Field Experiences with Different Methods of Controlling PRRS … · Field Experiences with...

Field Experiences with Different Methods of Controlling PRRS Virus

Management Changes to Reduce Exposure to Bacteria andEliminate Losses (McREBELTM)

by M McCaw

Control in Large SystemsMA FitzSimmons and CS Daniels

Control Using Oropharyngeal Scraping InoculationG Allison

Control with Modified-Live Virus (MLV) PRRS VaccineTG Gillespie

Control with Inactivated Virus PRRS VaccineE Thacker, B Thacker, W Wilson, and M Ackerman

Eradication Using Herd ClosureM Torremorell, S Henry, and WT Christianson

These approaches and techniques have not necessarily been rigorously tested under scientifically valid conditions and may not beappropriate for all herds. Therefore, readers are strongly encouraged to fully consider the merits, drawbacks, and implications of thesemethods prior to applying them in the field. These views are solely those of the author, and are not approved by the National Pork Board.

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Management Changes to Reduce Exposure to Bacteria andEliminate Losses (McREBELTM)

by M McCaw

Introduction

Optimization of herd health and productionefficiency begins at birth. Set-backs to the pigletduring lactation, particularly by PRRS virus incombination with secondary infections, will affectlater stages of production and may predispose pigs toadditional health problems. McREBELTM

management initially evolved from an attempt tocontrol pre-weaning mortality and regain healthygrowth during an outbreak of reproductive PRRS thathad lasted for 18 months (McCaw, 1995). Theunderlying philosophy of this approach is thatoptimization of suckling piglet growth requiresminimizing interventions and maximizing supportivecare. McREBELTM facilitates both and optimizes thegrowth of the suckling pig, as evidenced by increasedweaning weights, decreased pre-weaning mortalityand nursery mortality, and increased average nurseryclose-out weights vs traditional multiple cross-fostering management (McCaw, 2000a). Laterapplications of McREBELTM and field research haveshown its usefulness for meeting the needs of thesuckling pig, and, therefore, optimizing the survivaland growth of healthy pigs (McCaw, 2000b). Theseeffects are observed both in PRRS-affected andunaffected herds, although to different degrees,depending upon the herd’s general health status.

Control of Clinical PRRS

PRRS virus outbreaks were initially reported in NorthCarolina in the late 1980's (Dial et al., 1990).Clinical signs observed during the epidemic includedsows off-feed, mid- to late-term abortions occurringwith, and then followed by, increased numbers ofstillbirths and mummified fetuses of decreasing size(Loula, 1991). Concurrent with the reproductivebreaks was a marked increase in pre-weaningmortality among piglets born during the outbreak.Antibiotic treatments and supportive care of thesepiglets produced little or no response. Efforts thatcross-fostered poor-doing, sick piglets on to “good-milking” sows to minimize competition from largerpigs produced particularly poor results (McCaw,1995). Affected piglets and weaned pigs typicallyshowed signs of secondary bacterial infections withStreptococcus suis, Haemophilus parasuis, E. coli,Pasturella multocida type D, Bordetellabronchiseptica, Actinobacillus pleuropneumoniae,

and/or other opportunistic pathogens (Done andPaton, 1995; Stevenson et al., 1993).

In 1991, it was demonstrated that PRRS was causedby a virus that grew in swine lung macrophages.Koch's postulates were fulfilled when it was shownthat infecting susceptible pregnant sows with thevirus caused fetal death and the weak-born pigletsyndrome (Terpstra et al., 1991). Verticaltransmission by in utero infection of fetuses was alsoproven in those initial studies, although it was notrealized at the time how important in utero PRRSvirus infection was to subsequent acute and chronicPRRS in nursery pigs and finishers ( Benfield, 1997;Feng et al., 2001; Segalés and McCaw, 2002) Earlyempirical evidence came from the observation that itwas necessary to stop virus circulation (horizontaltransmission) in sow herds in order to improvenursery health. Keffaber et al. (1992) found nurserydepopulation alone to be ineffective in the controlPRRS virus-associated disease losses. Nurserydepopulation for controlling PRRS-associateddiseases was only successful in "stable" sow herds(Dee and Joo, 1994). The lesson to be learned wasthat stopping horizontal transmission between sowsdecreased the occurrence of infected sowstransmitting the virus vertically to their unborn orsuckling offspring. Afterwards, it became possible tosuccessfully eliminate PRRS virus by nurserydepopulation and subsequently sustain the PRRSvirus-free status of the nursery.

An approach was needed to help swine producerscontrol PRRS-associated losses in the farrowinghouse and nursery during the early phases of a PRRSoutbreak. Obviously, nursery depopulation didnothing to improve PRRS-related morbidity andmortality in suckling piglets. In addition, on-goingnursery pig disease losses needed to be controlledduring the four months or more required for the sowherd to “stabilize” so that depopulation of the nurserycould be successful (Dee and Joo, 1994). Aggressiveantibiotic treatment of piglets and heroic efforts tocross-foster unhealthy, weak piglets onto nurse-sowsfor intensive care failed miserably to control themeningitis, arthritis, or scours, much less returnpiglets to normal growth rates and deliver healthyweaned pigs to the nursery (M McCaw, personal


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observations). Frequent handling and treatment ofpiglets contributed to the problem by spreadingbacterial pathogens and PRRS virus to other littersvia pathogen-contaminated personnel and equipment(McCaw, 2000a; Otake et al., 2002). Lastly,“normal” appearing, but viremic piglets in the earlystages of bacterial infection carried disease problemsto healthy litters following “exchange” fostering ofvisibly sick piglets to nurse sows. Field observationsof ≥5-week-old, unhealthy piglets - unresponsiveafter multiple treatments and still suckling nurse sowsin a herd chronically affected with reproductivePRRS - led to the creation of a new pigletmanagement strategy (McREBELTM) designed tocontrol the occurrence of secondary bacterial diseaseand mortality in both suckling and weaned pigs(McCaw, 1995).

The Principles behind McREBELTM

By 1994, key facts about PRRS virus had becomeknown. These were incorporated into a method ofmanaging PRRS virus-affected piglets during acuteoutbreaks of reproductive PRRS. These factsincluded the following:

1. Piglets could become infected with PRRSvirus in utero (Terpstra et al., 1991).

2. PRRS virus infection alone did not killpiglets (Halbur et al., 1996).

3. PRRS-affected piglets were usuallyinfected with at least one of a variety ofsecondary bacterial infections (Done andPaton, 1995; Stevenson et al., 1993).Preweaning mortality and many of thesigns of disease during PRRS outbreaksresulted from secondary bacterial infectionsin PRRS virus-infected piglets.

4. Piglets born through caesarean section areborn nearly bacteria free, as demonstratedthrough the creation of specific pathogenfree (SPF) breeding stock (Twiehaus andUnderhaul, 1970).

To these research and diagnostic findings was addedthe field observation that extensive fostering ofpiglets and aggressive use of antibiotics failed tocontrol PRRS in suckling and weaned pigs.Therefore, a strategy was devised to control theselosses by limiting the exposure of PRRS virus-infected susceptible piglets to pathogenic bacteriaand making the litter the all-in/all-out (AIAO)production unit in the farrowing house. Theprocedure was named McREBELTM to reflect the

objectives, i.e., to protect piglets from the bacterialinfections and disease that seemed to result in theirpoor growth and death: Management Changes toReduce Exposure to Bacteria and Eliminate Losses.McREBELTM was also designed to meet productionobjectives, such as the need to use all functional teatsavailable in a farrowing room. This is achieved byallowing the fostering of piglets within the first 24hours after birth to litters with open teats. Fosteringis limited to moving the minimum number of pigletsto fill unused teats, and expressly not for equalizationof body-weights within litters. Limited fostering isallowed with the full knowledge that even this couldcompromise the few piglets that are moved during anactive PRRS outbreak.

McREBELTM Rules

The objective is to maximize the number of pigletsremaining on their birth mother and, secondly, tomaximize the number of piglets remaining on thecolostrum mother. The litter is the AIAO unit.

1. Do not cross-foster piglets after 24 hours ofage.

a. Move the minimum number of pigsnecessary to load functional teats.

b. Do not cross-foster for the purpose ofcreating uniform size or single genderlitters.

c. Prioritize assignment of functional teatsto larger and more vigorous piglets.

d. Smallest piglets are given the lowestpriority, usually leaving them in their birthlitter as “extras” if there are more pigletsthan available functional teats.

2. Do not move piglets between farrowingrooms and follow strict AIAO production.

3. A piglet held back from weaning (cross-fostered to a younger litter) takes a teataway from a younger, potentially healthierpig. Therefore, remove very sick,moribund, or poor body condition pigsfrom the system.

a. Eliminate piglets that do not improveafter treatment.

1. Extended antibiotic treatmentperiods may be needed to treatbacterial diseases of PRRSvirus-infected piglets.


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2. Change needles between littersor pens of treated pigs.

b. Eliminate very thin, starve-out, lame,swollen-jointed, light body weight, long-haired, chronically sick, and scouringpiglets as they are found.

c. Eliminate piglets at weaning that are toolight to survive in the nursery and havepoor body condition

4. In the nursery, implement practices tomaximize piglet survival and performance:

a. Size piglets into pens carefully.

b. Place the smallest piglets in a warm,non-drafty part of room.

c. Hand-feed the smallest piglets 4 to 6times a day for 5 days.

d. Switch rations based upon weight ofpigs in the pen, not the room.

e. Use heat lamps and/or plastic lying padsfor small piglets.

f. Lower one water nipple per pen indesignated small piglet pens and jam itopen for 24 hours.

McREBELTM Farrowing RoomManagement

The overall goal is to minimize mortality (pre-weaning mortality and nursery mortality combined)and maximize the average weight of the farrowingroom and nursery for each farrowing or productiongroup.

