Research News
Experimental models of secondary bacterial infection
following PRRSV infection have now been established. Mycoplasma
hyopneumoniae infection or challenge after PRRSV infection increases
the duration of PRRSV pneumonia lesions in weaned pigs. The reported
slowing of PRRSV pneumonia lesion healing caused by Mycoplasma
infection may be one type of pathogen cooperation that contributes
to Porcine Respiratory Disease Complex. The time at which pigs
were infected with Mycoplasma relative to PRRSV infection did
not seem to matter for causing increased PRRSV pneumonia lesions.
We demonstrated last year that in utero infection
of piglets by PRRSV greatly increased their susceptibility to
Streptococcus suis disease after challenge at 5 days of age.
Only 1 or 4 pigs died following infection with either PRRSV or
Strep. suis alone. However, 20 of 22 pigs died which were infected
with PRRSV in utero and then challenged with Strep. suis at 5
days of age. This year we evaluated some of the immune system
cells and organs of piglets infected with PRRSV in utero. At
birth and up to two weeks of age the thymus (lymphocyte immune
cell maturing organ) of PRRSV infected piglets was only half the
size of the thymus of uninfected pigs. The distribution of lymphocytes
still in the thymus and also in the blood of the PRRSV infected
piglets was greatly reversed, showing a CD 8 : CD 4 ratio of 12
: 1. This shift in CD 4 : CD 8 ratio is similar to that which
occurs in AIDS patients who also become sick with many different
secondary bacterial diseases. These observations underscore the
need to not foster piglets between litters during PRRS outbreaks
as outlined by McREBEL PRRS management procedures. The observed
changes in immune cells may account for infected piglets' increased
susceptibility to secondary bacterial diseases. The infected
piglets are much less able to fight off additional infections
they may encounter after being moved to a new litter by fostering.
While the occurrence of secondary bacterial diseases following
the viral infection is similar between PRRSV and AIDS, PRRSV is
not an AIDS-type virus. We are continuing to study what changes
PRRSV causes in the function of the immune cells of the newborn
pig, and how long these changes will last. These studies have
been funded by a three-year cooperatively funded grant from the
North Carolina Pork Producer's Council as well as the College
of Veterinary Medicine and College of Agriculture and Life Sciences
of NCSU.
French researchers have just reported the ability
of PRRSV infection to block an innate defense mechanism of cells
to resist infection by viruses. This blockage also was shown
to "help" another virus (TGE) infect and grow in the
cell culture experiment. This ability to block the body's defense
against virus infection may be an important explanation of why
PRRSV can be found in the blood of pigs days or weeks after initial
infection. We have yet to see proof of whether this property
of PRRSV "helps" other virus infections that contribute
to the Porcine Respiratory Disease Complex such as Influenza
virus or Respiratory Corona Virus.
Acute PRRS has apparently stopped occurring (or being
reported), at least for the time being. A total of 31 herds participated
in a nation-wide study of management practices and herd characteristics
used in affected herds. The viruses isolated from these herds
will be released for scientific study early in 1999. Many other
affected herds chose to not participate in the study. Nearly
all of the affected herds had been vaccinated with one or both
(including the three herds in North Carolina) of the modified
live PRRSV vaccines. The existence of PRRSV strains that are
not covered by protection stimulated by the available vaccines
tragically highlights the need for appropriate biosecurity measures
to be established and followed even in vaccinated herds.
Clinical disease outbreaks of abortion and high preweaning
mortality were observed in Danish pig herds after vaccination
with the American strain vaccine, RESPPRRS. This vaccine was
not approved in Denmark (or in the US) for use in pregnant sows.
However, by vaccinating pigs in the nursery and finishers of
European strain infected herds in Denmark, the virus apparently
was introduced by vaccinated gilts into and spread among pregnant
sows in the gestation barn. It appears the Danish pigs had insufficient
protection against American strain PRRSV infection following their
initial infection by the European strain PRRS. Therefore, we must
use extreme caution when deciding to vaccinate PRRSV-free herds
for the first time since the vaccine virus is known to be shed
from recently vaccinated animals. The vaccine virus infection
could spread in naive herds to unvaccinated pregnant animals
and cause reproductive losses.
Researchers at South Dakota State University have
demonstrated that piglets infected in utero with PRRSV carry and
shed the virus much longer than pigs infected with the virus after
birth. Normally pigs have PRRSV in their blood up to 40 days
after infection. The new research found PRRSV by PCR in the blood
of in utero infected pigs up to 150 days of age. Obviously, this
is not yet breeding age, but the study was also only performed
on a limited number of pigs infected at a single stage of gestation.
To date, when study pigs were found to have virus in their blood,
they were also antibody positive by the PRRS ELISA. This study
suggests caution when buying breeding stock, particularly boars
for use in studs, from herds which had clinical signs of PRRS
when those animals were born. Much more work is needed before
we know all the limitations or abilities of PRRSV to cause long-term
or persistent infections in individuals and the ability of these
individuals to infect others long after the initial in utero infection.
