Porcine Reproductive and Respiratory Syndrome

Also known as: PRRS, blue eared pig disease

Description

Porcine reproductive and respiratory syndrome was first recognised in the USA in 1987 and spreadto Europe in 1990 and the UK in 1991. Infection in the UK was initially seen in the Humberside area, but despite restrictions being placed on the movement of breeding stock outwith the infected zone, the disease spread to many parts of the country. PRRS is caused by a virus, of which different strains occur in the USA and Europe. The european strains are much milder in terms of their pathogenic potential than the US strains. The acute phase of disease lasts approximately 4-16 weeks. The most consistent featurs are reproductive lossed in pregnant stoock, increased pre-weaning mortality and inluenza-like illness affecting all ages of pigs. American strains of virus are much more virulent than European strains, causing sow martality in addidion to pneumonia and reporductive failure.

• The syndrome is caused by a small enveloped RNA virus which belongs to the new Arteriviridae group
• Replicates in and destroys macrophages and endothelial cells causing vasculitis -> viraemia -> virus shedding (nasal secretions, faeces)
• Clinical signs: respiratory and reproductive failure, weaned pigs, tachypnoea, eyelid oedema, conjunctivitis
• Moderate to severe interstitial pneumonia in the cranial lobe
• Superimposed bacterial infections are common
• Infectious disease in swine that emerged 10 years ago
• Today, PRRS is endemic in many if not all the pig-producing countries

PRRS Porcine reproductive and respiratory syndrome virus (Lelystad virus). There is abortion late in gestation with respiratory tract illness in live piglets (interstitial pneumonia).

Aetiology

The etiologic agent is a virus in the group Arteriviridae. The virus is enveloped and ranges in size from 45 to 80 mm. Inactivation is possible after treatment with ether or chloroform; however, the virus is very stable under freezing conditions, retaining its infectivity for 4 mo at -70°C. As the temperature rises, infectivity is reduced (15-20 min at 56°C).

Transmission and Epidemiology

ollowing infection of a naive herd, exposure of all members of the breeding population is inconsistent, leading to the development of naive, exposed, and persistently infected subpopulations of sows. This situation is exacerbated over time through the addition of improperly acclimated replacement gilts and leads to shedding of the virus from carrier animals to those that have not been previously exposed. The primary vector for transmission of the virus is the infected pig. Contact transmission has been demonstrated experimentally, and the spread of virus from infected seedstock originating from a single source has been described. Introduction of infected seedstock can lead to the introduction and coexistence of genetically diverse isolates of PRRS virus on the same farm. Controlled studies have indicated that infected swine may be longterm carriers, with adults able to shed PRRS virus for up to 86 days after infection, while weaned pigs may harbor virus for 157 days. Experimentally infected boars can shed virus in the semen up to 93 days after infection. Aerosol transmission of the virus has been considered to be a potential route of transmission, particularly under conditions of high humidity, low temperatures, and low wind speeds; however, this has been difficult to consistently reproduce under controlled field conditions and in the laboratory. PRRS virus can also be transmitted by fomites, such as contaminated needles, boots, coveralls, transport vehicles, and shipping containers. Farm personnel are not a risk, unless hands are contaminated with blood from viremic pigs. Finally, transmission via certain species of insects (mosquitos [ Aedes vexans ] and house flies [ Musca domestica ]) has been reported. The role of migratory waterfowl has not been determined. While biologic transmission of PRRS virus has been documented in immature Mallard ducks, results have not been reproducible experimentally using adult Mallards, nor have infected pigs been able to transmit virus to adult Mallards housed under field conditions.

Pathogenesis

• Infects alveolar macrophages, followed by interstitial pneumonitis
• Persistent infection of Monocytes followed by leukopenia and thrombocytopenia
• Mostly affects piglets
• In adults, cyanotic appearance due to vascular lesions
• Transplacental spread leads to abortion, mummification, or resorption

Diagnosis

Clinical Signs

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.

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. Outbreaks of the reproductive form of PRRS have been reported to last 1-4 mo, depending on the facilities and initial health status of the pigs. In contrast, the postweaning pneumonic phase can become chronic, reducing daily gain by 85% and increasing mortality to 10-25%. Numerous other pathogens are commonly isolated along with PRRS virus from affected nursery or finishing pigs. Other bacteria such as Streptococcus suis , Escherichia coli , Salmonella choleraesuis , Haemophilus parasuis , and Mycoplasma hyopneumoniae have been reported, as well as viruses such as porcine respiratory coronavirus and swine influenza virus. Finally, differences in the clinical response to PRRS virus may also be due to strain variation. Studies have demonstrated the ability of different isolates to induce varying degrees of interstitial pneumonia in CD/CD (cesarean-derived/colostrum-deprived) piglets after intranasal inoculation.

Laboratory Tests

• ELISA for virus antibody
• Rising antibody titres as a retrospective diagnosis (4X increase)

Control

• Certified Specific Pathogen Free units exclude by quarantine
• Management: all in/all out, screening AI semen
• Vaccine available