Observations on viral tenosynovitis (viral arthritis) in Scotland

Macdonald, J. W.; Randall, CJ; Dagless, M.D.; McMartin, D.A.

doi:10.1080/03079457808418303

Cited by 32 publications

(12 citation statements)

References 21 publications

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“…In Expt. 1, while variation in severity was seen between strains, the histopathology of the lesions was similar to that described by Kerr and Olson (1969), van der Heide et al (1974) and Macdonald et al (1978). In contact-infected birds, the relatively early appearances of cellular abnormalities in joints and of virus in the tissues demonstrates the comparatively rapid lateral spread of the agent.…”

Section: Discussionsupporting

confidence: 62%

The pathogenicity of some avian reoviruses with particular reference to tenosynovitis

Jones

Guneratne

1984

Avian Pathology

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SUMMARYIn two experiments, 13 avian reoviruses from different sources were tested in specific pathogen-free (SPF) light hybrid chicks at 1-day-old for their pathogenicity with particular respect to tenosynovitis. All strains including two from commercial ducks and another from a wedge-tail eagle caused tenosynovitis. In most cases the lesions were macroscopic but in a few only microscopic abnormalities were observed after footpad or oral inoculation. In the first experiment with six British strains, infection by contact also resulted in tenosynovitis, and in most cases virus persisted longer in the hock joint/tendons than in the gut. Among the 13 viruses, two strains, R14 and Lasswade 126/75 were the mildest, producing only slight microscopic lesions of the disease, while strain WVU 2937 was the most virulent for joints/tendons.

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Section: Discussionsupporting

confidence: 62%

The pathogenicity of some avian reoviruses with particular reference to tenosynovitis

Jones

Guneratne

1984

Avian Pathology

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“…Cell-mediated immunity is considered to be involved in the development of synovitis due to M. synoviae (Powell, 1983). Whether this applies to viral tenosynovitis as well has not been investigated, but Olson (1959) and Macdonald et al (1978) suggested that the inflammatory process may continue when the virus is no longer demonstrable. The high isolation rate of reovirus associated with the low morbidity rate in light birds observed by us was also reported by Marquardt et al (1983) who noted the virus to persist in tendon tissue despite the presence of high titres of neutralising antibody.…”

Section: Body Weight Gainmentioning

confidence: 99%

“…However, one feature of experimental infections is that joint lesions are seldom as severe as those observed in naturally occurring tenosynovitis (Macdonald et al, 1978;R.C. Jones, unpublished observations) and it has been considered that other factors such as the route of infection (Glass et al, 1973;Sahu et al, 1979;Wood and Thornton, 1981), susceptibility of the chickens used (Jones and Onunkwo, 1978;Macdonald et al, 1978;Marquardt et al, 1983) and their age at infection (Kerr and Olson, 1964;Wood and Thornton, 1981 ;Jones and Georgiou, 1984), may influence the severity of reovirus-induced tenosynovitis.…”

Section: Introductionmentioning

confidence: 99%

Reovirus‐induced tenosynovitis in chickens: The effect of breed

Jones

Kibenge

1984

Avian Pathology

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SUMMARYThe effect of breed of chicken on infection with an arthrotropic avian reovirus strain R2 was studied by oral or footpad inoculation of 1-dayold chicks of the following breeds: (1) specific pathogen-free (SPF) light-hybrid, (2) commercial White Leghorn egg-layer, and (3) commercial Ross I broiler, and observed to 12 weeks of age. Although most inoculated birds of all three breeds developed swelling of one or both legs below the hock joint at 3 to 4 weeks of age, gross lesions of tenosynovitis became progressively more severe and extended above the joints only in broilers, whereas in most orally-infected SPF and commercial light chickens gross lesions were intermittently severe and regressed with time. Cloacal virus shedding continued up to 2 weeks in the lighter breeds and 3 weeks after infection in broilers. From a small proportion of infected chickens, reovirus was also reisolated from heart, pancreas and caecal tonsils. In all breeds, the tissue in which virus persisted longest was the hock joint/tendon. There was a poor correlation between isolation of virus and the presence of gross lesions in chickens of 12 weeks of age, especially in broilers. Virus-neutralisation tests demonstrated that seroconversion in the lighter breeds occurred predominantly at 3 weeks and in broilers at 4 weeks after infection. In all three breeds the footpad infection gave significantly lower growth rates than were found in the control and oral-infection groups. Oral infection had no apparent effect on growth rates.

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“…The P100 virus represents the 100th tissue culture passage of Sl133. The R19 and Lasswade isolates (MacDonald et al, 1978) were obtained from R. C. Jones, University of Liverpool, Wirral, U.K. Human reovirus type 1 (Lang) was obtained from B. N. Fields, Harvard Medical…”

Section: Discussionmentioning

confidence: 99%