Sow managementCount functional teats on each sow at farrowing andplace at least as many pigs on her as she hasfunctional teats. "Overloading" sows with piglets,i.e., more piglets placed than estimated number offunctional teats, is recommended when live born isvery high. This ensures that all potentially functionalteats are used, thus maximizing number of pigsraised. When in doubt, load sows with at least theaverage number of pigs weaned by her parity for theherd. Do not expect to wean any more quality pigletsthan there are functional teats in a farrowing room.To maximize the number of piglets weaned per room,maximize the number of functional teats in the roomby proper gilt selection and sow culling practices.When more sows farrow than the number of cratesavailable, keep sows with the best udders in the

crates for full-length lactation. Culling decisionsshould include the sow's nursing ability and averagenumber of pigs weaned.

At farrowing, the objective is to maximize thenumber of piglets remaining on their original motherand, secondly, to maximize the number of pigletsremaining on the colostrum mother. Therefore, fosterextra piglets to sows with extra functional teats in away that optimizes the benefits of colostrum. Do notwait until "processing day" to foster piglets to openteats on sows. A piglet's ability to absorb colostralantibodies across the gut wall is reduced by half(half-life) approximately each three hours (Wagstromet al., 2000). As a result, by 24 hours of age thepiglet's ability to absorb colostral antibodies isminimal. Therefore, foster piglets 2 to 4 hours afterbirth if they are moving to a just-farrowed sow sothat the foster mother provides the piglets colostrum.Alternatively, foster piglets at 6 to 12 hours of age ifthey are to be moved to a sow that farrowed the daybefore so that the piglets get colostrum from theirbirth mother. Mark these piglets to ensure they areprocessed the next day.

Piglet managementEnsure that crates are designed or adjusted to allowpiglets free access to teats. Bottom bow bar, fingerbar, or proctor type crates are best for thisrequirement. If you have adjustable straight-sidedcrates, make sure the crates are adjusted (or sowsloaded to the properly adjusted crate) to the size ofthe sow's udder, i.e., the piglets are not forced tocrawl over the bar to reach the top teats.

Prioritize placement of piglets to functional teats bysize. Give the highest priority to the largest pigs andthe lowest to under-sized piglets. If more pigs areborn than there are functional teats, make sure theunder-sized pigs are the "extra" piglets in each litter.Do not create litters of under-sized piglets. This onlyprioritizes them over the medium and large pigswithin farrowing rooms with too few functional teatsto feed the number of piglets born live. Foster extrapiglets based upon their ability to suck teats of theadopting sow, i.e., smaller pigs to young sows withsmall udders, larger pigs to older sows with large,heavy udders.

Do not foster piglets just to make litters of uniformpiglet size. Size does not matter after the piglets havewon and/or selected their teats at 36 hours of age.Cross-fostering after 36 hours of age will onlydisplace another pig from its functional teat, causefighting, and possibly carry new disease to the litter.


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There will be no more fighting if piglets are notfostered into or out of the litter. All pigs suckling afully functional teat will thrive regardless of bodysize differences within the litter.

Look closely for piglets not suckling with littermates.Examine these pigs immediately for fever, scours,swollen joints, bad feet, gums damaged from needleteeth clipping, etc. and treat them. Never movesmaller or sick piglets "back" to younger rooms.Moving the biggest and healthiest litters forward(early weaning) to open a sow for healthy "plateau"piglets within that room is acceptable.

If a sow dies or stops milking, keep the litter togetheras a group and in their original crate wheneverpossible. Wean the litter if the piglets are at least 14days old. Otherwise, move a "just weaned" sow or"just farrowed" sow to the piglets' crate. Move a"just weaned" sow to the intact orphan litter if thepiglets are 4 to 14 days old. Move a "just farrowed"and "zero weaned" sow (low number of live born) tothe intact orphan litter if piglets are less than 4 daysold.

Piglet body condition scoring may be used to monitorpiglet health in the farrowing room:

1. Good body condition - At weaning, thesepigs have sufficient body fat to make themappear round and smooth. Their shoulderblades, backbones, and pelvis bones cannotbe seen.

2. Fair body condition - At weaning, theoutline of the shoulder blade of these pigscan be seen, but not the backbone or pelvis.These pigs may have suckled a partiallyfunctional teat or been mildly affected bydisease, such as lameness or diarrhea.

3. Poor body condition - In these pigs,shoulder blades, backbones, and pelvisbones are clearly visible at weaning. Thesepigs have been fostered frequently, sucked apoorly functional teat, or been affected bydisease.

Expect 90% or more of the pigs to score “good” ifsows and piglets are not sick and sows are milkingnormally.

It is better to euthanize unhealthy piglets than to tryto save them. This would include small, weak, thinpiglets (shoulder blades, backbone, and pelvis clearly

visible), pigs that do not respond following 2 to 3days of treatment for scours, thumping, swollen jointsand lameness, and pigs in poor body condition atweaning.

Summary

The objective of McREBELTM management is tooptimize the health and growth of piglets and nurserypigs during and following PRRS outbreaks.McREBELTM was developed in 1994 as a method tocontrol PRRS-associated disease and mortality insuckling and nursery pigs. By that time, it hadbecome apparent that extensive cross-fostering andantibiotic treatment did not control the high pigletmorbidity and preweaning mortality seen duringPRRS outbreaks. Furthermore, control of continuednursery pig losses could only be achieved by nurserydepopulation months after the outbreak, i.e., whenvirus circulation stopped among the sows and theherd “stabilized.” Critical information known by thattime included:

1. Piglets could be born alive and infectedwith PRRS virus.

2. Clinically-affected PRRS virus-infectedpiglets submitted to diagnostic laboratoriesdied because of secondary bacterial disease.

3. Experimental infection with PRRS virusfield isolates alone did not kill germ-freepigs.

4. Piglets were born nearly bacteria-free.

McREBELTM evolved from these facts and theunderlying premise that we needed to minimize thefrequency and level of bacterial exposure to pigs inorder to control clinical disease during PRRSoutbreaks. Since conventional methods of caring foryoung pigs, such as antibiotic treatment and crossfostering, had consistently failed, the intention was tocontrol clinical disease by minimizing piglethandling, treatment, and piglet fostering amonglitters. Ultimately, it was determined that groups ofpiglets raised using McREBELTM managementduring PRRS outbreaks returned to normal levels oftotal mortality (preweaning mortality plus nurserymortality) and achieved nearly normal growth ratesthrough the nursery. McREBELTM may also offereconomically significant production improvements inherds unaffected by PRRS and which foster pigletsbetween litters frequently throughout lactation.


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References

Benfield DA. 1997. Persistent fetal infection of porcine reproductive and respiratory syndrome virus (PRRS) virus.Proceedings of the American Association of Swine Practitioners, 455-458.

Dee SA, Joo HS. 1994. Prevention of the spread of porcine reproductive and respiratory syndrome virus in endemicallyinfected pig herds by nursery depopulation. Vet Rec 135:6-9.

Dial GD, Hull RD, Olson CL, et al. 1990. Executive Summary, Mystery Swine Disease: Implications and needs ofthe North American swine industry. Proceedings of the Mystery Swine Disease Committee Meeting,Livestock Conservation Institute, Denver, Colorado, pp. 3-6.

Done SH, Paton DJ. 1995. Porcine reproductive and respiratory syndrome: Clinical disease, pathology andimmunosupression. Vet Rec 136:32-35.

Feng W-H, Laster SM, Tompkins M, et al. 2001. In utero infection by porcine reproductive and respiratorysyndrome virus is sufficient to increase susceptibility of piglets to challenge by Streptococcus suis type 2. JVirol 75:4889-4895.

Halbur, PG, Paul PS, Meng X-J, et al. 1996. Comparative pathogenicity of nine US porcine reproductive andrespiratory syndrome virus (PRRS virus) isolates in a five-week-old cesarean-derived, colostrum-deprived pigmodel. J Vet Diagn Invest 8:11-20.

Keffaber KG, Stevenson W, Van Alstine C, et al. 1992. SIRS virus infection in nursery/grower pigs. AmericanAssociation of Swine Practitioners Newsletter 4(4):38-40.

Loula T. 1991. An update for the practitioner: Mystery pig disease. Agri-Practice 12(1):23-34.McCaw MB. 1995. McREBELTM PRRS: Management Procedures for PRRS control in large herd nurseries.

Proceedings of the Allen D. Leman Swine Conference 22:161-162.McCaw MB. 2000a. Effect of reducing cross-fostering at birth on piglet mortality and performance during an acute

outbreak of porcine reproductive respiratory syndrome. Swine Health and Production 8(1):15-21.McCaw MB. 2000b. Impact of McREBEL (minimal cross-fostering) management upon nursery pig sale weight

and survival under production conditions in PRRS asymptomatic herds. Proceedings of the International PigVeterinary Society Congress, p. 333.

Otake S, Dee SA, Rossow KD, et al. 2002. Transmission of porcine reproductive and respiratory syndrome virusby needles. Vet Rec 150:114-115.

Segalés J, McCaw M.B. 2002. Bacterial infections are potentiated by porcine reproductive and respiratorysyndrome virus (PRRSV) infection: Fact or fiction? In: Trends in Emerging Viral Infections of Swine.Morilla A, Yoon K-J, Zimmerman J (eds). Iowa State Press, Ames, Iowa, pp. 359-364.

Stevenson GW, Van Alstine WG, Kanitz CL, Keffaber KK. 1993. Endemic porcine reproductive and respiratorysyndrome virus infection of nursery pigs in two swine herds without concurrent reproductive failure. J VetDiagn Invest 5:432-434.

Terpstra C, Wensvoort G, Pol JMA. 1991. Experimental reproduction of porcine epidemic abortion and respiratorysyndrome (mystery swine disease) by infection with Lelystad virus: Koch’s postulates fulfilled. Vet Q 13:131-136.

Twiehaus MJ, Underhaul NR. 1970. Control and elimination of swine diseases through Repopulation with SpecificPathogen-Free (SPF) stock. In: Diseases of Swine (3rd edition). Dunne HW (ed). Iowa State University Press,Ames, Iowa, pp. 1096-1110.

