Porcine reproductive and respiratory syndrome (PRRS) continues to be an economically significant disease for the global swine industry. First identified in the late 1980s, it still frustrates pork producers and veterinarians around the world.
The PRRS virus can produce both a reproductive form of the disease in the breeding herd and a respiratory form in nursery and finishing pigs. Clinical signs of PRRS virus-induced reproductive disease include third trimester abortion, premature farrowing, higher levels of stillbirths, mummies and preweaning mortality.
The focus of this article, the respiratory form of PRRS, has been documented to induce annual losses of approximately $228/inventoried sow, secondary to poor growth rates, elevated mortality, reduced feed efficiency and increased postweaning treatment costs/pig.
The respiratory form of PRRS typically includes concurrent infection of PRRS virus and any number of opportunistic pathogens of a viral and/or bacterial nature. Common clinical signs include elevated levels of meningitis and septicemia in the nursery, due to PRRS virus co-infection with Streptococcus suis, Actinobacillus suis or Haemophilus parasuis.
In finishing, pneumonia may be due to infection with PRRS virus and swine influenza virus, Mycoplasmal pneumonia, Salmonella choleraesuis, or Actinobacillus pleuropneumonia.
The essential element in controlling the respiratory form of PRRS is the production of pigs that are free of the virus at weaning. In order to consistently achieve this high level of health, we must understand how PRRS is transmitted throughout the breeding herd and weaned pig populations, and how to accurately diagnose the point of infection in the pig's life.
In most chronically infected farms, uncontrolled circulation of PRRS virus occurs in the breeding herd. These farms experience repeat outbreaks of PRRS-related reproductive disease that is often specific to gilt parities, along with the respiratory form of PRRS in weaned pigs.
PRRS infection of the nursery pig typically begins early in life, either by transplacental transmission (vertical spread) or from sow-to-pig (horizontal transmission) before weaning. Litters of infected pigs then provide a source of virus for older pigs in the nursery, leading to continuous cycling of virus throughout the population. Understanding these transmission factors is key to “stabilizing” the breeding herd.
Stability for PRRS is a frequently misunderstood concept and is often an improperly used term. In this article, a stable breeding herd is defined as a population of adult swine and their offspring, within which there is no detectable evidence of sow-to-sow or sow-to-pig transmission of the virus.
Following is a summary of current scientific work and review of “take home messages” from eight studies.
PRRS virus persists in boars.
PRRS virus produces persistent infections of the male reproductive tract and can be shed through semen. The increasing world dependence on the use of artificial insemination makes this a key point in PRRS control.
PRRS virus subpopulations exist in chronically infected breeding herds.
Within infected breeding herds, PRRS-positive and PRRS-naïve adult hogs can coexist. PRRS antibody testing of randomly selected sows has shown that while certain animals remain seronegative, others become seropositive. This suggests that while viral transmission occurs in the breeding herd, it is very sporadic and viral exposure is inconsistent. This is particularly evident in large, 1,000-plus-sow breeding herds.
Improper replacement gilt management plays a major role in the maintenance of PRRS virus spread.
Similar to porcine parvovirus, uncontrolled introduction of PRRS-naïve or acutely infected gilts perpetuates circulation of the virus within the breeding herd. The result is repeat cases of PRRS reproductive disease and the preservation of PRRS subpopulations — groups of uneven health status within the herd.
Closing the breeding herd reduces PRRS virus circulation.
Field data suggests an internal multiplication program or a four-month ban on replacement stock entries, together with segregation of gilt and sow herds, reduced PRRS spread and exposure in both groups. This improved level of stability in the breeding herd allowed for successful depopulation of the nursery and improvement of pig performance.
Different PRRS strains can co-exist in a single infected farm.
Molecular sequencing of PRRS virus isolates from chronically infected farms has indicated that three genetically diverse strains of PRRS could co-exist and circulate within a farm. Further evidence from the University of Minnesota Veterinary Diagnostic Laboratory suggests that up to five different strains have been detected in a single farm.
The prevalence of PRRS-positive carrier sows in chronically infected breeding herds can be extremely low.
Results from an infected breeding herd that had been closed to introductions of breeding stock for more than six months indicated that the level of chronically infected breeding animals was low (1.7%). The virus was isolated from lymph nodes of an infected sow. Experimental infection of naïve, 95-day pregnant sows using this isolate produced either clinically affected litters of fetuses, or entire litters of fetuses that appeared normal but were infected with PRRS virus.
Persistently infected sows can shed PRRS virus to naïve sows.
Long-term, persistent PRRS infection can occur in sows, and these sows serve as a source of PRRS for naïve sows. In experimental infection of 12 sows, viral shedding was detected from infected sows to naïve sows that were separated from each other by a fence, 49, 56, and 86 days later. Nine sows that didn't shed were sacrificed; persistent PRRS virus was detected in multiple tissues of all nine sows.
PRRS spread occurs readily in weaned pigs.
There are a number of ways PRRS virus can spread between nursery rooms, even with all-in, all-out (AIAO) pig flow. This is particularly true if facilities contain multiple rooms and different ages of pigs.
A source of PRRS virus for recently weaned pigs is lateral transmission of PRRS from older, previously infected, 8- to 10-week-old pigs. Besides pigs, mechanical transmission of the virus can occur following exposure to contaminated coveralls, boots and needles.
Although people do not appear to serve as carriers, PRRS has been recovered from hands following direct contact with experimentally infected pigs. Following hand washing with soap and warm water, the virus was eliminated.
To control PRRS infections postweaning, it's crucial to use diagnostic testing to target when the pig is becoming infected. New tests such as polymerase chain reaction (PCR) and molecular sequencing have proven to be very helpful in understanding patterns of PRRS virus transmission within and between infected farms. The PCR test is much more sensitive than virus isolation, and results are available in a shorter period of time (24-48 hours). Molecular sequencing assists in identifying potential sources of new viral introduction to farms and differentiation of field isolates from vaccine virus.
