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260 Australian Veterinary Journal Volume 83, No 5, May 2005

Disease caused by the PorcineReproductive and RespiratorySyndrome (PRRS) virus is

widespread throughout much of the pigproducing world with the notableexception of Australia.

The disease is the cause of significantfinancial losses. The syndrome was firstrecognized in the mid-1980’s as “MysteryDisease” or “Blue-ear Disease” in NorthAmerica and Europe and was probablytransmitted to pigs from another hostspecies in about 1980. The aetiologicalagent was initially identified in theNetherlands (“Lelystad strain”or LV) in1991 and a similar but not identical strain(about 40% difference in amino acidsequences), was identified soon after inNorth America (VR-2332). The causativeenveloped RNA virus (50-65 nmdiameter) is in the genus Arterivirus andclassified in the family Arteriviridae;because of inherent errors in thetranscription of RNA there is considerableheterogenecity of the genome of the virus.Based on sequencing of the ORF5 gene atthe University of Minnesota, at least 800variant strains have been identified. Thisvariation is an important consideration inthe development and efficacy of vaccines.

Clinical SignsDepending on the class of animal infected,prior exposure history and the virulence ofthe strain of PRRS virus, the clinical signsvary widely. General signs include fever,lethargy, decreased appetite and respiratorydistress. Pregnant animals may abort inlate pregnancy or give birth to increasednumbers of mummified or stillbornfetuses. A typical sign in new born piglets

is an increased number of “weak” neonatesthat rarely survive to weaning. In grow tofinish age pigs the clinical signs are mostlyrelated to the respiratory tract with a peakof disease around 4 -10 weeks of age.Mortality and morbidity in this group isextremely variable.

Virus PropertiesPRRS virus is stable when stored attemperatures between -70oC and -20oCbut is rapidly inactivated when stored at40oC for 1 week or more. At 56oCinfectivity persists from 6 to 20 minutes (1).Infectious PRRS virus was recovered fromthe muscle of 2 of 14 pigs after 5 dayswhen the carcass was stored at 40oC (2).Two studies have demonstrated that PRRSvirus can be transmitted in raw pig meatfed to susceptible animals (3,4).

Current Australian regulations call forthe cooking of raw pork upon arrival inAustralia for 11 minutes at 70oC or for alonger time/lower temperaturecombination to inactivate PRRS virus.PRRS virus is stable within a pH range of6.5 – 7.5 and its infectivity is lost at a pHbelow 6.0 and greater than 7.5. In generalthe virus is unlikely to survive for longperiods in the environment. Isolation ofthe virus from aborted fetuses or stillbornpigs is difficult for the aforementionedreasons. Common disinfectants such asphenol or formaldehyde are effectiveagainst the virus.

Virus TransmissionTransmission of the virus under normalanimal production conditions is mostlikely by direct animal to animal contact asthe virus is present in urine, semen, faeces,

and nasal and mammary secretions. Thetime for which an animal is viraemic ishighly variable and some animals that arepersistently infected may shed virus for inexcess of 100 days; in practical terms theshedding period is usually shorter.However as the virus is highly infective,even shedding for only short periods oftime represents a significant disease risk.The speed at which the virus spreadswithin a herd is variable which may resultin “sub-populations” of sero-negative animals.

The issue of airborne spread iscontentious with little doubt that thevirus can be spread over distances ofaround 2km. The role of insects is evenmore contentious, however experimentalstudies in Minnesota USA have shownthat house flies may mechanicallytransport PRRS virus over a distance ofapproximately 1-1.7 km (5). These twomeans of spread may explain the spread ofthe virus where no other reason is obvious.

PathogenesisOnce the pig is infected the virus replicatesin the lymphoid tissues (spleen, tonsils,thymus, Peyer’s Patches and lymph nodes)and ultimately infects and compromisesthe function of pulmonary alveolarmacrophages (PAM) and intravascularmacrophages. This results in an interstitialpneumonia that may be worsened by thepresence of other pathogens such asMycoplasma hyopneumoniae,Mannheimia multocida, Actinobacilluspleuropneumoniae, swine influenza virusor porcine circovirus 2. Note that swineinfluenza virus is not present in Australia.

