In recent years, porcine circovirus associated disease (PCVAD) has spread rapidly across major swine-produc¬ing regions of North America. Before the vaccine became readily available, PCVAD caused devastating morbidity and mortality especially in post-weaned pigs. This was subsequently thought to be associ¬ated with the introduction of PCV2b genotype in affected areas.1
PCV2-associated reproductive failure in pregnant sows can manifest as either irregular return to estrus, abortion, or increased numbers of non-viable pigs at birth.7,9,12 Once PCV2 crosses the placenta, the virus has a tropism for fetal myocardial tissues and generally results in myocardial necrosis, in¬flammation, and fibrosis.7,10,12
With the overwhelming incidence of PCVAD, potential transmission routes of PCV2 across pig popu¬lations were re-evaluated. Currently, the main route of PCV2 transmission is thought to be fecal-oral.11 However, PCV2 can been detected in semen of infected boars.2,3,4,6 In boars, PCV2 infection is not typically associated with clinical disease or sperm morphology abnormalities; however, low amounts of PCV2 DNA are frequently detected in semen.3,4,6 Viral shedding in semen can be intermittent or continuous and last for extended periods of time with younger boars more likely to shed PCV2 in semen.3,4,6
Artificial insemination is a common practice in the swine industry, and semen may be transported over great distances. Recently it was de¬termined that PCV2 present in semen is infectious in a swine bioassay model.5 Thus, the
potential for semen transmission is apparent. However, when PCV2 PCR positive semen was extended and used to artificially inseminate PCV2 naive gilts, neither dam seroconver¬sion nor fetal infection occurred. To further investigate the role of semen in the transmission of PCV2, a study was designed with the following objectives: (1) determine if semen spiked with PCV2 has the ability to cause infection in PCV2 naïve mature female swine and (2) determine if delivery of PCV2 via artificial insemination causes reproductive failure or fetal infection.
Project Design
Nine conventional specific-pathogen-free (SPF) sows serologically negative for PCV2, porcine reproductive and respiratory syndrome virus (PRRSV), swine influenza virus (SIV), porcine parvovirus (PPV), and encephalomyocarditis virus (EMCV) were randomly divided into 3 groups with 3 sows in each group. Group 1 sows served as negative controls and were artificially inseminated with extended PCV2 DNA negative semen upon estrus detection. Groups 2 and 3 sows were artificially inseminated with extended semen spiked with PCV2a or PCV2b, respectively. Immediately prior to artificial insemination of group 2 and 3 sows, 5mls of PCV2a or PCV2b was added to the 80ml dose of extended semen and sow were inseminated once a day for 3 consecutive days. All sows were bled weekly and allowed to carry pregnancy to term and farrow naturally. At parturition, presuckle serum samples and tissues were obtained from all piglets.
Results
Group 1 sows remained seronega¬tive for PCV2 while sows in groups 2 (PCV2a) and 3 (PCV2b) developed PCV2 viremia within 14 days post-insemination and seroconverted. In addition, all sows remained serologically negative for PRRSV, PPV, SIV and EMCV. None of the sows in group 2 became pregnant while all the group 3 sows carried pregnancy to term without clinical signs of disease and farrowed at the expected due date. Colostral samples collected from group 3 sows contained PCV2 DNA, all group 3 live-born piglets (n = 8) were PCV2 viremic presuckle, stillborn fetuses (n = 2) had gross lesions of congestive heart failure, and mummified fetuses (n = 25) varied in crown-rump length ranging from 7-27 cm indicat¬ing fetal death between 42 and 105 days of gestation. PCV2 antigen was detected in myocardium by immu¬nohistochemistry (IHC) of 7/8 (88%) live-born piglets, 2/2 (100%) of the stillborn fetuses, and 25/25 (100%) of the mummified fetuses. In addition, 4/25 mummi¬fied fetuses had PCV2 antigen associated with smooth muscle cells and fibrocytes.
In conclusion, intrauterine placement of PCV2 is capable of causing dam viremia and fetal infection but may not result in abortion or clinical signs of disease in PCV2 naïve sows. It is unknown how much PCV2 virus can be shed in semen by a single boar or the amount of PCV2 that is needed in an artificial insemination dose to cause dam or fetal infection. However, semen transmission should be considered as a means for transmission of PCV2. Furthermore, reproductive issues associated with PCV2 should be considered if increased numbers of stillborn and mummified fetuses are expelled at parturition. Fetal myocardium is the preferred tissue for the diagnosis.
Editor’s Note: The research project described above was performed by Darin Madson1, DVM; Abby Patterson1, DVM, MS; Sheela Ramamoorthy1, DVM, PhD Narinder Pal1, PhD; Xiang-Jin Meng2, MD, PhD; Tanja Opriessnig1, Dr med vet, PhD1Department of Veterinary Diagnostic and Production Animal Medicine, Iowa State University, Ames, Iowa, 2Department of Biomedical Sciences and Pathobiology Virginia Polytechnic Institute and State University, Blacksburg, Virginia. It was supported by the National Pork Board Checkoff and by Boehringer Ingelheim Vetmedica, Inc. The study was presented at the 2009 AASV meeting. This commentary is sponsored by Boehlringer Ingelheim Vetmedica, Inc. For more information, go to www.bivi.com
References
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