In poultry species, the term "viral arthritis" is used to describe inflammation affecting leg joints and/or tendons that is attributable to reovirus infection. Clinical signs include lameness and ruptured tendons. Definitive diagnosis relies on isolation and/or identification of reovirus from the affected tissue via virus isolation or RT-PCR. For clinically affected birds, general supportive care is the only treatment option. Prevention of clinical signs relies on the generation of a protective, serotype-specific immune response.
Reoviruses are ubiquitous in commercial poultry worldwide. A variety of reoviruses can be found in the respiratory and/or GI tract of nonclinically affected poultry species and are apparently nonpathogenic; not all reoviruses cause viral arthritis. Viral arthritis in poultry is an inflammation of tendons and joints in the legs caused by virulent strains of reovirus.
The nature of the disease and clinical signs associated with viral arthritis depends on the type of bird (broiler, breeder, turkey), the bird's age and immune status, the virus pathotype, and the route of exposure.
Reoviruses are associated with various disorders in poultry, including the following:
immunosuppression
pericarditis
myocarditis
osteoporosis
hepatitis
The role of reoviruses as causative agents of viral arthritis has been well established.
Etiology and Pathogenesis of Viral Arthritis in Poultry
Reoviruses belong to the genus Orthoreovirus in the family Reoviridae. Avian reovirus is nonenveloped, with a 10-segmented, double-stranded RNA genome.
The sigma C protein, encoded on the S1 gene, is located on the outer capsid of the virus and is responsible for cell attachment and the induction of virus-neutralizing antibodies. The S1 gene sequence is the most variable within the viral genome and is the target for genetic characterization and diagnostic genotyping.
Reovirus strains differ in virulence, ranging from those that cause arthritis to those that exist harmlessly in the gut. The mechanisms that determine pathogenicity are poorly understood. Several antigenic types are known, and although there is some cross-protection between types, it is rarely complete. Most infections are acquired by ingestion.
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Transmission and Epidemiology of Viral Arthritis in Poultry
Reoviruses are transmitted vertically and horizontally. Infection after oral exposure allows the virus to gain access via intestinal epithelial cells. If viremia occurs, the virus can spread to multiple locations, such as the heart, liver, intestines, and tendons.
The outcome of exposure and infection by reoviruses depends on the age of the infected animal, its immune status, the viral pathotype, and the route of exposure. Birds < 2 weeks old are immunoincompetent, and in the absence of virus-specific maternal antibodies, viremia can occur unchecked.
In older or mature birds, infection by reoviruses can result in transient viremia that is halted by a functioning immune system and/or the presence of protective virus-neutralizing antibodies. Transient viremia in egg-producing flocks can result in vertical viral transmission, followed by horizontal transmission among immunologically naive offspring lacking maternal antibodies.
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In young and/or immunoincompetent birds, if viremia results in localization of the reovirus within tissues such as the heart and/or tendon, inflammation occurs. Subsequent cellular infiltration by heterophils, followed by lymphocytes, can lead to the development of hydropericardium. Edema and heterophilic inflammation, followed by lymphohistiocytic inflammation, occurs in the joints and tendons and coincides with the onset of lameness.
Clinical Findings of Viral Arthritis in Poultry
Although reovirus infection can occur early in life, the appearance of clinical signs depends on the type of bird, its immune status and age, and the pathogenicity of the virus.
Mild inflammation can go unnoticed in a flock, particularly in light breeds such as commercial layers or in birds with slowed growth rates, such as broiler breeders. Tendon damage (see ruptured tendon image) and subsequent fibrosis in broiler breeders can become apparent later, after birds move from a pullet facility into a typical breeder production system. In the henhouse, hens are expected to be able to jump up onto a slatted area, and this jumping motion can cause fibrotic tendons to rupture.
Courtesy of Ontario Veterinary College.
Inflammation within the joints and tendons of heavier or more rapidly growing meat poultry breeds can manifest as poor mobility, lameness, and slowed growth rates during the life of a flock. Alternatively, depending on slaughter age, clinical signs can go unnoticed until tendon damage and rupture are detected at processing.
Lesions of Viral Arthritis in Poultry
Examination of poultry legs affected by viral arthritis often reveals swollen tendons, hock joints, and shanks (see tendon lesion images). Necropsy might show increased fluid in the hock joint or edema of the digital flexor tendons and/or gastrocnemius tendon. In severe cases, the tibial condyles are flattened and the distal tibial cartilage shows pitted erosions. Additional findings can include rupture of the gastrocnemius tendon, pericarditis or epicarditis, and variable bird size within a flock.
Courtesy of Dr. Jenny Nicholds.
The synovial cells in poultry with viral arthritis are hypertrophied, hyperplastic, and infiltrated by lymphocytes and macrophages (see histological images). The synovia and tendon sheaths contain lymphoid aggregates with heterophils and macrophages. The heart can show nodular infiltration of lymphocytes in the epicardium and infiltration of heterophils or lymphocytes between myocardial fibers.
Courtesy of Dr. Jenny Nicholds.
Diagnosis of Viral Arthritis in Poultry
Demonstration of reovirus in affected tissue by virus isolation and RT-PCR
Diagnosis of reovirus infection causing viral arthritis in poultry ideally requires demonstration of reovirus in the affected tissue (the tendon or synovial fluid). Collecting whole legs from birds with clinical signs of reoviral arthritis is recommended for diagnostic purposes. Fresh tendon or synovial fluid can then be aseptically collected at a diagnostic laboratory to avoid contamination with other ubiquitous reoviruses.
