An Overview of Porcine Reproductive and Respiratory Syndrome

You've reached the Virginia Cooperative Extension Newsletter Archive. These files cover more than ten years of newsletters posted on our old website (through April/May 2009), and are provided for historical purposes only. As such, they may contain out-of-date references and broken links.

To see our latest newsletters and current information, visit our website at http://www.ext.vt.edu/news/.

Newsletter Archive index: http://sites.ext.vt.edu/newsletter-archive/

Porcine Reproductive and Respiratory Syndrome (PRRS) is considered the most economically important viral disease of intensive swine farms in Europe and North America. The disease may also be referred to as Swine Infertility and Respiratory Syndrome (SIRS) by some veterinary and swine industry professionals. The syndrome first began causing swine herd problems in the late 1980's and, prior to isolation of the causative agent, was often referred to as mystery swine disease. A European strain of the virus was first isolated by Wensvoort and coworkers (1991) in the Netherlands. A North American strain was isolated soon after in Quebec, Canada by Dea and coworkers(1992). The virus is classified as a Arterivirus (Dee et al.,1994) and there are multiple strains in Europe and North Americawith some variation in virulence potential (Done, 1995).

Acute outbreaks of PRRS within a swine herd can cause some dramatic symptoms. In the breeding herd, sows may display an elevated body temperature (103-105 F), reduced appetite and lethargy. The European reports also indicate an increase in bruising and a blue ear appearance of white sows (Done, 1995). Increases in the number of premature farrowings (abortions), stillbirths, mummified fetuses and weak piglets at birth are often reported. Agalactia may also occur among lactating sows. Stillbirths and mummies may increase to 35% and abortions can exceed 10% (Dee et al., 1994).

In young piglets, high mortality rates will occur and at the peak of an outbreak pre-weaning, death losses may reach 60 to 70% (Hill, 1996) with 30 to 50% losses more common (Dee et al.,1994). Suckling pigs often exhibit a "thumping" breathingpattern and morbidity is substantial. Mortality rates are also elevated in the post-weaning period, varying between 4 and 20%. Depressions in post-weaning weight gain of 60 to 65% have been reported (Dee and Joo, 1994a). Veterinary practitioners also report a greater incidence of secondary pathogenic diseases among PRRS infected nursery pigs including Salmonella cholerasuis, Haemophilus parasuis, Streptococcous suis, Mycoplasmahyo pneumonia and swine influenza virus (Hill, 1996). Infinishing pigs, acute PRRS has similar effects as in the nursery, however, the magnitude of the effects are not usually as severe as with younger pigs. Serum titers for PRRS infected finishing pigs often decline with advancing pig age.

The acute reproductive phase of PRRS typically lasts 30 to 60 days but occasional recurrence of reproductive failure does occur in PRRS positive herds (Dee and Joo, 1994b). It is not fully clear if chronic PRRS represents recurring bouts of symptoms among PRRS positive pigs or recurrent virus transmission from carrier pigs to disease naive pigs. It is likely that transmission to disease naive pigs plays an important role in the recurrence of PRRS symptoms because successful treatment strategies often involve isolation and alterations in the movement of pigs through facilities. After an outbreak, PRRS symptoms persist longer in nursery and grower pigs than among breeding animals. To some degree chronic persistence of the disease is concurrent with or masked by secondary pathogens(Done, 1995).

An important feature associated with the PRRS virus is the immunosuppressive effect it has, particularly in piglets and weanling pigs. An affinity for PRRS virus of sow origin to infect swine alveolar monocytes has been demonstrated (Voicu etal., 1994) and the virus causes death of pulmonary alveolar macrophages (Hill, 1996). This feature is consistent with the high incidence of secondary pathogenic infections among suckling and nursery pigs. It appears that normal levels of bacterial agents may become pathogenic when pigs contract a PRRS virus infection.

Swine appear to be the predominant host for PRRS infection but there is little data investigating alternative carriers. There view by Dee et al. (1994) discusses experimental infection and persistence in some species of waterfowl and European reports suggesting possible aerosol transmission across distances of 3 to 12 kilometers. A more recent study suggests that the virus is very sensitive to drying and air-born transmission beyond 2000 meters is unlikely (Blaha and Buker, 1995). Rats and mice do not appear to serve as carriers (Done, 1995).

