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PRRS
Elimination from Breeding Herds S. C. Henry, DVM, Dipl ABVP, Abilene Animal Hospital, P.A., Abilene, KS It
appears the swine industry and veterinarians have advanced beyond the
management of PRRS infections to the elimination of the virus from
herds. This adoption of
pathogen elimination as the best medical strategy reflects positively on
the progressive profession of swine veterinarians. The first published
suggestion that such a strategy might be possible was from an AASV
practitioner in 1993.1,2
While still far from a simple programmatic exercise, the
concepts, procedures and experiences in PRRSv elimination are being
spelled out by many workers.3-16 This is an astounding pace of progress in management of a
major disease with both high morbidity and mortality effects! PRRSv is
still less than 17 years old and elimination appears to be the impetus. While
we still lack some steps in the process and definition of
‘elimination’, the overarching premises behind the apparent
successes to date include: 1.
Individuals and groups of animals, especially adults, that
apparently develop a sterilizing immunity to the homologous challenge
strain of virus following natural infection. “Sterilizing immunity”
is an immune response that is sufficient to clear the organism from the
previously infected host and also prevents reoccurring infection.
“Sterilizing immunity” is the epitome of immune system barriers to
invading organisms. This ‘gold standard’ is uncommon in animal
immunology but is a most important power in the battle against PRRS. 2.
Development of sterilizing immunity in all animals in the
population is a process of many weeks time and confidence of exposure,
infection, recovery and immunity. 3.
Lengthy post-infection isolation of the target population,
preventing new transmission/infection in naïve additions, is absolutely
necessary. 4.
Subsequently, only animals known to be naïve to PRRSv can be
added to the population. Research
Advances: PRRSv workers recognized early on that understanding
mechanisms of immunity would be key.17 The
significant deficiencies in and risks associated with US PRRSv vaccines
stimulated a study which produced breakthrough understanding of
immunity.18 Clearly,
the late arising neutralizing antibodies with coincidental increase in
cell mediated immunity represented an unconventional response. The
practical significance of this report is a possible explanation for the
observations on virus elimination from populations observed in the
field. In a subsequent
study Osorio supplied passive immunity to susceptible, pregnant sows
through administration of specific immunoglobulins. Complete protection
to challenge was obtained, demonstrating conclusively that neutralizaing
antibodies are a major correlate of protection in PRRSv.19 Clarification
of immunity and infection differences in adults, in contrast to juvenile
pigs is emerging from a whole group of studies underway at the
University of Minnesota. It has been clear for some years that great
variation in measurable antibody exists within sow herds.20
What this means and how it may relate to true sow herd immunity,
on the one hand, and risk as a reservoir of virus on the other are the
questions. Observations collected from these ongoing studies by Dee,
etal, offer several points of clinical importance to elimination efforts
on farms:21 1.
Persistence of
infection in sows and boars is abbreviated in adults in comparison to
congenitally infected piglets. Persistent infection can occur in sows,
although the prevalence of persistence is very low in contrast to
juveniles. Adults are most unlikely to be persistently infected and are
unlikely sources of virus except during acute phases of infection. 2.
Even in the immediate
post-infection period of a few weeks, few adults actually function as
carriers, thus a reduced period of transmission can be assumed during
adult infections in comparison to juvenile infections. Shedding can
occur from carrier sows to naïve contacts following fenceline contact,
and aggressive behavior appears to play a role. Documented periods that
sows can carry and transmit virus are short (49-56 days pi) as compared
to pigs infected congenitally. 3.
Diagnosis of carrier
status or infected status by tonsillar biopsy is unsuccessful. No
testing methodologies are yet available to confidently detect latently
or persistently infected adults, or even to define clearly if they exist
in populations. 4.
With duration of
infectivity being shorter and persistence unlikely, the effect is slow,
and sporadic, transmission of virus through a sow herd. This, obviously,
has increasing ramifications as sow herd size increases. A starting
point for elimination efforts is thus difficult to find if all animals
have not assuredly been infected and thus lack immunity. 5.
