Objective-To inoculate white-tailed deer (Odocoileus virginianus) during the sixth or seventh week of gestation with bovine viral diarrhea virus (BVDV) and observe for signs of reproductive tract disease during a 182-day period. Animals-10 pregnant white-tailed deer (8 seronegative and 2 seropositive [control deer] for BVDV). Procedures-Deer were inoculated with 1 of 2 deer-derived BVDV strains (RO3-20663 or RO3-24272). Serum anti-BVDV antibody titers were determined prior to and 21 or 35 days after inoculation. Virus isolation (VI) procedures were performed on tissues from fetuses and does that died and on blood samples collected from live fawns. Ear notch specimens obtained from live fawns were assessed by use of BVDV antigen-capture ELISA (ACE). Results-Both RO3-20663-inoculated seropositive deer gave birth to apparently normal fawns. Among the RO3-24272-inoculated seronegative deer, 1 died, and 1 aborted and 1 resorbed their fetuses; among the RO3-20663-inoculated seronegative deer, 3 died, 1 aborted its fetus, and 1 gave birth to 2 fawns that were likely persistently infected. On the basis of VI and ACE results, those 2 fawns were positive for BVDV; both had no detectable neutralizing anti-BVDV antibodies in serum. Conclusions and Clinical Relevance-Reproductive tract disease that developed in pregnant white-tailed deer following BVDV inoculation was similar to that which develops in BVDV-exposed cattle. Methods developed for BVDV detection in cattle (VI, immunohistochemical evaluations, and ACE) can be applied in assessments of white-tailed deer. Fawns from does that had serum anti-BVDV antibodies prior to inoculation were protected against BVDV infection in utero.

Virologic and pathologic investigations were done on prednisolone-treated bitches with a history of canine herpesvirus (CHV) infection. Reactivation of CHV was demonstrated in 5 Beagle bitches after daily administration of 600 mg of prednisolone for 5 days. The reactivation was confirmed in 4 of 5 bitches. Canine herpesvirus was recovered from nasal, oral, vaginal, and ocular secretions on the 5th to 2lst days after initiation of treatment with prednisolone, and also from nasal mucosa and tonsil tissues. Results indicated that latent CHV infections develop and that the virus may be reactivated, without clinical signs, in dogs with a history of CHV infection.

The purpose of this study was to experimentally reproduce swine infertility and respiratory syndrome (SIRS). Six multiparous sows were intranasally inoculated at 93 days of gestation with lung homogenates from clinically affected pigs, and 3 additional sows were similarly inoculated with a virus isolated in cell culture from the lung homogenate (SIRS virus, isolate ATCC VR-2332). Inoculated sows developed transient anorexia, farrowed up to 7 days prematurely, and delivered a mean of 5.8 live pigs and 6.0 dead fetuses/litter. Clinical signs of disease were not observed in 3 sham-inoculated control sows that delivered a mean of 12.7 live pigs and 0.3 stillborn fetuses/litter. The sirs virus was isolated from 50 of 76 live-born and stillborn fetuses from the 9 infected fitters. Virus was not isolated from 26 autolyzed fetuses or 15 control pigs. Six of 9 inoculated sows developed neutralizing antibodies to SIRS virus. The reproductive effects found in these experiments were identical to those found in field cases. On the basis of our findings, virus isolate ATCC VR-2332 causes the reproductive failure associated with SIRS.

Pregnant sows, immune against pseudorabies after vaccination, were inoculated at 70 days of gestation either with autologous blood mononuclear cells that had been infected in vitro with pseudorabies virus (PRV) or with cell-free PRV. The infected cells or cell-free PRV were inoculated surgically into the arteria uterina. Eight sows (A to H) had been vaccinated with an inactivated vaccine. The titer of seroneutralizing antibodies in their serum varied between 12 and 48. Five sows (A to E) were inoculated with autologous mononuclear cells, infected either with a Belgian PRV field strain or with the Northern Ireland PRV strain NIA. These 5 sows aborted their fetuses: 2 of them (B and C) 3 days after inoculation, and the other 3 (A, D, and E) 10, 11, and 12 days after inoculation, respectively. Sows F, G, and H were inoculated with a cell-free PRV field strain. They farrowed healthy Utters after normal gestation. Neutralizing antibodies were absent against PRV in the sera of the newborn pigs, which were obtained prior to the uptake of colostrum. The 23 fetuses that were aborted in sows B and C 3 days after the inoculation were homogeneous in appearance and size. Foci of necrosis were not detected in the liver. Viral antigens were located by immunofluorescence in individual cells in lungs, liver, and spleen of 15 fetuses. Virus was isolated from the liver, lungs, or body fluids of 12 fetuses. The 39 fetuses that were aborted in sows A, D, and E between 10 and 12 days after inoculation were of 2 types: 17 were mummified and 22 were normal-appearing. Foci of necrosis were found in the liver of all mummified fetuses and 13 of the normal-appearing fetuses. In fetuses with foci of necrosis in the liver, viral antigens were located in groups of cells in the liver, lungs, and spleen. Virus was isolated from 16 normal-appearing fetuses and from 11 mummified fetuses. Pseudorabies virus was isolated from vaginal excretions of sows A and D until 1 and 2 days after abortion, respectively, and of sows B and C until 4 and 5 days after abortion, respectively. Virus was not isolated from sow E. It was concluded that PRV can reach the uterine and fetal tissues, via infected mononuclear cells, in the presence of circulating antibodies induced on vaccination. This cell-associated spread led to abortion. Cell-free virus did not induce abortion under similar circumstances.