Yoon and coworkers (1993) have demonstrated viremia of nursery pigs experimentally infected with PRRS virus and subsequent infection of sentinel pigs exposed to principal carrier pigs at 3, 10 and 24 days after initial infection. Pigs placed in exposure 24 days after infection developed viremia which lasted for a shorter time than the groups exposed earlier. Virus shedding was demonstrated in nasal secretions and feces of all exposed groups. The data demonstrated that young pigs may serve as PRRS virus vectors for at least 35 days post-infection. This experimental data and the numerous observations of veterinarians treating PRRS cases indicate that the infected pig is the main vector for PRRS transmission.

Another potential route of transmission is through boar semen. Boars experimentally infected with PRRS were shown to shed virus in the semen for up to 43 days post infection. Furthermore, PRRS may be transmitted to gilts which are bred artificially using semen from carrier boars (Hill, 1996).

Finally, it is accepted that PRRS can infect fetuses in the uterus (McCaw, 1995). It is this cross placental transmission that results in increased stillbirths, mummies and weak viremic pigs.

The most commonly used serological test for PRRS diagnosis by U.S. swine practitioners is the indirect fluorescent antibody (IFA) test described by Yoon et al. (1992). The test proved reliable in detecting PRRS antibody in experimentally infected animals and in swine herds experiencing clinical PRRS symptoms. However, the test measures prior exposure to PRRS but does not definitively indicate if the animal is shedding virus. The guidelines provided by Dee and coworkers (1994) indicate that titer values ranging from 1:256 to 1:1024 suggest recent exposure and the potential for active shedding of virus. Follow-up samples from the same animals can indicate if titer values are increasing or decreasing to further assess potential for virus shedding. In addition to the IFA test, an enzyme linkedimmuno assay (ELISA) has become available for antibody detection (Done, 1995). Furthermore, specific virus isolation tests are available and positive isolation of PRRS virus indicates existing viremia. If the potential exists for either American or European PRRS strains to be involved, then virus isolation tests for both strains may be warranted (Dee et al., 1994). Veterinary practitioners also recommend that a single reliable laboratory be selected to conduct PRRS serology to avoid confusion with normal variation in results between laboratories.

In the U.S. only one PRRS vaccine is currently labeled for swine use. The product is a modified live virus vaccine, trade name RespPRRSr, manufactured by Nobl Laboratories. The vaccine is only approved for use in pigs from 3 to 18 weeks of age. However, significant "off-label" use is being prescribed by swine veterinarians working with large herds experiencing PRRS cases. In prescribing off-label use, veterinarians are accepting some risk that the modified live virus may increase disease risk among some classes of pigs (McCaw, 1995).

There is still debate among veterinarians as to when it is safe and effective to vaccinate various classes of pigs. One concern is the potential for problems in developing fetuses when pregnant sows are vaccinated with the modified live virus during late pregnancy (after 50 days). The universal opinion among swine health practitioners is that indiscriminate use of the vaccine should be avoided and that use without other herd management strategies to control PRRS will not be effective.

Freese and Joo (1994) reported on a case in which a 250-sow herd developed PRRS in early 1990 but by April 1993 production levels returned to normal and serology indicated that circulation of the virus had stopped. In reviewing management changes that occurred in the herd, the authors concluded that longer quarantines for replacement breeding stock, all-in all-out pig flows through facilities and a 2-week interval between pig groups entering the nursery were the main factors that produced recovery. Since that time, management protocols have focused on these areas with some encouraging results.

Strict biosecurity measures are important, not just for PRRS control, but for many economically important diseases. Visitation of existing farms by outside personnel should be strictly monitored. Fresh boots and coverall clothing should be provided to any visitors and their previous exposure to hogs should be known. All vehicle traffic should be monitored and bird and rodent populations controlled.

Incoming replacement breeding stock should be from as few sources as possible and should be compatible in PRRS status with the receiving herd. Proven negative herds should only receive replacements from a proven negative source (Hill, 1996). There commendation for isolation of replacement stock is typically 30 days but, in cases of PRRS risk, Dee and Joo (1994b) recommend extending isolation to 45 to 60 days. This allows for testing and retesting of the stock to determine serum status and a longer period of time to properly expose and stabilize the animals before placing in the herd. Vaccination may be used during isolation but serum evaluations will be confusing because vaccine titers are not distinguishable from natural titers. This method of replacement isolation may require more extensive facilities for quarantine and less frequent purchase of larger groups of gilts. However, it has proven effective in some PRRS infected herds in the U.S. The principle is to prevent introduction of viremic animals that are shedding virus and extremely naive animals that react poorly when exposed to the existing herd.

