal Clinical Sciences (Walz, Baker, Kaiser), the Animal Health Diagnostic Laboratory (Steficek, Bell), and the Department of Veterinary Pathology (Bell), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824-1314.

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John C. Baker From the Department of Large Animal Clinical Sciences (Walz, Baker, Kaiser), the Animal Health Diagnostic Laboratory (Steficek, Bell), and the Department of Veterinary Pathology (Bell), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824-1314.

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Lana Kaiser From the Department of Large Animal Clinical Sciences (Walz, Baker, Kaiser), the Animal Health Diagnostic Laboratory (Steficek, Bell), and the Department of Veterinary Pathology (Bell), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824-1314.

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Thomas G. Bell From the Department of Large Animal Clinical Sciences (Walz, Baker, Kaiser), the Animal Health Diagnostic Laboratory (Steficek, Bell), and the Department of Veterinary Pathology (Bell), College of Veterinary Medicine, Michigan State University, East Lansing, MI 48824-1314.

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Abstract

Objective

To evaluate platelet aggregation responses in calves experimentally infected with a thrombocytopenia-inducing type II bovine viral diarrhea virus (BVDV) isolate (BVDV 890).

Animals

9 neonatal male Holstein calves.

Procedure

5 calves were inoculated with BVDV 890, and 4 were used as controls. Platelet aggregation studies and attempts to isolate BVDV from platelets were performed 2 days before, the day of, and every 2 days for 12 days after inoculation. Platelet function was assessed by means of optical aggregometry, using adenosine diphosphate and platelet-activating factor as agonists. Bovine viral diarrhea virus was isolated from purified platelet preparations by use of an immunoperoxidase monolayer assay.

Results

Maximum percentage aggregation and slope of the aggregation curve decreased over time in calves infected with BVDV. Bovine viral diarrhea virus was not isolated from platelets from control calves, but it was isolated from infected calves from 4 through 12 days after inoculation.

Conclusions and Clinical Relevance

Results suggest that platelet function may be depressed in calves infected with type II BVDV. Although the mechanism for altered platelet function was not determined, it likely involved an increase in the percentage of aged platelets in the circulation, a direct virus-platelet interaction, or an indirect virus-platelet interaction. Platelet dysfunction, in addition to thrombocytopenia, may contribute to the hemorrhagic syndrome associated with acute type II BVDV infection in calves. (Am J Vet Res 1999;60:1396–1401)

Abstract

Objective

To evaluate platelet aggregation responses in calves experimentally infected with a thrombocytopenia-inducing type II bovine viral diarrhea virus (BVDV) isolate (BVDV 890).

Animals

9 neonatal male Holstein calves.

Procedure

5 calves were inoculated with BVDV 890, and 4 were used as controls. Platelet aggregation studies and attempts to isolate BVDV from platelets were performed 2 days before, the day of, and every 2 days for 12 days after inoculation. Platelet function was assessed by means of optical aggregometry, using adenosine diphosphate and platelet-activating factor as agonists. Bovine viral diarrhea virus was isolated from purified platelet preparations by use of an immunoperoxidase monolayer assay.

Results

Maximum percentage aggregation and slope of the aggregation curve decreased over time in calves infected with BVDV. Bovine viral diarrhea virus was not isolated from platelets from control calves, but it was isolated from infected calves from 4 through 12 days after inoculation.

Conclusions and Clinical Relevance

Results suggest that platelet function may be depressed in calves infected with type II BVDV. Although the mechanism for altered platelet function was not determined, it likely involved an increase in the percentage of aged platelets in the circulation, a direct virus-platelet interaction, or an indirect virus-platelet interaction. Platelet dysfunction, in addition to thrombocytopenia, may contribute to the hemorrhagic syndrome associated with acute type II BVDV infection in calves. (Am J Vet Res 1999;60:1396–1401)

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