Porcine reproductive and respiratory syndrome (PRRS) was first reported in the USA in 1987. Since then, outbreaks of PRRS and successful isolation of the virus have been confirmed throughout North America, Asia, South America, Africa, and Europe.
The etiologic agent of porcine reproductive and respiratory syndrome is a virus in the group Arteriviridae. The virus is enveloped and ranges in size from 45 to 80 mm. Inactivation is possible after treatment with ether or chloroform; however, the virus is very stable under freezing conditions, retaining its infectivity for 4 months at −70°C (−94°F). As the temperature rises, infectivity is reduced (15–20 minutes at 56°C [132.8°F]).
After infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to development of naive, exposed, and persistently infected subpopulations of sows. This situation is exacerbated over time through the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to those that have not been previously exposed.
The primary vector for transmission of the virus is the infected pig and contaminated semen. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, and weaned pigs able to harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection.
Aerosol transmission of the virus out to 9.1 km has been confirmed. Environmental factors, such as wind direction and velocity, significantly impact spread via this route as well. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, experimental transmission via certain species of insects (mosquitoes [Aedes vexans] and house flies [Musca domestica]) has been reported.
Porcine reproductive and respiratory syndrome appears to have two distinct clinical phases: reproductive failure and postweaning respiratory diseases. The reproductive phase of the disease includes increases in the number of stillborn piglets, mummified fetuses, premature farrowings, and weak-born pigs. Stillbirths and mummies may increase up to 25%–35%, and abortions can be >10%. Anorexia and agalactia are evident in lactating sows and result in increased (30%–50%) preweaning mortality. Suckling piglets develop a characteristic thumping respiratory pattern, and histopathologic examination of lung tissue reveals a severe, necrotizing, interstitial pneumonia. PRRS is capable of crossing the placenta in the third and possibly second trimester of gestation. Piglets may also be born viremic and transmit the virus for 112 days after infection. Performance after weaning is also affected.
Outbreaks of the reproductive form of PRRS have been reported to last 1–4 months, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10%–25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis, Escherichia coli, Salmonella Choleraesuis, Haemophilus parasuis, and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus.
The most commonly used serologic assay to help diagnose porcine reproductive and respiratory syndrome is the ELISA. It measures IgG antibodies to PRRS virus. It cannot measure the level of immunity in an animal or predict whether the animal is a carrier. Titers are detected within 7–10 days after infection and can persist for up to 144 days. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Nucleic acid sequencing of the open reading frame 5 region of the virus is an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites. Recently, oral fluid sampling has been widely applied as a means to sample a population of pigs.
Currently, there are no effective treatment programs for acute porcine reproductive and respiratory syndrome. Attempts to reduce fever using NSAIDs (aspirin) or appetite stimulants (B vitamins) appear to have minimal benefit. The use of antibiotics or autogenous bacterins to reduce the effects of opportunistic bacterial pathogens has also been reported; however, results have been mixed.
Prevention of infection appears to be the primary means of control. Understanding the PRRS status of replacement gilts and boars, as well as proper isolation and acclimatization of incoming stock, are critical measures to prevent viral introduction. Pigs should be retested on arrival at the isolation facility and 14 days later, before entry to the herd.
Commercial, modified-live vaccines have been licensed and have been effective in controlling outbreaks, reducing shedding, and preventing economic losses.
Elimination of PRRS virus has been demonstrated to be possible on an individual farm basis through the use of the herd closure technique. Following successful elimination, strict quarantine and testing programs, the purchase of PRRS virus-naive breeding stock and semen, sanitation of transport vehicles, and strict protocols of fomite and personnel movement between farms must be practiced to prevent reintroduction of virus. In addition, monitoring the status of artificial insemination centers by PCR analysis of blood samples collected from the auricular vein (blood swab), and the application of air filtration to artificial insemination centers and breeding herds are very effective means to reduce the entry of virus via contaminated semen and aerosols.