Reoviruses are ubiquitous in commercial poultry worldwide. A variety of reoviruses can be found in the respiratory and/or GI tract of asymptomatic poultry species and are apparently nonpathogenic; not all reoviruses cause viral arthritis.
The nature of disease and clinical signs associated with viral arthritis is influenced by type of bird (broiler, breeder, turkey), age of bird, immune status, virus pathotype, and route of exposure.
Reoviruses are associated with a variety of disorders in poultry, including:
The role of reoviruses as causative agents of viral arthritis has been well established.
Etiology and Pathogenesis
Reoviruses belong to the family Reoviridae in the genus Orthoreovirus. 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 induction of virus-neutralizing antibodies. It is the target for diagnostic genotyping.
Strains differ in virulence, ranging from those causing arthritis 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.
Transmission and Epidemiology
Transmission of reoviruses occurs vertically and horizontally. Infection after oral exposure allows the virus to gain access via intestinal epithelial cells. If a viremia occurs, the virus can spread to multiple locations such as the heart, liver, intestines, and tendons.
The outcome of exposure and infection will depend on the age, immune status, virus pathotype, and route of exposure. Birds less than 2 weeks of age are immune incompetent, and, in the absence of virus-specific maternal antibodies, viremia can occur unchecked. In older or mature birds, infection may result in transient viremia that is halted by a functioning immune system and/or the presence of protective virus neutralizing antibodies. A transient viremia in a flock in egg production can result in vertical transmission of the virus, which can then spread horizontally among naïve, maternal antibody-negative offspring.
In young and/or immune-incompetent birds, if viremia results in localization within tissues such as the heart and/or tendon, inflammation occurs. Subsequent cellular infiltration in the heart can lead to development of hydropericardium. Edema and heterophilic inflammation, followed by lymphohistiocytic inflammation, occur in the joints and tendons and coincides with the onset of lameness.
As mentioned previously, although infection with reovirus may occur early in life, the appearance of clinical signs will depend on the type of bird, immune status, age, and pathogenicity of the virus.
Mild inflammation may go unnoticed in a flock, particularly in light breeds such as commercial layers or where growth rates are slowed, such as broiler breeders. Tendon damage and subsequent fibrosis in broiler breeders may become apparent later, once 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 result in rupture of fibrotic tendons.
Inflammation within the joints and tendons of heavier or more rapidly growing meat breeds can manifest in the form of poor mobility, lameness, and retarded growth rates during the life of a flock. Alternately, depending on slaughter age, clinical signs may go unnoticed until tendon damage and rupture are detected at processing.
Examination of legs often reveals swollen tendons, hock joints, and shanks. At necropsy, increased fluid in the hock joint and/or edema of the digital flexor tendons and/or gastrocnemius tendon can be observed. In severe cases, pitted erosions of the cartilage of the distal tibiotarsus are seen, with flattening of the condyles. Additional findings may include rupture of the gastrocnemius tendon, pericarditis or epicarditis, and poor uniformity. Histologically, the synovial cells are hypertrophied, hyperplastic, and infiltrated by lymphocytes and macrophages. The synovia and tendon sheaths contain lymphoid aggregates with heterophils and macrophages. In the heart, nodular infiltration of lymphocytes in the epicardium and infiltration of heterophils or lymphocytes between myocardial fibers may be observed.
Demonstration of reovirus in affected tissue by virus isolation and RT-PCR
Diagnosis of reovirus infection causing viral arthritis ideally requires demonstration of reovirus in the affected tissue, the tendon, or synovial fluid. Fresh tendon or synovial fluid, collected aseptically, from clinically affected birds should be tested for the presence of reovirus using methods such as virus isolation or RT-PCR. Isolation of reovirus from other tissues in the context of trying to diagnose viral arthritis is meaningless due to the ubiquitous nature of this virus in poultry production. Samples of tendon collected from affected birds can be formalin fixed for histopathologic examination to confirm inflammatory changes consistent with reovirus infection. However, with chronicity, 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 also unlikely to be successful.
Commercially available ELISAs can be used to diagnose reovirus infection, but results are not definitive. Plates used in these tests are coated with whole virus. The ubiquitous nature of reovirus means that even unvaccinated flocks will demonstrate a serologic response for reovirus, and furthermore, many flocks receive vaccination against reovirus. Commercially available kits will 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 significantly greater compared with historic baseline levels. Virus neutralization assays can be used to detect type-specific antibodies. Definitive diagnosis should, however, rely on detection of virus from affected tissues.
Other differential diagnoses should be considered for the described clinical signs and lesions, including but not limited to nutritional deficiencies (calcium/phosphorus imbalance, rickets) or other infectious causes (eg, mycoplasmosis Mycoplasmosis read more , staphylococcosis Staphylococcosis read more , colibacillosis Colibacillosis in Poultry Colibacillosis is caused by infection with a pathogenic strain of Escherichia coli. Signs vary and can include acute fatal septicemia, airsacculitis, pericarditis, perihepatitis, and lymphocytic... read more , etc.).
Prevention, Treatment, and Control
Vaccination with commercial or custom-made vaccines
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. This humoral immune response is, however, serotype specific. Historically, clinical signs of viral arthritis attributed to reovirus infection have been prevented through the use of commercially available vaccines; vaccination prevented vertical transmission of virus and provided progeny with maternal antibody to prevent clinical disease. In recent years however, an increasing number of variant reoviruses, to which protection is not afforded with commercially available vaccines, have been detected.
Commercially available poultry vaccine strains for reovirus include S1133, 1733, 2408, and 2177. The vaccine strains are serologically related and therefore do not protect against disease caused by variant reoviruses. In 2012 and after, an increase in the number of viral arthritis cases in chickens and turkeys was observed in various parts of the world. Characterization of field isolates from clinical cases revealed viruses that differed, both genetically and antigenically, from commercial reovirus vaccine strains.
Current prevention of viral arthritis due to reovirus infection depends on whether variant field reoviruses have been detected within a given company or region. In the absence of variant reoviruses, vaccination with live, attenuated live, and/or inactivated commercially available products continues to be a viable option. Upon detection of variant reoviruses from clinical cases, use of custom-made vaccines (CMVs) can be considered as a control option where legislation permits. CMVs are a limited licensed, inactivated, noncommercially available product containing antigen produced from the field isolate. This is an option available in countries such as the USA and Canada. The optimal selection of an isolate or isolates to include in a CMV will depend upon 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 are beneficial to ensure appropriate selection.
There is no treatment for infected birds once clinical signs of viral arthritis are apparent, other than general supportive care. 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 areas of current exploration.
There have been no reported zoonotic risks associated with avian reovirus infections.
Reovirus is a well-established cause of viral arthritis. However, not all reoviruses will cause viral arthritis.
Diagnosis of reovirus causing viral arthritis requires viral detection in the affected tissues. In the context of 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.