Epidemiology
Porcine parvovirus is ubiquitous among swine throughout the world. In major swine-producing areas such as the midwestern United States, infection is enzootic in most herds, and with few exceptions sows are immune. In addition, a large proportion of gilts are naturally infected with PPV before they conceive, and as a result they develop an active immunity that probably persists throughout life. Collectively, the seroepidemiological data indicate that exposure to PPV is common. They also emphasize the high risk of infection and reproductive disease among gilts that have not developed immunity before conception. The most common routes of infection for postnatal and prenatal pigs are oronasal and transplacental respectively.
Pigs nursing immune dams absorb a high titer of antibody for PPV from colostrum. These titers decrease progressively with time by dilution as pigs grow as well as by biological degradation. They usually reach subdetectable levels in 3–6 months if sera are examined by the HI test. Sometimes passively acquired antibody persists for a longer interval. Moreover, levels of antibody too low to be detected by the HI test may be detected by the SN test. The primary significance of passively acquired antibody is that it interferes with the development of active immunity. High levels of such antibody can prevent infection, and lower levels can minimize dissemination from infected pigs. Consequently, some groups of gilts are not fully susceptible to infection and dissemination of virus until either shortly before conception or during early gestation.
Contaminated premises are probably major reservoirs of PPV. The virus is thermostable, is resistant to many common disinfectants, and may remain infectious for months in secretions and excretions from acutely infected pigs. It was shown experimentally that although pigs transmitted PPV for only about 2 weeks after exposure, the pens in which they were initially kept remained infectious for at least 4 months. The ubiquity of PPV also raises the possibility that some pigs are persistently infected and at least periodically shed virus. However, shedding beyond the interval of acute infection has not been demonstrated. The possibility of immunotolerant carriers of PPV as a result of early in utero infection has been suggested. When gilts were infected with PPV before day 55 of gestation, their pigs were born infected but without antibody. Virus was isolated from kidneys, testicles, and seminal fluid of such pigs killed at various times after birth up to the time they were 8 months of age; at which time the experiment was terminated. Results of another study, wherein dams were infected early in gestation and their pigs were born infected but without antibody, also suggest an acquired immunotolerance. A possible example of an infected, immunotolerant, sexually active boar was reported.
Boars may play a significant role in dissemination of PPV at a critical time. During acute infection the virus is shed by various routes, including semen, and the isolation of PPV from semen of naturally infected boars has been reported. Semen may be contaminated externally, as for example with viruscontaining feces, or within the male reproductive tract. The virus was isolated from a testicle of a boar 5 days after it was injected into the boar's prepuce and from testicles of boars killed 5 and 8 days after they were infected oronasally (Mengeling, unpublished data 1976). Virus was also isolated from scrotal lymph nodes of boars killed 5, 8, 15, 21, and 35 days after oronasal exposure. After day 8, isolation was accomplished by cocultivating lymph node fragments with fetal porcine kidney cells (Mengeling, unpublished data 1976). Irrespective of their immune status, boars can also function as a vehicle for mechanical dissemination of PPV among susceptible females.
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