The objectives of this study were to determine if vaccination against porcine circovirus type 2 (PCV2) or previous PCV2 infection of the dam are sufficient to prevent fetal infection when dams are artificially inseminated with PCV2-spiked semen. Nine sows (Sus domestica) were allocated into three groups of three dams each: The PCV2 naïve negative control Group 1 was artificially inseminated with extended PCV2 DNA negative semen during estrus, whereas the extended semen used in the vaccinated Group 2 (PCV2 vaccine was given 8 wk before insemination) and PCV2-exposed Group 3 (infected with PCV2 12 wk before insemination) was spiked with 5 mL of PCV2 inoculum with a titer of 10(4.2) tissue culture infectious dose (TCID(50)) per milliliter at each breeding. The dams in the vaccinated and PCV2-exposed groups were positive for PCV2 antibody but negative for PCV2 DNA in serum at the time of insemination. Three negative control dams, two vaccinated dams, and three dams with previous PCV2 exposure became pregnant and maintained pregnancy to term. After artificial insemination, viremia was detected in one of three vaccinated dams and in two of three dams with previous PCV2 exposure. At farrowing, PCV2 infection was not detected in any piglets or fetuses expelled from the negative control dams or from dams with previous PCV2 exposure. In litters of the vaccinated dams, 15 of 24 live-born piglets were PCV2 viremic at birth, with 6 of 26 fetuses having detectable PCV2 antigen in tissues. In conclusion, vaccine-induced immunity did not prevent fetal infection in this sow model using semen spiked with PCV2.
"Because most of the foetal exposure to virus occurs after a maternal viraemic episode, antibody levels play a role in reducing the amount of virus that can cross the placenta [14,15]. Furthermore, other studies [40,41] imply that anti-PCV2 antibodies seem to be a partial safeguard against in utero PCV2 infection. The present investigation also suggests anti-PCV2 antibodies play a role in foetal protection even in the case of a primary intrauterine infection. "
[Show abstract][Hide abstract] ABSTRACT: Background
Since 1999, field evidence of transplacental infection by porcine circovirus type 2 (PCV2) and reproductive failure has been reported in pigs. The objective of this study was to evaluate the clinical and pathological consequences of PCV2 infection in conventional PCV2-seropositive gilts by insemination with PCV2b-spiked semen.
Six PCV2 seropositive gilts were inseminated with PCV2b-supplemented semen (infected) and three animals with semen and cell culture medium (controls). Only three out of the six infected animals were pregnant by ultrasonography on day 29 after insemination, while two out of the three controls were pregnant. One control gilt aborted on day 23 after insemination but not due to PVC2. Viraemia was demonstrated in four out of six infected and in one control gilt that became infected with PCV2a. Anti-PCV2 antibody titres showed dynamic variations in the infected group throughout the study. Among infected gilts, the animal with the lowest anti-PCV2 titre (1/100) at the beginning of the experiment and another that reached a similar low value during the experiment showed evident seroconversion over time and had also PCV2 positive foetuses. One placenta displayed mild focal necrosis of the chorionic epithelium positively stained by immunohistochemistry for PCV2 antigen.
PCV2-seropositive gilts can be infected with PCV2 after intrauterine exposure and low maternal antibody titre may increase the probability of a foetal infection.
" detected in these dams during gestation . However , PCV2 in utero infection was detected at parturition in 10% ( 5 / 50 ) of the piglets born to vaccinated sows ( Madson et al . , 2009b ) . Similarly , in utero infection was observed in the spiked semen model when PCV2 naı¨ve dams were vaccinated ( Ingelvac 1 , CircoFLEX 2 ) 8 weeks prior to AI ( Madson et al . , 2009a ) . PCV2 vaccination at the breeding herd level benefits the dam which is actively vaccinated and protected , in utero fetuses which benefit by a reduction of PCV2 viremia in their dam , and piglets which receive higher amounts of anti - PCV2 antibodies via colostral intake ."
[Show abstract][Hide abstract] ABSTRACT: Porcine circovirus type 2 (PCV2) causes great economic losses in growing pigs and there are several reviews on disease manifestations and lesions associated with PCV2 in growing pigs. Reproductive failure in breeding herds, predominately associated with increased numbers of mummies and non-viable piglets at parturition, is one of the disease manifestations of PCV2 infection. Boars shed low amounts of infectious PCV2 in semen for extended time periods, and vertical transmission of PCV2 to fetuses during PCV2 viremia of the dam has been experimentally confirmed. However, intrauterine-infected piglets often are clinically normal. Nevertheless, pigs infected with PCV2 by the intrauterine route can be born viremic, possibly contributing to horizontal spread of PCV2 within the breeding herd and into the nursery. Shedding of PCV2 in semen and prevalence of intrauterine-infected piglets can both be greatly reduced by PCV2 vaccination well ahead of expected PCV2 exposure. This review is a discussion on current knowledge on the effects of PCV2 infection in the dam and in in utero fetuses, including clinical signs, lesions, diagnosis and prevention through vaccination. Infection of boars with PCV2, the potential for PCV2 transmission via semen and prevention of PCV2 shedding are also discussed.
Animal Health Research Reviews 06/2011; 12(1):47-65. DOI:10.1017/S1466252311000053
[Show abstract][Hide abstract] ABSTRACT: Porcine circovirus type 2 (PCV2) impacts global swine production, is economically important, and is associated with multiple disease entities that include multisystemic disease, wasting, pneumonia, diarrhea and reproductive failure. Transmission of PCV2 within or between swine populations is not well understood. We characterized semen shedding of PCV2a and PCV2b in Landrace boars and found that PCV2 viremia precedes semen shedding, clinical signs are absent, and peak PCV2 semen shedding occurs between 10-20 days post-infection. PCV2 can be continuously shed in semen for at least 90 days. We determined that PCV2 shed in semen is infectious when used in a swine bioassay model, but dam or fetal infection after artificial insemination with PCV2 positive extended semen does not necessarily occur. However, when nayve dams were artificially inseminated with PCV2-spiked semen, dam viremia and fetal infection occurred. Nayve dams inseminated with spiked semen did not show clinical signs of infection after PCV2 exposure, but increased numbers of mummified and stillborn fetuses were observed. Stillborn fetuses exhibited gross lesions of heart failure and myocardial tissue was determined to be the best sample for diagnosing in utero PCV2 infection. Using the PCV2-spiked semen model, we compared dam immunity associated with PCV2 vaccination to immunity associated with a previous infection to induce protection against subsequent PCV2-challenge. PCV2 antibodies induced by a homologous strain of PCV2 protected against in utero infection; however, 63% of the piglets from vaccinated dams were PCV2 viremic at birth suggesting that commercial vaccines may not prevent fetal infection. We also verified that PCV2 vaccination of dams is not protective against fetal infection following oro-nasal challenge during gestation, and affirmed that immunocompetent in utero fetuses are able to clear PCV2 infection prior to parturition.
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