PRRS CONTROL: WHOLE HERD MANAGEMENT CONCEPTS AND RESEARCH UPDATE

Monte McCaw
College of Veterinary Medicine
North Carolina State University
Raleigh, NC 27606

Introduction

It is 4 years since the discovery of the virus that causes PRRS and its reentry into the North Carolina Swine Industry. In its wake PRRS has killed countless piglets, caused undetermined levels of production losses and medication costs, and thoroughly frustrated and demoralized pork producers throughout the state. Producers are so frustrated with "the problems with PRRS" that ANY PROBLEM in their herd's production JUST HAS TO BE PRRS! The GOOD NEWS is that not all problems are due to PRRS. Several management tools are now available to prevent or greatly limit losses caused by PRRS and the associated disease complex. The challenge is to refocus our efforts on maximizing attention to production details that had originally placed the North Carolina Swine Industry at the lead and envy of the nation.

We will cover the Problems currently seen with PRRS infection of our herds, the proposed Mechanisms by which these problems occur, and currently practiced Solutions for these problems.

Acute (Explosive) Outbreaks

Problem

Explosive outbreaks of late-term abortions, stillbirths (SB), mummies, weak-born piglets, and astronomical preweaning / nursery mortality rates are less frequent than in past years. This is probably due to 1) a majority of breeding stock sources are now PRRS infected, 2) most hog farms are now PRRS infected (with or WITHOUT clinical signs), and 3) increasing use of the new modified live virus PRRS vaccine.

Mechanisms

Explosive outbreaks occur when the virus enters an uninfected sow herd OR when a new strain is introduced into an infected herd that has a large proportion of PRRS negative breeding animals. Smaller "outbreaks" reoccur in previously infected herds because the original virus has stopped circulating among breeding animals and gilts added to the herd for a year or more were remained PRRS negative. There is also some evidence that indicates that immunity to PRRS is not life-long even after natural infection by wild-type virus, particularly to a different strain. Therefore, clinical signs may also be seen in older parity sows and their litters if a new strain of the virus is introduced into the herd. PRRS enters swine herds most efficiently and frequently in infected breeding stock or feeder pigs. These pigs come from herds in which PRRS is actively circulating in the nursery or finisher, and they can be viremic upon arrival. Viremia lasts for up to 40 days in younger pigs, and viremic pigs are able to shed the virus to other pigs. PRRS can also be shed in the semen of viremic boars and infect sows even by artificial insemination. Therefore the virus can infect negative herds by purchase of semen from boar studs that have viremic boars. Contaminated equipment, especially transport trucks and busses, can also spread PRRS to uninfected herds.

Solutions: Acute outbreak PRRS

Isolation of incoming breeding stock, vaccination of new breeding stock and sows, and careful control of PRRS in boar studs will greatly reduce the risk of acute outbreaks of PRRS. Dr. Scott Dee of Morris, Mn recommends that new breeding stock should be isolated for a MINIMUM of 60 and preferably 90 days before being added to the herd. The time in isolation allows the new stock time to control the PRRS infection and stop shedding the virus and possibly eliminate the infection. During this time they can be bled for PRV and PRRS, exposed to manure from the herd, housed with cull animals from the herd, and finally vaccinated for PRV and PRRS prior to entry into the herd. If you produce your own gilt replacements, run the gilt grow-out buildings all-in all-out in an attempt to mimic isolation procedures. This will hopefully allow gilts to clear the infection by the time of selection. They can be vaccinated for PRRS and PRV near the end of the grow-out phase. Use of the NOBL modified live virus PRRS vaccine, RespPRRS, is only approved for pigs between the ages of 3 to 18 weeks of age. However, due to the devastating losses that occur with outbreaks of PRRS, many veterinarians and producers have decided to accept the risk that the vaccine itself, could under limited conditions, cause some disease losses. Vaccination of sows seems to be safest and most effective when they are vaccinated at 60 to 70 days gestation and at 14 days post-farrowing (field observations by many Midwest veterinarians). Gilts should be vaccinated twice, once before entry into the herd, a second time 21 days later, and then bred 42 days after the first injection.

Boars can apparently be vaccinated at entry (or before) and a second time 21 days later, waiting at least 28 days before using them for breeding. Recent research by David Benfield and others at South Dakota State University indicates vaccine virus can be detected in their semen for up to 28 days after vaccination. The significance of this finding is unknown, but waiting for 1 month after the second vaccination before using new boars for breeding may be prudent. Vaccination of boars in Benfield's study and two others prevented virus excretion in semen or reduced the number of days PRRS was found in semen after challenge.

Chronic (long-term or reoccurring) PRRS-associated disease complex

Problem

Currently the most common problem with PRRS is long-term farrowing house / nursery disease and death losses. These pigs have scours, pneumonia, rhinitis, or brain infections / central nervous system signs. Sick pigs respond poorly, if at all, to antibiotic treatment. Preweaning mortality runs 15 to 30% and nursery mortality runs between 4 to 15%. Average nursery close-out weights fall to 40 pounds instead of 50 pounds at ten weeks of age. More pigs have to be held back because of reduced rate of gain.