Wagstrom EA, Yoon K-J, Zimmerman JJ. 2000. Immune components in porcine mammary secretions. ViralImmunol 13:383-397.


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Control in Large SystemsMA FitzSimmons and CS Daniels

*Adapted from a chapter in Trends in Emerging Viral Infections of Swine. 2002. A Morilla, K-J Yoon, JZimmerman (eds). Iowa State Press, Ames, Iowa.

Introduction

PRRS has been raising havoc with swine productionfor over a decade, but there is still little consensusamong producers and veterinarians regarding controlprocedures in production systems. The confusionstems from the lack of concrete information in twoareas: PRRS virus transmission and protectiveimmunity.

Although the U.S. swine industry has threecommercial vaccines at the time of this writing, noone has yet described how PRRS virus, either fieldvirus or vaccine virus, elicits protective immunity.Furthermore, there is no practical way to evaluatecross-protection between the modified live virus(MLV) vaccines and heterologous field strains ofPRRS virus. Vaccine has been used extensively insome swine production systems, but with mixedeffects. Some systems report good results; othershave blamed vaccines for creating even more severedisease problems. These highly dissimilar outcomessuggest one of two possibilities: 1) a lack of crossprotection, or 2) no protection at all. If vaccines werecross protective, many herds should have improveddramatically when vaccinated. Since the problemsthe industry has had with PRRS have continued in theface of multiple vaccinations, it is easy to concludethat, in many cases, the vaccine has not createdheterologous protection. That is, if the field viruswere similar to the vaccine strains, the MLV productswould have provided protection. In addition, thereare many examples of farms returning to normalproduction without any vaccine use after severeoutbreaks.

Therefore, our conclusion is that the long-termstability of PRRS virus-infected farms depends onconsistent acclimatization. Acclimatization meanspreparing PRRS virus-naïve gilts for entry into thesow herd through the development of activeimmunity against field virus. For farms to maintainlong-term stability, it is important that all PRRSvirus-susceptible sows in the herd develop activeimmunity and that all replacements are immune priorto entry. The use of vaccine in these cases maycreate populations of sows that have not beenexposed to the field strains within the herd. These

unprotected populations can result in small re-breaksthat show up as affected pigs in the nursery.

The following description details what may havehappened over the past decade in the industry andhelps explain why problems have escalated in the lastfive years.

A Clinician’s Perspective on CyclicOutbreaks of PRRS

Since the initial breaks, it was observed that the rapidstabilization of the sow farm resulted from the rapidspread of the virus through an entirely susceptiblepopulation. If the original source of virus wereincoming gilts, the continued introduction of thesepreviously exposed, naturally protected replacementsstopped the virus spread due to the absence ofsusceptible animals in the population. Ultimately,stabilization of the sow herd depended on one ofthree things occurring:

1. The entry of previously exposed, naturallyprotected gilts meant no susceptiblepopulation would redevelop.

2. The acclimatization (infection) of PRRSV-naïve replacements through exposure toinfected nursery pigs maintained herdimmunity.

3. The virus completely stopped circulating.

Over time, these stable farms eventually producedPRRS virus-negative pigs, these susceptible animalswould then be moved into positive nursery/finishingsystems, where they would become infected.

After a few years of unacceptable nursery/finishingperformance, the industry implemented procedures toclean up the downstream pig flow, i.e.,partial/complete depopulation (Dee, 1994, 1997a,b),all-in/all-out facilities (Dee, 1993), and/orunidirectional pig flow (Dee, 1998). The use ofPRRS virus-positive replacement gilts eventually ledto the near elimination of PRRS virus from thesystem. This situation resulted in naïve, completely


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susceptible gilts being produced for entering into thesow farm. The sow herd dynamics then began tochange as the population started to differentiate intoresistant and susceptible classes in regards to PRRSimmunity. Some farms rolled through this phase andbecame PRRS virus negative. Other herds, after anuncertain length of time or number of naïve animalintroductions, began to re-circulate virus andeventually classical, clinical PRRS reappeared.There were even re-breaks in cases where systemsbelieved they were properly acclimating gilts byexposure to infected sows or nursery pigs. This wasbecause the gilts they received were already positive,but to a heterologous strain of PRRS virus. Thesegilts were susceptible to the "resident" PRRS virusstrain because the acclimatization process had failed,perhaps because the contact sows or nursery pigs towhich they were exposed were no longer sheddingvirus. The use of MLV vaccines further confused theissue by creating antibodies that could not bedifferentiated from field virus. Therefore,seropositivity or seroconversion to PRRS virus couldnot be used to confirm exposure to field virus duringacclimatization.

Some of these farms ended up in cycles: clinicaloutbreaks in the sow farm prompted procedures toacclimatize gilts, which lead to a clinically quietphase, the production of negative pigs, anddepopulation of nursery/finishing stages. Success incontrolling PRRS virus circulation in the sow herdled to the production of negative “seeder” pigs, whichresulted in the failure to transmit the endemic virus toresident gilts. The ultimate result was theintroduction of PRRS virus-naïve replacementanimals into the sow herd. Once in the breedingherd, these unprotected replacements eventuallymade contact with infected sows and became infectedwith the endemic PRRS virus. The result of theinfection depended on her stage of gestation, but onepossible outcome was weaning viremic pigs into thenow-negative nursery. These cycles revolved aroundone main flaw, the failure to continually expose andprotect incoming gilts to the resident PRRS virus.Several things led to this failure, including

1. The use of PRRS MLV vaccine in someacclimatization programs eliminated thesystem’s ability to determine by means ofserology whether homologous field virusexposure had occurred.

2. The vaccine may have restricted thetransmission of field virus to all intendedreplacements.

3. All in/all out gilt acclimatization required aconsistent source of viremic sows or seederpigs.

This last point is very important because it holds thekey to successful long term stabilization of PRRSpositive sow herds.

Methods of PRRS Control in Swine Units

DefinitionsA few definitions are necessary before discussing anappropriate system for control of PRRS in large sowunits. For simplicity, only gilt sources will bediscussed, but the same concepts apply to boars. Forclarity, "PRRS virus-naïve" is defined as an animalthat has never been infected with either field strain orvaccine strain PRRS virus. In contrast, PRRS virus-negative is based on serum antibody status asdetermined by an ELISA or indirect fluorescentantibody (IFA) test. Within the specificity limits ofthe tests, PRRS virus-naïve animals will testnegative, but infected or vaccinated animals may alsotest negative as antibody levels decline over time postinfection.

Incoming animals can be put into two categories asderived by source: PRRS virus-naïve sow herds orpositive sow herds. Naïve sow farms, by definition,produce PRRS virus-naïve replacement gilts. Thesegilts may be entering either PRRS virus-positive ornaïve commercial farms. If entering naïve herds,these animals only need to be isolated; there is noneed for off-site acclimatization (at least with regardto PRRS virus). If these animals are going to a PRRSvirus-positive sow farm, they must be acclimatized toa PRRS virus homologous to the virus endemic onthe farm before entering the sow herd. It is essentialthat these animals match the status of the sow herdbefore introduction.

The second category is animals sourcing frompositive sow farms. Individual animals from thesefarms may be either naïve or PRRS virus-positive,depending on the production system and the successof the source sow farm’s PRRS stabilization protocol.The concept of making naïve pigs from previouslyinfected sow herds has been debated extensively inthe past five years, particularly in the context of giltsales. There is no doubt that positive stable sowherds will make a lot of PRRS virus-naïve pigs. Theproblem with these systems is that they are always atrisk of breaking down due to the unexpectedintroduction of naïve gilts or the circulation ofanother PRRS virus that is already present. Either


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way, the result is PRRS virus-infected offspringmoving downstream. If these pigs flow out tocommercial finishing, there is no subsequent effect,except directly on that pig population. However, ifthese are replacement gilts, they could infectdownstream sow herds and their production as well.Therefore, as a customer of that multiplicationsystem you have to be concerned not only with thebiosecurity of the source, but also their managementof the PRRS stabilization process. It is the opinion ofthis author that, if you have a negative sow herd, youshould only receive naïve replacements from naïvesow herds. If your gilt source was the origin of yourresident PRRS virus but they have succeeded inmaking negative gilts, it would be acceptable tocontinue to purchase replacements from them, thenacclimatize them to the resident virus via methodsdescribed later. However, if you have a positive sowherd and the gilts will originate from a herd otherthan the one that was the source of your virus, itwould be preferable to only accept gilts from a trulynegative source. It is important to understand that thesame principles applied at the commercial level tocreate negative nursery/finisher populations areoccurring upstream at the source farm. The successof their program and the consistency of that successare paramount to the success of the acclimatizationprocedures in place in the commercial herd.

With these definitions in mind, we can turn to theissue of introducing animals into recipient sow farms.

Receiving naïve gilts from naïve sourcefarmsThe ideal procedure is to receive naïve replacementsfrom naïve source farms. This allows the option ofacclimating the replacements to specific sow herdsand their farm-specific strains of PRRS virus. It alsodecreases the chance of clinical breaks resulting fromthe introduction of a different PRRS virus into theherd.

When naïve gilts are to be introduced to a positivesow farm, they must first develop immunity to the"resident" (endemic) strain of PRRS virus. This isthe point at which differences in opinion arise. Aprocedure that has been widely publicized involvesthe use of a commercially available PRRS vaccine incombination with cull animal exposure in all-in/all-out off-site facilities to acclimatize incoming animals.The acceptance of this procedure has varieddepending on past experience and perceived success.The system that will be described in this paper isquite dïifferent. This system is based on two simplepremises:

1. Field virus infection results in effectivelong-term protection.

2. Successful PRRS acclimatization willdecrease or eliminate the amount of viruscirculating in the sow farm.

If acclimatization is managed as all-in/all-out andrelies on exposure to cull sows to introduce virus toeach group, unprotected gilts will eventually enter thesow farm because cull sows will not consistentlyshed and/or transmit the resident PRRS virus to naïvegilts. If gilts are vaccinated upon entry to theisolation/acclimatization site, it will be impossible toknow if field virus exposure has occurred. Previousexperiences suggest that commercial vaccines havenot been completely cross protective (Benson et al.,2000). Without the ability to definitively determineif field virus infection has occurred, it is not possibleto know whether successful PRRS acclimatizationhas occurred.

