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Avian Insight Vol3 2013

Avian Insight Vol3 2013

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Published by Bryan Nicoll

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Published by: Bryan Nicoll on Oct 15, 2013
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Further Viral Arthritis/Tenosynovitis Updates
Within the past few years,there has been no shortageof discussion concerningviral arthritis andtenosynovitis across theindustry. This has beenfueled by an increase inthe “classic” forms of thedisease both well-definedand well-diagnosed inchickens, but also by the emergence of similar signsand lesions in meat-type turkeys proven to beassociated with avian reovirus. Several issues can beassociated with avian reoviruses in chickens such asstunting syndrome, immunosuppression, entericdisease, and respiratory disease. Of these, viralarthritis/tenosynovitis is the most readily diagnosedand arguably of the most economic importance.
 Although reoviruses have been associated with otherdiseases in commercial turkeys, tenosynovitis hashistorically been a very uncommon finding.
Economic Losses
Since the reoviruses that cause tenosynovitis arepresent worldwide in most commercial poultryoperations, the potential for large economic losses isa constant threat in unprotected flocks.
 Both acute and chronic cases produce a varyingdegree of lameness which leads to increased cullrates and mortality in broiler and hen flocks alike. Inaffected flocks, clinical signs and lesions are muchless pronounced at younger ages but increase inseverity as the age increases. Uniformity and feedconversion also suffer partially due to the physicallameness, but also due to the intenseimmunosuppressive nature of the virus which cancause the birds to be more susceptible to disease.Hens exhibit decreased weights and uniformity whichdirectly affects egg production. Breeding malesundergo the same weight challenge which directlyaffects fertility.As broiler flocks approach processing age, otherlosses become more obvious resulting in higher feedconversions, lower average daily gains, and sometimeshigher medication costs.
Automated eviscerationequipment relies on a certain level of flock uniformity.Poor flock uniformity results in higher contaminationand condemnation rates due to physical damage tothe carcasses.
Gastrocnemius tendon ruptures
Volume 3, 2013
Since approximately2008, the incidencerate of “classic”tenosynovitis inhens and broilerflocks has beenon the increase,even in the faceof comprehensivevaccinationprograms.
Further Viral Arthritis/TenosynovitisUpdates,
Notes from the Director of Sales,US & Canada,
Jim Stockam,
 Technical Services Veterinarian
often very pronounced in these flocks andproduce increased condemnation rates of leg quarters due to the
green color observed
 after picking.
Disease Control History
 The role of immunization in attempts tocontrol viral arthritis/tenosynovitis is welldocumented and has been generallysuccessful. Vaccination programs aredesigned to protect breeders and broilersthrough the use of multiple vaccinations.
 Protection from ongoing challenges istypically acquired through the application of three live vaccines given to pullets andmales within the first 6 weeks of agefollowed by one or two inactivated vaccinesbetween 10 and 18 weeks of age. Programssuch as these have historically inducedadequate protection for production hensand provided early parental immunityprotection to broiler chicks. The fact thatsevere forms of the disease have rarely beenencountered for several years in well-protected flocks is clear evidence that thevaccine strains have delivered sufficientcross protection to the general population of field strains commonly found in the industry.
Current Issues
Since approximately 2008, the incidence rateof “classic” tenosynovitis in hens and broilerflocks has been on the increase, even in theface of comprehensive vaccination programs. The flocks present with pronounced clinicallameness, swollen hocks, joint immobility,ruptured gastrocnemius/
digital flexor tendons
- and mortality in the same manneras has been seen in unprotected flocks.Flocks in question usually exhibit reovirustiters much higher than clinically normalflocks that have received the samevaccination protocols. Also, reovirus canreadily be isolated from both acute andchronic lesions. During the same time frame,the Midwest turkey industry has witnessedthe emergence of a similar syndromeaffecting tom turkeys. This condition ischaracterized by many of the same clinicalsigns and lesions seen in chickens with viralarthritis/tenosynovitis.
