Explore the vast range of titles available.

Porcine reproductive and respiratory syndrome (PRRS) severely impacts global swine production. While studies have revealed host genetic factors and molecular mechanisms of fetal response to PRRSV infection, the relationship between fetal genotype, thymic transcription and PRRS susceptibility remains unclear. This study integrates genomic and thymic transcriptomic analyses of fetal pigs from a maternal PRRSV-2 challenge model. Fetuses were categorized by susceptibility to PRRS, following maternal inoculation at gestation day 84–86 into four groups: complete resistance (CR), partial resistance (PR), viable susceptible (VS), and meconium-stained susceptible (MS). CR and PR fetuses exhibited 0 or less than 4 viral loads in serum and thymus, respectively, despite maternal exposure, while VS and MS fetuses had high viral loads with MS showing signs of compromise. Thymic transcriptome analyses revealed a strong interferon response and downregulation of cell cycle and DNA repair pathways in VS and MS fetuses compared to CR and PR fetuses. Severe infection (MS) was further associated with downregulation of genes involved in early thymocyte development, suggesting disrupted T cell development in the thymus. Interaction expression quantitative trait loci (ieQTLs) were identified, where the association between genetic variants and expression levels of differentially expressed genes (DEGs) varied by fetal PRRS susceptibility. Notably, ieQTLs were identified for genes critical for T cell development, including TMEM98 (involved in Th1 cell differentiation) and PTCRA (expressed in early stages of thymocyte development). These findings highlight the complex interplay between fetal genotype, thymic gene expression, and PRRS susceptibility, offering potential genetic markers for breeding programs for replacement gilts.

The bacterium Coxiella burnetii has been detected in the fetal membranes, birth fluids and vaginal mucus, as well as in the milk and other excretions of several domestic mammals. The finding of C. burnetii in association with abortion, parturition and in the postpartum period has led to the hypothesis that C. burnetii causes a range of reproductive diseases. This review critically evaluates the scientific basis for this hypothesis in domestic mammals. The review demonstrates a solid evidence for the association between C. burnetii infection and sporadic cases of abortion, premature delivery, stillbirth and weak offspring in cattle, sheep and goats. C. burnetii induced in-herd epidemics of this complete expression of reproductive failure have been reported for sheep and goats, but not for cattle. The single entities occur only as part of the complex and not as single events such as generally increased stillbirth rate. Studies show that C. burnetii initially infects the placenta and that subsequent spread to the fetus may occur either haematogenous or by the amniotic-oral route. The consequences for the equine, porcine, canine and feline conceptus remains to the elucidated but that infection of the conceptus may occur is documented for most species. There is no solid evidence to support a hypothesis of C. burnetii causing disorders such as subfertility, endometritis/metritis, or retained fetal membranes in any kind of domestic animal species. There is a strong need to validate non-pathology based methods such as polymerase chain reaction for their use in diagnostic and research in relation to establishing C. burnetii as the cause of abortion and to adapt an appropriate study design and include adequate control animals when linking epidemiological findings to C. burnetii or when evaluating effects of vaccination in production herds.

Uterine natural killer (uNK) cells play crucial roles in pregnancy, impacting maternal–fetal immune tolerance, angiogenesis, and immune responses. While extensively studied in humans and mice, porcine uNK cells’ functional properties remain relatively underexplored in both healthy uterine environments, as well as during viral infection. This study examined the functional properties of porcine uNK cells isolated from the maternal endometrium (ME) and fetal placenta (FP) in late gestation, comparing healthy gilts to those experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV), one of the most economically damaging reproductive viruses of the swine industry. Flow cytometry analyses identified three uNK cell subsets based on NKp46 expression to assess subpopulation frequencies and functional variations. Results showed that PRRSV infection did not significantly alter the total NK cell counts but affected NK cell proliferation. NKp46 high subsets showed increased Ki-67 expression in samples from experimentally infected gilts. An upregulation of perforin was observed in NKp46 high cells, indicating potential immune responsiveness to PRRSV. CD107a degranulation capacity of the examined NK cells was lower in FP uNK cells, possibly due to the fetal immune environment's immaturity. Despite PRRSV exposure, CD107a expression did not significantly change in uNK cells. PRRSV infection led to a suppression of interferon (IFN)-γ expression in most uNK cell subsets. This study provides a look into a previously unstudied aspect of the immune response to PRRSV infection in the porcine uterus and gives new insights into porcine NK cell subsets in an important non-lymphoid organ.