When introducing naïve gilts into positive farms thegoal is exposure to a homologous field virus in anoff-site acclimatization facility. For the purposes ofthis paper, the definition of acclimatization isinfection of a susceptible animal with a specificdisease organism. Natural infection and recovery isthe surest way to elicit protection to PRRS virus andcan be accomplished by one of three methods:

1. Exposure to viremic cull sows or nurserypigs.

2. Adding naïve pigs to a PRRS virus-infected, continuous pig flow.

3. Injection with live virus.

In the first method, the long-term risk is thatshedding of PRRS virus in the sow farm eventuallystops, thereby resulting in acclimatization failure.Continuous flow acclimatization is one way toaddress this eventuality. PRRS virus will continue tocirculate in the population as long as susceptible giltsare continually introduced, but maintaining viruscirculation is a function of population size, mixingprocedures, and the interval between theintroductions of susceptible gilts. Of these three, theintroduction interval appears to be the most importantfactor. It is critical that the virus continues tocirculate and successfully infects the next group. Iftoo much time is left between introductions of gilts,the virus may stop circulating and populations ofnaïve gilts will again enter the sow herd. In practice,the clinical disease experienced duringacclimatization is least severe in 10- to 14-week-old


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pigs. Vaccination programs for the control ofcommon secondary infections can minimize theclinical aspects of these diseases. It is important tohave at least 60 to 90 days of off-siteisolation/acclimatization in these continuous flowsystems to allow for complete recovery from PRRSvirus.

A theoretical concern with continuous flowacclimatization is viral mutation. The virus goesthrough many replications, which may increase thechance for mutations that could create instability inthe sow herd due to cross protection failure. Inaddition, it is impossible to control all the otherinfectious diseases circulating in the continuous flowpopulation well enough to avoid increases inmortality and culling rates. Over time, some of thesesystems will become progressively worse andpartial/complete depopulation may be necessary. Ifan acclimatization/isolation site is to be depopulated,it is important to maintain a source of virus to restartPRRS virus circulation. This can be accomplished byharvesting serum from viremic pigs and laterinjecting it into naïve gilts. An alternative to thisprocedure is to leave a few viremic pigs in thefacility. Serologic testing is required to confirmexposure and infection when acclimatization isrestarted.

The last method deals with intentionally exposingnaïve gilts to live virus by injection. This isequivalent to using a live autogenous vaccine. Thisprocedure may be necessary to allow sufficient "cooldown" after infection if isolation/acclimatization islimited to 60 days. That is, in continuous flowsystems, it may require three weeks for the virus tomove through the population and expose every pig,which results in a delay of the "cool down" period.With injection, the "cool down" period startsimmediately. Other advantages of this systeminclude control of the dose and exact time ofinfection. If this system is used in conjunction withall-in/all-out pig flow, exposure to other pathogenicmicroorganisms can be reduced. This will lead todecreased mortality and culling. This procedure alsorequires less testing to confirm infection of the entirepopulation because a few PRRS virus-positive giltsare sufficient to demonstrate that the inoculum wasinfectious at the time of injection. It should beacknowledged, that there are safety issues concerningthis method that should be discussed by producersand veterinarians prior to its implementation. Use ofthis method has been challenged on ethical grounds,but it shares a striking similarity to other methodsthat are currently in use, e.g., intentional exposure of

animals to materials contaminated with porcineparvovirus or transmissible gastroenteritis virus.Regardless of the method employed, the ultimategoal of acclimatization is to infect and consequentlyprotect naïve replacement gilts against an endemicPRRS virus prior to entry into a positive sow farm.Acclimatization needs to consistently achieve thegoal of infection/protection now and well into thefuture.

Receiving gilts from positive farmsAll replacements from PRRS virus-positive sourcefarms should be viewed as positive gilts until provenotherwise. Some groups of gilts from positive farmsare PRRS virus-naïve, but farms are known to re-break. What does this mean to the recipient sowfarm? If the stability of the source farm is disrupted,virus may find its way downstream to your farm.This virus will not create significant clinicalproblems as long as it is sufficiently similar to thePRRS virus on your farm and susceptible sowpopulations have not developed due to failure toacclimatize naïve gilts. If the strain of PRRS virusthe gilts introduce is sufficiently different, the resultwill be instability in the recipient herd.

“Naïve” gilts from positive sow farms need to beisolated and tested to prove they are actually PRRSvirus-naïve. After their naïve status has beenconfirmed, they must be exposed to a homologousvirus and prepared for entry into the sow herd. Thisprogram may consist of isolating weaned pigs in anursery and, if they test negative (naïve) at 10 to 12weeks of age, acclimating them. The quality ofdiagnostic testing techniques available todaydetermines the risk of receiving these animals. If theoriginal gilt source sends positive and negativegroups over time, as long as the virus is similar andcontinues to circulate in acclimatization there shouldnot be a problem.

Acclimatization may not be needed if the source farmwas the original-and-only source of your PRRS virusand it continues to allow PRRS virus to circulatethrough the finishing phase. Acclimatization mayconsist only of a "cool down" period of 60 to 90 daysto decrease the risk of introducing a large level ofvirus into the sow farm. Actually, this systemworked well until source farms started implementingtechniques to create PRRS negative nursery/finishers– which then become your replacement gilts. Theirreasoning was perfectly understandable when lookingat nursery/finishing performance, but it createdinstability problems in the recipient commercialfarms. This instability was due to a change in


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replacement gilt status from infected/protected toPRRS virus-naïve and the recipient farms' failure toadjust to the changing gilt status and take measures toassure acclimatization.

In summary, receiving gilts into positive farmscreates two challenges. First, naïve gilts must beacclimatized to the "resident" PRRS virus. Second, ifthe gilts are PRRS virus-positive, the virus to whichthey were exposed must be the same as the virusendemic in the recipient herd to assure protection.Sufficient "cool down" time is important to allow theanimals to respond immunologically and reduce thevirus load. If the gilt source was not the originalsource of the endemic PRRS virus, additionalproblems may arise due to inadequate cross-protection. Receipt of seropositive gilts makes itimpossible to measure if farm-specific PRRS virusexposure occurs.

Summary

Porcine reproductive and respiratory syndrome(PRRS) virus was identified over a decade ago. Evenso, basic PRRS virus information, particularly in thearea of immunity and transmission, is conspicuous byits absence. Controlling clinical cases in commercialproduction systems is a constant problem forproducers and veterinarians. Although vaccines areavailable, the protection they confer is inconsistent.In this section, we discuss strategies for controllingPRRS, with an emphasis on methods for establishingand maintaining herd immunity. This overview is notintended to give answers to an individual farm orsystem PRRS problem. The intent is to stimulatethinking and to challenge popular paradigms. Thesepractices may seem risky or radical to some, but notto the producers who have successfully used thesetechniques to protect their livelihood.

References

Benson JE, Yaeger MJ, Lager KM. 2000. Effect of porcine reproductive and respiratory syndrome virus (PRRSV)exposure dose on fetal infection in vaccinated and non-vaccinated swine. Swine Health and Production 4:155-160.

Dee SA, Joo HS. 1994. Prevention of PRRSV spread in endemically infected swine herds by nursery depopulation.Vet Rec 135:6-9.

Dee SA, Joo HS, Polson DD, et al. 1997a. Evaluation of the effects of nursery depopulation on the persistence ofporcine reproduction and respiratory syndrome virus and the productivity of 34 farms. Vet Rec 140:247-248.

Dee SA, Joo HS, Polson DD, Marsh WE. 1997b. Evaluation of nursery depopulation on the profitability of 34farms. Vet Rec 140:498-500.

Dee SA, Morrison RB, Joo HS. 1993. Eradication of PRRSV using multi-site production and nursery depopulation.Swine Health and Production 1:20-23.

Dee SA, Phillips R. 1998. Using vaccination and unidirectional pig flow to control PRRSV transmission. SwineHealth and Production 1:21-25.


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Control Using Oropharyngeal Scraping InoculationG Allison

Introduction

Natural exposure to infectious agents in a controlledfashion has long been used to infect swine andestablish immunity. Typically, these methodsinvolve exposure to acutely infected animals, and/orpathogen-contaminated tissues and manure.However, controlled PRRS virus infection in the fieldhas proven to be a difficult or unreliable process.Exposure of susceptible animals to PRRS virus bycontact with infected animals is successful in someinstances and not in others. Exposure tocontaminated materials is generally unsuccessfulbecause PRRS virus is thermal and pH labile and,therefore, does not survive outside of the host forextended periods. The virus is unstable inenvironments containing low levels of detergents(Plagemann, 1996), it is easily in activated in a dryenvironment (Blomraad et al., 1994), and will notsurvive on fomites commonly found in the barn(Pirtle and Beran 1996). Somewhat ironically, aninoculation of 10 or fewer PRRS virus particles byintranasal or intramuscular routes easily infects swine(Yoon et al., 1999). Thus, PRRS virus is frequentlydescribed as highly infectious but not overlycontagious.

In this chapter, we describe a practical method forexposure of susceptible animals to PRRS virus. Thismethod is appropriate in herds where the strategy forpreventing clinical PRRS involves maintaining aPRRS virus-positive breeding herd. In brief, themethod involves exposing naive replacement animalsto a virus-contaminated inoculate collected fromPRRS virus-infected grower pigs. As is true with allmethods involving natural exposure, there is adistinct possibility of unknowingly transmitting notjust PRRS virus, but also other pathogens. Whetherthis is a detriment or a benefit will depend on theherd and the circumstances, but should always bekept in mind and discussed with the herd owner. Theadvantages of oropharyngeal scraping inoculation areits reproducibility, simplicity, and the fact thatanimals establish immunity to PRRS virus strainscirculating in the herd prior to their introduction.

