Occurrence: Worldwide, a few countries still free.
Age affected: All ages.
Causes: Strains of Porcine Reproductive and Respiratory Syndrome virus (PRRSv) management and other infections are important.
Effects: Illness, conjunctivitis, inappetence, mummies, stillbirth, abortion, pre-weaning mortality, cough, infertility.
Occurrence: Worldwide, a few countries still free.
PRRS is caused by an arterivirus. The virus strains found in Europe (Lelystad virus EU1 and also EU2, 3 and 4) are related to those found in the US and Canada (NA types), but the differences between them are sufficient to affect diagnosis and protection from vaccines. Differences in the viral nucleic acid sequence affect diagnosis by Polymerase Chain Reaction (PCR), and the viral proteins are sufficiently different so that monoclonal antibody to one strain cannot always be used to diagnose infections with the other.
Vaccines made from North American strains do not always protect against European strains for the same reason In addition to the two types of PRRS virus, a high pathogenicity (HP) strain of the NA virus has emerged in China and is a deletion mutant which is capable of causing 20% mortality.
The virus can be grown in the laboratory in alveolar macrophages (lung defence cells) and artificial cell cultures and lyses (kills) some types of cells but not all cells within 12 hours. The virus infects pigs via the respiratory tract or by insemination and multiplies in the cytoplasm of alveolar macrophages and many other related cells including those lining the blood vessels (endothelial cells).
It rapidly reaches the blood where it can be found, even after immunity has developed. It multiplies in and kills alveolar macrophages, leading to loss of defences in the lung and thus contributing to pneumonia. The virus may penetrate the reproductive tract to enter foetuses from 72 days of pregnancy and enter the semen in boars. Recovered pigs develop antibody but may carry virus for up to 12 weeks and shed virus in secretions.
The most important mode of transmission is by contact between infected and uninfected pigs, when the virus is inhaled from infected respiratory secretions and infects the respiratory tract. Indirect transmission by aerosol can occur over long distances in suitable conditions (9-20 km), and transfer of infection on drinkers and feeders is possible. The virus can be found in the semen and venereal infection can take place. Transmission between farms is generally by the introduction of affected or carrier pigs, but can be from transport, clothing, aerosol and through semen.
Clinical signs of PRRS are most severe when infection enters a non-immune conventional health herd, but may cause no obvious disease. Disease in sows and boars begins with inappetence lasting up to 4 days. They may become listless with laboured breathing but fever rarely exceeds 40°C and is transient. Reddening of the skin or a purple colour of the ears occur in 1-2%. Abortion occurs in 2-3% sows and is first apparent at 22 days, but most cases occur later. Lactation may be affected and anoestrus and returns to service may also occur. Antepartum deaths result in birth of large mummified piglets.
A rise in stillbirths (to 18%) and increased mortality in piglets aged up to 1 week occurs due to premature farrowing, weakness and play leg. Oedema of the eyelids, conjunctivitis, bleeding from tail docking, bruising after iron injection and bleeding into the gut may occur resulting in pre-weaning mortality of up to 33%. An increase in respiratory disease and skin changes may be seen in weaners and growers 5-7 days after infection to raise post-weaning mortality to 9%. The outbreak gradually resolves until near normal production is regained after 26 weeks. There is an overall loss of 2.54 pigs/sow/year.
Inappetence followed by an increase in stillbirths to 20%, abortions to 8% and pre-weaning mortality to 26% should lead to suspicion of PRRS. Lesser levels of these parameters and the other clinical signs described may suggest PRRS. Respiratory disease which is difficult to control and a consequent increase in medication and mortality in weaners or growers may also be associated with PRRS infection.
HP strains can result in higher mortality (20%). Diagnosis is most commonly confirmed by detecting antibody. Antibody to PRRS virus can be best demonstrated in the serum of sucking pigs soon after birth and at 10-12 weeks of age in chronically-infected herds. Herd antibody profiles allow infected houses to be identified. Saliva samples collected on a pen basis using ropes can be used to determine the presence or absence of antibody.
Post-mortem examination cannot confirm the disease, but changes in the anterior lung lobes, swollen lymph nodes and the presence of haemorrhages in the carcase may occur. Haemorrhage is particularly obvious where HP strains are involved. Microscopic findings include an interstitial pneumonia and the absence of alveolar macrophages. The presence of the virus may be confirmed by demonstration of the viral nucleic acid in tissue directly, and by immunofluorescence or immunoperoxidase using specific antibody reagents. A reverse Polymerase Chain Reaction (PCR) has been described which detects the viral nucleic acid. Virus may be isolated from tissue, alveolar macrophages and from blood.
PRRS is a viral disease so there is no specific treatment. Supportive measures can reduce losses and include the use of aspirin for 7 days prior to farrowing in an outbreak, checking all sows for pregnancy for 4-5 weeks gestation, promptly re-serving sows aborting early, allowing 21 days before re-service of sows aborting after 72 days and, following weaning, supplementing sow rations to reduce loss of condition and the use of AI to supplement natural service as semen quality may be reduced.
Induction of farrowing should stop, iron injection and teeth clipping should be delayed and artificial colostrum may improve piglet survival. Electrolytes may aid weak or diarrhoeic piglets. Disease in the feeding herd should be treated. Control is based on vaccination. Modified live and killed vaccines can be given to gilts or sows at service and to piglets at 3 or 6 weeks.
Protection reduces losses, but may not prevent colonisation with wild-type virus. Infection may be eradicated by depopulation and restocking or by extension of uninfected areas within farms coupled with herd antibody profiles to identify the location of active infection. Eradication has been carried out by closing herds to the introduction of new stock for periods of several months. Mass vaccination with or without herd closure may also be effective. Isolation prevents infection, but aerosol transmission is common for up to 500 m and sometimes occurs over greater distances. Breeding stock should be purchased from antibody-free herds and semen sourced from antibody free boar studs. Regional eradication has been successful in the short term, but herd breakdowns have occurred in some programmes.
PRRS is one of the most damaging porcine diseases in economic terms.