Free access
Issue
Vet. Res.
Volume 31, Number 1, January-February 2000
Page(s) 56 - 57
DOI http://dx.doi.org/10.1051/vetres:2000043
How to cite this article Vet. Res. (2000) 56-57
Vet. Res. 31 (2000) 56-57

Pathogenesis of porcine reproductive and respiratory syndrome virus (PRRSV) in gestating sows

C. Prieto and J.M. Castro

Dpto. Patología Animal I. F. de Veterinaria. U.C.M., Avda. Puerta de Hierro s/n, 28040 Madrid, Spain

Abstract - Porcine reproductive and respiratory syndrome (PRRS) is a newly described swine disease. Since the time the PRRS virus (PRRSV) was first identified, it has become a significant pathogen of swine herds worldwide. It has recently been classified in the Arteriviridae family, in the order of Nidovirales. The first reports of field cases of PRRSV induced reproductive failure described a sudden increase in early farrowings, late-term abortions and dead and mummified fetuses, along with severe drops in conception rate and fertilisation rate. The purpose of this presentation is to review the scientific data on the pathogenesis of PRRSV in the female reproductive tract. Gilts and sows are susceptible to PRRSV when they are inoculated by any route. The incubation period varies greatly, but the first clinical signs usually appear between two and seven days post-inoculation (p.i.). They are usually moderate or absent, consisting of an occasional depression, lethargy, anorexia and hyperthermia. The virus primarily replicates in alveolar macrophages, although others have described the first replication in the nasal and bronchial epithelia. The virus is able to spread from the lungs to the rest of the body, either in the blood alone or in association with leukocytes or monocytes which will then migrate to different tissues to become tissular macrophages. Through this dissemination, PRRSV can reach the reproductive tract, leading to the development of clinical signs associated with reproduction. Regarding the effects of the virus in early gestation, the first thing to take into account is the possibility of venereal transmission of the disease. It is now generally accepted that insemination of sows or the use of infected boars to breed them can result in the transmission of PRRSV, as was demonstrated by seroconversion or reisolation of PRRSV from different organs after slaughtering of the sows. In some studies, however, it was impossible to reproduce the infection, and the gilts remained clinically normal during the whole experimental period and seroconversion was not demonstrated. Finally, some authors also obtained inconsistent results. The discrepancy of the results obtained in the different studies might be due to a number of reasons, including differences in the virulence of the strains used in the different studies and a possible failure in reaching the minimum infective dose necessary to produce infection by this route. Once the possibility of transmission has been accepted, the next step is to study the effects of the infection at the time of breeding on conception and fertilisation rates. There is again some discrepancy over this matter. Although some authors have described cyclic returns to oestrus, others could not reproduce this effect. In any case, the differences in conception and fertilisation rates between infected animals and controls have never been statistically significant. In conclusion, it can be assumed that the presence of PRRSV at the moment of breeding may have an insignificant effect or no effect on conception and fertilisation rates. Focusing on the reproductive performance of infected sows, it is generally accepted that the importance of infection in early and mid-gestation is relatively low as compared with the effects in late-gestation. In this sense, it has been proven that, when infection takes place between days 1 and 21 of gestation no effect on reproductive performance can be demonstrated. However, when infection occurs later on, the effect of the virus increases as gestation progresses and a reproductive failure characterised by early farrowings and late-term abortions has consistently been reproduced in late-term pregnant sows. Besides, the stillborn rate and newborn mortality are also affected by the moment of infection. Regarding the effects of dam exposure to PRRSV at different stages of gestation, the first matter to consider is whether PRRSV can infect developing conceptuses or not. It has been reported that early pig embryos are not susceptible to productive infection neither in vitro nor in vivo. From about 14 to 20 gestation days onwards it however, becomes possible to isolate PRRSV from some embryos or fetuses, although it is generally admitted that the likelihood of transplacental infection increases as gestation progresses. This means that when the dams are exposed to PRRSV at the beginning of gestation the proportion of infected embryos is relatively low as compared to the proportion affected when infection takes place later on. This fact led investigators to inquire whether the embryos were equally susceptible to PRRSV at any time. To solve this question, in some studies fetuses were infected directly, by transuterine inoculation during gestation. The results obtained suggest variable susceptibilities in relation to gestational age, with older fetuses dying earlier than younger ones. On the contrary, a recently discovered, remarkable finding is the detection of persistent infections related to in utero infections. It has been possible to obtain a great proportion of viremic pigs at birth by infecting sows in late gestation. PRRSV was able to be isolated from these viremic pigs after 60 to 130 days. These kinds of animals can easily develop a marked respiratory distress and are more susceptible to secondary diseases. Some lesions of the placenta and umbilical cord have been described that could help to explain the great proportion of dead fetuses and weak piglets delivered during natural outbreaks of the disease. These lesions consist of degenerative changes with multifocal microseparations on the epithelial layers of the materno-fetal union of the placenta that can lead to the premature separation of the maternal and fetal sides and areas of necrotising arteritis of the umbilical cord. These alterations can play an important role in the development of a placentary insufficiency leading to fetal hypoxia that can cause late-term abortions, stillborn and weak piglets. In conclusion, PRRSV may cause reproductive failure at any time during gestation. The inoculation of susceptible gilts with PRRSV at the onset of gestation has little or no effect on conception and fertilisation rates, although it can result in transplacental infection and embryo death. The infection is, however, relatively unimportant in early and mid-gestation compared to late-gestation and the likelihood and incidence of embryonic infection at the beginning of gestation is markedly lower than in sows infected later on, with it being impossible to isolate the virus before implantation has taken place. Failure to detect the virus before implantation could be due to a number of reasons. One possibility is that the virus is unable to cross the zona pellucida or that the undifferentiated blastomeres may not be suitable for viral replication and a specific cell population would have to differentiate in order for the embryos to become infected by the virus. Finally, the possibility of conceptuses being infected by PRRSV during early gestation could be affected by the fact that the pig conceptus does not begin to attach to the endometrium until days 13 or 14 of gestation. From that moment onwards, as gestation advances, the vascular bed of the placenta is brought closer together by taking on a subepithelial position and by invasion of the trophoblast by embryonic capillaries. As a consequence, the materno-fetal capillary interrelationship of the placenta becomes a more efficient organ for exchange as gestation progresses. In an attempt to explain the pathogenetic mechanism of PRRSV on the female reproductive tract, it has been postulated that this phenomenon would increase the likelihood of transplacental infection with PRRSV. The virus could cross the placenta in the free form or be associated with maternal cells that migrate through it, i.e. macrophages or monocytes. These findings could help to explain why many natural outbreaks of PRRSV-induced reproductive failure are manifested principally as late-term abortions and early farrowings.


Corresponding author: C. Prieto Tel.: (34) 913943714; fax: (34) 913943908;
    e-mail: Marie@eucmax.sim.ucm.es

© INRA, EDP Sciences 2000