Porcine Reproductive and Respiratory Syndrome (PRRS)

Definition

PRRS is an acronym (porcine reproductive and respiratory syndrome) for a relatively new viral disease of pigs that is characterized by two overlapping clinical presentations - reproductive impairment or failure in breeding animals, and respiratory disease in pigs of any age.

The causative agent

The causative agent of PRRS is the PRRS virus, which is an RNA virus classified under the order Nidovirales, family Arteriviridae and genus Arterivirus. There are two related but antigenically and genetically distinguishable strains: genotype 1, with the prototype Lelystad virus representing the viruses predominating in Europe and genotype 2, represented by VR 2332, the prototype of strains originally mostly found in North America. In 2006, a clinical outbreak characterized by high body temperature, rubefaction on the skin, respiratory disorder, and high mortality and morbidity in the affected pig herds attacked on the pig-producing areas of China. It has been proven that this outbreak of atypical PRRS occurred in China in 2006 was caused by a highly pathogenic variant of type 2 PRRSV with 90 nucleotides deletion, namely 30-amino-acid (30-aa in 481 and 533–561) deletion in its Nsp2- coding. There have also been descriptions of East European strains of type 1 PRRSV with a high degree of polymorphism. The PRRS virus is only moderately resistant to environmental degradation. The virus is easily inactivated by phenol, formaldehyde, and most common disinfectants. Strains of PRRSV vary markedly in virulence.

Susceptible species

The pig (Sus scrofa), whether domestic or feral, is the only species known to be naturally susceptible to this disease. Other species of wild pig and members of family Suidae may be susceptible.

Occurrence

PRRS is probably the most important swine disease of the last half-century. Although reported initially in only a few countries in the late 1980s, PRRS now occurs worldwide in most major swine-raising countries, except for a few countries including Sweden, Switzerland, New Zealand, and Australia which claim to be free of this disease.

 Clinical signs

Serological testing has revealed there are many infected herds in which signs are not apparent. Where signs are apparent, they vary and are influenced by several factors such as virulence of the virus, the age of animals, herd size and management practices, whether it is an initial infection or ongoing (endemic with herd immunity, presence of other disease causing agents in the population, etc.

Porcine reproductive and respiratory syndrome virus (PRRSV) occurs in all age groups. Reproductive impairment or failure, more obvious in sows or gilts, also affects some boars. The respiratory syndrome is seen more often in young growing pigs but also occurs in naïve finishing pigs and breeding stock.

Breeding age gilts, sows, and boars: Clinical signs may include a period of anorexia, fever, lethargy, depression, and perhaps respiratory distress or vomiting. Mild cyanosis of the ears, abdomen and vulva has been reported in some outbreaks. Reproductive problems, often the most obvious signs, include a decrease in the number of dams that conceive or farrow. There is usually an increase in premature farrowings, late term abortions, stillborn or weak piglets and mummified fetuses. Preweaning mortality is high. Nursing pigs may have dyspnea (“thumping”). The period for reproductive signs varies with herd size but is usually two to three months in duration. A slow improvement in reproductive performance then begins. In larger operations, signs may be cyclical, especially if naïve gilts or sows continue to be introduced into the herd. There is evidence that subpopulations within large breeding herds escape initial infection but are infected when exposed later and serve as sources of continued virus shedding. Also, herds may be infected with multiple, heterologous strains of PRRS virus that are not completely cross-protective. In boars, clinical signs are similar to sows and are accompanied by a decrease in semen quality.

Young, growing and finishing pigs: Primary clinical signs among young pigs are fever, depression, lethargy, stunting due to systemic disease, and pneumonia. Sneezing, fever and lethargy are followed by expiratory dyspnea and stunting. Peak age for respiratory disease is four to ten weeks. Post-weaning mortality often is markedly increased, especially with more virulent strains and the occurrence of ever-present concurrent and secondary infections. Older pigs, especially naïve, high-health swine, have similar respiratory signs. Heterologous infections may lead to prolonged or repeated outbreaks of respiratory disease.

Diagnosis

Although there are no pathognomonic symptoms, clinical signs and history often suggest PRRS, especially in acute outbreaks. Characteristic microscopic lesions in lungs and several other tissues also are suggestive but not pathognomonic. Any tentative clinical diagnosis should be confirmed by detection of the PRRS virus. This can be by virus isolation (VI), detection of PRRS antigen by fluorescent antibody tests (FAT) or immunohistochemistry (IHC), or detection of PRRS virus genome by polymerase chain reaction (PCR). Serology provides indirect evidence of infection but does not determine if there is actual disease caused by PRRS virus.

Antibody can be detected by ELISA and by the indirect staining of pre-prepared monolayers of infected cells (Immunoperoxidase monolayer assay (IPMA) and IFA). Commercially available ELISA kits are also commonly being used for PRRSV antibody detection. All serological tests can give rise to false positives and false negatives on individual animals, but on a group basis, they are reliable in indicating whether the herd has been infected or not.

In PRRSV test and removal programs, RTPCR has been used to detect viremic animals or carriers, primarily using serum, tonsil biopsy, or oropharyngeal scrapings. This assay has also been used to detect PRRSV RNA in semen samples, with an advantage over the virus isolation technique because of the toxicity of semen on the cells used for virus isolation. Although seldom used for diagnostic purposes, in-situ hybridisation is capable of detecting and differentiating type 1 and 2 PRRSV genotypes in formalin-fixed tissues. The sensitivity and specificity of the methods for detection of PRRSV genome or antibody are compromised by the very high genetic diversity of PRRSV.

Collection of specimens for laboratory diagnosis 

The following specimens should be collected and sent to the laboratory.

 For virus isolation and RT-PCR: whole blood (in EDTA) and serum, lung, lymph nodes, respiratory tract, spleen and tonsils of affected animals. Samples from mummified or aborted litters are unlikely to yield virus, but can still be useful for RT-PCR.

For antibody testing (serology): Serum from up to 20 exposed animals in the herd. Specimens should be chilled and forwarded unfrozen on water ice or with frozen gel packs.

For immunohistochemistry: Lung, tonsil, heart, brain, and nasal turbinate fixed in 10% neutral buffered formalin should be submitted for histologic examination

Specimens should be chilled and forwarded to the laboratory unfrozen on water ice or with frozen gel packs.

Control

There is no single successful strategy for control of PRRS, largely because of genetic and antigenic variability between viruses, large swine populations, and unresolved issues of transmission. Intervention strategies to prevent PRRSV spread are the keys to success. In some smaller herds, immunity may be sufficient so that infection is not causing significant economic losses, in which case no intervention is necessary. Often, there are sufficient losses to consider some or all of the following points for control.

Once the disease is confirmed, a strategy should be decided either to eliminate the disease or to control (or “live with”) PRRS. Current control measures include the management of incoming replacement gilts, the use of vaccines and implementation of biosecurity protocols validated to reduce the risk of PRRSV spread within and between herds. Methods of eliminating virus from endemically infected herds include whole herd depopulation/repopulation, test and removal and herd closure.

There is no specific treatment for PRRS. Broad-spectrum antibiotics may be useful in controlling secondary infections. Anti-inflammatory products are commonly administered during acute disease. Other helpful techniques include early weaning and isolation of piglets, regular serologic monitoring, testing (ELISA, PCR and IFA) and removal of persistent carriers in herds with <10% infection, and improving biosecurity.

Since the PRRS virus, the control strategies, and the specific farm situations are so variable, it is important that field veterinarians, diagnosticians and research workers continue to objectively expand their knowledge for better control and eventual elimination of this financially devastating disease.