Dee and Joo (1994a) have documented cases in which sow herds were stabilized based on IFA serum tests but chronic PRRS related problems persisted in the farm's nursery pigs. Their approach to correcting this problem involved total nursery depopulation followed by recurrent washing and disinfection for 3 times during a 14-day period. The manure slurry was removed twice from the collection pit during this 14 day period as well. After the 14 day depopulation time, normal pig flow into the nurseries was resumed. For the 6-month evaluation period after the treatment, mortality and performance were markedly improved and no seropositive pigs were identified. With this method of control, the authors caution that there is much less chance for success unless the breeding herd and suckling piglets are stable and not shedding virus. If sows and piglets are shedding virus, PRRS will simply be reintroduced into the nurseries with subsequent weaning groups. Under any circumstance, managing all the facilities with an all-in all-out pig flow as much as feasible is important to PRRS control.

Dr. Monte McCaw (1996) has also described a set of management procedures for piglets and nursery pigs which has been effective in large herd cases in the U.S. The process has actually been patented as a management system called McRebelr for control of PRRS and associated diseases in young pigs. The system is based on the principle that handling and moving sick pigs increases the spread of PRRS and other diseases. It is not designed to work effectively unless nurseries can be operated as all-in all-out rooms. The general principles of the McRebelr management system are as follows:

Porcine Reproductive and Respiratory Syndrome (PRRS) is an economically important swine herd disease that is receiving a great deal of attention by swine veterinarians. At this point in time, vaccine use to control and prevent PRRS has had only limited success in the U.S. The most successful documented approaches to controlling PRRS has been by avoiding introduction of infected replacement stock, controlling and stabilizing the disease in the breeding herd and utilizing strict all-in all-out management in nursery pig facilities. Holding sick pigs back with younger pig groups and excessive cross-fostering of sick pigs has contributed to recurring PRRS problems on intensive farms. Use of diagnostic serology and consultation with experienced swine veterinary practitioners is important in development of a PRRS control program.

Blaha, T. and E. Buker. 1995. Risk factors for the spread and the severity of PRRS. Second International Symp. on PRRS, pp.29, Copenhagen, Denmark.

Dea, S., R. Bilodeau, R. Athanassions, et al. 1992. Swine infertility and respiratory syndrome in Quebec: Isolation and characterization of an enveloped virus serologically related to Lelystad virus. Can. Vet. J. 33: 801-808.

Dee, S., H. S. Joo, and C. Pijoan. 1994. Control of porcine reproductive and respiratory syndrome virus transmission: Handling infected seedstock. Compendium of Continuing Education for Practicing Veterinarians 16(7): 927-933.

Dee S. A. and H. S. Joo. 1994a. Prevention of the spread of porcine reproductive and respiratory syndrome virus in endemically infected pig herds by nursery depopulation. Veterinary Record 135: 6-9.

Dee, S. A. and H. S. Joo. 1994b. PRRS in the United States: there-education of the swine practitioner. Swine Health and Production 3(2): 81-84.

Done, S. H. 1995. Porcine reproductive and respiratory syndrome. Misset-PIGS, June 1995, pp. 12-17.

Freese, W. R. and H. S. Joo. 1994. Cessation of porcine reproductive and respiratory syndrome (PRRS) virus spread in a commercial swine herd. Swine Health and Production 2(1): 13-15.

Hill, H. 1996. PRRS: Practical strategies for prevention and management of a positive herd. Proceedings of the 1996 North Carolina Pork Producers Conference pp. 1-7, January 9-10, 1996, Fayetteville, North Carolina.

McCaw, M. 1995. PRRS control: whole herd management concepts and research update. Proceedings of the North Carolina Healthy Hogs Seminar, pp. 57-64, Greenville, North Carolina, U.S.A.

Voicu, I. L., A. Silim, M. Morin, et al. 1994. Interaction of porcine reproductive and respiratory syndrome virus with swine monocytes. Veterinary Record 134: 422-423.

Wensvoort, G., C. Terpstra, JMA Pol, et al. 1991. Mystery swine disease in the Netherlands: The isolation of the Lelystad virus. Vet. Quarterly 13: 121-130.

Yoon, I. J., H. S. Joo, W. T. Christianson, et al. 1992. An indirect fluorescent antibody test for the detection of antibody to swine infertility and respiratory syndrome virus in swine sera. J. Veterinary Diagnostic Investigation 4: 144-147.

Yoon, I. J., H. S. Joo, W. T. Christianson, et al. 1993. Persistent and contact infection in nursery pigs experimentally infected with porcine reproductive and respiratory syndrome (PRRS) virus. Swine Health and Production 1(4): 5-8.