Comparison of the virulence of two isolates of porcine parvovirus in 72-day-old porcine fetuses.

Two strains of porcine parvovirus (PPV), designated Kresse and NADL-8, were compared for relative virulence in porcine fetuses. Strain Kresse was injected into the amniotic fluid of all fetuses of 1 uterine horn of each of 2 pregnant gilts at 72 days of gestation. Strain NADL-8 was administered similarly to fetuses of 4 other gilts at the same stage of gestation. All gilts were killed and necropsied 35 days later. Selected tissues of all fetuses were tested for infectious virus and viral antigen. Sera from live fetuses were tested for antibody to PPV. These tests confirmed that most fetuses exposed to PPV by intra-amniotic injection became infected. All of 11 fetuses exposed to strain Kresse by intra-amniotic injection were alive at the time of necropsy, and all appeared clinically normal. In contrast, 8 of 24 fetuses exposed similarly to strain NADL-8 were dead. Many of the fetuses from the uterine horns contralateral to the uterine horns inoculated with virus were infected after 72 days of gestational age by intrauterine spread of the virus. Four such fetuses, 3 infected with the NADL-8 strain and 1 infected with the Kresse strain, were dead at the time of necropsy. These findings were inconsistent with those of a previous report, which indicated that the Kresse strain of PPV was markedly more virulent than the NADL-8 strain of PPV for porcine fetuses. A possible reason for this apparent discrepancy is discussed.     

Safety and efficacy of vaccination of pregnant gilts against porcine reproductive and respiratory syndrome.

OBJECTIVE: To determine the safety and efficacy of vaccination of pregnant gilts with an attenuated strain of porcine reproductive and respiratory syndrome virus (PRRSV). ANIMALS: 16 pregnant gilts. PROCEDURE: Pregnant gilts free of antibodies for PRRSV were assigned (4 gilts/group) to the following groups: group I, untreated controls; group II, vaccinated on day 60 of gestation; group III, vaccinated on day 60 of gestation and exposed to virulent PRRSV on day 90 of gestation; and group IV, exposed to virulent PRRSV on day 90 of gestation. Safety and efficacy of vaccination was evaluated by group comparisons of prenatal and postnatal survival of fetuses and pigs, respectively, and by the condition and rate of weight gain of liveborn pigs. RESULTS: Collective (prenatal and postnatal) death losses up to day 15 after farrowing (conclusion of study) were similar for groups I (7/47, 14.9%) and II (7/44, 16.9%) but were greater for group III (18/49, 36.7%) and were greater still for group IV (23/37, 62.2%). Mean body weight 15 days after farrowing was greatest for pigs in litters of group I (4.46 kg) and progressively less for the other groups (3.87, 3.76, and 2.18 kg for groups II, III, and IV, respectively). CONCLUSIONS: Using these conditions, vaccination of gilts during midgestation appeared to be safe. However, it provided only partial protection against subsequent exposure to virulent virus. CLINICAL RELEVANCE: Attenuated-PRRSV vaccines may have to be administered to naive gilts > 30 days before conception to provide maximum protection throughout gestation.     

The relationship of fetal weight to serum albumin and alpha-fetoprotein in swine

The within-litter relationship of fetal weight to fetal serum albumin and alpha-fetoprotein (AFP) was investigated at d 30 to 40, 45 to 50, 50 to 60, 75 to 85 and 90 to 105 of gestation in swine. Regression equations were calculated on individual litters and regression coefficients pooled across litters within each gestational age group. Coefficients for the regression of albumin on fetal weight (microgram . ml-1 . g fetus-1) were significant over all groups and ranged from 22.5 +/- 6.6 to d 45 to 50 to .7 +/- .2 at d 95 to 105. There was no significant relationship between AFP levels and fetal weight at any gestational age. Unilateral ovariectomy-hysterectomy was performed before mating to study effects of uterine crowding on the relationship of fetal weight to AFP and albumin. Although the total number of ovulations was not different from controls, this treatment resulted in only about 1.3 more fetuses/uterine horn compared with controls at either d 40 or 60 of gestation. Fetal weights in crowded litters were not different from controls. However, AFP levels in fetuses from crowded litters were lower than in control fetuses at d 40 (4.5 +/- .1 vs 6.7 +/- .5 mg/ml). Albumin levels in crowded fetuses were significantly lower than in controls at d 60 (342 +/- 50 vs 653 +/- 41 micrograms/ml). Because none of these differences in albumin or AFP could be attributed to variation in fetal weight or fetal number at the time of sample collection, it is possible that more extreme uterine crowding earlier in development resulted in these differences. These results demonstrate that fetal serum albumin concentrations are related to fetal weight when analyzed on a within-litter basis and that unilateral ovariectomy-hysterectomy may affect serum concentrations of both AFP and albumin early in fetal development. Future studies involving the regulation of synthesis of these proteins at the cellular level during development should provide information as to how factors affecting overall fetal growth and development influence the expression of a single gene. Previously, such markers that are amenable to study early in development have been lacking.     

