We evaluated the effectiveness of 2 dopamine antagonists as treatments for fescue toxicosis in horses. Sixteen gravid mares were assigned by breed and expected foaling date to 1 of 3 treatment groups: endophyte-infested control 1.1 mg of domperidone/kg of body weight/d; and 3.3 mg of sulpiride/kg/d. Mares were pastured on endophyte-infected fescue and received 0.454 kg of a corn and dried molasses carrier containing the drug treatment. Treatment started 30 days prior to expected foaling date and continued until parturition. Blood samples were collected, and mammary gland scores were recorded every 5 days. Body weight and body condition scores were obtained every 28 days. Serum was analyzed for prolactin, progesterone, and estradiol-17beta concentrations. Domperidone-treated mares had shorter (P = 0.09) gestation duration and foaled closer (P = 0.07) to their expected parturition date than did control mares. Mammary gland scores were higher (P < 0.05) for domperidone-treated mares than for control mares. By 4 and 9 days after the start of treatment, serum prolactin concentration was higher P < 0.05) in domperidone-treated mares and sulpiride-treated mares, respectively, than in control mares. Domperidone- and and sulpiride-treated mares had higher (P < 0.05) serum progesterone and lower (P < 0.01) estradiol-17beta concentrations than did control mares. These results indicate that domperidone may offer considerable potential as a treatment for fescue toxicosis in horses.

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 X 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus. Age at puberty was similar between gilts exposed to low or moderate concentration of ammonia (208 vs 205 days; SEM, 1.3 days), even though weight at puberty was less (P < 0.03) for gilts exposed to low concentration of ammonia than for gilts exposed to moderate concentration of ammonia (109.7 vs 118.2 kg; SEM, 4.5 kg). At day 30 of gestation, number of live fetuses (10.6 vs 11.7), fetal length (2.53 vs 2.57 cm), and fetus-to-corpus luteum ratio (0.85 vs 0.78) were similar between gilts at low and moderate ammonia environments. These data indicate that exposure of gilts to mean aerial ammonia concentration of 35 ppm in environmentally regulated rooms depressed MDG for 2 weeks, but failed to alter onset of puberty or litter size at day 30 of gestation.

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.

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.

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.

Three experiments were conducted to investigate experimentally the occurrence of periparturient nematode egg rise in ewes and the hormonal modulation of Haemonchus contortus infections. In the first experiment, fall-bred and winter-bred pregnant (n = 4 and 14, respectively) and nonpregnant (n = 5 and 29, respectively) ewes were treated with anthelmintic and were pastured together on fields that were contaminated with H contortus. Three weeks before lambing, all ewes were placed in concrete pens; fecal egg counts for the winter-bred group were obtained on alternate days. Pregnant and lactating ewes had significantly larger numbers (P < 0.01) of H contortus eggs than did the nonpregnant controls 1 week before and after lambing. Lactating, fall-bred ewes had significantly (P < 0.01) more adult worms in their abomasum through natural acquisition than the nonpregnant controls. In the second experiment, fall-bred and winter-bred helminth-free, pregnant (n = 4 and 8, respectively) and nonpregnant (n = 3 and 15, respectively) ewes were inoculated on 5 alternate days, beginning 70 days after breeding with 20,000 infective H contortus larvae. The ewes were maintained on concrete pens throughout pregnancy. Fecal egg counts were significantly (P < 0.05) greater in pregnant ewes, beginning 1 week before lambing until 1 week after lambing. Abomasums of lactating ewes from both lambing seasons yielded significantly (P < 0.01) more adult worms at necropsy than nonpregnant ewes. In the third experiment, ewes were ovariectomized (n = 15) or sham-operated (n = 9); half of the control ewes were bred. Beginning on day 70 of pregnancy, all ewes were inoculated orally with 20,000 infective H contortus larvae on 5 alternative days. Abomasums were removed from all ewes after lambing, and adult worms were recovered. Pregnant ewes and half of the ovariectomized ewes had significantly (P < 0.05) more worms than did the sham-operated ewes.

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.

