PORCINE REPRODUCTIVE AND RESPIRATORY SYNDROME

FRANCISCO RUIZ-FONS

Instituto de Investigacion en Recursos Cinegeticos IREC (CSIC-UCLM-JCCM), Ciudad Real, Spain

Porcine reproductive and respiratory syndrome virus (PRRSV) of swine causes respiratory disease in young animals and reproductive disorders in adults.

PRRSV is an enveloped, single-stranded positive-sense RNA virus. Viruses are 50—65 nm in diameter and repli­cate in macrophages producing long-lasting viraemia and persistent infections. Two different PRRSV prototypes are recognized, one from North America and one from Europe, and they show approximately 60% nucleotide homology.

A reproductive and respiratory syndrome first observed in pigs in the USA in 1987 was later recognized in central Europe. More recently, PRRSV has spread over Europe. PRRSV was detected in free-roaming European wild boar from Germany, Italy and France and in farmed wild boar from France. Studies carried out in Croatia, Germany, Russia, Slovenia, Sweden and other eastern European countries did not detect PRRSV infection. Recent inves­tigations in wild boar populations in Spain have shown a low seroprevalence to the virus.

PRRSV is considered as a swine pathogen and has not been detected in other species, including rodent, carni­vores and birds. In domestic pigs, spread of PRRSV within a farm may occur in 2 to 3 months; when 85 to 90% of the animals become seropositive. The density of pigs and pig farms influences the rate of spread of PRRSV within a farm or geographic region. In a study in European wild boar the seroprevalence was slightly higher in young (6.4%) than in adult (4%) animals(³⁷), whereas in another study the age and population density did not affect the prevalence⁽³⁸⁾.

PRRSV survival in aerosols is higher at lower tempera­tures and at lower relative humidity⁽³⁹⁾, which suggests that aerosol transmission in nature is influenced by climate. Arthropod vectors can maintain PRRSV for short periods, but they are not considered to be important reservoirs.

The current panorama of PRRSV status in European wild boar and domestic pig populations suggests that wild boar are spillover hosts of a virus maintained by domestic pigs. However, where wild boar population densities and infection rates are high PRRSV may be maintained in these populations. There is little information on the trans­mission pathways of PRRSV between wild boar individu­als, groups or populations.

In domestic pigs PRRSV is excreted in blood, semen, saliva, aerosols, milk, colostrum and, depending on the study, faeces. Vertical transmission from females to their offspring has also been demonstrated. The routes for PRRSV excretion in wild boar and the infective viral titre are unknown, although the high prevalence found in wild boar lung⁽³⁸⁾ suggests that respiratory transmission is important.

The PRRSV targets cells within the monocyte/ macrophage lineage. After replication of PRRSV in mac­rophages at the primary site of infection, the virus is dis­tributed by these cells to the rest of body tissues. There is significant variation in the development of infection in individual animals. A humoral immune response appears in infected domestic pigs after a week post-infection (pi), with maximum antibody titres 30 days pi.

PRRSV infection may persist in the host at low titres for a variable period. Vertically infected pig fetuses had PPRSV infection 210 days after birth and sentinel animals developed PRRSV antibodies 14 days later.

Macroscopic lesions associated with PRRSV infection may vary with the age of the host and concurrent infec­tions, and in general consist of moderate to severe lym­phadenopathy. Histologically, mild to severe interstitial pneumonia and hyperplasia of lymphatic follicles with cellular necrosis and lymphoid depletion is observed. Other lesions may be observed in piglets, including rhini­tis, encephalitis and myocarditis.

No lesions associated with PRRSV infection have been described in European wild boar.

PRRSV causes a marked increase in return to oestrus, late- term abortions, stillborn and weak piglets. In many cases, severe respiratory disease in suckling and weaned pigs also occurs. No clinical cases of PRRS have been described in wild boar.

Diagnosis of PRRSV infection in wild boar may be performed by using common techniques of virus isolation or by RT-PCR. Antibody detection in wild boar has been carried out mainly with ELISA tests designed for the domestic pig, but the tests have not been validated in wild boar.

Prevention of PRRSV introduction to domestic pig premises requires implementation of strict hygiene proto­cols in order to avoid accidental introduction by fomites or aerosols from nearby infected farms. Once the disease has entered a farm, control can be achieved by testing and slaughter, herd slaughter or vaccination. Currently, control and management measures are not applied to wild boar populations even though there is evidence of low circula­tion of PRRSV in many populations. Nonetheless, evalu­ating available commercial vaccines and other control measures in prevention of future outbreaks of PRRSV in wild boar populations should be considered.

There are no known concerns for public health associ­ated with PRRSV.

No link between domestic pig and wild boar with regard to PRRSV prevalence has been demonstrated.