Reovirus infections are ubiquitous in commercial poultry flocks. They are global in distribution, although the virulence of viruses appears to differ between regions. Most strains are nonpathogenic and appear to survive harmlessly in the intestine, whereas others have been associated with several disease conditions, including malabsorption and other enteric disorders, hydropericardium, and occasionally respiratory disease. In many instances, the association of the reovirus with disease is uncertain. An exception to this is viral arthritis, or tenosynovitis, because it can be reproduced experimentally by infecting birds with reovirus alone.
Viral arthritis results in severe lameness in heavy broiler breeds of chickens and occasionally in laying breeds. Although lameness in turkeys has sometimes been reported to be associated with avian reoviruses, experimental evidence in the past has been unable to confirm that turkeys are as susceptible to these viruses as chickens. However, recent field evidence from the USA indicates the presence of novel reoviruses causing arthritis and tendon rupture clinically identical to that in chickens. Reoviruses have been isolated from a range of other avian (including wild) species, and it is possible that cross-infection occurs, although ducks and geese have reoviruses that differ genetically from those of chickens.
Etiology and Pathogenesis
Viral arthritis is caused by avian reoviruses, which are RNA viruses related to but distinct from mammalian reoviruses. Strains differ in virulence, ranging from those causing arthritis and sometimes death to those that exist harmlessly in the gut. The mechanisms that determine whether a reovirus is pathogenic or harmless are poorly understood. Several antigenic types are known, and although some cross-protection occurs between types, it is rarely complete. Most infections are acquired by ingestion. After intestinal replication, the virus spreads via the bloodstream to all parts of the body. Pathogenic viruses localize in the hock joint, where they cause arthritis. Other organs, such as the liver, may be affected.
Transmission and Epidemiology
Avian reoviruses can be egg transmitted, so infected breeder hens pass virus to chicks. Transmission is short-lived, and only a small nucleus of chicks carry virus. Infection is spread locally to hatch mates by the fecal-oral route. The virus is quite resistant to inactivation and can persist on farm materials for many days or weeks. Fomites are important.
Serious outbreaks of viral arthritis are followed by a decreased incidence in later hatch groups of birds from the same parent flock and may be related to decreased egg transmission and development of maternal immunity. Day-old chicks are more susceptible than older birds when exposed by natural means. The younger the chick when infected, the more likely it is that disease will develop.
Viral arthritis usually is seen in broilers 4–8 wk old as unilateral or bilateral swellings of the tendons of the shank and above the hock. It can also be found in much older chickens, usually at peak of production or beyond, probably because of reactivation of persistent virus at sexual maturity. Affected birds walk with a stilted gait or prefer not to move. In the most severe form, rupture of the gastrocnemius tendon is common, although digital flexor tendons are sometimes affected and many cull birds are seen around the feeders and waterers. The most severely affected birds do not recover; less severely affected birds may recover in 4–6 wk. Infection is asymptomatic in many birds. Feed efficiency and rate of weight gain are decreased. Mortality is 2%–10% and morbidity 5%–50%.
An acute, fulminating infection is occasionally seen in young chicks and embryos with cardiomegaly, hepatomegaly, and splenomegaly with necrotic foci. Edema around the tendons of the leg is marked, petechial hemorrhages develop in the synovial membranes above the hock, and fusion and calcification of the tendon bundles are common. Blood clots and hemorrhages are seen accompanying rupture of the gastrocnemius tendon. In the most severe cases, pitted erosions of the cartilage of the distal tibiotarsus are seen with flattening of the condyles. Histologically, the synovial cells are hypertrophied, hyperplastic, and infiltrated by lymphocytes and macrophages. The synovia contain lymphoid aggregates with heterophils and macrophages. In the heart, infiltration of heterophils or lymphocytes between myocardial fibers is a consistent finding.
A presumptive diagnosis can be based on unilateral or bilateral swelling of the tendons of the shank and tendon bundle above the hock and on the inflammatory changes in the tendons and synovia described above. However, other causes of lameness such as Mycoplasma synoviae or Escherichia coli should be considered. Reovirus can be isolated from affected joints in primary chick embryo kidney, liver, or lung cell cultures, or via the yolk sac or chorioallantoic membrane of embryonated chicken eggs. In view of the widespread nature of reovirus infections without disease, isolation from the gut is not significant. In many laboratories, PCR is used for virus identification and is more rapid and sensitive than isolation. Avian reoviruses are now classified according to their sigma surface proteins, and the indications are that the novel USA turkey and European chicken viruses are different from the common ones associated with viral arthritis. The turkey isolates are genetically related to the turkey enteric reoviruses, but further molecular analysis is awaited. In view of the ability of avian reoviruses to recombine, it is possible these new arthritogenic variants in both species have evolved by this means. ELISA is the serologic test of choice, and most birds are positive early in infection. Virus neutralization tests and challenge of immunized chickens can be used to identify the specific serotype. However, serologic results can be difficult to interpret in view of the ubiquity of reovirus infections. Culture procedures should be used to differentiate mycoplasmal and other bacterial infections.
Treatment and Control
There is no treatment. Live and killed vaccines are available. Maternal antibodies prevent early infection in chicks and minimize or prevent egg transmission. In view of egg transmission and the greater susceptibility of baby chicks, the main objective of vaccination is to ensure good immunity in the parent flock. Vaccination programs should be directed to the serotype(s) present in local flocks. Adult birds are less susceptible to clinical disease if exposed by natural routes. Currently available commercial vaccines against viral arthritis are not effective against the newly encountered chicken viruses described in Europe or against those causing arthritis in turkeys.
There have been no reported zoonotic risks associated with avian reovirus infections.
Last full review/revision September 2013 by Richard C. Jones, BSc, PhD, DSc, FRCPath