The consequences of inoculation of bluetongue virus (BTV) serotype 11 into 16 susceptible cows either at the time of breeding or at specified stages of pregnancy were studied. The cows were free of BTV or epizootic hemorrhagic disease virus, and none had antibodies to BTV before virus inoculation. A group of 4 cows was mated naturally to a bull reported to shed BTV (CO75B300 strain) in the semen. The bull was suspected of infecting cows at mating with BTV-11, which subsequently transplacentally infected the developing fetuses and induced persistently infected and congenitally malformed progeny. Two groups of 4 pregnant cows were inoculated with an insect-derived strain of BTV-11 (CO75B300), one group by direct deposit into the uterus at estrus, the other, by intradermal and sc administrations. A 90-day fetus was inoculated in utero with virus from the same pool. Four pregnant cows were inoculated with sheep blood-passaged virus of the same BTV-11 strain (CO75B300) by intradermal and sc routes. Three cows were inoculated with BTV-free suspending fluids and ovine erythrocytes by the intrauterine and intradermal-sc routes and were used as in-contact controls.Infection with insect-derived BTV-11 was confirmed in 3 cows of 1 group by virus isolation and by detection of serum antibodies. The 4 cows inoculated with sheep blood suspension of BTV-11 developed viremia and produced antibodies to the virus. None of the cattle had clinical signs of bluetongue, other than 2 cows that had a slight rectal temperature increase on postinoculation day 4.All cows and fetuses that ranged in gestational age from 69 to 217 days appeared grossly normal at necropsy. Antibodies were not detected in fetal blood. Viral antigen was not detected in fetal tissues by inoculation into sheep or by immunofluoerscence, and viral RNA was not detected by use of the polymerase chain reaction. Developmental deformities were not seen in any fetus. The BTV-11 was not transmitted via the bull semen after natural mating. The BTV-11 strain CO75B300, isolated from this bull and passaged either as insect-derived or ovine erythrocyte suspensions, infected 8 cows. However, the virus was not transplacentally transmitted to their fetuses. It was concluded that there was no evidence for congenital BTV-11 infection in this study.

Effects of the endophyte Acremonium coenophialum in tall fescue on pregnant mares and foal viability were evaluated. Twenty-two mature pregnant mares were randomly chosen to graze either Kentucky-31 tall fescue that was free from A coenophialum (endophyte-free, EF) or tall fescue infected with A coenophialum (endophyte-present, EP) after the first 90 days of pregnancy through parturition. Concentrations of pyrrolizidine and ergopeptine alkaloids were significantly greater in EP grass, compared with EF pasture. Ten of 11 mares grazing EP pasture had obvious dystocia. Mean duration of gestation was significantly greater for the EP group, compared with the EF group. Foal survivability was severely reduced among mares grazing Ep fescue with only 1 foal surviving the natal period. Udder development and lactation were low in mares grazing EP grass. The absence of clinical problems in mares grazing EF grass implicated the endophyte as the causative agent of reproductive problems and perinatal foal mortality in pregnant mares grazing endophyte-infected fescue grass. Caution should be exercised in allowing pregnant mares to graze pastures infected with the endophyte A coenophialum.

Seventy-nine cattle in all stages of gestation were inoculated with a low dose (2.5 X 10(8) colony-forming units) of Brucella abortus strain 19, then challenge exposed with pathogenic B abortus strain 2308 during the subsequent gestation. A brucellosis case was defined by isolation of strain 2308 from dam or calf samples. Cumulative incidence of brucellosis cases was 48, 33, 25, or 47% for cattle that were, respectively, not pregnant, or 19 to 87, 100 to 167, or 190 to 253 days in gestation at vaccination. The cumulative incidence was 56% in 27 nonvaccinated controls. The 95% confidence intervals for risk ratios included 1 in all cattle, except those that were 100 to 167 days in gestation at vaccination (ie, second trimester); the confidence interval for this group was 0.21 to 0.97. The prevented fraction (1-risk ratio) attributed to strain 19, in ascending order, was 0.14, 0.16, 0.4, or 0.55, respectively, for cattle that were not pregnant, or were 190 to 253, 19 to 87, or 100 to 167 days in gestation at vaccination. Potential confounders of breed, pen effect, and gestation days at challenge exposure did not significantly affect results. Results supported the hypothesis that stage of gestation at vaccination will affect the prevented fraction of brucellosis, or efficacy of strain 19, in cattle vaccinated with a low dose and, therefore, is one factor that may explain variation in strain 19-induced protection.