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===Clinical Signs===
 
===Clinical Signs===
 
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The clinical signs of PRRS vary with the strain of virus, the immune status of the herd and management
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.
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factors. Infection may also be asymptomatic. Clinical disease in a herd is a consequence of acute viraemia in
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individuals and transplacental transmission of virus from viraemic dams to their foetuses, which can occur at
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any time, though infections in the last third of pregnancy can result in severe disease. Concurrent infections
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with other pathogens are also common.
    
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.
 
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.
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