Exclusive to turkeys,however, is the dramatic increase in aorticruptures and the distinctive correlationbetween ruptured digital flexor tendonsand aortic rupture mortality in the sameanimal. Avian reovirus strains have beenisolated from turkey lesions but are reportedto be antigenically different from S1133.Also, the turkey isolates have been shownto be pathogenic to both turkeys andchickens when introduced into the foot pad.
  There appears to be considerable variationin disease severity in both the chicken andturkey outbreaks. Some flocks exhibitvarying degrees of lameness but very littlemortality. Other flocks suffer an increase inmortality of 2-5%. The same inconsistencieshave also been noted in weight gain, feedconversion, and susceptibility to secondaryinfection. Resistance to reovirus infectionsdoes increase with age and hens willeventually seroconvert to field challengeswhich may provide an insight as to thevariability of outbreaks.
Possible Explanations
 The question remains as to why previousimmunization methods appear to haverecently lost some of their efficacy. Onepossible explanation is that variant strainsof reoviruses have always been present butare just now beginning to play a prominentrole as etiologies of the disease. Anotherconsideration could be that previouslyknown pathogenic strains may haveundergone genetic reassortment much inthe same way as influenza viruses do.Orthoreoviruses are double strandedRNA viruses that are non-enveloped andpossess a genome consisting of 10 segments.Due to these properties, they could maintainthe ability to undergo reassortment andproduce viruses that may be different inantigenicity or pathogenicity. In other words,they have the ability to “reshuffle” geneticmaterial in order to produce a different viruswhile maintaining similar characteristics of the old one. The new virus may cause thesame “disease” with the same clinicalsigns and lesions, but is antigenically
different enough that conventional reovirusvaccines are not as effective in immunizingthe animal against the new virus.Although there is no hard evidence tosubstantiate the role of reassortment as itrelates to the current situation, virusneutralization assays used to compare thestrains have shown that while some of theseviruses are of the same serotype, they differantigenically from the chicken viral arthritisstrain S1133.
Further attempts areunderway to characterize these novel strainsin hopes of gaining knowledge that will leadto effective live and inactivated vaccines.
Poultry operations should strive to attain anaccurate diagnosis of lameness thought tobe caused by reoviruses. The goal should beto avoid clouding the issue with thosefactors unassociated with viral arthritis/tenosynovitis, so that a true diseaseassessment can be made. A combination of serology, histopathology, virus isolation, andantigen specific testing can be employed torule in or rule out the presence of a variantfield strain. Once determined, integratorsmay opt to use an inactivated autogenousproduct in hopes of creating some level of immunity to the new virus strains. However,due to the variability of disease severity andlack of field information, evaluation of theseproducts is difficult and more specificchallenge studies need to be completed.Also, without an effective live primer, thelevel of immunity derived from autogenousproducts may not be as effective asimmunization programs geared towardtraditional strains. Hopefully, with a greaterunderstanding as to the characteristics of these novel strains, more effective vaccinescan be developed to assist in control of thechanging viral arthritis/tenosynovitis issue.
1. Rosenberger, J.K. and N.O. Olson. 1997. InB.W. Calnek, H.J. Barnes, C.W. Beard, L.R.McDougald, and Y. M. Saif (eds.). Diseasesof Poultry, 10
ed. Iowa State UniversityPress, Ames, IA, 711-718.2. Dobson, K.N., and J.R. Glisson. 1992.Economic impact of a documented caseof reovirus infection in broiler breeders.Avian Diseases 36:788-791.3. Jones, R.C. Reovirus Infections. 2010.In: Diseases of Poultry. Y. M. Saif, J. R.Glisson, A. M. Fadly, L. R. McDougald, L. K.Nolan, and D. E. Swayne (eds). BlackwellPublishing, Ames, IA, 311-___4. Johnson, D.C. and L. Van der Heide. 1971.Incidence of tenosynovitis in Mainebroilers. Avian Diseases 15:829-834.5. Schat, K.A., and M.A. Skinner. 2008. AvianImmunosuppressive Diseases andImmunoevasion. In: Avian Immunology. G.Davison, B. Kaspers and K. A. Schat (eds).Elsevier, Ltd., London, U.K. pp 314-337.6. J. Rosenberger, J. Trites, D. Mills, J. Stockam,S. Rosenberger, and M. Markis. 2012.Characterization of reoviruses isolatedfrom tendons of turkeys presenting withtenosynovitis and digital flexor tendonrupture. Proceedings of the 61st WesternPoultry Disease Conference. p 13.

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