Sporadic spikes of late term abortion, mummies and stillbirths are also reported. Regular (21 days) and irregular returns to estrus are reported from infected herds, but there is no evidence that PRRS can directly cause early embryonic death. PRRS has been shown to cause a temporary decrease in sperm quality after initial infection of boars. Fever associated with PRRS infection may prevent gilts from becoming pregnant. However, these two factors are very unlikely to continue occurring in a herd for weeks or months, like the reported regular return problems apparently have. Regular returns are almost exclusively a problem with breeding management which is tightly tied to worker morale, according Drs Glen Almond and Jack Britt, reproductive physiologists in the College of Veterinary Medicine.

Mechansims

PRRS can infect fetuses in utero ("vertically") causing direct death of the fetus (stillbirths or mummies) or the birth of weakborn and viremic (infected) piglets. The piglets infected in utero can shed the virus and infect other penmates "horizontally" after birth. However, PRRS VIRUS INFECTION AFTER BIRTH DOES NOT KILL PIGLETS!! PRRS seems to help secondary bacteria to infect, cause disease, and kill piglets after birth by infecting and killing important immune system cells called macrophages. This conclusion appears obvious, since herds have severe disease losses when they get infected with PRRS. Also, PRRS is frequently isolated from sick pigs in these herds seeing long-term farrowing / nursery disease losses. However, the "hypothesis" that PRRS makes pigs more susceptible to secondary bacterial infections cannot be proven experimentally.

Another critical concept in trying to control PRRS in chronically diseased herds is PIGLETS ARE BORN BACTERIA FREE. Therefore piglets are getting secondary bacterial diseases and are dying because of bacterial infections they get AFTER they are born.

These two principles become very important in light of our observation that a litter in a herd experiencing severe losses during a PRRS outbreak was left untreated so the piglets could be submitted to the diagnostic laboratory. When other treated litters were having severe disease and mortality, this litter remained perfectly healthy! Subsequently more "test" litters were left untreated, and were much healthier than the litters given antibiotic treatment. Therefore, in that herd, handling piglets to give them antibiotic treatments actually increased the amount of disease in those litters! The workers probably got large amounts of bacteria on their hands after handling severely sick piglets, like the sticky material on scouring piglets, which they then rubbed on other piglets. More importantly, while moving piglets between litters to match body size to help sick piglets survive, workers probably infected other, healthy piglets with massive amounts of bacteria. These healthy piglets subsequently become sick from these bacterial infections because of 1) increased susceptibility or "immunosuppression" apparently caused by PRRS infection or 2) overwhelming bacterial exposure from crossfostered "Typhoid Mary" sick pigs. The increased number of sick pigs and mortality caused by crossfostering "Typhoid Mary's" may not be seen until they reach the nursery.

The source of continued virus circulation in the herds comes from two sources, the nursery where pigs transmit the virus horizontally to younger pigs, and from the sow herd where sows, gilts, and boars exchange the virus horizontally and viremic sows then infect their piglets vertically.

Sporadic spikes of reproductive disease (late-term abortions, stillbirths, and mummies) occur when potentially new strains of the virus (by animals or semen) or just viremic animals are introduced into the sow herd. This is particularly true if many PRRS negative gilts were previously introduced into the herd resulting in a group of susceptible sows. These susceptible animals become infected, shed virus to other sows, and show signs of reproductive disease or their piglets have typical PRRS-associated disease and mortality.

Solutions: Chronic PRRS-associated disease complex

Very rapid control of farrowing house disease losses, and control of nursery losses once the new, "healthy" groups of pigs enter the nursery can be obtained using the following "McREBEL" management procedures developed at the NCSU College of Veterinary Medicine. These procedures work in herds that have individual rooms for different age groups in both farrowing and nursery that can be operated all-in all-out.

McREBEL Procedures:

(Management Changes to Reduce Exposure to Bacteria to Eliminate Losses for PRRS-associated disease control in farrowing and nursery pigs)

Control / prevention of sow herd virus circulation

See SOLUTIONS for Acute Outbreak of PRRS above

New Research Developments

Distinct differences (genetic and antigenic) have been demonstrated between different isolates of PRRS across North America and across Europe. These differences definitely affect PRRS diagnosis (false negative results are possible on most antibody tests) and probably affect immune response (protection by vaccination against different strains).

Six of eight segments of the PRRS virus genome have been isolated. The proteins these segments code for have been produced experimentally in pure preparations, a major accomplishment!. Pure viral protein preparations produced in this manner are being used to study which proteins are important for protective immunity. Once the protective proteins are identified they may be combined in high tech "safe" killed vaccines or genetically engineered modified live PRRS virus strains can be produced that will be safe and that will protect across many different strains of PRRS.