Procedure

Animals to be sampled should be selected frompopulations with laboratory confirmation of PRRSvirus infection. Oropharyngeal scraping samples are

collected by using age-appropriate restraint andscraping the tonsil of the soft palate with a sterile,long-handled spoon. Typically, restraint involvessnaring the animal and using an oral speculum tohold the mouth open. Collection spoons may befashioned from standard stainless steel flatware towhich an extension of appropriate length is welded tothe handle. Sufficient pressure should be appliedduring scraping to obtain a quantity of saliva, mucus,and cellular debris in the bowl of the spoon. Thisgenerally requires 4 to 6 passes of the spoon. Pigswith excess feed in the oral cavity should not besampled. In animals of 150 pounds (68 kilograms) orless, the entire procedure requires 15 seconds or less.

Once collected, the scrapings are removed from thespoons using a swab. The sample material can thenbe prepared, using simple laboratory techniques, forinjection into susceptible animals. Prior to use, thematerial should be tested to confirm the presence ofPRRS virus by PCR.

Summary

Oropharyngeal scraping inoculation has been utilizedas a method to manage PRRS virus since May 1999in a variety of clinical settings. The immunity thatdevelops from PRRS virus infection protects theconvalescent animal from subsequent challengeagainst the homologous viral strain. For that reason,this technique can be an important herd-specificcomponent in the control of PRRS. As is shown inTables 4.4.1 and 4.4.2, seroconversion of 100 percentof the inoculated animals is possible in the field. Inboth genders and in both mature and immature swine,the technique has reliably induced an antibodyresponse that seems consistent with a stablepopulation. Failure of the inoculation procedure, aswas seen in Herd E, resulted from collectingoropharyngeal samples from swine subsequentlyfound to be negative for PRRS virus infection.Accordingly, the inoculum should be tested for PRRSvirus by PCR prior to use. Likewise, evaluation ofanimals for pre-existing infectious diseases, such assalmonellosis, is strongly advised as PRRS virus canact synergistically with concurrent infections. Theadvantages of this technique are its reproducibility,the development of immunity to herd-specific viralstrains, and the ability to inoculate swine under


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controlled circumstances and allow for a "cool down"period prior to introduction into the herd.

References

Pirtle EC, Beran GW. 1996. Stability of porcine reproductive and respiratory syndrome virus in the presence offomites commonly found on farms. J Am Vet Med Assoc 208:390-392.

Plagemann PGW. 1996. Lactate dehydrogenase-elevating virus and related viruses. In: Field's Virology (3rdedition). Fields BN, Knipe DM, Howley PM (eds). Lippincott-Raven Publishers, Philadelphia, pp. 1105-1120.

Yoon K-J, Zimmerman JJ, Chang C-C, et al. 1999. Effect of challenge dose and route on porcine reproductive andrespiratory syndrome virus (PRRSV) infection in young swine. Vet Res 30:629-638.


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Control with Modified-Live Virus (MLV) PRRS VaccineTG Gillespie

Introduction

Effectively controlling PRRS virus is one of the mostchallenging tasks facing veterinarians and swineproducers today. Effective control of the PRRS viruscan be complicated, and may involve many factors:

1. Number and type (identification bysequence) of viruses present in a farm orsystem.

2. Risk of new virus introductions.

3. Management strategies to combat PRRS.

4. Pig flow.

The objective of this paper is to focus on the role ofMLV vaccine and immune management in thecontrol of PRRS virus. Discussion will also includethe use of MLV vaccine in an off-label use thatrequires a valid veterinarian-client-patientrelationship (VCPR) and the use of all diagnostictools available to understand virus activity prior toimplementing the program and monitoringthroughout.

Basics in PRRS Virus Control

Effective PRRS virus control requires a systematicapproach that utilizes diagnostic investigations todetermine where, and at what stage of production thevirus is actively circulating in a farm or system.Once the pattern of viral circulation is understood,intervention strategies can be systematicallyemployed in an effort to minimize PRRS viralcirculation and its impact on the production system.

Among the tools implemented in the PRRS viruscontrol formula is effective use of modified-live virus(MLV) PRRS vaccine for the control of the PRRSvirus. There are two modified-live PRRS vaccinesavailable in the U.S.: Ingelvac® PRRS MLV, andIngelvac® PRRS ATP (Boehringer IngelheimVetmedica, Inc., St. Joseph, Missouri). Ingelvac®PRRS MLV is licensed for use in pigs 3 weeks of ageor older and in non-pregnant gilts or sows 3 to 4weeks prior to breeding in PRRS virus positivefarms. Ingelvac® PRRS ATP is licensed for use inpigs 3 weeks of age or older, up to 18 weeks of age inPRRS virus positive farms.

A new technology being attempted in the swineindustry is to utilize MLV PRRS vaccine in apopulation based approach for PRRS control. Thisprotocol is often referred to as “mass vaccination”and implements modified-live vaccine to an entirepopulation of growing pigs or a breeding herdpopulation at a point in time. The objective of thisapproach is to establish a uniform or homogenousimmune status within a population, by eliminatingnaïve susceptible subpopulations of pigs within thatpopulation.

The spread of field PRRS virus is enhanced whencarrier pigs shed virus to subpopulations of naïvepigs that coexist within the same population (Dee etal., 1996). Published reports have also demonstratedthat regularly introducing seronegative, naïve pigsinto infected populations enhances the spread of virusand maintains the cycle of infection (Dee and Joo,1994). The existence of susceptible subpopulationsis a factor in the maintenance of persistent PRRSviral transmission from carrier animals in chronicallyinfected populations. Vaccination has been used as ameans to eliminate naïve subpopulations and tocontrol the spread of field virus within infected herds(Dee and Philips, 1998).

Field Studies

A study to evaluate mass vaccination in the control ofPRRS virus transmission demonstrated the concept tobe an effective method for controlling, andpotentially eliminating, PRRS virus in a segregatedfinishing population of pigs (Dee and Philips, 1998).This study incorporated mass vaccination of afinishing population of pigs and herd closure for aperiod of 60 days. The finishing population wasvaccinated en masse with MLV vaccine. Vaccinationwas repeated 30 days later. The finishing facility wasclosed to any new animal entries from the nursery fora period of 60 days starting from the first vaccinationby diverting pigs to an alternative finishing facility orselling animals as feeder pigs. Following the 60-dayperiod of facility closure and diverted nursery pigflow, the flow of non-vaccinated PRRS-negative pigsfrom the nursery to the finishing facility was re-established. The initial protocol was based on fourhypotheses:


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1. Eliminating negative subpopulationsthrough the process of mass vaccinationwill prevent the continued spread of fieldvirus within the population.

2. Mass vaccination of the entire populationwill prevent the pig-to-pig spread ofvaccine virus.

3. Establishing a period of herd closure andunidirectional pig flow for a controlledperiod of time, thereby preventing naïvepigs from being introduced into thevaccinated population, will produce anoninfectious population.

4. Once established, the noninfectiouspopulation will be incapable of transmittingfield virus or vaccine virus, allowing bothstrains to be eliminated as vaccinated,infected pigs are marketed and naïvereplacements are introduced over time.

The implications of this study were that the use of aprotocol of mass vaccination and a period of herdclosure eliminated naïve subpopulations and thespread of PRRS virus creating a noninfectiouspopulation. Mass vaccination and a 60-day period ofclosure and diverted pig flow enabled the entry ofnonvaccinated PRRS negative pigs into the finishingphase of production to remain negative and led to thesuccessful control and elimination of virus from thesite.

This protocol has been repeated in other finishingpopulations with identical results (Philps et al., 2000;Wonderlich et al., 2002). Mass vaccination and herdclosure has also been compared to a protocol thatutilized herd closure alone for the control of PRRSvirus in finishing populations of pigs (Philips andDee, 2002). The results of the study suggested thatmass vaccination with herd closure is an effectivestrategy for the control and elimination of PRRSvirus from targeted finishing populations. This studyclearly demonstrated that MLV vaccine could besuccessfully used in a PRRS virus control andelimination program. Finishing populations thatemployed mass vaccination and herdclosure/unidirectional flow were successful incontrolling and eliminating the PRRS virus (4successes of 4 attempts). The results were consistentwith the creation of a noninfectious population viamass vaccination. The finishing populations thatemployed only herd closure/unidirectional flowwithout the use of vaccine all failed to eliminate thePRRS virus (zero successes of four attempts). In thelatter case, the results showed continued transmission

of PRRS virus from infected pigs to naïve susceptiblepigs, which resulted in the failure to control andeliminate the virus. Thus, site closure andunidirectional pig flow alone did not control oreliminate transmission of PRRS virus, againsuggesting that immunization with an effective MLVPRRS vaccine was an essential component forachieving PRRS virus elimination.

Recent studies have investigated applying the massvaccination and herd closure protocol to breedingherds (Flores and Dufresne, 2002; Gillespie et al.,2002; Philips et al., 2002; Turner and Dufresne,2002). The strategy employed mass vaccination witha MLV PRRS vaccine and a period of herd closurewith the goal of eliminating naïve subpopulationswithin the breeding herd and developing a protectiveimmune response. The objective was to create ahomogeneous immune status within the breedingherd population and minimize the spread of PRRSvirus. The use of MLV vaccine in an off-label userequires a valid veterinarian-client-patientrelationship (VCPR) with risk assessment activity,although on going research is being conducted toevaluate the use of MLV in all reproductive stages.

