Introduction

Porcine reproductive and respiratory syndrome virus (PRRSv) can be devastating to breeding herds due to losses resulting from reproductive failure, i.e., reduced fertility, abortions, and premature farrowing, as well as delayed return to estrus. In addition, piglets born to affected dams suffer from increased weakness at birth, decreased growth rates, increased susceptibility to respiratory infections, and higher pre-weaning mortality. Vaccination is of value for decreasing these detrimental effects.

Under field conditions, García-Monte et al, (2019) demonstrated that the farm where that they operated had a history of PRRSV circulation and outbreaks despite regular vaccination of the sows with a PRRS Modified Live Vaccine (MLV). Two months before they started a safety and efficacy study, sera were obtained from 150 sows of different parity and tested for serology and viremia. Results confirmed seropositivity in 94.7% and PRRSV Type 1 viremia in 11.3% of the sampled sows. Sequencing of the gene open reading frame 5 (ORF 5) revealed the presence of two distinct PRRSV strains; one matching the vaccine strain and the other one considered a wild PRRSV Type 1.

PRRS exists in two distinct forms, reproductive and respiratory, and infected farms may experience one or both. A variety of factors, including swine genetics, the specific PRRS virus variants in the herd, health status of the herd, ages of the animals involved, and pregnancy status, may influence the clinical signs.

Clinical signs

Zimmerman, (2019) described the mains symptoms of PRRS in pig production. In the present post we will focus on gilts/sows clinical signs. Gilts and sows infected with PRRS virus may show inappetence (off feed) and fever, or may show no clinical signs.

Gilt/Sow

Acute stage

“Rolling inappetence” and fever (40ºC to 40.6ºC) are often observed and may involve up to 30% of the infected animals. During this acute stage, abortions may occur in 1 to 3% of pregnant animals, with abortion most common in females infected during the last trimester of pregnancy. An increase in the number of open sows, irregular returns to heat, and reduction in farrowing rate may be observed. Some PRRS virus variants are more virulent than others; highly virulent variants may cause abortion rates of 10 to 50% and mortality in up to 10% of gilts and sows. Signs of central nervous system involvement, including ataxia, circling, and falling to one side, may follow early abortions.

Second evolution phase

The acute infection enters a second phase approximately one week after the onset of clinical signs. As a result of PRRS virus infection of the fetuses, late-term reproductive failure occurs; both in pregnant females with and those without previous clinical signs. This phase typically lasts 1 to 4 months and causes 5 to 80% reproductive failure in pregnant females at 100 to 118 days of gestation. Most affected sows abort or farrow prematurely, but some farrow at full term. The number of premature farrowing may increase 1 to 4 weeks after the outbreak begins. These litters will contain variable numbers of normal, weak, and dead pigs in various stages of mummification.

Over the course of this 1 to 4 month phase, the pattern of abnormal pigs in affected litters shifts. Initially, affected litters contain stillborn and large, partially mummified late-term fetuses. With time, this shifts to smaller, more completely mummified pigs; then to small, weak-born pigs; and finally, to pigs of normal size and vigor. Typically, 1 to 2% of litters are born dead. Gilts/sows infected with PRRS virus that progress through this four-stage disease process are difficult to rebreed. Often, these animals exhibit delayed return to estrus and low conception rates, resulting in depressed farrowing rates.

Boars

In general, few clinical signs are observed in boars infected with PRRS virus. If present, signs include fever, lethargy, inappetence, decreased libido, and occasionally, respiratory signs. Infrequently, boar deaths have been attributed to highly virulent PRRS virus variants. Some field and experimental studies report a decline in semen quality (reduced motility and proximal and distal cytoplasmic droplets) 2 to 10 weeks after infection. PRRS virus in semen from infected boars can be transmitted to susceptible females by natural mating or artificial insemination, so producers need to monitor sources of boars and semen for PRRS virus infection. The likelihood of transmission of PRRS virus via semen is dependent on the quantity of virus. As compared to intranasal inoculation, a 100 to 1000-times higher dose of PRRS virus is required to infect gilts by virus-contaminated semen. Of course, infected boars also shed virus in saliva and other secretions and excretions.

Diagnosis

In respiratory cases in which PRRS virus is suspected, serum, lung, and lymphoid tissues from pigs with clinical signs or increased body temperatures should be submitted for testing. In abortion cases, live weak-born pigs should be submitted, rather than stillborn and mummified fetuses, because the virus is rapidly inactivated in necrotic tissues. In suckling, weaned, or growing pigs, virus may be isolated from serum for 4 to 6 weeks post infection; 1 to 2 weeks in sows and boars. In adults, virus can usually be detected for an additional 2 to 4 weeks after infection in cells that have been washed from the lungs (lung lavage). The following techniques are recommended for diagnosis:

Enzyme-Linked Immunosorbent Assay (ELISA)

ELISA is the most common method used to determine if a herd has become infected or to monitor infection in endemically-infected herds, is detection of serum antibodies using the commercial PRRS ELISA. It is a rapid and inexpensive method of detecting and monitoring of PRRS virus infections on a herd basis. The test detects the presence of antibodies in serum as early as 7 days after infection, but more commonly by 14 days. The ELISA reports results in the form of a sample-to-positive (S/P) ratio and S/P ratios of 0.4 or higher are considered positive.

The polymerase chain reaction (PCR)

The PCR is a test that detects and amplifies a small, specific segment of the PRRS virus genome. PCR is more sensitive than virus isolation and results are available in a shorter period of time. Samples suitable for analysis by PCR include serum, semen, and tissue. Once collected, samples should be kept cool and shipped to the diagnostic laboratory overnight on ice. Chilling (refrigeration) is preferable to freezing. DNA obtained from the PCR reaction can be sequenced to differentiate infection with field virus from modified-live virus vaccine.

Immunohistochemistry (IHC)

IHC can be used for directly visualizing PRRS virus antigens in tissues. IHC is less sensitive than other tests and lung, lymph nodes and tonsil are usually the preferred specimens because these tissues contain higher amounts of virus.

Control and Eradication

A variety of management strategies have been used to reduce clinical PRRS or stop the circulation of virus in susceptible populations of pigs. The most important component of a control program is the proper use of diagnostic tests to accurately determine the pattern of virus transmission within an infected production system. Serum samples for serologic profiling should be collected from the breeding herd across all parities, recently weaned pigs, 8- to 10-week old nursery pigs, and 5- to 6-month old finishers.

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