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Suppurative, ulcerative endometritis associated with bovine herpesvirus-4 (BHV-4) infection was identified in 15 postparturient dairy cows from 5 separate dairies. Characteristic eosinophilic to amphophilic intranuclear viral inclusion bodies were identified within degenerate endometrial lining epithelium and endothelial cells. Bovine herpesvirus-4 was confirmed as the etiology by a combination of fluorescent antibody assays, viral isolation, heminested PCR, ultrastructural examination of the uterus and inoculated tissue culture cells, and negative-stain electron microscopy of tissue culture supernatant. Viral particles measuring 70-95 nm were demonstrated in uterine epithelial and endothelial cells by electron microscopy. Bacteria including Arcanobacterium pyogenes, Escherichia coli, and an alpha-Streptococcus isolate were isolated from all uteri. Bovine herpesvirus-4-associated endometritis has been previously reported in sporadic cases in Europe but has not been previously reported in the United States. Endometritis associated with BHV-4 appears to be an emerging syndrome in Georgia dairy herds.

Despite the importance of congenital viral infections in both veterinary and human medicine, only limited experimental work has been carried out to elucidate the mechanisms involved in transplacental virus infections. To further an understanding of fetal infection with pestiviruses, the distribution of bovine pestivirus in the uterine and fetal tissues of ewes in early pregnancy, following a natural route of infection, was investigated. On the 18th day of pregnancy, nine ewes were inoculated by the intranasal route with 1 x 10(5) 50% tissue culture infective doses of an Australian isolate of noncytopathic bovine pestivirus (bovine viral diarrhea virus genotype 1). All ewes were ovariohysterectomized at approximately 100 hours postinfection. Samples from the reproductive tract and conceptus were examined histologically and tested for bovine pestivirus by nested reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry and for interferon-tau mRNA expression by nonnested RT-PCR. Although no histopathologic changes were observed in the maternal or fetal tissues, virus was detected in the reproductive tract of all nine ewes and in all of the conceptuses examined. At the time of surgery, only two of the nine ewes were demonstrably viremic. This study demonstrates that bovine pestivirus can spread from a natural site of infection to the ovine fetus within 4 days in the absence of maternal immunity and despite the presence of interferon expression in the reproductive tract.

Economic loss from infection with bovine viral diarrhea virus (BVDV) is of worldwide concern. The unique pathogenesis and antigenic variability of BVDV have made this virus challenging to control. Vaccination programs are a major component of control and prevention strategies. Both killed and modified live vaccines are commercially available. Choice between killed and modified live vaccines is controversial. Of major concern is the safety of modified live vaccines. Little information is available on their tissue tropism and potential for causing pathology, especially with respect to the reproductive system. The objective of this study was to determine if BVDV could be detected in the ovary of cattle following immunization with a modified live BVDV vaccine. In 2 separate trials, 6 heifers and 4 mature cows were immunized with a modified live BVDV vaccine and ovaries were removed between 7 and 30 days postvaccination. Cytopathic BVDV was isolated from ovaries removed on days 8, 10, and 12. BVDV antigen was detected using immunohistochemistry on days 10-30. These findings are significant because replication of virus in the ovary could cause ovarian dysfunction, resulting in reduced fertility.

Diagnosis of porcine reproductive and respiratory syndrome virus (PRRSV)-induced reproductive failure in swine is difficult because of the rapid inactivation of virus in fetuses that have died prior to abortion or farrowing. In this report, we describe gross and microscopic lesions of diagnostic value found in fetuses transplacentally infected with PRRSV during late gestation. Seven sows free of PRRSV-specific antibody and 1 sow (#8) that had been previously infected with PRRSV were oronasally exposed to a PRRSV inoculum at or about 90 days of gestation (DG). One control sow (#9) was oronasally exposed to a sham inoculum at 90 DG. Sows were euthanized 21 days postexposure, and fetuses were tested for virus. Transplacental infection was detected in litters 1-7, and gross lesions of the umbilical cord were observed in some fetuses in 6 of the 7 litters. No transplacental infection or fetal lesions were found in litters 8 and 9. The gross lesions in the umbilical cords ranged from segmental hemorrhagic areas 1-2 cm in length to a full length involvement of the cord, which was grossly distended with frank hemorrhage. All live fetuses that had gross lesions in the umbilical cord were viremic, and histopathologic examination revealed a necrotizing umbilical arteritis with periarterial hemorrhage. This was the most consistent microscopic lesion in fetuses infected with PRRSV. Sows 1-7 had endometritis and myometritis of various degrees, suggesting PRRSV also may induce these lesions. Careful gross and microscopic examination of the umbilical cord may aid in the diagnosis of PRRSV-induced reproductive failure.

Six female dogs (four pregnant and two nonpregnant) were inoculated with bluetongue virus (BTV), serotype 11. Pregnant animals and one nonpregnant dog received 5.5-6.3 log10 of cell culture-adapted virus. The other nonpregnant dog received a modified live vaccine contaminated with bluetongue virus. The non-pregnant animals never became clinically ill and were euthanatized 35 days post-inoculation. Three of the four pregnant dogs aborted, and all four died or were euthanatized 5-10 days post-inoculation. The predominant pathologic feature in the adults was severe pulmonary edema. Various tissues from the bitches and fetuses were examined by in situ hybridization using a digoxigenin-labeled probe corresponding to the nonstructural protein-1 gene of BTV-17. By this technique, viral nucleic acid was detected predominantly in endothelial cells of lung of all four dogs, with lesser amounts in capillaries of uterus, spleen, and kidney in some of the dogs. In two adult dogs, bluetongue viral nucleic acid was detected in mononuclear cells of the periarteriolar lymphoid sheaths of spleen. There was minimal staining of capillaries in placenta in three of the five fetuses examined. There was no viral nucleic acid detected in any of the other fetal tissues.