Systematic PRRS virus control in a farm or systembegins with the breeding herd. Control of viralcirculation in the breeding herd is fundamental to theprocess of reducing the prevalence of infectedoffspring and their impact on “down-stream” nurseryand finishing populations. The goal of most farms orsystems today is to “stabilize” the breeding herd as itregards PRRS virus status resulting in a reduction ofPRRS virus prevalence in offspring and minimizingPRRS virus circulation in the nursery and finishingpopulations of pigs. PRRS stability in the breedingherd is defined as “the lack of evidence of detectableviral transmission; horizontally or vertically, fromsow to offspring”. The mass vaccination protocol isimplemented in an effort to achieve these objectives.Modified-live vaccine used in a mass vaccinationprotocol provides:

1. Consistent and controlled exposure of thebreeding herd population.

2. Continued maintenance of a homogenouslevel of immunity.

3. Minimization of susceptiblesubpopulations.

4. Reduction of the risk of chronicreplication/circulation of field virus.


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The basic protocol employed in the mass vaccinationstrategies for breeding herds is:

1. Closure of the breeding herd for aminimum of 60 days.

2. Mass vaccination of the herd with MLVvaccine twice at 30-day intervals.

3. Implementation of a maintenance massvaccination strategy that occurs on aquarterly interval or less, depending on theneeds and level of challenge within the herdand specific herd risk factors.

4. Replacement gilts are routinely vaccinatedwith MLV PRRS vaccine inisolation/acclimatization beginning at least42 days before introduction into the sowherd.

Results from studies that have utilized this protocolin breeding herds have demonstrated success inattaining PRRS stability and in the reduction inprevalence of field virus in “down-stream” nurseryand finishing flows. These, in turn, result inimproved health and production performance.

The reduction in prevalence of PRRS virus ingrowing pigs following stabilization of the breedingherd often allows control of the PRRS virus by pigflow strategies, such as all-in/all-out movement ofpigs by facility or site. In situations where pig flowin the growing pig population is continuous byairspace, PRRS virus can continue to circulate in achronic/endemic fashion. In these situations, it maybe necessary to employ strategic vaccination in aneffort to control viral circulation and minimize theimpact of clinical disease. The use of MLV PRRSvaccine for the control of the PRRS virus in growingpigs for the respiratory form of the disease is aneffective tool in these cases. Timing of vaccination isextremely important in order to optimize protectiveimmunity offered by vaccination. It has beendemonstrated that at least 4 weeks is requiredbetween vaccination and field virus exposure in orderfor the pig to generate a good protective immuneresponse (Halbur and Roof, 1999). This suggests thata diagnostic investigation may be warranted in order

to determine when pigs are being exposed to fieldvirus so that optimum placement of vaccine can beaccomplished. Diagnostic tools used in bothmonitoring and diagnostic investigations include theuse of PCR tests on nursing piglets and early nurserypigs, as well as the ELISA on older nursery pigs andnegative populations, such as sentinel replacementanimals.

Summary

In summary, use of MLV PRRS vaccine can besuccessfully utilized to stabilize and control PRRSvirus in conjunction with additional managementtechniques. A systemic approach is the mosteffective method in developing an immunemanagement program. Points to bear in mind are thefollowing:

1. Controlling PRRS virus is a challenging task andinvolves many factors.

2. Effective control requires a systematic approachthat implements multiple PRRS virusmanagement tools.

3. Modified-live PRRS vaccines can be effectivelyemployed as an immune management tool in aneffort to minimize field virus circulation inpopulations of pigs.

4. The first goal is to attain stability of the breedingpopulation using strategic monitoring andimmune management. Breeding herd stabilitywill, in turn, influence the PRRS virus status ofthe nursery and finishing populations.

5. Strategic monitoring, including the use of PCRand ELISA, will indicate when stability has beenachieved.

6. Immune management includes viral exposureinternally (within the herd) and viral exposureexternally (prevent new entry of virus into theherd).

7. Replacement gilt management is important inPRRS virus control programs. The animals mustbe properly prepared and stable/non-infectiousprior to entry into the sow herd. In some cases,naïve replacements can be used in a monitoringprogram to detect virus activity (sentinels).

References

Dee SA, Joo HS, Henry S, et al. 1996. Detecting subpopulations after PRRS virus infection in large breeding herdsusing multiple serologic tests. Swine Health and Production 4(4): 181-184.

Dee SA, Joo HS. 1994. Recurrent reproductive failure associated with porcine reproductive and respiratorysyndrome in a swine herd. J Am Vet Med Assoc 205:1017-1018.


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Dee SA, Philips R. 1998. Using vaccination and unidirectional pig flow to control PRRSV transmission. SwineHealth and Production 6(1):21-25.

Flores J, Dufresne L. 2002. Ingelvac® PRRS MLV mass vaccination: performance of two farrow to finish herds.Proceedings of the International Pig Veterinary Society Congress 2:131.

Gillespie T, Polson DD, Holck JT, et al. 2002. PRRS negative offspring from a positive herd using massvaccination. Proceedings of the International Pig Veterinary Society Congress 2:125.

Halbur PG, Roof M. 1999. Efficacy of a killed and modified live porcine reproductive and respiratory syndromevirus vaccine when used alone or in combination in growing pigs. Proceedings of the Allen D. Leman SwineConference, pp. 29-30.

Philips R, Dee SA, et al. 2000. Elimination of porcine reproductive and respiratory syndrome virus following aclinical PRRS outbreak in a negative herd. Proceedings of the International Pig Veterinary Society Congress.

Philips R, Dee SA, Jordan D. 2000. Elimination of PRRS virus from a 250 sow continuous flow farrow to finishfarm using a MLV PRRS vaccine, unidirectional flow, and test and remove procedures. Proceedings of theInternational Pig Veterinary Society Congress, p. 590.

Philips R, Dee SA. 2002. Evaluation of mass vaccination and unidirectional flow for elimination of PRRS.Proceedings of the International Pig Veterinary Society Congress 2:130.

Turner M, Dufresne L. 2002. A MEW program to eliminate PRRS, APP, and Mycoplasma Hyopneumonia.Proceedings of the International Pig Veterinary Society Congress 1:279.

Wonderlich AL, Michels T, Philips R. 2002. MV/UF to eliminate PRRSV from a gilt multiplier farm. Proceedingsof the International Pig Veterinary Society Congress 2:129.


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Control with Inactivated Virus PRRS VaccineE Thacker, B Thacker, W Wilson, and M Ackerman

Introduction

Porcine reproductive and respiratory syndrome(PRRS) virus continues to be one of the mostimportant swine diseases in the world. Strategies forPRRS virus control and eradication vary amongproduction systems and veterinary advisors, but thereis growing sentiment that a PRRS virus-free herd isthe “gold standard,” especially for herds that producebreeding stock. In the case of PRRS virus, the goldstandard has not been easy to achieve.

Inactivated Virus PRRS Vaccines

Only one inactivated vaccine product (PRRomiSe,Intervet Inc., Millsboro, DE) is currently licensed inthe U.S. Several manufacturers produce autogenousinactivated vaccines, but little data is availableregarding their use, efficacy, or immune response.Use of an inactivated PRRS virus vaccine in Europewas reported to significantly reduce the number ofstillborn and mummies following experimentalchallenge (Charreyre et al., 1998; Reynaud et al.,1998). Current label directions for the licensedinactivated vaccine specify an initial 2.0 ml dose tobreeding females 5 to 8 weeks after service and asecond 2.0 ml dose 14 to 28 days later. Themanufacturer recommends that this two-dosevaccination regimen be repeated at subsequentgestations. The vaccine has not been approved foruse in pigs at other stages of production.

Studies with a Commercial InactivatedPRRS Vaccine

Iowa field studyA recent field study funded by the National PorkBoard investigated the eradication of PRRS virusthrough intensive vaccination of sow herds andyoung pigs with PRRomiSe. Three herds in Iowathat had recently experienced PRRS outbreaksparticipated in the project. Herd T contained 80sows, farrowed 5 times per year, and all phases ofproduction were contained on one site. Herd Scontained 60 sows, farrowed 4 times per year, and allphases of production were housed on one site, withthe exception of several small adjacent sites used forbreeding stock. Herd K consisted of 150 sows andfarrowed every 28 days (5 groups of sows, 3 weeklactation). For this herd, one site contained thebreeding herd and nursery pigs and another site

contained the finishing pigs in one barn with 4rooms.

The inactivated vaccine was administered accordingto the manufacturer’s recommendations with regardto dose and injection site. At the start of the study,all breeding animals were vaccinated twice at 3 to 4week intervals. Thereafter, gilts were vaccinatedtwice prior to breeding, sows and boars oncequarterly, and the pigs at weaning and again 3 to 5weeks later.

All herds noted improvements in overall healthstatus, especially related to respiratory disease. HerdK reported time-to-market decreased by 3 to 4 weeks.All producers were interested in continuing thevaccination program, including the pig vaccinations,although the expense of vaccinating the weaned pigsis probably prohibitive in the long term. In all herds,vaccination of sows appeared to increase serumantibody titers and most sows tested wereseropositive following the initial intensivevaccination program. All herds were successful inproducing PRRS virus-free pigs from the breedingherd. Herds S and T began producing negative pigsas soon as the intensive vaccination program hadbeen instituted. Herd K, the herd with the mostintensive pig flow, did not produce PRRS virus-freepigs until the third monthly weaning group afterinitiation of the program. Only Herd S wassuccessful in maintaining a PRRS virus-free statusthrough the finishing phase. Twice during the study,it appeared that the finishers in Herd K would staynegative, but the situation reversed to a pattern inwhich the pigs becoming infected within one monthafter entering the finisher.

Although there is no single definitive method forcontrolling or eliminating PRRS virus from herds orproducing PRRS virus-free pigs, the results of thisfield study suggested that an inactivated PRRSvaccine could be beneficial in producing PRRS virus-free pigs from infected sow herds.

