Histomorphometric and scanning electron microscopic analyses were performed on 74 embryos and fetuses and 20 sheep (early postnatal to adult age). Histologic differentiation of the omasum took place at 33 days of fetal life, with the appearance of first-order laminae. Second-, third-, and fourth-order laminae appeared at 39, 50, and 59 days, respectively. Neutral mucopolysaccharides first appeared in epithelial cells at 46 days of fetal life, decreasing quantitatively until birth, before subsequently stabilizing in postnatal life. Acid mucopolysaccharides, mucins, and mucoid compounds were not detected. Growth curves and formulas were constructed for each tissue layer. Initial tests involved multiplicative (y = axb), exponential (y = EXP [a + bx]), linear (y = a + bx), and polynomial models [y = a + bx + cx(2) + dx(3)].

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.

Two experiments were undertaken to evaluate whether porcine reproductive and respiratory syndrome (PRRS) virus was able to cross the placenta and infect midgestation fetuses following intranasal inoculation of sows and whether PRRS virus directly infected fetuses following in utero inoculation. In experiment 1, eight sows between 45 and 50 days of gestation were intranasally inoculated with PRRS virus (ATCC VR-2332), and four control sows were inoculated with uninfected cell culture lysate. Virus inoculated sows were viremic on postinoculation (PI) days 1, 3, 5, 7 and 9, shed virus in their feces and nasal secretions, and became leukopenic. Sixty-nine of 71 fetuses from principal sows euthanized on PI day 7, 14 or 21 were alive at necropsy and no virus was isolated from any of the fetuses. Two principal sows that farrowed 65 and 67 days PI delivered 25 live piglets and three stillborn fetuses. The PRRS virus was isolated from two live piglets in one litter. In experiment 2, laparotomies were performed on five sows between 40 and 45 days of gestation and fetuses were inoculated in utero with either PRRS virus alone, PRRS virus plus a swine serum containing PRRS antibodies, or uninfected cell culture lysate. Three sows were euthanized on PI day 4 and two sows on PI day 11. Viral replication occurred in fetuses inoculated with virus alone and was enhanced in fetuses inoculated with virus plus antibody. No virus was isolated from control fetuses. The results indicate that sows and fetuses are susceptible to PRRS virus infection in mid-gestation, that viral replication is enhanced by the addition of serum with PRRS virus antibody, and that the virus does not readily cross the placental barrier during mid-gestation.

Albendazole, administered orally at a dose rate of 25 mg/kg of body weight to presumed pregnant cows or heifers on days 21, 31, 41, 51, and 61 of gestation, did not induce toxicosis in embryos or fetuses, and all calves born were structurally normal. Albendazole administration at a rate of 25 mg/kg to cows at 7 and/or 14 days of gestation decreased the apparent conception rate (ie, embryolethality), but did not have a teratogenic effect. Apparent embryolethality was greater in cows administered 25 mg/ kg only on day 14, compared with those administered the drug only on day 7. Single dosage of 25 mg/kg given in the final 3 months of gestation did not induce abortion. There were no adverse effects of albendazole at a dosage of 10 or 15 mg/kg on developing embryos or fetuses when administered to presumed pregnant cows at various times in early gestation.

Both ovaries from 88 bovine fetuses in the fifth month or later of gestation were studied histologically to determine the prevalence, origin, and time of appearance of atretic corpora lutea (ACL). Ovaries from 36 (41%) fetuses had ACL; fetuses < 6 months of gestation did not have ACL. Six fetuses had more than 25 ACL, but there was no apparent relationship between fetal age and number of ACL. Formation of ACL involved disintegration of the stratum granulosum of secondary follicles, concomitant with proliferation and invasion by vascularized elements of the theca. Fully developed ACL consisted of a large primary oocyte surrounded by a prominent zona pellucida and encased in a well-vascularized, largely thecal, fibrocellular wall. They measured approximately 0.5 to 1.0 mm in diameter. Empty, collapsed zona pellucidas were seen in many of the degenerating ACL.

Akabane virus (AKV) strain OBE-1 was inoculated IV into 17 pregnant sheep. Ten fetuses infected at 29 to 45 days of gestation and examined 29 to 30 days later had AKV antigen in the following groups of cells: neuroglial cells in the brain and spinal cord, ganglion cells in the cranial and abdominal ganglia, layer of ganglion cells in the retina, ganglion cells (Auerbach's plexus) in small intestine, hepatocytes, cells in the arterial wall of mesenteric membrane, and trophoblast cells in the placenta. Prior to detection of circulating virus-neutralizing antibody, immunoglobulin-containing cells were found initially at 59 days of gestation in the peripheral portion of white pulp tissue in the spleen. After that, numbers of immunoglobulin-containing cells gradually increased. These results indicated that AKV may have strong affinity for neuronal and ganglional cells in infected fetuses and immunoglobulin-containing cells might be considered the earliest immunologic response to AKV replication in the fetus.

Five cows in the last month of gestation, provided with uterine electrodes and in which catheters had been chronically installed in the fetal aorta, were used to study patterns of fetal heart rate (FHR) and the influence of periods of myometrial electrical activity during gestation (contractures) on FHR. The FHR was calculated by counting the number of blood pressure pulses on the tracings during alternate periods of 12 seconds. Three 1-hour recordings without contractures and 10 recordings during the time of a contracture were randomly selected for each cow. The calculated data points were plotted on a graph to display FHR patterns. In 41 periods associated with single contractures, FHR data points were taken every 72 seconds. Changes in absolute and relative FHR in these periods were determined to analyze a possible effect of contractures on FHR. Three types of variation in FHR patterns could be distinguished: a short-term, low-amplitude variation of basal FHR; a second type in which the duration was < 4 minutes and the amplitude was greater than or equal to 15 beats/min; and prolonged periods with increased or decreased FHR values (> 4 minutes and greater than or equal to 15 beats/min). The relationship between these types of variation and fetal activity states remains to be established for cows. During the 60 hours of recordings that were analyzed, a period of several minutes during which FHR values were extremely high (> 180 beats/min) was found 3 times. There were no significant differences in absolute or relative FHR before, during, or after a contracture.

Labor and delivery stimulate increased release of catecholamines and endogenous opioid peptides in neonates. Catecholamines promote adaptation to the extrauterine environment after birth. Enkephalins are stored together with catecholamines in the adrenal medulla and have an inhibitory effect on catecholamine release. We investigated the influence of labor and neonatal hypoxia on epinephrine, norepinephrine, and met-enkephalin release in calves. Blood samples were taken from the umbilical artery before rupture of the umbilical cord and from the jugular vein repeatedly after birth. Highest plasma norepinephrine concentration was found in calves delivered at the end of gestation (term calves) before umbilical cord rupture. In calves delivered before the physiologic end of gestation (preterm calves), norepinephrine values increased after cord rupture, but remained lower than values in term calves. Epinephrine release followed a similar pattern, but norepinephrine was clearly predominant. In term calves, met-enkephalin values were significantly higher than values in preterm calves. In calves of both groups, met-enkephalin release increased after cord rupture. During birth, the increase in catecholamine release seems to take place earlier than that of enkephalins. Norepinephrine-dominated stimulation during expulsion of the calf might be followed by increasing enkephalinergic inhibition after cord rupture and onset of respiration. Reduced release of catecholamines and enkephalins in preterm calves may be connected with delayed adaptation to the extrauterine environment.