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Since approximately 2008, the incidence rate of classic tenosynovitis in hens and broiler ocks has been on the increase, even in the face of comprehensive vaccination programs.
Introduction Within the past few years, there has been no shortage of discussion concerning viral arthritis and tenosynovitis across the industry. This has been fueled by an increase in the classic forms of the disease both well-defined Jim Stockam, Technical Services Veterinarian and well-diagnosed in chickens, but also by the emergence of similar signs and lesions in meat-type turkeys proven to be associated with avian reovirus. Several issues can be associated with avian reoviruses in chickens such as stunting syndrome, immunosuppression, enteric disease, and respiratory disease. Of these, viral arthritis/tenosynovitis is the most readily diagnosed and arguably of the most economic importance.1 Although reoviruses have been associated with other diseases in commercial turkeys, tenosynovitis has historically been a very uncommon finding. Economic Losses Since the reoviruses that cause tenosynovitis are present worldwide in most commercial poultry operations, the potential for large economic losses is a constant threat in unprotected ocks.2 Both acute and chronic cases produce a varying degree of lameness which leads to increased cull rates and mortality in broiler and hen ocks alike. In
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often very pronounced in these ocks and produce increased condemnation rates of leg quarters due to the green color observed after picking.4
Current Issues Since approximately 2008, the incidence rate of classic tenosynovitis in hens and broiler ocks has been on the increase, even in the face of comprehensive vaccination programs. The ocks present with pronounced clinical lameness, swollen hocks, joint immobility,
to be antigenically different from S1133. Also, the turkey isolates have been shown to be pathogenic to both turkeys and chickens when introduced into the foot pad.6 There appears to be considerable variation in disease severity in both the chicken and turkey outbreaks. Some ocks exhibit varying degrees of lameness but very little mortality. Other ocks suffer an increase in mortality of 2-5%. The same inconsistencies have also been noted in weight gain, feed conversion, and susceptibility to secondary infection. Resistance to reovirus infections does increase with age and hens will eventually seroconvert to field challenges which may provide an insight as to the variability of outbreaks. Possible Explanations The question remains as to why previous immunization methods appear to have recently lost some of their efficacy. One possible explanation is that variant strains of reoviruses have always been present but are just now beginning to play a prominent role as etiologies of the disease. Another consideration could be that previously known pathogenic strains may have undergone genetic reassortment much in the same way as inuenza viruses do. Orthoreoviruses are double stranded RNA viruses that are non-enveloped and possess a genome consisting of 10 segments. Due to these properties, they could maintain the ability to undergo reassortment and produce viruses that may be different in antigenicity or pathogenicity. In other words, they have the ability to reshufe genetic material in order to produce a different virus while maintaining similar characteristics of the old one. The new virus may cause the same disease with the same clinical signs and lesions, but is antigenically
Disease Control History The role of immunization in attempts to control viral arthritis/tenosynovitis is well documented and has been generally successful. Vaccination programs are designed to protect breeders and broilers through the use of multiple vaccinations.5 Protection from ongoing challenges is typically acquired through the application of three live vaccines given to pullets and males within the first 6 weeks of age followed by one or two inactivated vaccines between 10 and 18 weeks of age. Programs such as these have historically induced adequate protection for production hens and provided early parental immunity protection to broiler chicks. The fact that severe forms of the disease have rarely been encountered for several years in wellprotected ocks is clear evidence that the vaccine strains have delivered sufficient cross protection to the general population of field strains commonly found in the industry.
ruptured gastrocnemius/ digital exor tendons - and mortality in the same manner as has been seen in unprotected ocks. Flocks in question usually exhibit reovirus titers much higher than clinically normal ocks that have received the same vaccination protocols. Also, reovirus can readily be isolated from both acute and chronic lesions. During the same time frame, the Midwest turkey industry has witnessed the emergence of a similar syndrome affecting tom turkeys. This condition is characterized by many of the same clinical signs and lesions seen in chickens with viral arthritis/tenosynovitis.6 Exclusive to turkeys, however, is the dramatic increase in aortic ruptures and the distinctive correlation between ruptured digital exor tendons and aortic rupture mortality in the same animal. Avian reovirus strains have been isolated from turkey lesions but are reported
different enough that conventional reovirus vaccines are not as effective in immunizing the animal against the new virus. Although there is no hard evidence to substantiate the role of reassortment as it relates to the current situation, virus neutralization assays used to compare the strains have shown that while some of these viruses are of the same serotype, they differ antigenically from the chicken viral arthritis Further attempts are strain S1133.6 underway to characterize these novel strains in hopes of gaining knowledge that will lead to effective live and inactivated vaccines. Summary Poultry operations should strive to attain an accurate diagnosis of lameness thought to be caused by reoviruses. The goal should be to avoid clouding the issue with those factors unassociated with viral arthritis/ tenosynovitis, so that a true disease assessment can be made. A combination of serology, histopathology, virus isolation, and antigen specific testing can be employed to rule in or rule out the presence of a variant field strain. Once determined, integrators may opt to use an inactivated autogenous product in hopes of creating some level of immunity to the new virus strains. However, due to the variability of disease severity and lack of field information, evaluation of these products is difficult and more specific challenge studies need to be completed. Also, without an effective live primer, the level of immunity derived from autogenous products may not be as effective as immunization programs geared toward traditional strains. Hopefully, with a greater
understanding as to the characteristics of these novel strains, more effective vaccines can be developed to assist in control of the changing viral arthritis/tenosynovitis issue. References 1. Rosenberger, J.K. and N.O. Olson. 1997. In B.W. Calnek, H.J. Barnes, C.W. Beard, L.R. McDougald, and Y. M. Saif (eds.). Diseases of Poultry, 10th ed. Iowa State University Press, Ames, IA, 711-718. 2. Dobson, K.N., and J.R. Glisson. 1992. Economic impact of a documented case of 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). Blackwell Publishing, Ames, IA, 311-___ 4. Johnson, D.C. and L. Van der Heide. 1971. Incidence of tenosynovitis in Maine broilers. Avian Diseases 15:829-834. 5. Schat, K.A., and M.A. Skinner. 2008. Avian Immunosuppressive Diseases and Immunoevasion. 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 isolated from tendons of turkeys presenting with tenosynovitis and digital exor tendon rupture. Proceedings of the 61st Western Poultry Disease Conference. p 13.
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