Study in a 600-sow multiplier herdIn a separate field study, PRRomiSe vaccine wasused to control PRRS in a 600-sow gilt multiplierherd with 3-site production (M. Ackerman, personalcommunication). In December of 1999, the entire


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sow herd, which had previously been vaccinated witha modified-live virus (MLV) PRRS vaccine, wasvaccinated once with the inactivated vaccine and allgilts in isolation were vaccinated twice, two weeksapart. Starting three weeks later, sows and giltsreceived a second dose of vaccine at 60 days ofgestation. Vaccination of all sows and gilts at 60days of gestation was continued thereafter. Thepractice in this herd has been to obtain gilts from aPRRS virus-free herd at 6 months of age. Allincoming gilts are maintained inisolation/acclimatization facilities for 30 days prior tointroduction into the sow herd. Gilts are vaccinatedwith the inactivated vaccine upon arrival and again 2weeks later. Upon entry into the sow herd, nearly allgilts (over 96%) are seronegative for PRRS virus,although they have been vaccinated twice with theinactivated vaccine. Sow and gilts are given abooster dose at 60 days of gestation. At thebeginning of the program, 40 percent of the sow herdwas seropositive, the nursery pigs were seronegative,and the finishers were seropositive. Testing in May2000 revealed seropositive nursery pigs, withantibody levels decreasing in a pattern suggestive ofmaternal antibodies. Nursery pigs were seronegativeby 8 to 10 weeks of age and remained negativethrough the finisher. Since September of 2000, thesow herd has been tested monthly (36 to 45 animalsper month) and the percentage of seropositive sows ateach testing has ranged from 10.0 to 52.3 percent. Asof April 2002, through natural attrition and continuedvaccination with the inactivated vaccine, the herd isnow 85 percent seronegative for PRRS virus. Olderanimals have been gradually replaced, as are all sowsor gilts testing positive for serum antibodies. Thisregimen appears to be proceeding successfully withregard to eradicating PRRS virus from the herd basedon serology and the production of PRRS virus-negative replacement gilts through the finisher.

Summary

PRRS virus vaccination is as a tool for decreasing theimpact of PRRS virus on the breeding herd. TheNAHMS 2000 survey reported that 53.5 percent ofbreeding females were vaccinated for PRRS virus,with MLV vaccine being the most commonly used(37.7%). MLV vaccines are typically thought to

induce a more effective immune response comparedto inactivated virus vaccines due to their ability toinfect and replicate in cells.

Using an inactivated PRRS virus vaccine has severalsafety-related advantages, including no shedding ofvaccine virus and no possibility of reversion tovirulence. In the field, efficacy of either theinactivated or the MLV vaccine has been difficult toconfirm. In the U.S., most PRRS virus vaccination isperformed in the breeding herd and vaccination ofsows with either inactivated virus or MLV is donerepeatedly. Accordingly, these vaccines are mainlyused to booster pre-existing immunity to wild typevirus. Vaccine use in young pigs is low. TheNAHMS 2000 study reported that only 6.4 percent ofpigs in the survey were vaccinated for PRRS virus.

Studies evaluating the immune responses, as well asability of the inactivated virus vaccine to producePRRS virus-negative pigs from PRRS virus-positivesows, have been described. The immune responseinduced by the inactivated virus vaccine differs fromthat of the MLV product. Two of the studies reportedhere suggested that repeated vaccination with theMLV vaccine does not booster the immune responseto PRRS virus. This lack of an anamnestic or recallresponse suggests that repeated chronic exposure toPRRS virus antigen through MLV vaccination maydiminish the ability of lymphocytes to respond to thevirus. However, the studies described here did notdefinitively demonstrate a complete lack oflymphocyte response to PRRS virus antigen. Theefficacy of a vaccine cannot be determined bymeasurement of an immune response alone.Ultimately, challenge studies are required todetermine the ability of a vaccine to induceprotection against clinical disease. The results of thestudies reported here highlight the need for moreinvestigation of the immune responses induced bychronic exposure to wild-type virus and repeatedvaccination. Increased understanding of the immuneresponses induced by repeated vaccination is requiredfor not only PRRS virus but other pathogens, as well,in order to develop appropriate strategies forcontrolling disease in breeding herds where animalscan be kept as long as 4 to 5 years.

References

Charreyre C, Burn A, Aeberle L, et al. 1998. Vaccination challenge with an inactivated vaccine against PRRS.Proceedings of the International Pig Veterinary Society Congress, 2:139.

Reynaud G, Zimmerman M, Charreyre C, et al. 1998. Field evaluation of an inactivated vaccine against PRRS.Proceedings of the International Pig Veterinary Society Congress 3:301.


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Eradication Using Herd ClosureM Torremorell, S Henry, and WT Christianson

Introduction

PRRS virus infection can be costly, is difficult tocontrol, and presents a major limitation to efficientproduction in intensive swine units. For thesereasons, PRRS virus eradication strategies haverecently received close attention from the U.S. swineindustry. Various strategies have been described forPRRS eradication: total depopulation/repopulation,partial depopulation (Dee et al., 1993), Isowean®(Gramer et al., 1999) or segregated early weaning(Rajic et al., 2001), test and removal (Dee, 1998),mass vaccination with unidirectional pig flow (Deeand Philips, 1998) and herd closure are among theprocedures that have been tried. In this section, wedescribe a procedure for PRRS eradication withoutdepopulation based on herd closure. This procedurehas also been described as PRRS elimination by rollover, flow-through, or normal attrition.

The success rate attributed to the herd closureprogram is estimated to be above 85 percent. Theprogram should be implemented in fairly wellisolated three site production systems where the sowherd can be left standing alone. Implementation ofthis program in continuous flow, farrow-to-finishfarms, or in farms with poor and inconsistent giltexposure programs may result in failure.

Control vs. Eradication

In PRRS virus control, the objective is to limit virusdamage in the various stages of production. This isprimarily achieved through management stepsinvolving the gilt pool. Serologically positive ornegative replacements are exposed to PRRS virus inthe acclimatization or isolation unit and are allowedto recover from infection. These animals are thenintroduced into the breeding herd after they becomeimmune, i.e., after when they are no longer viremicand a source of infection to herd mates. Therefore,replacement animals are introduced into the sow farmas PRRS virus seropositive animals.

In PRRS virus elimination, the objective is to removethe virus from infected herds. The virus must beeliminated from all stages of production in order toconsider a production system negative and the systemmust demonstrate its negative status over time. Withthis objective, it is imperative to have negative gilts

and boars available from the source farm(s) asreplacements.

Herd Closure vs. Closed herd

Herd closure, or closing a farm, refers to a period oftime during which replacement animals are notintroduced. Closure applies to both internalreplacements and replacements purchased fromoutside. An interruption of this type is an essentialpart of the PRRS virus eradication program describedin this section.In a closed-herd system, replacements are producedinternally and are introduced into the sow herddirectly from the grower or finisher independently oftheir PRRS virus infection status. In general,“closed-herd systems” do not achieve PRRS viruselimination, although they do bring a measure ofdisease control because replacements usually haveprior exposure to pathogens circulating in the herd.

Overview of the Process

Naïve, seronegative replacement animals areintroduced into seropositive breeding herds whenvirus transmission has ceased. These negativeanimals replace the seropositive herd through normalattrition or by scheduled culling of the previouslyinfected animals. This strategy results in a negativepopulation of breeding animals over time.

To begin, a general evaluation of the farm or systemdetermines whether PRRSV eradication is needed forthe farm, whether it can be done, and if so, if it iseconomically practical.

Location - The farm should be sufficientlyisolated from other farms so as to limit the riskof reinfection after the program is complete.

On-farm biosecurity - Strict on-farmbiosecurity measures are needed to prevent theintroduction of new PRRS viruses and to preventmovement of the virus within the farm orsystem.

Negative source of semen - Only semen from aroutinely monitored PRRSV negative boar studis used.


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Replacement animals - Only naïve,seronegative replacements are used. Availabilityof an isolation area to hold and test thereplacements is mandatory.

Transport - It is important to have a goodunderstanding of how pigs are moved within thesystem and how the trucks are cleaned anddisinfected. Special attention should be paid tocull and slaughter trucks.

Type of production system - Farrow-to-finishfarms are at a disadvantage when using herdclosure because of the risk of PRRS virusspreading from grower animals in proximity tothe breeding herd.

The Principles Behind the Process

Evidence to support the herd closure strategies comesfrom field observations showing that, in closedpopulations, viral infections can be naturallyeliminated over time (Freese and Joo, 1994; Harris etal., 1987; Torremorell et al., 2002). The principlessupporting PRRS virus eradication by this methodwere recently summarized (Torremorell et al., 2000).These principles are summarized as follows:

Immunity. Pigs previously infected with, andrecovered from, PRRS virus are immune toexperimental, homologous challenge for anextended period of time. This suggests thathomologous immunity is protective (Lager et al.,1997). In addition, preliminary data suggeststhat animals with a strong cellular immuneresponse no longer harbor infectious virus(Meier et al., 2000). Importantly, this immunitymay take up to six months to fully develop(Meier et al., 2000); thus, the need to close theherds for an extended period of time. Thepurpose of closure is to allow adequate time forsuch immunity to develop in all the adultanimals.

Biosecurity/transmission. At the beginning ofa PRRS virus elimination project, populations ofpigs with differing immune status (immune vs.susceptible) coexist in the herd. During thistime, it is essential to identify all possiblesources of virus within the farm and to establishoptimal biosecurity measures between thedifferent populations to accommodate pig flowand prevent transmission. Biosecurity measures

to prevent the possible introduction of new viralstrains need to be recognized and strengthened.

Assessment and definition of the population.Defining the dynamics of the viral infection as itoccurs within the farm is a prerequisite toimplementing biosecurity and stoppingtransmission. It is important to identify thepopulations in which the virus circulates, the ageat which pigs become infected, and the serologicand infection status of current replacements.From this information, it can be determinedwhether animal flow can be adequately managedto allow the needed segregation.

Replacement animal introduction. Aconsistent and dependable source of negativereplacement animals and semen is required.