Exotic Animal Diseases Bulletin

No. 92

Compiled by Disease Preparedness Section Office of Chief Veterinary Officer

Porcine Reproductive and RespiratorySyndrome (PRRS) Virus - A significant

disease of pigsBy William Hall BVSc MS - Program manager, Research and Innovation Division - Australian Pork Limited

Photos courtesy of Pat Halbur - American Association of Swine Veterinarians

261Australian Veterinary Journal Volume 83, No 5, May 2005

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DiagnosisDiagnosis of PRRS virus infection is basedon typical clinical findings described aboveincluding enlargement of lymph nodes,typical histo-pathological lesions ofinterstitial pneumonia, virus isolation,serology (commonly ELISA) andPolymerase Chain Reaction (PCR) testingof fixed tissues, serum and fresh tissuesusing real-time PCR. Strain variationsmay be identified using RestrictionFragment Length Polymorphisms (RFLP)of the ORF5 gene or by sequencing the gene.

The Search for an EffectiveVaccineA huge effort has been expended over thelast 15 years to develop an effective vaccineand control methods for PRRS virus.Regrettably methods for control are notuniversally available. Both killed andmodified live vaccines have been used in alarge number of combinations in breedingand growing animals.

The vaccines appear to be highlyeffective in the presence of a homologouschallenge but as indicated earlier thenumber of strains of the virus is large andmany farms harbour one or more strainsof virus.

In the event of an outbreak of PRRSvirus in Australia the use of a vaccinewould be considered a measure of lastresort. Genetically engineered replicationdefective viruses may offer some hope forthe future. The use of serum inoculationhas become a widespread practice inNorth America that upon firstexamination appears to have achievedsome degree of control over PRRS inclosed herds by the production of PCRnegative pigs at weaning.

At present import control measures inAustralia have kept PRRS virus out of theAustralian pig herd. If a diagnosis ofPRRS were to be made in Australia rapidand significant measures would berequired to eradicate the virus including astamping out program, quarantine andmovement controls supported by strictbiosecurity measures. In countries wherePRRS has established itself, the virus hasproved to be a very costly disease to thepig industry.

For more information on PRRS andthe AUSVETPLAN strategy endorsed todeal with the disease please seehttp://www.aahc.com.au/ausvetplan/prrsinterim.pdf

References1. Benfield D et al (1999): Porcine

reproductive and respiratory syndrome.In: Diseases of Swine. 8th Ed. PubBlackwell Science 201-232.

2. Bloemraad M et al (1994): Porcinereproductive and respiratory syndrome:Temperature and pH stability ofLelystad virus and its survival in tissuespecimens from viraemic pigs. VetMicrobiol 42: 361-371.

3. Magar R, Larochelle R (2004):Evaluation of the presence of porcinereproductive and respiratory syndromevirus in pig meat and experimentaltransmission following oral exposure.Can J Vet Res: 68:4; 259-266.

4. Van der Linden IF et al (2003): Oraltransmission of porcine reproductiveand respiratory syndrome virus bymuscle of experimentally infected pigs.Vet Microbiol: 97: (1-2): 45-54.

5. Schurrer JA et al (2004): Spatialdispersal of porcine reproductive andrespiratory syndrome virus-contaminated flies after contact withexperimentally infected pigs. Am J VetRes: 65: 1284-92

Co-infection of PRRS virus and Actinobacilluspleuropneumoniae and subsequent lung

lesions.

Detection of PRRS virus byimmunohistochemistry.

High virulence PRRS virus and subsequentpulmonary lesions.

Lymphadenopathy caused by PRRS virus.

Depressed and anorexic pigs showing typicalsigns of PRRS virus infection.

Co-infection of PRRS virus and Mycoplasmahyopneumoniae and subsequent lung lesions.