Regarding the detection of PRRS antibodies, the IDEXX ELISA test is a serologic test used routinely in diagnostic laboratories worldwide. The ELISA (enzyme-linked immunosorbent assay) test detects the formation of PRRS virus antibodies 9-13 days after virus exposure. Results are reported in the form of a sample to positive (s/p) ratio; levels of 0.4 or higher are considered positive. Cross-sectional sampling by ELISA according to stage of production can be useful to determine the point of infection in the pig's life.
For a serological profile, collect 10 samples from the breeding herd, from recently weaned pigs, from 8- to 10-week-old nursery pigs and 5- to 6-month-old finishers. Larger breeding herds (>1,000 sows) may require larger sample sizes, such as 30 or 60. Sampling by parity may indicate whether a specific subpopulation within the herd, such as gilts, is susceptible to infection.
Your veterinarian can assist you in determining the proper number of samples to collect, according to herd size and your available budget.
Finally, realize that PRRS infection alone may have little impact on performance. Therefore, it is important to use clinical observations and production records, in conjunction with diagnostic data, to properly evaluate the impact of PRRS in your herd. Once the pattern of virus spread and the age in which the pigs are infected is determined, intervention strategies can be initiated.
Vaccine Control of PRRS
Due to the need for cell-mediated immunity to control PRRS, modified-live virus (MLV) vaccines are far superior to killed preparations.
While MLV products have the potential to shed in naïve populations following first herd vaccination, transmission of vaccine virus is not readily detected following revaccination with the same (homologous) vaccine strain.
Diagnostic profiling is especially critical when vaccinating to avoid immunizing pigs already infected, and to start vaccination at least four weeks before infection.
Proper handling of MLV vaccines is important to enhance viability and efficacy of the vaccination process.
As well, an adequate needle length is vital to insuring proper intramuscular administration. A 1½-in. needle is required for adult breeding animals; a 1-in. needle is required for finishers and a ½-in. needle for nursery pigs. The product must be rehydrated using the proper diluent, and administered within 24 hours following hydration. Using a designated syringe, rinsed with only with hot water (not disinfectant), is important to vaccine efficacy.
Besides the introduction of PRRS virus by infected pigs at weaning, PRRS can circulate in the nursery by the shedding of the virus from older, infected pigs to younger, susceptible pigs.
Nursery depopulation is a cost-effective way to stop lateral PRRS spread and control of the respiratory form of PRRS. Major advances in nursery pig daily gain, mortality, treatment cost and profitability have been published, following implementation of this strategy (Table 1).
The protocol of nursery depopulation consists of emptying all nursery rooms on a given day, washing and disinfecting each room and allowing the entire facility to remain empty for at least two days.
Due to the poor viability of PRRS virus outside the pig, extended periods of downtime can be avoided, enhancing facility utilization and still succeeding in virus elimination.
Disinfectants recommended include phenolic- or formaldehyde-based products, shown to reduce survivability of the virus in the environment. This strategy also works in PRRS-infected finishing groups.
The positive response to nursery depopulation has resulted in the practice of flowing eight-week batches of weaned pigs into facilities designed for AIAO, allowing for a regularly scheduled depopulation of the nursery every eight weeks.
Due to the potential of contaminated boots, coveralls, needles and hands to serve as mechanical vectors of PRRS, producers should frequently change needles, ideally between every sow, litter of nursing piglets and between pens of weaned pigs. This is especially critical in times of high susceptibility to PRRS infection, such as sows in the third trimester of gestation, or during periods of high virus load, when nursery pigs are 6-8 weeks old.
Furthermore, when producers are finished working with clinically affected pigs, they should change clothes, boots, and wash hands prior to contacting susceptible animals.
Producers should also avoid mixing poor-doing, older animals with younger stock, to reduce viral spread from room-to-room, and avoid disruption of AIAO pig flow.
Finally, ensure that nursery room ventilation systems are functioning properly for adequate air flow to pigs of all ages throughout the year.
While nursery or finisher depopulation is very effective in eliminating postweaning PRRS infection, reinfection can occur following addition of infected weaners.
Therefore, elimination of persistently infected breeding animals, in conjunction with nursery and/or finisher depopulation can eliminate PRRS.
Test and removal was the first successful strategy for PRRS elimination. Test and removal consists of blood-testing the entire breeding herd in a single day, identifying PRRS-infected animals using both an antibody (ELISA) and a virus (PCR) test, and immediately removing positive animals from the farm. Limitations of this approach include a high degree of labor involved in a whole herd test, and diagnostic costs that approach $10/tested sow. Furthermore, a low seroprevalence (<10 %) of ELISA positive sows is required to reduce the impact of animal removal.
Postweaning PRRS infection still plays a major role in the porcine respiratory disease complex. Multiple tools for the diagnosis, control and eradication, along with new information on the epidemiology of the virus have enhanced the ability of producers and practitioners to reduce the economic impact of the disease.
Yet many questions still remain unanswered, and scientists throughout North America must work together to bring the knowledge to the industry as quickly as possible.
More information regarding the immunology and transmission of the virus, the availability of diagnostic tests to detect carriers and differentiate antibody responses produced from vaccine (vs.) infection are just a few critical, missing puzzle pieces.
Table 1. Mean Differences in Pig Performance from 34 Nurseries 12 Months Before and 12 Months After Nursery Depopulation.
|Group||#Farms||ADG (lb.)||Mortality||Feed:Gain||Treatment cost/pig**|
|**= Total cost of injectable and water soluble antibiotics and vaccines on a per pig basis.|