Diagnostic investigation of chronic porcine reproductive and respiratory syndrome virus in a breeding herd of pigs

Forty-five sows and 15 boars were selected at random from a breeding herd known to be chronically infected with porcine reproductive and respiratory syndrome virus (PRRSV) and lymphoid, immune-privileged, and non-lymphoid/non-immune-privileged tissues were tested for the presence of the virus by PCR, virus isolation, and immunohistochemistry. The virus was isolated from the lateral retropharyngeal lymph node of one sow; the isolate was nucleic acid sequenced and determined to be of field origin, and it was inoculated into two PRRSV-naive pregnant sows (A and B) at 95 days of gestation. They were necropsied 14 days later and samples of maternal and fetal tissue and blood samples were collected. Sow A had 10 fresh, six partially autolysed, and two mummified fetuses, and sow B had six fresh and viable fetuses. Viral nucleic acid was detected by PCR in tissue pools from each sow and also from pooled fetal tissues, and the virus was isolated from fetal pools from sow A.     

Strain predominance following exposure of vaccinated and naive pregnant gilts to multiple strains of porcine reproductive and respiratory syndrome virus

Two studies were performed in order to test the relative ability of different strains of porcine reproductive and respiratory syndrome virus (PRRSV) to replicate and cross the placental barrier in pregnant gilts. Study 1 comprised 6 nonvaccinated gilts. Study 2 comprised 8 nonvaccinated gilts and 12 gilts that were vaccinated twice before conception. On, or about, gestation day 90 all gilts were simultaneously exposed to 20 field strains of PRRSV (all strains were distinguishable by restriction fragment length polymorphism (RFLP) patterns). Gilts of study 1 were euthanized on day 7 postpartum. Gilts of study 2 were euthanized on, or about, gestation day 111. All gilts, pigs, and fetuses were tested for the presence and type of strain of PRRSV. Of 128 samples shown to contain PRRSV, 118 contained a single strain, 4 contained 2 strains, and 2 contained a strain or strains for which the RFLP pattern was undecipherable. Only 8 of the 20 strains were isolated from nonvaccinated gilts and their litters. And only 2 of the 20 strains (notably 2 of the same strains isolated from nonvaccinated gilts and their litters), were isolated from vaccinated gilts and their litters. Moreover, 1 of the 2 strains accounted for most (31 of 37; 84%) of the isolates from the vaccinated group. Collectively these results indicate that strains differ in their ability to replicate in pregnant gilts and cross the placental barrier. And they suggest that maternal immunity, although sometimes insufficient to prevent transplacental infection, can exert additional selective pressure.     

In utero infection of swine fetuses with infectious bovine rhinotracheitis virus (bovine herpesvirus-1)