PRRS virus infection is combining with Swine Influenza Virus and / or Porcine Respiratory Corona Virus to produce respiratory disease complexes in nursery and finishing pigs. These respiratory disease complexes can be very severe, and do not respond to vaccination with PRRS vaccine alone.

It is very difficult to experimentally recreate the PRRS and secondary bacteria disease complexes that are found in production swine herds. This difficulty may slow the development of proper control methods for the PRRS disease complexes. Some researchers questioned whether PRRS acts alone in triggering the secondary bacterial disease problems that producers have to fight.

Gilts were infected with PRRS by using EXTENDED SEMEN from experimentally infected boars or using semen to which PRRS virus was added after collection from uninfected boars. This infection had no effect on the gilt's ability to become pregnant.

PRRS virus can be detected from semen of infected AND vaccinated boars by PCR (polymerase chain reaction test for viral RNA or genes). Vaccine virus can be found up to 28 days after initial infection. Wild-type virus can be found for over 90 days after infection in semen by PCR. Vaccination before infection with wild-type virus either prevented or greatly reduced the number of days that virus was detected in semen after challenge.

Successful management procedures were reported that controlled PRRS associated disease losses in production swine herds. The procedures were severely limiting cross-fostering or total nursery depopulation.

PRRS ELISA developments (Dr. Gene Erickson, Rollins Laboratory)

Positive samples have S/P (sample-to-positive) ratios greater than 0.40.

S/P ratios greater than 2.25 may come from animals that are viremic (have virus in their blood and can transmit the virus to other animals). Gilts or boars with S/P ratios greater than 3.5 are usually viremic, and are the most likely type of animal to spread PRRS to other animals in your herd.

Vaccinated sow herd S/P ratios range from 0.7 to 2.0. Approximately 20% of animals will be seronegative within 60 days after vaccination. Nearly all vaccinated pigs will be seronegative by 4 months after vaccination IF they have not been exposed to wild-type virus.

Weaned pigs that have not become infected with PRRS will have S/P ratios of 0.4 to 0.7 at 4 weeks of age due to passive antibody from colostrum, and will be antibody or ELISA S/P negative at 6 weeks of age. If virus is circulating in the nursery, ELISA S/P ratios will begin to be positive at 7 weeks of age with many pigs carrying PRRS antibody. By 9 to 10 weeks of age all pigs will be ELISA positive with S/P ratios greater than 2.0 and most pigs are viremic and shedding virus.

Take-Home Message

Cross-fostering can increase spread of PRRS-associated disease problems.

McREBEL management procedures or limiting cross-fostering in herds with PRRS-associated disease complex can rapidly control disease losses and return your herd to normal levels of production quickly.

Piglets need to be vaccinated once or twice (depending on at what age and how severe the PRRS exposure level is in the nursery), commonly at 7 days and / or at weaning. Piglets have been vaccinated intranasally or intramuscularly at 7 days old and intramuscularly at weaning.

Virus circulation in the sow herd can cause sporadic abortions or restart piglet disease losses in lactation or the nursery.

Virus circulation in the sow herd can reoccur after the original outbreak because of introduction of new viremic gilts and boars that infect a built-up group of PRRS susceptible gilts and sows in the breeding herd.

Isolation of breeding stock for 60 days minimum before introduction into your herd is critical. If you produce your own gilt replacements try to operate gilt developers as close to all-in all-out as possible to allow them time to control the PRRS infection.

Vaccination of the sow herd attempts to make sure sows are immune and resistant to the disease. The immunity stimulated by vaccination is not life-long. Vaccination twice per reproductive cycle seems to be necessary.

Vaccination of sows seems to be safest and most effective when they are vaccinated at 60 to 70 days gestation and at 14 days post-farrowing. This is not an approved use of the vaccine. A new vaccine approved for use in sows may be available early in 1996.

No evidence exists to show that vaccination of viremic (recently infected) animals reduces the likelihood of shedding the virus to other animals or reduces the clinical signs seen in viremic pigs. I.E., depend more upon isolation than vaccination of incoming breeding stock to protect your herd from recently infected viremic gilts and boars.

Vaccination of boars reduces the number of days they shed virus (or prevented virus shedding) in their semen after infection with wild-type virus. Vaccine virus is found in the semen for up to 28 days after the first vaccination in some boars.

Isolation of new breeding stock, vaccination of the sow herd, controlling virus circulation in boar studs, and sanitation of delivery trucks should help control long-term or endemic PRRS-associated disease losses.

PRRS is NOT the cause of all, or probably most, of the current disease problems seen in North Carolina swine herds!! A thorough diagnostic work-up of your farm's problems and an evaluation of your management procedures are needed before you can conclude that PRRS is the cause of your herds' problems.