Turkey Arthritis Reovirus (TARV) and aortic rupture in Ontario turkeys
Emily Martin, Davor Ojkic, Marina Brash, Emily Brouwer and Helen Wojcinski
Animal Health Laboratory, University of Guelph, Guelph, ON (Martin, Ojkic, Brash, Brouwer); Wojcinski Poultry Health Consulting, Michigan, USA. (Wojcinski).
AHL Newsletter 2020:24(2):12.
Reovirus was isolated from joints and ruptured tendons of turkeys with tenosynovitis/arthritis as early as 1980; however, while reovirus was shown to cause the disease, it could not be reproduced experimentally. In 2011, reovirus-associated lameness in turkeys re-emerged with experimental infection causing tendon lesions by 10 days of age and rupture of tendons by 8 to 10 weeks of age. This reovirus, identified as turkey arthritis reovirus (TARV), has been reported from all turkey-producing states of the USA and other countries. The lameness affects male turkeys 12-17 weeks of age (occasionally hens) and is characterized by recumbency with wing tip bruises (“wing walkers”), and uni- or bilateral swelling of the hock (tibiotarsal) joints (Fig. 1). Gross lesions include hock swelling, periarticular edema and fibrosis, increased fluid in the tendon sheaths and hock joints, tenosynovitis, and occasional rupture of the gastrocnemius or digital flexor tendon (Fig. 2). Lameness affects 15%-70% of a flock, resulting in economic losses due to excessive culling, diminished carcass quality and reduced market weights. The severity of clinical signs is believed to depend on the virus pathotype, route of exposure (vertical or horizontal), age of infection (<2 weeks), maternal antibody (breeder vaccine or field exposure), plus environmental management and nutrition.
Experimentally, the lesions start as lymphocytic infiltration at 4 weeks, progressing to fibrosis by 16 weeks post infection. Tendon fibrosis results in decreased tendon tensile strength, and tendon adhesions may contribute to tendon rupture in older, heavier birds. In addition, there is evidence that aortic ruptures are associated with TARV infection with increased mortality for 2 or more weeks in older birds (>13 weeks). One theory for this association is that there may be damage to collagen/elastin of tendons and aorta; however, no histologic evidence of vascular inflammation has been reported in diagnostic cases or experimental challenge studies. Another theory is when barns housing heavy birds have lights turn on, large birds may have pain on rising, causing increased blood pressure and subsequent aortic rupture.
Based on the USA experience, the National Turkey Federation (USA) has a TARV economic summary and case definition:
Ontario’s TARV situation is currently under investigation. Lameness in Ontario turkey flocks can be multifactorial. TARV infection is an additional differential diagnosis that is based on gross lesions, compatible histologic lesions and positive reovirus PCR. Other causes of lameness including osteomyelitis, synovitis/tenosynovitis, tibial dyschondroplasia, muscle/tendon rupture from other causes, footpad dermatitis, Mycoplasma synoviae, Mycoplasma iowae and dietary deficiencies need to be ruled out. Subsequent reovirus genotyping and phylogenetic analysis will provide further information on strains in Ontario.
The most likely source of TARV is the turkey enteric reovirus (TERV), as they share a high degree of homology. Chickens are not believed to be the reservoir for TARV infection in turkeys. Although turkey arthritis reoviruses are extremely hardy, lasting 2 weeks in unsanitized water and 6 – 8 days in litter, they are susceptible to most commonly-used disinfectants.
There is no specific serological test for TARV. Current commercially-available reovirus ELISA tests are chicken-based and detect both TERV and TARV. The degree of the ELISA response or seroconversion may indicate exposure to TARV and can be used for surveillance purposes. Turkey-validated PCRs are available; however, in many cases, older turkeys showing typical clinical and postmortem signs may test negative by PCR or virus isolation. TARV is best detected prior to or as soon as lameness develops. Follow up testing of subsequent flocks at an earlier age is recommended.
Collecting your own samples for submission to AHL:
Swabs: Aseptically swab the hock joint and/or digital flexor tendon for reovirus PCR, mycoplasma PCR and bacterial culture (individual swabs or in pools of no more than 5).
Histology: Collect gastrocnemius tendon and/or digital flexor tendon (3 to 5 maximum). If applicable, collect the area of aortic rupture (3 to 4 maximum).
Submitting intact legs to AHL for sample collection (submit 5 intact legs maximum):
a) Swabbing and histology only: reovirus PCR, mycoplasma PCR, bacterial culture, and tissue collection (histology).
Fees: Pathologist tissue collection (per 15 minutes), testing fees, and decalcification charge.
b) Full leg dissection for evaluation of bacterial infections, tibial dyschondroplasia (TD), and swabbing: reovirus and mycoplasma PCR, bacterial culture, and tissue collection (histology).
Fees: Full PM charge, testing fees, and bone/tendon decalcification charge.
Virus isolation is available as a send-out test and can be arranged if requested.
If you have any questions, please contact AHL to discuss your sample submission. AHL
Fig 1. Unilateral (left) hock Fig 2. Tendon rupture. (Photo: D. Pyle)
swelling. (Photo: D. Pyle)
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