Sentinels as biologic indicators of infection.PRRS virus-naïve, seronegative sentinel animalscan be used as biologic indicators to verify thatvirus is no longer circulating on the farm.Certainty in determining the time for safelybeginning the introduction of negativereplacements relies on the testing results fromsentinels and the demonstration of continuedfreedom from PRRS virus infection. Differentsentinel programs exist, but basically they can begrouped in two strategies: 1) sentinel animalscan be mixed in an off-site location with weanedor cull sows and young gilts to assessseroconversion after proper contact; 2)vasectomized heat check boars can also be usedas sentinels. In this case, by allowing thevasectomized boars to perform the daily heatdetection activities, exposure to previouslyinfected animals is assured. In some systems,the first groups of negative gilts may also beused as the sentinels.

Attrition effects on sow population. Allpreviously exposed and/or infected animals needto be removed as the elimination processprogresses. Whether removal of previouslyinfected pigs is done by test-and-removal,accelerated culling based on age, or herd closure,the fact is that previously exposed animals are arisk factor for transmitting infection tosusceptible animals.


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Implementation of Elimination by HerdClosure

At this time, although elimination by herd closure isattractive, data is lacking to recommend this methodover others. However, clinical experiences indicatethat this method may be a safe, effective, costefficient method to achieve successful PRRS viruselimination.

As discussed previously, candidate farm must standalone, i.e., not house any growing animals other thannursing pigs. Three-site farms are good candidates.Farrow-to-finish farms face the problem of activevirus infection in the growing pig population and therisk of re-introducing the virus into the negativebreeding herd. A summary of the timeline involvedin the implementation of the PRRSV eliminationprogram by herd closure is provided in Table 1.

1. The first step in elimination by herd closure isto ensure that all reproductive animalsundergo PRRS virus infection and recovery.This is achieved by managing the gilt pool andexposing replacement animals to PRRS virus inthe isolation/quarantine area prior tointroduction in the breeding herd . This step iscritical since it will create a population ofimmune animals. In addition this step isconsidered preliminary to the eradicationprogram and it is part of achieving control toPRRS virus infection.

2. The second step is to close the farm to theintroduction of replacement animals. As arule of thumb, the farm should be closed for aminimum of six months, although this willdepend on the production flexibility of the farmand the clinical situation. Methods to decreasethe period of closure are discussed in item c(below). In most cases, the period of closurewill be longer. By closing the farm, naturallydeveloping immunity eliminates virus infectionfrom the herd.To manage a period without animalintroductions and, simultaneously, minimize thecosts associated with the program, off-sitebreeding of negative replacements should beconsidered. If replacements are not available,breeding targets, parity structure, and overallproduction will be affected. In order tominimize the cost associated with theinterruption of gilt introduction, three strategiescan be implemented:a. Use off-site breeding. This strategy will

allow the farm to hit breeding targets in an off-site location. The pregnant gilts will beintroduced into the sow farm at farrowing orlate in gestation. The extra costs incurred arethe lease of an off-site facility, added labor, andadditional animal transport. The breedingproject requires negative gilts, thus at the end ofthe closure period, production is resumed withnegative replacement animals.The economic and operational differencesbetween this and total repopulation are several.Fewer gilts are needed for herd closure;essentially the same number of gilts that wouldbe used in normal flow are required overall.Younger parity animals are not being culled(wasted) and normal replacement flow remainsthe same. An external site will have to berented and, although breeding labor can be doneby personnel already present on site one, therewill be increased labor costs for the project. Incontrast to depopulation, downtime costs areavoided and an extensive clean-up procedure onthe sow farm is not required.b. Add extra replacements to the sow herdprior to closure. This is recommended insystems where virus is actively circulating inthe sow herd as, for instance, immediatelyfollowing an outbreak. These replacements canbe exposed and develop immunity to the viruswhile the sow farm is closed. This strategy maynot work in situations where the sow farm isconsidered very stable and virus circulation isminimal, as the infection of replacementinfection cannot be assured. This strategymimics TGE elimination procedures (Harris etal., 1987) and requires active, on-goinginfection at the time the process is initiated.c. Use replacements infected in the nursery.Farms in which replacements were infected asnursery-aged pigs have an additional option. Aconsistent nursery infection and recoverypattern, accompanied by freedom from clinicalsigns and verified by serologic monitoring, mayreduce the closure time to 2 to 4 months. Thiscan be achieved by changing the giltintroduction schedule to quarterly introductions.The decision to implement a shorter closureperiod depends on the number of viral strains inthe herd, the sow farm stability, theacclimatization program, and the farm’sbiosecurity.

3. Select a source of negative replacements.After initiation of an elimination project, allfuture replacements must be negative when


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introduced into the sow farm. The semensource must also be negative.

4. Introduce negative replacements into the sowfarm. The initial introduction of naïve,seronegative, animals into the sow farmrepresents the point of greatest risk in theprocess. The degree of risk at this stage isdependent upon the degree of assurance thatvirus circulation has ceased. Unfortunately, it isdifficult to determine with certainty that viruscirculation has stopped because laboratorytechniques applied to large swine populationsare not sufficiently sensitive to absolutelyeliminate the possibility of virus transmission.One way to limit this risk is by using naïve,seronegative, sentinel animals prior to theintroduction of negative replacements. Sentinelanimals should be commingled withseropositive sows and gilts in a separate facilityto determine whether virus is still being shed.The replacement animals that enteredimmediately prior to the closure of the herdwere, of course, PRRS positive and, therefore,the animals most likely to remain infected.Since they present the greatest risk of sheddingvirus, careful measures should be taken tosegregate them from the naïve replacements forthe longest time possible

At farrowing, farrowing seropositive andseronegative gilts in the same rooms should beavoided. Additionally, cross-fostering of pigletsbetween these two populations should also beavoided. This will be achieved by delayingbreeding of the negative replacements for at leastthree weeks after the last positive gilt was bred.

5. Eliminate PRRS virus from the growing pigs.This is the last step in the process and requiresdepopulation of the nursery. This, in turn, willcreate an “empty bubble” that will be movedthrough the finisher leaving a population ofPRRS negative pigs behind it. Vigorouscleaning and disinfection is mandatory. Viruselimination in the pig flow should not beattempted at the beginning of the eradicationprogram; it should be performed towards theend, if not after, herd closure and when there are

indications that the pig flow will remainnegative.

6. Eliminate exposed adult animals throughnormal attrition. Removal of previouslyexposed animals is by the normal, or in somecases accelerated, culling of all seropositivefemales present at the time the farm was closed.This makes herd closure very attractive, since itallows for the preservation of the breeding herd,its economic value, and genetics. Overall, theprogram optimizes the value of herd age andproductivity and minimizes the costs associatedwith premature removal of previously infectedanimals.

Throughout the process, routine serologic monitoringis required: sentinels at the beginning of the programand, after the introduction of naive replacements, thenegative breeding stock and the growing pig flow.Monitoring in the production flow is best performedat least on a monthly basis and with adequatestatistical power to detect infection if present.Monitoring should be continued on an on-goingbasis. The purpose of monitoring is to confirm thatthe farm has become, and then remains, seronegative.

Summary

Although it is recognized that PRRS virus can beeradicated from farms, most of the PRRS eliminationprograms that have been described were implementedin farms associated with breeding stock companies.In general, these farms have good biosecurityprograms and are located in low-density pig areas.Without any doubt, these circumstances have alsocontributed to the success of the programs. Thequestion remains whether we can keep farmsnegative in large commercial production systems orin high-density pig areas. So far, it has been verydifficult to keep farms negative that are part of largercommercial systems. In production systems, asystem-wide approach versus a single-farm approachneeds to be explored. Ultimately, the adoption ofPRRS virus elimination programs on a large scale byswine producers will depend on successfullydemonstrating the ability to keep farms negative afterthey are cleaned up.

References

Dee SA. 1998. Elimination of PRRS virus using a test-and-removal process in conjunction with serology and PCRdiagnostics. Proceedings of the American Association of Swine Practitioners, pp. 117-118.

Dee SA, Morrison RB, Joo HS. 1993. Eradicating porcine reproductive and respiratory syndrome (PRRS) virususing two-site production and nursery depopulation. Swine Health and Production 1(5):20-23.


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Dee SA, Philips R. 1998. Using vaccination and unidirectional pig flow to control PRRSV transmission. SwineHealth and Production 6(1):21-25.

Freese WR, Joo HS. 1994. Cessation of porcine reproductive and respiratory syndrome (PRRS) virus spread in acommercial swine herd. Swine Health and Production 2(1):13-15.

Gramer ML, Christianson WT, Harris DL. 1999. Producing PRRS negative pigs from PRRS positive sows.Proceedings of the American Association of Swine Practitioners, pp. 413-416.

Harris DL, Bevier GW, Wiseman BS. 1987. Eradication of transmissible gastroenteritis virus withoutdepopulation. Proceedings of the American Association of Swine Practitioners, p. 555.

Lager KM, Mengeling WL, Brockmeier SL 1997. Duration of homologous porcine reproductive and respiratorysyndrome virus immunity in pregnant swine. Vet Microbiol 58:127-133.

Meier WA, Wheeler J, Husmann RJ, et al. 2000. Characteristics of the immune response of pigs to wild-type PRRSvirus or to commercially available vaccines: an unconventional response. Proceedings of the AmericanAssociation of Swine Practitioners, pp. 415-418.

Rajic A, Dewey CE, Deckert AE, et al. 2001. Production of PRRSV-negative pigs commingled from multiple,vaccinated, serologically stable, PRRSV-positive breeding herds. J Swine Health Prod 9(4):179-184.

Torremorell M, Henry S, Moore C. 2000. Producing PRRSV negative herds and systems from PRRSV positiveanimals: the principles, the process and the achievement. Proceedings of the American Association of SwinePractitioners, pp. 341-347.

Torremorell M, Moore C, Christianson WT. 2002. Establishment of a herd negative for porcine reproductive andrespiratory syndrome (PRRSV) from PRRSV-positive sources. J Swine Health Prod. 10(4):153-160.

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