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latent orthoreovirus infections which complicates the course of possibly following initial avian orthoreovirus induced tendon
the disease (Tang et al., 1987a). The virulence of orthoreovirus damage. However, bacteria were not present in all clinical out-
infections in chickens was synergistically enhanced by coinfec- breaks of tenosynovitis (Kibenge et al., 1982a). Tenosynovitis
tion with Eimeria spp. (Ruff and Rosenberger, 1985a) whereas was experimentally reproduced in chickens by infecting them
Staphylococcus aureus (MacKenzie and Bains, 1977; Kibenge et with avian orthoreoviruses via intra-muscular, intra-peritoneal,
al., 1982a), Mycoplasma synoviae (Bradbury and Garuti, 1978), intra-abdominal, subcutaneous, respiratory, and footpad inocula-
Cryptosporidium baileyi (Guy et al., 1988), and infectious bursal tion routes as well as horizontally in non-infected birds in contact
disease virus (IBDV) (Springer et al., 1983; Moradian et al., with infected conspecifics (Kerr and Olson, 1969; Johnson, 1972;
1990) have been reported to exacerbate disease caused by avian Olson and Khan, 1972; van der Heide et al., 1974, 1980; Sahu and
reoviruses. Avian reovirus may also enhance disease conditions Olson, 1975; Jones and Onunkwo, 1978). Tenosynovitis or viral
caused by other pathogens including chicken anaemia virus arthritis lesions have been identified in varying degrees of severity
(CAV) (McNeilly et al., 1995), Escherichia coli (Rosenberger et in affected birds, and the severity of lesions depends on the breed
al., 1985), IBDV (Moradian et al., 1990), and common respira- of chicken (Jones and Kibenge, 1984), the age at the time of
tory viruses (Rinehart and Rosenberger, 1983). Moreover, it has infection (Carboni et al., 1975; Wood and Thornton, 1981), route
been demonstrated that co-infections of avian reoviruses with of inoculation (Wood and Thornton, 1981; Islam et al., 1988),
other immunosuppressive pathogens of chickens, including avian and presence of secondary bacterial infections (MacKenzie and
reticuloendotheliosis virus, CAV, and avian leucosis virus, lead to Bains, 1977; Kibenge et al., 1982a; Hill et al., 1989).
diminished weight gain, poor feed conversion and reduced mar- The clinical signs of infection following oral inoculation of
ketability of affected birds (Xie et al., 2012). one day old SPF light hybrid chickens included depression and
lameness (Kibenge and Wilcox, 1983), prostration (Jones and
Georgiou, 1984), and anorexia at day 2 PI (Tang et al., 1987b),
Clinical features but by day 8 PI the chicks in all these studies appeared normal.
Known pathogenic avian orthoreoviruses, the diseases caused The tenosynovitis lesion consisted of a unilateral swelling on the
by them, and their isolation history is given in Table 6.2. Dinev plantar aspect of the leg, below the hock joint by 3–4 weeks PI
(2010) has excellent pictures of the different clinical conditions. (Jones and Georgiou, 1984) which decreased by 8 weeks PI.
Mortality, poor growth, decreased feed conversion efficiency,
Tenosynovitis/viral arthritis and carcass condemnation were associated with acutely infected
Arthritis was first recognized as a major cause of leg weakness in flocks (Schwartz et al., 1976). Viral mortality of chicks began day
poultry by Olson (1959). Arthritis of chickens with a definite 4 PI (Tang et al., 1987b; Afaleq and Jones, 1991) and continued
viral aetiology was first described in the USA by Olson and Kerr until day 10 PI (Kibenge and Dhillon, 1987). The growth rates
(1966) and the aetiology was identified as an orthoreovirus by observed by measuring body weight were found to be significantly
electron microscopy (Walker et al., 1972). A similar condition lower in inoculated chickens than in the corresponding control
was reported in the United Kingdom, which was called tenosyno- group at 5 weeks PI (Kibenge and Dhillon, 1987). Affected
vitis (Dalton and Henry, 1967). The term avian tenosynovitis was birds usually had difficulty accessing feed and water and became
originally used to describe an inflammation of the tendon sheaths emaciated (Kibenge and Wilcox, 1983). However, another
and tendons caused by Mycoplasma synoviae (Dalton and Henry, experiment using a different strain of avian orthoreovirus showed
1967), whereas the orthoreovirus associated disease was referred no significant differences between the weights of the infected and
to as viral arthritis (Olson, 1973). Later, both terms were used control groups within 2–6 weeks PI (Jones and Kibenge, 1984).
to describe the orthoreovirus-associated disease (Kibenge and Sometimes no clinical signs were observed until 3 or 5 weeks PI
Wilcox, 1983), but the true arthritic lesions were present only in (Kibenge et al., 1985; Kibenge and Dhillon, 1987). In field condi-
the late stages of the disease (Kerr and Olson, 1969). Isolation tions, orthoreovirus associated lameness is seldom encountered
of an avian arthrotropic orthoreovirus from broiler chickens with before 7 weeks of age (Jones and Onunkwo, 1978), even though
ruptured gastrocnemius tendons was reported in Britain by Jones the affected birds were infected at a very young age or through egg
et al. (1975), and the disease was experimentally reproduced in transmission (van Loon et al., 2001).
light breed chickens by Jones and Onunkwo (1978). Although The macroscopic lesions of orthoreovirus induced tenosynovi-
many pathogens such as adenoviruses (MacKenzie and Bains, tis are mainly confined to the hock joints and leg tendons (Rhyan
1976), Staphylococcus aureus (Johnson, 1972; MacKenzie and and Spraker, 2010) and are characterized by swelling of the hock
Bains, 1976; Macdonald et al., 1978), Mycoplasma synoviae (Kerr joints and lesions in the gastrocnemius tendons (Benavente and
and Olson, 1969), and Mycoplasma iowae (Dobson and Glis- Martínez-Costas, 2007). The most prominent findings in the
son, 1992) were commonly isolated from tenosynovitis lesions disease are swelling of the tibiotarsal-tarsometatarsal region and
of affected chickens, avian orthoreoviruses were considered to extensive swelling of the digital flexor and metatarsal extensor ten-
be the primary aetiological agent that caused the tenosynovitis dons. Jones and Georgiou (1984) noted tendon swelling below
(van der Heide, 1977). MacKenzie and Bains (1976) suggested the hock at 3 weeks PI and above the hock by 6 weeks PI. Inflam-
Staphylococcus aureus was a secondary pathogen that exacerbated mation of the swollen tendon areas often proceeds to a chronic
the primary avian orthoreovirus lesion, and similarly other bac- hardening and fusion of the tendon sheaths (Stott, 1999) at 9
teria were more likely to be secondary opportunistic pathogens weeks PI (Jones and Georgiou, 1984). As the tendons become