Coxiella burnetii is an intracellular bacterial pathogen that causes Q fever. Infected pregnant goats are a major source of human infection. However, the tissue dissemination and excretion pathway of the pathogen in goats are still poorly understood. To better understand Q fever pathogenesis, we inoculated groups of pregnant goats via the intranasal route with a recent Dutch outbreak C. burnetii isolate. Tissue dissemination and excretion of the pathogen were followed for up to 95 days after parturition. Goats were successfully infected via the intranasal route. PCR and immunohistochemistry showed strong tropism of C. burnetii towards the placenta at two to four weeks after inoculation. Bacterial replication seemed to occur predominantly in the trophoblasts of the placenta and not in other organs of goats and kids. The amount of C. burnetii DNA in the organs of goats and kids increased towards parturition. After parturition it decreased to undetectable levels: after 81 days post-parturition in goats and after 28 days post-parturition in kids. Infected goats gave birth to live or dead kids. High numbers of C. burnetii were excreted during abortion, but also during parturition of liveborn kids. C. burnetii was not detected in faeces or vaginal mucus before parturition. Our results are the first to demonstrate that pregnant goats can be infected via the intranasal route. C. burnetii has a strong tropism for the trophoblasts of the placenta and is not excreted before parturition; pathogen excretion occurs during birth of dead as well as healthy animals. Besides abortions, normal deliveries in C. burnetii-infected goats should be considered as a major zoonotic risk for Q fever in humans.

Porcine reproductive and respiratory syndrome (PRRS) is the most economically significant disease impacting pig production in North America, Europe, and Asia, causing reproductive losses such as increased rates of stillbirth and mummified piglets. The objective of this study was to explore the genetic basis of host response to the PRRS virus (PRRSV) in a commercial multiplier sow herd before and after a PRRS outbreak, using antibody response and reproductive traits. Reproductive data comprising number born alive (NBA), number alive at 24 h (NA24), number stillborn (NSB), number born mummified (NBM), proportion born dead (PBD), number born dead (NBD), number weaned (NW), and number of mortalities through weaning (MW) of 5,227 litters from 1,967 purebred Landrace sows were used along with a pedigree comprising 2,995 pigs. The PRRS outbreak date was estimated from rolling averages of farrowing traits and was used to split the data into a pre-PRRS phase and a PRRS phase. All 641 sows in the herd during the outbreak were blood sampled 46 d after the estimated outbreak date and were tested for anti-PRRSV IgG using ELISA (sample-to-positive [S/P] ratio). Genetic parameters of traits were estimated separately for the pre-PRRS and PRRS phase data sets. Sows were genotyped using the PorcineSNP60 BeadChip, and genome-wide association studies (GWAS) were performed using method Bayes B. Heritability estimates for reproductive traits ranged from 0.01 (NBM) to 0.12 (NSB) and from 0.01 (MW) to 0.12 (NBD) for the pre-PRRS and PRRS phases, respectively. S/P ratio had heritability (0.45) and strong genetic correlations with most traits, ranging from -0.72 (NBM) to 0.73 (NBA). In the pre-PRRS phase, regions associated with NSB and PBD explained 1.6% and 3% of the genetic variance, respectively. In the PRRS phase, regions associated with NBD, NSB, and S/P ratio explained 0.8%, 11%, and 50.6% of the genetic variance, respectively. For S/P ratio, 2 regions on SSC 7 (SSC7) separated by 100 Mb explained 40% of the genetic variation, including a region encompassing the major histocompatibility complex, which explained 25% of the genetic variance. These results indicate a significant genomic component associated with PRRSV antibody response and NSB in this data set. Also, the high heritability and genetic correlation estimates for S/P ratio during the PRRS phase suggest that S/P ratio could be used as an indicator of the impact of PRRS on reproductive traits.

Porcine circovirus 3 (PCV-3) has been detected in cases of reproductive failure but the pathogenesis of such infection is poorly understood. So far, experimental PCV-3 inoculations have been performed only in piglets. Therefore, through the experimental inoculation of pregnant gilts at two different time points (second and last third of gestation), this study aimed to evaluate the outcome of PCV-3 infection in dams and their offspring until weaning age. Two weeks postinoculation, all gilts became viremic and the infection lasted until the end of study. Farrowing occurred naturally, without evidence of reproductive disorders, and piglets showed no significant clinical signs from farrowing to weaning (21 day-old). However, majority of the delivered piglets were viremic, mostly until weaning age. Both newborn and weaned pigs showed different degrees of systemic, lymphohistiocytic arteritis and periarteritis. Lesions were more severe in the piglets infected during the second third of gestation and worsened at weaning. Additionally, PCV-3 detection in nervous and cardiac tissue and development of histopathological lesions in these tissues were gestational dependent, as only occurred in piglets infected at second third of pregnancy. Piglets with lesions raised to weaning age had less body weight than those without them. This study represents the first description of a PCV-3 experimental infection in pregnant gilts, which resulted in transplacental infection, histological lesions in piglets mimicking those of natural occurring disease, and lesser body weight in piglets with vascular lesions at weaning age. Obtained results allowed proposing a potential pathogenesis model for PCV-3 infection in swine.