Ten multiparous sows were inoculated between 46 and 50 days of gestation with a fetal swine isolate of encephalomyocarditis virus (EMCV) to investigate the ability of the virus to cause transplacental infection and fetal death. Four sows (group 1) were inoculated IM with EMCV MN-25 that had been passaged 4 times on baby hamster kidney-21 line cell monolayers. Two sows were euthanatized at postinoculation (PI) day 23, and the other 2 sows at PI day 44. An additional 6 sows (group 2) were inoculated IM with the same virus that had been passaged 5 additional times in pigs. Two sows were euthanatized at 14 days, and the remaining 4 sows at PI day 28. Clinical signs were not observed in any of the sows, whereas all sows seroconverted to EMCV. In group 1, only 2 of 50 fetuses were mummified. Virus was not recovered, although EMCV antibodies were detected in the 2 mummified fetuses. In group 2, the 2 sows that were euthanatized at PI day 14 had 26 normal fetuses and there was no evidence of fetal infection. However, in the 4 sows euthanatized at PI day 28, 20 of 48 fetuses were mummified, hemorrhagic, or edematous. Encephalomyocarditis virus was recovered from 21 of 48 fetuses. Transplacental infection and fetal deaths in pregnant sows was achieved following infection with EMCV passaged in pigs.

Nucleic acid hybridization, bacteriologic culture, and a fluorescent antibody test were compared for detection of Leptospira interrogans serovar hardjo type hardjo-bovis in bovine urine. Seventy-five urine samples were collected from pregnant cows challenge exposed with type hardjo-bovis. Twenty samples were collected from steers not exposed to hardjo-bovis. Sediments from each sample were examined, using fluorescent antibodies and a repetitive sequence element nucleic acid probe, to detect the presence of leptospires. Urine samples were processed for bacteriologic culture, using standard techniques. Under laboratory conditions typically used for these techniques, leptospires were detected in 60 of 75 urine samples from challenge exposed cows by nucleic acid hybridization, in 24 samples by fluorescent antibody test, and in 13 samples by bacteriologic culture. Leptospires were not detected in the urine of steers not exposed to hardjo-bovis.

Sarcocystis capracanis, pregnant dairy goats immunized with a subclinical dose of sporocysts and subsequently challenged with lethal doses, concluded that: i) subclinical dose given in early pregnancy can cause fetal death without causing clinical disease in doe; ii) abortion can occur prior to development of 2nd-generation meronts; and iii) Sarcocystis-induced immunity is impaired during pregnancy

Six pregnant gilts were purchased from a high health herd and were found to be serologically positive for swine influenza virus (SIV) subtype H3N2. Three of the gilts, at 80 to 82 days of gestation, were experimentally exposed a second time to the same SIV subtype --- H3N2. No clinical signs resulted from the second exposure to SIV and hemagglutination-inhibition (HI) titers for SIV at 4 weeks postexposure were unchanged suggesting that the gilts had not been reinfected. However, the second exposure to SIV affected the number of pigs born alive. Each of the 3 litters from the twice exposed gilts suffered 2 or 3 stillborn piglets per litter. In contrast the 3 matched, sero-positive gilts that were not exposed to SIV (controls) had no stillborn piglets. These differences were statistically significant using a t-test for unequal variances (P = 0.0086). Sera from 2 of the stillborn piglets were negative for HI antibodies and there was no indication from the pigs born alive that the H3N2 virus had crossed the placenta.

Fetal infectivity of Ehrlichia risticii was investigated in 19 ponies that were E risticii negative on the basis of results of an indirect fluorescent antibody (IFA) test. Thirteen pregnant ponies were infected by IV administration of E risticii between 90 and 180 days of gestation. Six pregnant ponies served as noninfected controls. Each infected pony had clinical signs of equine monocytic ehrlichiosis, was confirmed to be ehrlichemic, and developed an IFA titer to E risticii. Two infected ponies became recumbent, were unresponsive to supportive care, and were euthanatized. After recovery from clinical illness, the remaining ponies were observed throughout gestation for reproductive abnormalities. On abortion, each fetus was necropsied and tissue specimens from the liver, bone marrow, spleen, colon, and mesenteric lymph nodes were inoculated into canine monocyte cell cultures. Six infected ponies aborted at a mean 217 days of gestation, which was between postinoculation days 65 and 111. Five fetuses were recovered for evaluation, and E risticii was isolated from 4 of them. All 5 fetuses recovered had similar histologic findings, including enterocolitis, periportal hepatitis, and lymphoid hyperplasia with necrosis of the mesenteric lymph nodes and spleen. All fetuses tested negative for IgG to E risticii, although 3 had low IgM titer to E risticii. The remaining 5 infected ponies had normal parturition. Presuckle IFA titer to E risticii was measured in 4 of the term foals, and results for 3 were positive. Two foals from infected ponies were monitored for 6 months and daily gain in body weight was comparable to that of a control foal. None of the control ponies became ill or seroconverted during the clinical illness phase, and none aborted throughout gestation. Two control ponies seroconverted to E risticii 6 weeks before parturition. Results of this study indicate that E risticii is a primary abortifacient under experimental conditions.

Inoculation of 53 ewes after 35, 45, 60, or 80 days of gestation with bluetongue virus serotypes 10, 11, 13, or 17, or with epizootic hemorrhagic disease virus serotypes 1 or 2, resulted in overt clinical disease in the 47 ewes inoculated with bluetongue virus but not in the 6 ewes inoculated with epizootic hemorrhagic disease virus. None of the lambs produced by these ewes had developmental defects or any evidence of persistence of viremia.