The pathogenesis of infectious bovine rhinotracheitis (IBR) virus (bovine herpesvirus-1) was studied in porcine fetuses after in utero inoculation. Laparotomies were performed on 8 seronegative pregnant sows at 34 to 86 days of gestation, and all fetuses in 1 uterine horn of each sow were exposed to IBR virus via inoculation into the amniotic sacs. Fetuses in the other horn served as controls. Clinical signs of infection were not observed in the sows, except for 2 sows that aborted at postinoculation days (PID) 11 and 15. Fetuses of the remaining 6 sows were collected at slaughter on PID 15 to 28. Fetuses were examined for gross abnormalities, presence of IBR virus in tissues, and the formation of neutralizing antibodies to IBR virus. Of 33 inoculated fetuses from 6 sows, 10 were mummified, 11 were hemorrhagic and/or edematous, and 12 were alive. Necrotic lesions were observed on the skin and in the liver of dead and live fetuses. Virus was recovered from 29 of 33 inoculated fetuses. Infectious bovine rhinotracheitis virus was isolated from fetal skin, liver, lungs, kidney, spleen, stomach contents, brain, amniotic fluid, and placenta. Virus was isolated from 4 of 11 fetuses recovered from 1 aborting sow. Antibodies to IBR virus were not detected in sera from the sows. However, antibodies were detected in 6 of 15 fetuses inoculated at 63 to 86 days of gestation and collected at slaughter at 86 to 112 days of gestation. The youngest fetus with detectable IBR antibody was estimated to be 74 days of gestation by measuring crown-rump length of the fetus.     

Efficacy of an inactivated virus vaccine for prevention of porcine parvovirus-induced reproductive failure.

Gilts vaccinated IM either once (4 gilts) or twice (2 gilts) with an acetylethyleneimine-inactivated porcine parvovirus (PPV) vaccine before they were bred were subsequently exposed intranasally and orally to virulent PPV at about the 40th day of gestation (from 37 to 43 days). At 2 weeks after vaccination, all had hemagglutination-inhibiting (HI) titers for PPV (from 20 to 80) which decreased by the time the immunity was challenged with virulent virus (from 10 to 40), but increased thereafter (from 160 to 1,280). Titers of singly and doubly vaccinated gilts were similar throughout the experiment. The gilts were killed at about the 84th day of gestation (from 80 to 87 days), and their litters were examined. Litters were comprised of 68 live fetuses and 1 dead fetus (7 to 14 fetuses/litter). Neither viral antigen, PPV, nor homologous HI antibody was found in any of the fetuses. In addition, 4 gilts were kept in contact with the vaccinated gilts and were treated similarly except for vaccination. These 4 gilts remained free of HI antibody until after they were exposed to virulent PPV during gestation. At the time the gilts were killed the titers were 1,280 to 2,560. Their litters were comprised of 11 live fetuses and 26 dead fetuses (8 to 11 fetuses/litter). Virus was isolated from fetuses of all litters. Viral antigen was found in 24 of the dead fetuses and 10 of the live fetuses. All infected live fetuses also had HI antibody for PPV. The 2 boars used to breed vaccinated and nonvaccinated gilts (usually each gilt was bred to each of the 2 boars), but not exposed to virulent PPV, remained free of HI antibody for PPV.     

Evaluation of protective immunity in gilts inoculated with the NADC-8 isolate of porcine reproductive and respiratory syndrome virus (PRRSV) and challenge-exposed with an antigenically distinct PRRSV isolate.

OBJECTIVES: To determine whether intrauterine inoculation of porcine reproductive and respiratory syndrome virus (PRRSV) interferes with conception and whether exposure to one strain of PRRSV provides protection against challenge-exposure (CE) with homologous or heterologous strains of PRRSV. ANIMALS: 40 gilts. PROCEDURE: Gilts were inoculated by intrauterine administration of a PRRSV isolate (NADC-8) at breeding. Inoculated and noninoculated gilts were exposed oronasally to homologous (NADC-8) or heterologous (European isolate) PRRSV during late gestation. Specimens from gilts and fetuses were tested against CE virus. Lack of virus in gilts indicated protective immunity for the dam, in fetuses indicated protection of gilt from reproductive losses, and in both groups indicated complete protection. RESULTS: In the homologous CE group, interval from inoculation to CE ranged from 90 to 205 days, and protection was complete. In the heterologous CE group, interval from inoculation to CE ranged from 90 to 170 days, and protection was incomplete. The CE virus was detected in gilts necropsied 134 to 170 days after CE and in a litter necropsied 170 days after CE. CONCLUSIONS: Homologous protection can be induced in gilts by exposure to live PRRSV. Heterologous protection from reproductive losses can be induced in gilts by exposure to live PRRSV; however, this protection is incomplete and may have a shorter duration than homologous protection. CLINICAL RELEVANCE: Exposure of swine to enzootic PRRSV will provide protection against homologous PRRSV-induced reproductive losses. Extent and duration of protection against heterologous PRRSV may be variable and dependent on antigenic relatedness of the virus strains used for inoculation and CE.     