Tendon/synovial fluid can be tested for the presence of reovirus using methods such as virus isolation or RT-PCR. If the viral load in the tissue could be diminishing, virus isolation followed by RT-PCR might be preferable. Isolation of reovirus from other tissues is not useful for diagnosing viral arthritis, because this virus is ubiquitous in poultry production.
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Samples of the contralateral tendon in affected birds can be collected and fixed in formalin for histological examination to confirm inflammatory changes consistent with reovirus infection. With chronicity, however, microscopic changes associated with reoviral arthritis become indistinguishable from other joint insults that result in progressive tendon fibrosis. Isolation and detection of reovirus from chronically affected tissue is unlikely to be successful.
Commercially available ELISAs can be used to diagnose reovirus infection; however, results are not definitive. Plates used in these tests are coated with whole virus. The ubiquitous nature of reovirus means that even unvaccinated flocks show a serological response for reovirus; furthermore, many flocks are vaccinated against reovirus. Commercially available kits detect group-specific antibodies but cannot differentiate between reovirus serotypes.
ELISA can be used to determine whether a flock has been exposed to a field virus if a rapid increase in antibody titers is observed between acute and convalescent serum in the absence of recent vaccination or if titers are substantially greater compared with historic baseline levels.
Virus neutralization assays can be used to detect type-specific antibodies. However, definitive diagnosis should rely on the detection of virus in affected tissues.
Other differential diagnoses that should be considered for the described clinical signs and lesions include nutritional deficiencies (calcium/phosphorus imbalance, rickets) or other infectious causes (eg, mycoplasmosis, staphylococcosis, colibacillosis, etc).
Prevention, Treatment, and Control of Viral Arthritis in Poultry
Vaccination
The humoral immune system generates a protective immune response to reovirus after exposure to the sigma C protein on the outer capsid of the virus. However, this humoral immune response is serotype specific.
Historically, clinical signs of viral arthritis in poultry that were attributed to reovirus infection were prevented by administration of commercially available vaccines; vaccination prevented vertical transmission of the virus and provided progeny with maternal antibody to prevent disease.
Beginning in 2012, the number of viral arthritis cases in chickens and turkeys increased in various parts of the world. Characterization of field isolates from clinical cases revealed variant reoviruses—viruses that differed, both genetically and antigenically, from commercial reovirus vaccine strains.
Analysis of the sigma C sequence of reoviruses enables genetic characterization of viruses into genetic clusters (GCs). To date, seven GCs (GC1–GC7) have been identified in clinical samples. In addition, some clinical isolates contain mixed populations of reoviruses belonging to several distinct GCs.
Nearly all commercially available modified live and inactivated poultry reovirus vaccine strains in North America are contained in GC1, including strains S1133, S1733, S2408, and S2177. One exception to this grouping is a vaccine consisting of three variant reovirus serotypes.
In general, because reoviral vaccine strains are serologically related, they do not protect against disease caused by variant reoviruses. In 2012–2014, many variant reovirus isolates belonged to GC5. As a result, many US companies began incorporating GC5 isolates into their autogenous (custom-made) vaccine programs. Since then, the detection of GC5 isolates has diminished; however, other variant reoviruses belonging to multiple other GCs continue to be detected.
Current prevention of viral arthritis due to reovirus infection depends on whether variant field reoviruses have been detected within a given poultry production operation or region. In the absence of variant reoviruses, vaccination with any commercially available product—whether live, live-attenuated, or inactivated—continues to be a viable option.
If variant reoviruses from clinical cases are detected, autogenous vaccines can be considered as a control option where legislation permits. Custom-made vaccines are conditionally licensed, inactivated, non–commercially available products that contain antigen produced from the field isolate. Autogenous veterinary vaccines are available in the US, Europe, and several Latin American, Asian, and African countries.
The optimal selection of isolate(s) to include in a custom-made vaccine depends on the collection and characterization of clinically relevant isolates from the field. Additional laboratory work to identify the most prevalent circulating genotype(s) and to confirm pathogenicity helps to ensure appropriate selection.
Other than general supportive care, there is no treatment for viral arthritis in poultry once clinical signs are apparent. Birds that are lame and unable to reach feed and/or water should be euthanized.
Future control of viral arthritis due to reovirus infection will rely on new vaccination technologies and strategies. Quadrivalent, recombinant, and subunit vaccines are all being investigated.
Zoonotic Risk of Viral Arthritis in Poultry
No reported zoonotic risks are associated with avian reovirus infections.
Key Points
Reovirus is a well-established cause of viral arthritis in poultry. However, not all reoviruses cause the disease.
Diagnosis of reovirus as the cause of viral arthritis requires detection of the virus in affected tissues. Given the ubiquitous nature of reoviruses, isolation from other tissues does not confirm viral arthritis.
There is no treatment for birds clinically affected with viral arthritis. Prevention of clinical signs relies on the generation of a protective, serotype-specific immune response.
For More Information
Pitcovski J, Goyal SM. Avian reovirus infections. In: Swayne DE, ed. Boulianne M, Logue CM, McDougald LR, Nair V, Suarez DL, associate eds. Diseases of Poultry. 14th ed. Wiley Blackwell; 2020:382-400.
van der Heide L, Vaillancourt J-P. Reovirus infections. In: Brugère-Picoux J, Vaillancourt J-P, Shivaprasad HL, Venne D, Bouzouaia M, eds. Manual of Poultry Diseases. AFAS; 2020:chap 27.
Sellers HS. Avian reoviruses from clinical cases of tenosynovitis: an overview of diagnostic approaches and 10-year review of isolations and genetic characterization. Avian Dis. 2022;66(4):420-426.
Gamble TC, Sellers HS. Field control of avian reoviruses in commercial broiler production. Avian Dis. 2022;66(4);427-431.