Infection of individual
herds with multiple variants of PRRSv virus is documented. The impact of
dual or multiple variant infection on development of the effective,
sterilizing heterologous immunity necessary for elimination is a study
in progress.22 6.
Sequencing of virus
isolates for later reference is advised; lacking such a determination
failures in elimination attempts cannot be characterized as to possible
reasons for failure. Lacking the sequences, one cannot tell if the cause
of infection was failure to eliminate or if a new variant had been
introduced. 7.
Injections are a very
efficient way by which to transmit PRRSv. Contamination of needles
during injection procedures disseminates virus to other animals
subsequently injected with the same needle. Finally,
as PRRSv infections are integrally linked with other pathogens, the
documentation of multi-pathogen mechanisms and disease effects
fundamentally changes prevention and therapy decisions. The relationship
of PRRSv to mycoplasma and streptococci, often clinically concurrent
pathogens, is now much more clearly understood.25,26 Field
observations from our practice: Many client herds in our practice
participate in a systematic approach that we hope will eliminate the
virus from their operations. These herds are diverse in size, genetic
base, operational type and location but all have experienced clinical
PRRSv disease in both adults and in growing animals. Our process in
elimination of PRRSv is actually an outgrowth of earlier control
methods: 1.
PRRSv vaccines are
strongly discouraged. No client herds have been exposed to vaccine, live
or killed, since October of 1996.23 2.
Replacement breeding
animals, whether reared or purchased, male or female, are entered into
the herd at as young an age as possible, preferably as weaned pigs. 3.
Operating, where
possible, nursery through finishing on sites removed from the breeding
herd; in all cases employing conscious segregation. 4.
Minimizing unnecessary
procedures that might transmit infectious body fluids among pigs,
examples being injections, identification and surgery. Our
assessment of these efforts is on several levels. Freedom from clinical
signs of PRRSv infection is a primary evaluation, combined with the
production record. Secondarily, laboratory evidence of infection or lack
thereof is considered. While extensive laboratory evaluations on all
herds would be desirable, it is not economically feasible. Results are
most promising in many herds under a variety of production methods. Most
gratifying of all has been the lack of new cases in sow herds and the
great reduction in nursery infection. While progress is slow, it has
been steady. Premise:
Immunity to homologous PRRS variants appears to be very strong and
effect. Based on work with specific antiserum, protection appears to
provide a “sterilizing immunity” of extended duration. The
development of this level of protection occurs quite late in comparison
to most other immunologic responses with which we are familiar. Thus the
goals are that all animals are infected with, and recover from, the
specific endemic PRRS variant at an early age. Obviously, multiple
variant infections in herds complicate the situation. Yet the process,
to be described in this presentation, continues to be effective in our
practice. Additionally,
some producers are choosing repopulation as a method to eliminate PRRS
but it should be noted this is NOT the primary reason behind the
decision. Instead, there is a desire to both improve genetics as well as
eliminate other diseases, generally App, from the herds. Present
assessment of the effort: Based on serologic screening of nursery pigs
and the testing of sero-negative sentinels, added to the sow herds, we
work with 32 herds that have been affected by PRRS and are now negative
to the best of our assessment through the nursery phase. Twenty-seven of
these herds have become negative through the process of herd roll-over
with immune animals and some have now completed the process of sow herd
replacement with negative animals. Five herds are negative due to
repopulation. At
this point, there are only 2 herds, in addition to these 32, which
failed in the process and experienced reoccurring PRRS infections, in
both cases herds with known multiple variant infections. These herds had
achieved negative nursery flow before reoccurrence of clinical disease. Conclusions:
While the process still lacks sophistication, it appears the simple
steps outlined above are consistently leading to PRRSv negative flow
and, by attrition, negative sow herds. A great deal of caution is still
warranted as the experience of many producers and veterinarians
demonstrates. Avoiding the cost and pathology associated with vaccine,
reduction in medication use and improved performance have all been most
appreciated by producers. We believe this is a disease to eliminate and
not just to manage. These are the early days and additional tools will
be most welcome when they are developed. Nonetheless, we are encouraged
by the success. References
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