Occurrence: Worldwide, a few countries still free Age affected: All ages
Photo: Animal Health Service - the Netherlands

Effects: Illness, conjunctivitis, inappetence, mummies, stillbirth, abortion, pre-weaning mortality, cough, infertility.

• Detailed causes
• Clinical signs
• Diagnosis
• Treatment and control

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Detailed causes

PRRS is caused by an arterivirus. The virus strain found in Europe (Lelystad virus) is related to those found in the US and Canada, 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. 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.

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Clinical signs

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.

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Diagnosis

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. 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. 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. 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.

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Treatment and control

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 reserving 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 in some countries. 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 no prevent colonisation with wild-type virus. Infection may be eradicated by depopulation and restocking or by extension of uninfected areas within farms. Isolation prevents infection, but aerosol transmission is common for up to 500m and sometimes occurs over greater distances. Experts recommend that breeding stock are purchased from antibody-free herds.

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