A plan for eradicating PRRSV from infected sow herds
has been reported by Dr. Scott Dee. He has used three PRRSV diagnostic
tests in combination to first find antibody positive animals,
and then confirm current infection in the animals by using PCR
on blood samples. He has apparently eliminated PRRSV from a large
sow herd using these techniques. However, two major points must
be recognized. First, one must be certain they have a very solid
biosecurity program to prevent reintroduction of PRRSV into the
herd. Secondly, the herd that Dr. Dee worked with was unvaccinated
at the time of the original outbreak of clinical disease. Therefore,
that particular strain of PRRSV could have moved rapidly between
animals in the herd, potentially infecting and therefore "immunizing"
all of them at the same time. This situation may have contributed
significantly to the necessary end of virus circulation between
sows of the herd. We have observed sows in two different UNVACCINATED
large sow herds in North Carolina return to basically seronegative
status after outbreaks of PRRS. Introduction of new gilts into
the herd in Dr. Dee's report was strictly controlled following
the outbreak as well. Therefore, his technique is not yet proven
to work (remove virus infected sows faster than they are "created")
within herds which have been vaccinating for long periods of time
that still have repeated losses of PRRS. Also, candidate farms
should have been practicing successful acclimatization of new
gilts for at least a year before attempting PRRSV eradication
by this method. Finally, serologic testing of all sows in the
herd and the necessary follow-up with PCR is very expensive.
We must be certain that we can recover these costs by increased
production and profitability over that obtainable with traditional
PRRS control measures of McREBEL, vaccination, nursery depopulation,
and gilt isolation / acclimatization.
On-farm PRRS Control Measures
New breeding stock introductions MUST be ISOLATED
for a MINIMUM of 60 DAYS in an isolation unit run strictly All
In - All Out. Acclimatization of these animals can be accomplished
at the same time without any need to move them after 30 days.
These "units" do not need to be fancy, but they must
be separate from the herd. Two separated units are best to supply
gilts on a monthly basis. Adding new animals into the same room
30 days after entry of the first group of gilts appears to neutralize
any advantages obtained by isolation for PRRS control. To acclimatize
new animals, add culled gilts, sows, or nursery pigs from your
farm (if PRRSV is known to be circulating there) to the isolation
unit when new gilts and boars arrive. These cull animals will
hopefully expose, infect, and immunize the new stock to the strain
of PRRS (and any other significant pathogens) in your herd.
You are attempting to make sure these gilts are not "susceptible"
when they enter and therefore contribute to continuation of virus
circulation within the breeding herd. These practices are NECESSARY
for long term PRRSV prevention and control since there are certainly
new strains of PRRS present which are not "covered"
by currently available vaccines. Also, it appears that viremic
piglets born to sows recently infected by PRRSV are likely sources
of virus and bacteria that initiate disease losses in the nursery.
Therefore, control of virus circulation in the sow herd is critical
to long-term nursery disease control.
Minimize the number of different breeding stock source
farms that you purchase your replacements from. This will maximize
the likelihood these animals will be immune to the strain of virus
already in your herd, and minimize the chance they will introduce
new strains into your herd. If you must change source herds,
try to get diagnostic confirmation that the herd has not experienced
virus circulation within the past year in either the breeding
herd or growing pigs.
During PRRS outbreaks do not vaccinate sows or piglets.
Late-term vaccination of sows can lead to fetal infection by
vaccine strain virus. Piglets will often be born virus infected
during PRRS outbreaks. McREBEL management in the farrowing house
will minimize the amount of death and disease without the cost
of vaccination. If the herd was already vaccinated it is obvious
that the vaccine was not effective anyway. It may be best to
let the infection spread uninhibited through even unvaccinated
herds at the time of the outbreak. It appears that if most sows
and replacement gilts get infected during the outbreak, they all
become immune at the same time. We observed an end of virus circulation
(sows went seronegative within 6 months) within two large North
Carolina sow farms which had allowed the disease to spread. This
method of disease management is similar to the control measures
recommended for TGE outbreaks. Taking some increased short term
losses during the PRRS outbreak as a result of spreading the infection
throughout the herd may prove to be successful for LONG TERM PRRS
control within herds that successfully acclimatize future gilt
additions.
To determine whether your PRRS control program is
working, you must have your veterinarian regularly test for antibody
levels of pigs in several different age groups. Test sows of
all parities just prior to farrowing (if you are vaccinating during
lactation), 10 week old nursery pigs, and developing gilts at
16and 24 weeks old. Test 30 sows and 10 to 20 pigs per age group
quarterly. Test all incoming breeding stock as they enter isolation
and again 2 weeks prior to ending isolation / acclimatization.
The long-tern goal is to develop a management program that will
end virus circulation among sows in the breeding herd. Once this
occurs, virus circulation among nursery pigs can also stop.
