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 venereally via infected semen. Blood, saliva, urine, milk and semen from infected animals have all been shown to contain PRRS virus. Fomites, such as contaminated needles, boots, overalls and transport vehicles can also transmit PRRS, as can certain species of insects including house flies. Aerosol transmission is thought to 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. This lengthy persistence of infection is an important factor in the maintenance of infection within a herd.

Pathogenesis

Once PRRS virus gains entry to the host, primary replication occurs in regional or mucosal macrophages such as in the tonsil and the nasal and respiratory epithelium. After around twelve hours, viraemia occurs and the virus is disseminated systemically. The PRRS virs then seconarily replicated in the moncytes and macrophages in a wide variety of tissues. Other cells, such as fibroblasts, endothelial cell and smooth muscle may acqure PRRS infection, but only cells of the macrophage lineage have been shown to unequivocally support replication. Viraemia persists for around 4-6 weeks in most infections, but lymphoid tissues can remain infected for extended periods of time: following experimental innoculation, PRRS virus has been detected for up to 225 days. Both cell mediated and humoral immune responses are induced by PRRS virus infection, and pesistance of infection occurs despite this.

Diagnosis

In the field, suspicion of PRRS is based on clinical signs of reproductive failure and high levels of neonatal mortality. Farm records may provide useful information for confirming reproductive failure.

The differential diagnoses for PRRS include those of respiratory and reproductive signs. Respiratory differentials include swine influenza, enzootic pneumonia, Haemophilus parasuis infection, porcine respiratory coronavirus and porcine circovirus-associated disease. Reproductive differentials include porcine parvovirus, porcine enterovirus, and Aujesky's disease.

Clinical Signs

There appears to be two distinct clinical phases to PRRS: reproductive failure and post-weaning respiratory diseases. When sows are infected, a period of acute disease is seen which is characterised by lethargy, inappetance and pyrexia. These signs are generally mild, but occasionally severe infections can occur which are associated with vestibular signs, and death of up to 10% of the sow stock. The reproductive aspects of the syndrome are seen when sows become infected in the last trimester of pregnancy. Reproductive signs include increased numbers of stillborn piglets, mummification, abortions, premature farrowings and the birth of 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 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%. Mortality in growing pigs can be increased by up to 25% when PRRS is present in the herd. Lethargy and a loss of appetite is seen in weaned pigs, as well as a failure to thrive. Breathing is laboured and there may be obvious respiratory distress. The skin can appear red and blotchy, with a rough hair coat.

Secondary infections commonly occur concurrently to PRRS. 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.

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

Laboratory Tests

The most frequently used diagnostic tests are an ELISA and an indirect fluorescent antibody test. Both of these tests measure IgG antibodies against PRRS virus, which can be detected from 7-10 days post-infection. Titres persist for up to 144 days. High titers may indicate recent exposure, and viral shedding may be occurring within the sampled population.

Tests for the PRRS virus itself also exist. These include PCR and virus isolation on clinical samples, and immunohistochemistry on tissues. Nucleic acid sequencing of the 5' end of the virus is commercially availabe ans is useful for comparing isolates recovered from different sites in order to facilitate epidemiological investigations.

The following specimens should be collected. – For virus isolation and RT-PCR — whole blood (EDTA) and also serum, lung, respiratory tract, spleen and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can still be useful for RT-PCR. – For antibody testing (serology) — serum from up to 20 exposed animals in the herd. Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs. 􀂃 Virus isolation Buffy coat, serum, lung, lymph nodes, spleen and tonsils are the specimens of choice. The virus replicates well on swine pulmonary alveolar macrophages and some strains, particularly those of genotype 2, on Marc 145 cells. Cytopathic effects are evident in 1–4 days. Perform two 7-day passages for maximum sensitivity. 􀂃 RT-PCR Whole blood (EDTA), buffy coat and clarified homogenates of the above tissues are best. At this time, there is no fully validated PCR that has international acceptability. Please consult the OIE Manual for suggested methods. 􀂃 Serological tests IgM can be detected within 7 days of infection and IgG can be detected within 14 days. Humoral antibody titres reach a maximum about 5–6 weeks after infection. Antibody can be detected by ELISA and by the indirect staining of pre-prepared monolayers of infected cells (IPMA and IFA). Antibody levels can drop quite quickly in the absence of circulating virus.

Pathology

PRRS virus produces a multisystemic infection in pigs, but gross lesions are usually only observed in respiratory and lymphoid tissues. Both gross and microscopic lesions are most marked in neonatal and young weaned pigs. The gross pathology observed after uncomplicated infection of PRRS virus in finishing pigs may be anything from severe to unremarkable. In severe disease, lungs are mottled, tan and red, and fail to collapse; the cranioventral lobes are most affected. Lymph nodes are moderately to severely enlarged and tan in colour and, for some strains of virus, may be haemorrhagic. Under field conditions, most PRRS virus infected pigs are co-infected with one or more pathogens, which complicates the diagnosis of PRRS based on pathology.

Gross necropsy lesions are minimal in the uncomplicated respiratory form of PRRS. Microscopically, interstitial pneumonia is the typical finding. There is a mononuclear infiltration of the alveolar walls with type 2 pneumonocyte proliferation, and necrotic debris and macrophages accumulate in the alveolar spaces. In lymph nodes, follicular hyperplasia and necrosis may be seen. Non-suppurative meningoencephalitis and choroiditis is commonly present, but severity is highly variable.

There are no gross lesions noted in aborted or stillborn fetuses, but histopathology inconsistently interstitial pneumonia, myocarditis anr pulmonary arteritis. However, these changes are not specific or diagnostic for PRRS.

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.