Pathogenesis and prevention of placental and transplacental porcine reproductive and respiratory syndrome virus infection

Porcine reproductive and respiratory syndrome virus (PRRSV)-induced reproductive problems are characterized by embryonic death, late-term abortions, early farrowing and increase in number of dead and mummified fetuses, and weak-born piglets. The virus recovery from fetal tissues illustrates transplacental infection, but despite many studies on the subject, the means by which PRRSV spreads from mother to fetus and the exact pathophysiological basis of the virus-induced reproductive failure remain unexplained. Recent findings from our group indicate that the endometrium and placenta are involved in the PRRSV passage from mother to fetus and that virus replication in the endometrial/placental tissues can be the actual reason for fetal death. The main purpose of this review is to clarify the role that PRRSV replication and PRRSV-induced changes in the endometrium/placenta play in the pathogenesis of PRRSV-induced reproductive failure in pregnant sows. In addition, strategies to control placental and transplacental PRRSV infection are discussed.     

Change of porcine circovirus 2 target cells in pigs during development from fetal to early postnatal life

Change of porcine circovirus 2 (PCV2) target cells during development from fetal to postnatal life in pigs was examined. PCV2 inoculation was performed in fetuses in utero at either 57, 75 or 92 gestational days and in piglets at 1 day of age. Twenty-one days after virus inoculation, PCV2-infected cells in the heart, lungs, liver, spleen and inguinal lymph nodes were localized and immuno-phenotyped by double-immunofluorescence labeling using different cell markers and PCV2-antibodies. During fetal life, viral antigens were detected in cardiomyocytes, hepatocytes and macrophages and infected cell numbers decreased with increasing fetal age at inoculation. The heart contained the highest number of infected cells and cardiomyocytes were the main target cell. Postnatally, macrophages were the only target cell type in different organs and infected cell numbers were similar to those of fetuses inoculated at 92 days of gestation. One piglet showed exceptionally high number of infected cells in different organs with values 13-513-fold higher compared to littermates. In this piglet, the majority of infected cells in lymphoid tissues could not be typed. This study reveals that PCV2 target cells change from cardiomyocytes, hepatocytes and macrophages during fetal life to only macrophages postnatally.     

Viremia and effect of fetal infection with porcine viruses with special reference to porcine circovirus 2 infection

This publication reviews some pathogenetic features of the transplacental infection with porcine viruses in sows. Viremia either with virus freely circulating or associated to peripheral blood mononuclear cells (PBMC) is an essential part of such pathogenesis. Virus replication occurs either in fetal tissues only or both in fetal and maternal tissues and the outcome may be different.Since porcine circovirus 2 (PCV2) has been associated with reproductive failure in sows, the question was asked what type of viremia PCV2 causes and what the effect of PCV2 is on the pregnant uterus. Seronegative gilts were oronasally inoculated and plasma and PBMC were monitored for infectious virus and for quantity of viral DNA copies. Infectious virus was found in plasma only at 21 days post-inoculation (DPI). Virus associated to PBMC was detected between 14 and 49 DPI. Viral DNA was found in plasma between 14 and 49 DPI and associated to PBMC between 7 and 63 DPI (end of experiment). Direct intra-fetal inoculation at 57, 75 and 92 days of gestation and collection of fetuses 21 days later showed that the virus replicates highly in fetal tissues, particularly in the heart. Fetal death occurred in the 57 days sows while virus and antibodies were observed in the 75- and 92-day inoculated sows. Inoculation at 57 and 75 days of gestation and collection of the piglets at the end of pregnancy showed that intrauterine spread had occurred to fetuses adjacent to the inoculated ones and that fetal death occurred also in the presence of antibodies. The pregnancy was not interrupted.This study shows that PCV2 causes viremia which is largely cell-associated and that virus replication in fetuses causes fetal death with mummification. Whether such transplacental infection occurs in the immune sow population is questionable.     

