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http://www.merckvetmanual.com/generalized-conditions/porcine-reproductive-and-respiratory-syndrome/overview-of-porcine-reproductive-and-respiratory-syndrome

http://www.thepigsite.com/pighealth/article/142/porcine-reproductive-and-respiratory-syndrome-prrs/

http://www.thepigsite.com/diseaseinfo/97/porcine-reproductive-respiratory-syndrome-prrs/

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modified live virus (MLV) vaccines appear to be more efficacious than killed preparations

modified live vaccines should not be used in PRRS virus -negative herds, pregnant females, or breeding age boars

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Manage and treat sick animals

Separate healthy and sick pigs.

Treatment of adult pigs

medicate with antibiotics (in the feed or water or byindividual injections) for up to sixweeks

Treatment of piglets

Piglets should be injected with eitherlong-acting oxytetracyclineor amoxicillin on days 3, 7 and 14 after farrowing.

Give artificial colostrum if needed.

Give electrolytes to counteract dehydration.

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REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION (RT-PCR)

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REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION (RT-PCR)

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•Whole blood, buffy coat and clarified homogenates of the above tissues are best.

•At this time, there is no fully validated PCR that has international acceptability.

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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

Cytopathic effects are evident in 1–4 days.

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measures IgG antibodies to PRRS virus.

cannot measure the level of immunity in an animal or predict whether the animal is a carrier.

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.

Antibody levels can drop quite quickly in the absence of circulating virus.

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The characteristic lesions of acute infection include lymph node enlargement and interstitial pneumonia, the severity of which reflects the virulence of the infecting virus strain.

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PRRS virus infects only domestic and wild pigs.

Initially characterized by anorexia, fever, and lethargy.

Clinically affected animals are

hyperpneicor dyspneic

exhibit transient hyperemia or cyanosis of the extremities.

Nursery pigs have roughened hair coats and reduced growth rates.
Infection of sows in early to mid gestation

have little adverse consequence

Infection of sows in late gestation

results in reproductive failure characterized by abortion, premature births, stillbirths, and mummified fetuses.

Piglets that are born alive after in-utero infection are often weak and die quickly, typically with respiratory distress.

Other types of infectious diseases are more common in herds with enzootic porcine reproductive and respiratory syndrome virus infection.

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Virus spread by means of direct contact including pugilism.

The virus is shed from infected pigs in all type of secretions and excretions.

Transplacental transmission

commonly in full susceptible sows.

Transmitted indirectly by air for up to 3km.

Aerosol transmission

Environmental factors

Direction and velocity of the wind

Transmit via fomites.

Transmission via mosquitoes;

Aedesvexans

house flies; (Muscadomestica has been reported).

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Agent: Virus in the group of Arteriviridae.

enveloped,

replicate by means of in vitro only and in macrophages

Identified as “Lelystad virus” (major pathogen in swine population worldwide).

Field strains of PRRS are genetically heterogeneous.

Also affect other animals as well;

Equine arteritis virus in horse

Lactate dehydrogenase-elevating virus in mice

Simian haemorrhagic fever virus in Macaques