Viral Arthritis: Introduction
(Reoviral infection, Tenosynovitis) |  |
| Reoviruses are ubiquitous in chickens and turkeys; some strains become viremic and localize in the large joints, resulting in arthritis, tendinitis, and synovitis. Most birds are thought to be susceptible to respiratory-intestinal strains of reoviruses. Chickens and, to a lesser degree, turkeys are susceptible to viral arthritis, which is seen worldwide. Reoviruses also have been associated with pericarditis and myocarditis, hydropericardium, pasting, malabsorption, and femoral
head necrosis, although further study is needed to define their role. (See also
malabsorption syndrome,
Malabsorption Syndromes .) |
| Transmission and Pathogenesis: |
| The disease is egg-transmitted and is of short duration except when lateral transmission in a flock is prolonged. Respiratory and digestive infections may occur but are of short duration; however, the virus survives in tendon sheaths for extended periods. The virus is spread via aerosols, fomites, and mechanical means, and is resistant to heat and chemical inactivation. |
| Several antigenic subtypes of avian reoviruses have been identified; however, there appears to be significant cross-protection among most of the isolates or subtypes. Pathogenicity of the isolates varies widely. Serious outbreaks of viral arthritis are followed by a decreased incidence in later hatch groups of birds from the same parent flock. This may be related to decreased egg transmission and development of parental immunity. Day-old chicks are more susceptible than older
birds when exposed by natural means. The earlier in life the chick is infected, the longer the virus persists in the tissues. |
|  |
| Clinical Findings: |
|
The arthritic form (tenosynovitis) 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. The birds walk with a stilted gait. In severely affected flocks, rupture of the gastrocnemius tendon is frequent, and many cull birds are seen around the feeders and waterers. Mortality is 2-10% and morbidity 5-50%. Severely affected birds
rarely recover; less severely affected birds recover in 4-6 wk. The infection is inapparent in many birds. Feed efficiency and rate of gain are decreased. |
Lesions:
| An acute, fulminating infection is occasionally seen in young chicks and embryos with cardiomegaly, hepatomegaly, and splenomegaly with necrotic foci. Edema of 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 with rupture of the gastrocnemius tendon. 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 heterophils and macrophages. Infiltration of heterophils or lymphocytes, or both, between myocardial fibers is a constant finding. However, the infiltrating heterophils are difficult to distinguish from the clusters of young, proliferating heterophils (ectopic myelopoiesis) that are present in the heart muscle
of all young, rapidly growing broiler chickens. |
| |
| Diagnosis: |
| 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. Virus from affected tissues can be isolated in primary kidney, liver, or lung cells, or in the yolk sac or chorioallantoic membrane of embryonating chicken eggs. The agar-gel-precipitin test is usually positive, and most birds are positive early in the infection. Virus
neutralization tests and challenge of immunized chickens are used to detect the specific serotype. Culture procedures should be used to differentiate mycoplasmal and other bacterial infections. Other causes of lameness should be considered. |
| |
| Treatment and Control: |
| There is no treatment. Maternal antibody prevents early infection in chicks and should reduce or prevent egg transmission. Because egg transmission is the principal means of spread, it is desirable to have the breeder flock immune. Such a program should be directed to the serotypes present in the flock. Adult birds are less susceptible to clinical disease if exposed by natural routes. |
| |
;)