猪繁殖与呼吸综合征病毒垂直传播及其危害研究进展

猪繁殖与呼吸综合征病毒(PRRSV)感染引起的繁殖障碍在妊娠早期表现为母猪受胎率低、不规律返情及孕早期流产;怀孕后半期流产、早产,产死胎、木乃伊胎及弱仔等。先天感染的仔猪抵抗继发感染的能力低,可持续排毒并感染周围的阴性动物。PRRSV穿过胎盘屏障感染胎儿很可能是经巨噬细胞/单核细胞介导的,并在母胎界面造成病理损伤,病毒在胎儿着床点的复制可能是导致胎儿死亡和母猪流产的原因。预防PRRSV垂直传播必须控制母猪感染PRRSV,缩短已感染母猪的病毒血症持续时间,此外,通过生物安全、限制猪群流动和严格的消毒措施控制水平传播,通过疫苗免疫和药物保健消除易感动物。作者概述了妊娠各阶段母猪感染PRRSV发生垂直传播的情况及其后续的繁殖障碍。     

Research Progress on Porcine Reproductive and Respiratory Syndrome Virus Vertical Transmission and its Hazards

Productive disorder induced by porcine reproductive and respiratory syndrome virus (PRRSV) is characterized by low conception rate, irregular return to estrus and abortion during early gestation sow; Later-term abortion, early farrowing, stillborn, mummies and weak-born piglets are generally happened at second half of gestation.Piglets with congenital infection become more sensitive to secondary infection, and there exists excreted virus which infects the negative animals on every side.PRRSV passes through the placenta mediated by macrophages/monocytes, which cause pathological damage in the maternal-fetal interface, and virus replication in the fetal implantation sites plays a role in the fetal death and sow abortion.PRRSV infection prevention and viremia shortening for sow are conductive to reduce PRRSV vertical transmission.In addition, biosafety measures, reasonable pig flow and strict disinfection are carried out to control horizontal transmission, and vaccine immunization and medicine administration are done to protect susceptible animals.The main purpose of this review is to summarize PRRSV vertical transmission during each stage of gestation and subsequent reproductive failure.     

Lymphoid tissue tropism of porcine reproductive and respiratory syndrome virus replication during persistent infection of pigs originally exposed to virus in utero

The ability of porcine reproductive and respiratory syndrome virus (PRRSV) to establish a persistent infection is the principal contributing factor to the world-wide spread of the disease. Several studies have documented the course of viral infection in postnatally infected pigs; however, very little is known regarding sites of virus replication during persistent infection of pigs exposed to PRRSV in utero. In this study, virus replication and PRRSV-specific antibody were followed for several hundred days in a group of pigs derived from three sows infected at 90 days of gestation with PRRSV isolate VR-2332. Eighty-four percent of pigs were born viremic with a mortality of 54% within 21 days after birth. At approximately 60 days sera from pigs were negative for virus by virus isolation. Analysis of virus replication in the tissues of pigs randomly sacrificed between 63 and 132 days showed no evidence of virus in lung and other non-lymphoid organs. However, virus was easily recovered from tonsil and lymph nodes and in situ hybridization identified these tissues as sites of virus replication. Even though replication was at a low level, virus was easily transmitted to sentinel pigs. By 260 days pigs became seronegative and did not transmit virus to sentinel pigs. Sacrifice of remaining pigs after 300 days showed no evidence of virus in blood and tissues. This study shows that congenital PRRSV-infected pigs can support virus replication for an extended period during which virus replication is primarily restricted to tonsil and lymph nodes.     

Experimental fetal infection with bovine viral diarrhea virus. I. Virological and serological studies.

The serological and virological results of an experimental infection of bovine fetuses with bovine viral diarrhea virus are presented. Four fetuses, 120-165 days gestational age, were inoculated in utero with a second passage virus strain. Two fetuses received a sham-inoculum. A humoral immune response in the virus-inoculated fetuses, was demonstrated three weeks later. In three fetuses only IgM and IgG1 were detectable. The serum from the fourth fetus also contained IgG2 and IgA. Bovine viral diarrhea virus-neutralizing antibodies were detected in two fetuses. These two fetuses inoculated at 135-150 days gestational age, represent the youngest reported bovids, giving a specific response in three weeks following an experimental infection with bovine viral diarrhea virus. The fetal sera did not contain heat-labile factors, which could mediate the neutralization. The virus was not reisolated from any of the fetuses, but viral antigen was nevertheless demonstrated by immunocytochemical methods in sections of several of the fetal organs, primarily lymphoid tissues.     

