Porcine Reproductive and Respiratory Syndrome

Also known as: PRRS, blue eared pig disease

Description

Porcine reproductive and respiratory syndrome (PRRS) first appeared in the USA in 1987, although subsequent serologic evidence indicated that it had been circulating for some time prior to being recognised. The disease was seen in Europe in 1990 and reported in Humberside in the UK in 1991. PRRS is caused by an arterivirus, and leads to abortions, mortality and reduced growth, significantly impacting pig welfare and production economics worldwide.

Aetiology

The virus that causes PRRS is an aterivirus, within the Arteriviridae family. The arteriviruses are the only genus contained within the Arterivirdae family, and other members include the agent responsible for equine viral arteris and lactate dehydrogenase-elevating virus of mice. The viruses are host-specific and antigenically distinct, and establish persistent infections after invasion.

Arteriviruses are enveloped viruses of 45 to 80 nm in diameter with a spherical appearance due to the shape of the envelope. However, the icoshedral nucelocapsid that contains the positive-sense single-stranded RNA genome is actually icosohedral. The lipoprotein envelope has ring-like structures on its surface, but there are no gross surface spikes. Arteriviruses have a tropism for macrophages and endothelial cells, where they reproduce in the cytoplasm. The genome is 13Kb in length, and is infectious itself without the capsid or envelope.

Arteriviruses are inactivated by traetment with chloroform or ether. They are very resistant to freezing, althouth infectivity is in reduces as temperature risees.

Transmission and Epidemiology

ollowing infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to the 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. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. 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, while weaned pigs may 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 has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. 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, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

Pathogenesis

• Infects alveolar macrophages, followed by interstitial pneumonitis
• Persistent infection of Monocytes followed by leukopenia and thrombocytopenia
• Mostly affects piglets
• In adults, cyanotic appearance due to vascular lesions
• Transplacental spread leads to abortion, mummification, or resorption

Diagnosis

Clinical Signs

Clinical signs include non-specific illness (anorexia and dullness) in sows, with reproductive losses occuring 1-2 weels later. In piglets, PRRS is characterised by inthriftiness, respiratory illness and mortality. Signs are similar in all ages of growing stock. Effects on neonatal piglets can be severe. Respiratory distress is seen, in addition to scour, unthriftiness and high mortality. Infection of boars may lead to impaired semen quality. Blue ears, snout and vulva can be seen in 1-5% of sows. Reproductive problems include infertility (normal oestrus delated, retuns to service increased), premature farrowing, stillbriths and weakly piglets.

RRS appears to have 2 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. Infection with PRRS virus results in destruction of mature alveolar macrophages, which has led to the hypothesis that infection results in the suppression of the immune system; however, controlled studies indicate that the virus may actually enhance specific parameters of the immune response. Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, 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. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

Laboratory Tests

The most commonly used tests are the ELISA or the indirect fluorescent antibody test. These tests measure IgG antibodies to PRRS virus. They 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. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population. Tests for PRRS virus include PCR, virus isolation, and immunohistochemistry. Recently, nucleic acid sequencing of the open reading frame 5 region of the virus has become commercially available, and has proved to be an excellent tool for epidemiologic investigations in the field to confirm similarity between isolates recovered from different sites.

Pathology

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS, but interstitial pneumonitis is a consistent histopathologic finding. There are no gross or histopathologjc lesions noted in aborted or stillborn fetuses,sup>viro.

Control

Currently, there are no effective treatment programs for acute PRRS. Attempts to reduce fever using NSAID (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 have 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 45-60 days later, before entry to the herd. Elimination of existing infection by multisite production and segregated early weaning has also been described. While these strategies have had some success, the longterm risks of reinfection appear high. Prevention of viral spread by nursery depopulation has been described. This is successful when virus transmission is not occurring in the sow herd (usually 12-18 mo after initial outbreak), but the nurseries and growing/finishing pigs are still infected. All nursery pigs are removed from the farm to be finished elsewhere. The nurseries are then aggressively washed and disinfected and left empty for 7-14 days, after which they can be used normally. The technique has successfully eliminated PRRS virus from several herds, in which pigs have remained seronegative (for >1 yr) to market age, and production in the nurseries has improved, both in growth rate and mortality. Commercial vaccines, both modified live and killed, have been licensed and have been effective in controlling outbreaks and preventing economic losses. Recently, eradication of PRRS has been demonstrated to be possible on an individual farm basis. Methods such as whole herd depopulation-repopulation, test and removal, and herd closure have been documented as effective methods for eliminating PRRS virus from endemically infected herds. Unfortunately, a number of eradication efforts have failed due to the introduction of new isolates through unidentifiable routes.

Links

• The Pig Site: Porcine Reproductive and Respiratory Syndrome

References

1. Wise, D J and Carter, G R (2005) A Concise Review of Veterinary Virology, IVIS.
2. Merck & Co (2008) The Merck Veterinary Manual (Eight Edition), Merial.
3. Done, S and White, M (2003) Porcine respiratory disease and complexes: the story to date. In Practice, 25(7), 410-417.
4. OIE (2008) PRRS: the disease, its diagnosis, prevention and control. Report of the OIE ad hoc Group on Porcine Reproductive and Respiratory Syndrome.
5. Laegreid, W(2006) Porcine Reproductive and Respiratory Syndrome. Proceedings of the Annual Meeting of the American College of Veterinary Pathologists and American Society for Veterinary Clinical Pathology.