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

The virus is spread by contact with infected pigs, and infection also be transmitted by infected semen. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. It has been thought that aerosol transmission may occur, particularly under conditions of high humidity, low temperatures, and low wind speeds, but this has been difficult to reproduce in the field and experimentally. Once infected, adult animals shed PRRS virus for up to 86 days, and younger, weaned pigs for 157 days. Virus excretion in semen can persist for up to 93 days after infection.

Pathogenesis

Transmission of PRRS virus to swine occurs most efficiently through direct contact. Blood, saliva, urine, milk and semen from infected animals have been shown to transmit PRRS virus to susceptible swine (Wills et al., 1997). Aerosol transmission may occur but has proven difficult to demonstrate even over relatively short distances (meters). Transmission by semen, either through natural service or artificial insemination is well established (Yaeger et al., 1993). Following exposure to PRRS virus, primary replication occurs in regional or mucosal macrophages (Rossow, 1998; Rossow et al., 1996a). Typically macrophages of the tonsil, nasal and respiratory epithelium are sites of primary replication after oronasal exposure. Viremia can occur within 12 hours following exposure resulting in systemic dissemination of the virus. Lymphatic transport of PRRS virus and virus-infected macrophages to regional lymph nodes is also thought to occur. Secondary replication of PRRS virus occurs in monocyte/ macrophages in many tissues. While other cell types, including fibroblasts, endothelial cells, seminiferous epithelium and smooth muscle, have been reported to be PRRS virus-positive by in situ hybridization and/or immunohistochemistry, only cells of macrophage lineage have been unequivocally shown to support PRRS virus replication (Sur et al., 1997). In most swine, viremia resolves within 4-6 weeks following infection. However, PRRS virus can persist in lymphoid tissues, such as tonsil, for extended periods of time and be transmitted to susceptible swine (Zimmerman et al., 1992). PRRS virus has been detected for up to 225 days following inoculation, though the proportion of positive animals appears to drop off between 80 and 100 days (Albina et al., 1994; Allende et al., 2000; Wills et al., 2003). Persistence occurs in the face of neutralizing and other antibodies, and cell mediated immune responses, as indicated by gamma-interferon producing cells. Studies indicate that a low T cell response contributes to prolonged PRRS clearance (Xiao et al., 2004). Persistence is of epidemiologic significance since persistently infected animals are capable of transmitting PRRS virus to susceptible pigs via direct contact (Albina et al., 1994). This is likely an important mechanism by which PRRS virus is maintained within, and transmitted between, swine herds.

Diagnosis

Clinical Signs

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. Severe infections may also be associated with vestibular signs, and death of up to 10% of the sow stock can occur. Reproductive failure is results in increased numbers of stillborn piglets, mummified foetuses, abortions, premature farrowings and weak piglets. Lactating sows often display anorexia and agalactia, which leads to a rise in preweaning mortality. Signs are also seen in the piglets themselves, including a "thumping" respiratory pattern which on post-mortem examination is revealed to be associated with ls a severe, necrotising, interstitial pneumonia. Oedema may be seen around the eyes, and there is considerable variation in the size of piglets within litters.

Post-weaning performance is also affected, with daily live weight gain reduced by up 85% and increases in mortality by up to 25%. Lethargy and a loss of appetites is seen as in adult pigs, and weanling fail to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Outbreaks of the reproductive form of PRRS reportedly last between one and four months, depending on the initial health status on the pigs and the management of the outbreak. However, the post-weaning respiratory phase can become chronic, creating major production problems.

Secondary infections commonly occur. Bacteria previously reported to be associated with PRRS include Streptococcus suis, Escherichia coli, Salmonella choleraesuis, Haemophilus parasuis and Mycoplasma hyopneumoniae. Viral infections such as porcine respiratory coronavirus and swine influenza virus are also possible.

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.

Microscopic lesions of the fetus and placenta include umbilical vasculitis, interstitial pneumonia, myocarditis and pulmonary arteritis but are inconsistent and not diagnostic for PRRS (Lager and Ackermann, 1994; Lager and Halbur, 1996; Rossow et al., 1996b). There may be residual effects of PRRS virus infection in sows manifest as a reduced conception rate (Lowe et al., 2006).

Microscopically, interstitial pneumonia with mononuclear septal infiltration, type 2 pneumonocyte proliferation and accumulations of necrotic debris and macrophages in alveolar spaces is evident. Follicular hyperplasia and necrosis may be present in lymph nodes. Nonsuppurative meningoencephalitis and choroiditis is commonly present, with highly variable severity

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.