The shedding of Coxiella burnetii in bovine, caprine, and ovine milk was measured using PCR, in 3 herds for each species, the bulk tank milk samples of which were positive at the time of their selection. Milk samples of 95 cows, 120 goats, and 90 ewes were sampled over 16 wk, as was the bulk tank milk. The shedding of C. burnetii in vaginal mucus and feces was checked at the beginning of the experiment and 2 mo later. The clinical signs in the selected herds as well as the duration and the shedding routes differed among the 3 species. The cows were asymptomatic and shed C. burnetii almost exclusively in milk. In one of the caprine herds, abortions due to C. burnetii were reported. The goats excreted the bacteria mainly in milk. In contrast, the ewes, which came from flocks with abortions due to Q fever (C. burnetii infection), shed the bacteria mostly in feces and in vaginal mucus. This could explain why human outbreaks of Q fever are more often related to ovine flocks than to bovine herds. These excretions did not seem more frequent when the samples were taken close to parturition. The samples were taken from 0 to 421 d after parturition in bovine herds and from 5 to 119 d and 11 to 238 d after parturition in the caprine and ovine herds, respectively. The shedding in milk was sometimes intermittent, and several animals shed the bacteria but were negative by ELISA: 80% of the ewes were seronegative, underscoring the lack of sensitivity of the ELISA tests available for veterinary diagnosis. The detection of antibodies in milk seems more sensitive than it is in serum.

Background For the first time, a case of vertical transmission of TBEV in a dog associated with foetal death is described. Case presentation A six-year-old beagle bitch experienced foetal death from day 49 in pregnancy. A caesarean section was performed on day 56, and one live and three dead pups in different stages of resorption were delivered. Black mucoid, non-smelling foetal membranes surrounded the dead foetuses. The live-born foetus died despite efforts to save it and was sent for autopsy together with the placenta. Autopsy demonstrated lung atelectasis and no malformations. A mild acute necrotizing placentitis was diagnosed on histopathology. Selective bacteriological cultures for Brucella canis from blood, vagina and the foetus were all negative, as was PCR for canine herpes virus (CHV). Viral metagenomics analysis identified the presence of tick-borne encephalitis virus (TBEV) in the placental tissue and in situ hybridization revealed TBEV in the trophoblasts. The bitch had antibodies to TBEV. One year later, the bitch had a normal pregnancy and whelping. Conclusion With the spread of both ticks and TBEV, infection with TBEV should be given further consideration as a potential differential diagnosis in cases of foetal death in dogs.

Congenital Zika virus (ZIKV) infection can result in birth defects, including malformations in the fetal brain and visual system. There are two distinct genetic lineages of ZIKV: African and Asian. Asian-lineage ZIKVs have been associated with adverse pregnancy outcomes in humans; however, recent evidence from experimental models suggests that African-lineage viruses can also be vertically transmitted and cause fetal harm. To evaluate the pathway of vertical transmission of African-lineage ZIKV, we inoculated nine pregnant rhesus macaques (Macaca mulatta) subcutaneously with 44 plaque-forming units of a ZIKV strain from Senegal, (ZIKV-DAK). Dams were inoculated either at gestational day 30 or 45. Following maternal inoculation, pregnancies were surgically terminated seven or 14 days later and fetal and maternal-fetal interface tissues were collected and evaluated. Infection in the dams was evaluated via plasma viremia and neutralizing antibody titers pre- and post- ZIKV inoculation. All dams became productively infected and developed strong neutralizing antibody responses. ZIKV RNA was detected in maternal-fetal interface tissues (placenta, decidua, and fetal membranes) by RT-qPCR and in situ hybridization. In situ hybridization detected ZIKV predominantly in the decidua and revealed that the fetal membranes may play a role in ZIKV vertical transmission. Infectious ZIKV was detected in the amniotic fluid of three pregnancies and one fetus had ZIKV RNA detected in multiple tissues. No significant pathology was observed in any fetus; and ZIKV did not have a substantial effect on the placenta. This study demonstrates that a very low dose of African-lineage ZIKV can be vertically transmitted to the macaque fetus during pregnancy. The low inoculating dose used in this study suggests a low minimal infectious dose for rhesus macaques. Vertical transmission with a low dose in macaques further supports the high epidemic potential of African ZIKV strains.

Zika virus infection during pregnancy is associated with miscarriage and with a broad spectrum of fetal and neonatal developmental abnormalities collectively known as congenital Zika syndrome (CZS). Symptomology of CZS includes malformations of the brain and skull, neurodevelopmental delay, seizures, joint contractures, hearing loss and visual impairment. Previous studies of Zika virus in pregnant rhesus macaques (Macaca mulatta) have described injury to the developing fetus and pregnancy loss, but neonatal outcomes following fetal Zika virus exposure have yet to be characterized in nonhuman primates. Herein we describe the presentation of rhesus macaque neonates with a spectrum of clinical outcomes, including one infant with CZS-like symptoms including cardiomyopathy, motor delay and seizure activity following maternal infection with Zika virus during the first trimester of pregnancy. Further characterization of this neonatal nonhuman primate model of gestational Zika virus infection will provide opportunities to evaluate the efficacy of pre- and postnatal therapeutics for gestational Zika virus infection and CZS.