A current assessment of the role of porcine parvovirus as a cause of fetal porcine death.

One hundred one litters containing 1 or more dead porcine fetuses were collected at an Iowa abattoir during a 2-month interval and examined for evidence of viral infection. Each of 1,137 fetuses (302 dead, 835 alive) of these litters was tested for porcine parvovirus (PPV) antigens by direct immunofluorescence microscopy (FA) of fetal lung. Antigens of PPV were detected in the lungs of most of the fetuses of 11 of the litters. The 11 FA-positive litters contained 105 dead (100 FA-positive) and 14 live (12 FA-positive) fetuses. Infectious PPV was isolated from 10 of the 11 FA-positive litters and from 3 of the 90 FA-negative litters. No cytopathogenic agents other than PPV were isolated from any of the litters. Eleven of 101 (11%) litters examined and 100 of 302 (33%) dead fetuses examined were FA positive for viral antigen, indicating that PPV remains as a major cause of porcine fetal death.     

Transplacental infection of porcine fetuses following experimental challenge inoculation with encephalomyocarditis virus.

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.     

Transplacental infection following exposure of gilts to porcine reproductive and respiratory syndrome virus at the onset of gestation

Twenty-five gilts without measurable porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) serum antibody titres were used for this experiment. All of them were randomly assigned to one of the treatment groups at the time of artificial insemination. Twelve gilts were exposed to PRRSV, of these, six were slaughtered on day 10 after exposure and constituted group A. The remaining six were slaughtered on day 20 after infection and constituted group C. Thirteen gilts were used as controls, six of these were slaughtered on day 10 after treatment and constituted group B. The remaining seven were slaughtered on day 20 after treatment and constituted group D. The infected gilts were inoculated with PRRSV intranasally and intravenously in the ear vein. They were observed for clinical signs of infection and the effects on conception and fertilization rates were studied, while the gilts and their embryos were tested for PRRSV and homologous antibodies. The infected animals developed signs of PRRS associated with anorexia and slight pyrexia. Infection was verified by reisolation of the virus from serum and other tissue samples and also by seroconversion. Ten out of 12 infected gilts and 10 out of 13 controls were pregnant at the time of slaughter and the ratio of embryos to corpora lutea was the same in both, infected and control groups (0.75). Therefore, infection with PRRSV at the onset of gestation did not appear to interfere with conception and fertilization rates and subsequent pregnancy. The PRRSV was not isolated from any of the embryos collected at day 10 postexposure, but was present in 20-day-old embryos of group C gilts. In this group, 60% of litters were infected prenatally, with 16% of embryos infected. The proportion of dead embryos was three times greater than in control group D (35.4% and 9.8%, respectively). The results of this report indicate that exposure of susceptible gilts to PRRSV at the onset of gestation has no significant effect on conception and fertilization rates. However, although infection does not appear to have any effect on the embryos before implantation, it can result in transplacental infection and embryo death.     

An inactivated, oil-emulsion vaccine for the prevention of porcine parvovirus-induced reproductive failure

Pig fetuses inoculated at 45 days gestation with virulent porcine parvovirus (PPV) were harvested 10 days later. Virus was extracted, inactivated with binary ethylenimine and the antigen suspension emulsified with mineral oil adjuvant. One dose of this vaccine, or two doses with a 14 day interval, stimulated high and long lasting serum antibody titres in gilts. Vaccination caused no clinical reactions and lesions at injection sites were minor. Vaccination of seronegative gilts at 40 days gestation caused no adverse effects on fetuses. Six gilts which had been vaccinated five to nine weeks before mating were challenged intravenously with live, virulent PPV at 40 days gestation. At 98 days gestation 78 out of 84 (93 per cent) fetuses were alive and normal and no evidence of PPV infection was found in the six dead (mummified) fetuses. In four unvaccinated gilts similarly challenged with PPV at 40 days gestation only five out of 51 (10 per cent) fetuses survived to 98 days gestation and the virus was detected in 41 of the 46 dead (mummified) fetuses. This vaccine appears to be safe and effective for prevention of PPV-induced fetal loss in gilts.