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
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.
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
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
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.
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
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.
(Management Changes to Reduce Exposure to Bacteria to Eliminate Losses for PRRS-associated disease control in farrowing and nursery pigs)
Nursery depopulation has been shown by Dr. Scott Dee, Morris MN, to be very effective in eliminating PRRS and the associated bacterial disease losses, particularly in continuous flow nurseries (McREBEL will probably not work in continuous flow nurseries). Depopulation eliminates the virus as well as the bacterial disease problems from these nurseries. McREBEL management will usually eliminates the disease losses, but it does not immediately eliminate the virus from the nursery. PRRS virus circulation returned in 50% of the nurseries that were depopulated, but disease losses so far have not returned if all-in all out management procedures are followed.
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
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
PRRS ELISA developments (Dr. Gene Erickson, Rollins Laboratory)
Positive samples have S/P (sample-to-positive) ratios greater
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.
Cross-fostering can increase spread of PRRS-associated disease
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
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
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
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
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.