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  • Author or Editor: Thomas G. Bell x
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Abstract

Objective

To test the effect of thiacetarsamide and melarsomine on vascular responses in isolated rings of pulmonary artery from heartworm-infected dogs.

Animals

18 heartworm-infected dogs.

Procedure

Isolated rings of pulmonary artery from heartworm-infected dogs were randomly treated with thiacetarsamide (30 μg/ml) or melarsomine dihydrochloride (30 μg/ml) for 30 minutes; untreated rings from the same dog served as control. Cumulative dose-response relations to norepinephrine, nitroglycerin, and methacholine were determined.

Results

Norepinephrine-induced constriction was not altered by treatment with either thiacetarsamide or melarsomine. Treatment with thiacetarsamide depressed nitroglycerin-induced relaxation, compared with values for untreated control rings and rings treated with melarsomine. Treatment of rings with thiacetarsamide or melarsomine depressed methacholine-induced relaxation, compared with values for untreated rings. Histologic examination of rings indicated that treatment with thiacetarsamide or melarsomine resulted in loss of endothelial cells.

Conclusion

Endothelial cell loss as a direct drug effect may be responsible for impaired endothelium-dependent relaxation in pulmonary artery from heart-worm-infected dogs. Thiacetarsamide appears to have additional effects on vascular smooth muscle, which may explain why fewer complications are observed in dogs treated with melarsomine.

Clinical Relevance

Melarsomine may be a safer drug than thiacetarsamide and could be a better treatment for dogs with heartworm infection. (Am J Vet Res 1997;58:389–393)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To determine whether viral involvement with platelets obtained from cattle persistently infected (PI) with bovine viral diarrhea virus (BVDV) is associated with altered platelet function or decreased platelet counts.

Sample Population—Platelets obtained from 8 cattle PI with BVDV and 6 age-, sex-, and breed-matched uninfected control cattle.

Procedure—Manual platelet counts were determined, and platelet function was assessed through optical aggregometry by use of the aggregation agonists ADP and platelet-activating factor. Identification of BVDV in serum and preparations of purified platelets was determined by use of virus isolation tests.

Results—No significant difference in platelet counts was detected between cattle PI with BVDV and control cattle. In response to the aggregation agonists, maximum aggregation percentage and slope of the aggregation curve were not significantly different between cattle PI with BVDV and control cattle. We isolated BVDV from serum of all PI cattle and from purified platelets of 6 of 8 PI cattle, but BVDV was not isolated from serum or platelets of control cattle.

Conclusions and Clinical Relevance—Isolation of BVDV from platelets in the peripheral circulation of cattle immunotolerant to BVDV does not result in altered platelet function or decreases in platelet counts. (Am J Vet Res 2005;66:1738–1742)

Full access
in American Journal of Veterinary Research

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)

Free access
in American Journal of Veterinary Research

Abstract

Objective—To compare degree of viremia and disease manifestations in calves with type-I and -II bovine viral diarrhea virus (BVDV) infection.

Animals—16 calves.

Procedure—Colostrum-deprived calves obtained immediately after birth were assigned to 1 control and 3 treatment groups (4 calves/group). Calves in treatment groups were inoculated (day 0) by intranasal instillation of 107 median tissue culture infective dose BVDV 890 (type II), BVDV 7937 (type II), or BVDV TGAN (type I). Blood cell counts and virus isolation from serum and leukocytes were performed daily, whereas degree of viremia was determined immediately before and 4, 6, 8, and 12 days after inoculation. Calves were euthanatized on day 12, and pathologic, virologic, and immunohistochemical examinations were performed.

Results—Type-II BVDV 890 induced the highest degree of viremia, and type-I BVDV TGAN induced the lowest. Virus was isolated more frequently and for a longer duration in calves inoculated with BVDV 890. A parallel relationship between degree of viremia and rectal temperature and an inverse relationship between degree of viremia and blood cell counts was observed. Pathologic and immunohistochemical examinations revealed more pronounced lesions and more extensive distribution of viral antigen in calves inoculated with type-II BVDV.

Conclusions and Clinical Relevance—Degree of viremia induced during BVDV infection is associated with severity of clinical disease. Isolates of BVDV that induce a high degree of viremia may be more capable of inducing clinical signs of disease. Strategies (eg, vaccination) that reduce viremia may control clinical signs of acute infection with BVDV. (Am J Vet Res 2001;62:1095–1103)

Full access
in American Journal of Veterinary Research