Abortion in the later stages of pregnancy is the clinical manifestation of PRRS virus infection that causes most concern to farmers. Although aborted material is sent to the lab in an attempt to detect the virus, the result is often frustrating.
Even though much research has been done, the pathogenesis of intrauterine PRRS virus infection remains largely unknown. Results from recent studies and judicious observation of the aborted material, however, can help to increase the success rate in detecting the PRRSV in the laboratory.
Determining the cause of late abortions in sows is a challenge, as they may be infectious or not depending largely on herd management, the overall health status, the region where the farm is located, the specific prevention measures against abortogenic pathogens, etc. Pregnancy itself is a risk status for the sow; if they are subjected to sudden changes in the environment, abortion can occur spontaneously. If the herd management and housing conditions are adequate, outbreaks of late abortions are usually attributed to an acute PRRS virus infection. In these cases the sample used to confirm the presence of the virus in the laboratory is the aborted material, usually accomplished by the polymerase chain reaction assay (PCR).
Although this is the standard procedure for PRRS virus identification in clinical material coming from abortion, a high proportion of PCR-negative results are the most common outcome from the diagnostic laboratory, as was reported in a large-scale study in Germany. The German3 researchers analyzed not only fetuses, but also samples collected from the affected sows. However, infection with the PRRS virus was confirmed in only 8.6% of the samples. These results contrast sharply with those reported from a similar field investigation of late-term abortions in sows in Thailand4, with up to 65.6% of the samples being PCR-positive. Taking into consideration the differences in the development of the pig industry in the two countries, in particular the difference in the rate of vaccination against PRRS, which is much higher in Germany, it seems plausible that the characteristics of the farm and overall health management greatly influence the success of PRRS virus detection in this kind of sample.
The selection of samples to confirm the presence of the PRRS virus in cases of abortion may also influence the outcome of the PCR, as can be deduced from the accumulated scientific evidence on the distribution of the PRRS virus in maternal and fetal tissues in cases of transplacental infection. A recent study1 suggests that meconium-stained fetuses, along with those decomposed but not autolytic, are the best samples for detection of the PRRS virus in the thymus, lungs and serum of fetuses using PCR. The results further indicate that fetuses in advanced autolysis and those of normal appearance are usually negative in the PCR, and therefore should not be used for diagnosis. Meconium staining was the most consistent gross abnormality observed in fetuses infected with the PRRS virus in another study2, suggesting that this is a reliable indicator of intrauterine infection.
Because aborted fetuses are by definition autolytic samples, since death occurs hours or days before they are delivered, it is likely that the autolysis has a negative impact on the PCR as a consequence of viral RNA degradation. However, there is little information about the stability of RNA virus in samples of pig origin in advanced autolysis. A recent study5 revealed an average half-life of viral RNA in pig tissues stored at room temperature for up to 21 days, ranging from 0.95 to 2.55 days. This indicates that there is a very short timeframe between detection of abortion on the farm, and sample submission for PCR analysis in the laboratory.
All in all, demonstration of PRRS virus infection in late-term aborted fetuses can be improved by sampling both meconium-stained and decomposed (non-autolytic) fetuses, umbilical cord and placenta on the farm. Sampling should be performed as soon as the abortion occurs, and should be delivered under refrigeration by express transport, when possible.
1. Ladinig A., et al., 2014. Variation in Fetal Outcome, Viral Load and ORF5 Sequence Mutations in a Large Scale Study of Phenotypic Responses to Late Gestation Exposure to Type 2 Porcine Reproductive and Respiratory Syndrome Virus. PLoS ONE, 9(4), e96104.
2. Lager K. M. and Halbur P.G., 1998. Gross and microscopic lesions in porcine fetuses infected with porcine reproductive and respiratory syndrome virus. J Vet Diagn Invest. 8(3):275-82.
3.Nathues H., et al., 2011. Infectious agent detection in reproductive disorders in swine herds. Retrospective evaluation of diagnostic laboratory examinations. Tierarztl Prax Ausg G Grosstiere Nutztiere. 39(3):155-61.
4.Olanratmanee E., et al., 2015. Prevalence of porcine reproductive and respiratory syndrome virus detection in aborted fetuses, mummified fetuses and stillborn piglets using quantitative polymerase chain reaction. J. Vet. Med. Sci. 77(9): 1071–1077.
5. Weesendorp, et al., 2008. The effect of tissue degradation on detection of infectious virus and viralRNAto diagnose classical swine fever virus, Vet Microbiol. 2009.09.028.