Table 1. Effect of PPV infection in seronegative pigs in different stages of pregnancy. Infection of the sow
Infection time of the foetus
Result of the infection
Clinical disease
10-30
Death and reabsorption of embryo
Large number of sows returning to oestrus
30-70
Foetal death and mummification
Smaller litters with mummified foetuses
70-tĂŠrmino
Normally there are no harmful effects. Infected immunocompetent foetuses produce antibodies
Habitually none
Days of gestation <56
>56
PATHOGENY PPV infects pigs via the oronasal or venereal routes and reaches the bloodstream about 10 days after infection causing transient leucopoenia (Taylor, 2006). Viraemia facilitates the passage of the virus to the reproductive tract of the animal 10-14 days after infection. The virus can be found in sperm of boars by days 5-9 post-infection, and in seminal vesicles and testicular tissue by 8-21 dpi (Taylor 2006). PPV adheres to the pellucid area of ovocytes and infects and makes non-immunocompetent embryos and foetuses unviable by about day 67 of gestation. The virus does not affect females infected 1-4 weeks before insemination but crosses the placenta in those that become infected during insemination or in the following 90 days. Embryos and foetuses that die before days 33-35 of pregnancy can be reabsorbed completely, whereas those that die after that time may become mummified, be stillborn or be aborted (abortions from PPV do not occur when the infection is after 70 days of gestation). The infection spreads from pig to pig along the uterus. In pigs infected at the end of gestation, piglets that do not die may develop high levels of serum neutralizing antibodies or become immunotolerant and remain infected for more than 8 months after birth (Johnson and Collings 1971). Infected piglets that recover from infection show a significant reduction in growth. Serum antibodies appear in the mother at 7-10 days post-infection and their titres rapidly increase. The virus is shed in low con-
centrations in urine, faeces, tonsillar peeling and nasal secretions as of the second week post-infection. In persistently infected pigs, this shedding occurs for approximately two weeks. Affected pigs recovering from the infection have strong humoral immunity (antibodies) transmitted via colostrum to offspring that can be detected up until 4-6 months of age (this varies according to the diagnostic techniques). Pigs are susceptible to reproductive failure induced by PPV if they become infected at any time during the first two trimesters of gestation. This range of maternal susceptibility is supported by numerous experimental studies (Joo et al. 1976; Mengelin 1979; Mengelin and Cutlip 1976; Mengelin et al. 1980). If the sow is infected in the first 56 days of pregnancy, embryonic death and resorption (10-30 days gestation) or death and mummification (30-70 days gestation) may occur. After day 56 of gestation, the infection in sows moves to the placenta, when the foetus is at about day 70 of gestation, and there may be an immune response and survival of the future piglet.
EPIDEMIOLOGY The most common routes of infection in pigs in the postnatal and prenatal period are the oronasal and transplacental routes, respectively. Infection is endemic on most farms in areas of high concentration of swine. A large proportion of primiparous pigs are infected with PPV before insemination. Gilts that have not been exposed to infection before their first pregnancy are at high risk of infection and reproductive disease. Piglets