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190 | Kibenge et al.

it is among the first tissues infected during viraemia (Pantin- and persisted for a longer period in young chicks, suggesting that
Jackwood et al., 2008). Intestine and bursa are primary entry and young chicks are more susceptible to orthoreovirus infection than
replication sites for orthoreoviruses in chickens (Kibenge et al., older chickens (Ellis et al., 1983). Subramanyam and Pomeroy
1985; Jones et al., 1989; Pantin-Jackwood et al., 2008) and tur- (1960) reported similar findings with the Fahey-Crawley virus.
keys (Pantin-Jackwood et al., 2008). The intestinal tract is also a The age of birds at infection was a crucial factor in determining
principal route of excretion of the virus (Jones et al., 1989). the viral virulence, and the mechanism involved was related to the
The pathogenesis of mammalian orthoreovirus infection has ability of the birds to mount an effective immunological response
been studied in detail. Mammalian orthoreovirus type 1 crosses to infection with orthoreovirus (Gouvea and Schnitzer, 1982b).
the mucosal barrier via M cells at the Peyer’s patches (Tyler and According to Roessler and Rosenberger (1989), the increased
Fields, 1990). Subsequently, the virus spreads to the mesenteric resistance in older chickens may be associated with maturation of
lymph nodes and spleen (Kauffman et al., 1983) or is trapped by humoral immune response, as younger birds produced antibodies
hepatic Kupffer cells and excreted in the bile (Tyler and Fields, against orthoreovirus later than older birds. Jones and Georgiou
1990). The pathogenesis of avian orthoreovirus infection is like (1984) noted the relative inability of a young chicken to mount
that described for mammalian orthoreoviruses. Natural avian an effective humoral immune response may influence the severity
orthoreovirus infection occurs mainly via the oral-faecal route of avian orthoreovirus infection and tissue dissemination of the
(Sahu and Olson, 1975; Jones and Onunkwo, 1978). Following virus. The high resistance of older birds to infection with avian
oral inoculation of day-old SPF light hybrid chicks with strain orthoreovirus may be related to maturation of the T-cell medi-
R2 of avian orthoreovirus (Jones et al., 1975), the virus was re- ated immune responses (Roessler and Rosenberger, 1989). von
isolated from the pancreas, oesophagus, ileum, caecal tonsils, and Bülow and Klasen (1983) suggested that macrophages may be
cloaca at day 1 PI (Kibenge et al., 1985). Maximum virus titres target cells for avian orthoreovirus and the relatively mature mac-
were found in the liver at day 3 PI and declined by day 7 PI. Virus rophages found in older birds may be more effective in resolving
was re-isolated from the heart at day 10 PI and from hock joint at orthoreovirus infections. In addition, the susceptibility of one day
day 14 PI. Jones et al. (1989), using an arthrotropic orthoreovi- old chicks to oral infection by S1133 strain of orthoreovirus was
rus, reported that the virus entered and replicated primarily in the related to the immune status of their dams (Wood et al., 1986).
intestinal epithelium and bursa of Fabricius within 12 hours PI There is a wide variation in avian orthoreovirus pathogenicity
and spread to most tissues within 1–2 days PI, finally localizing in (Kibenge and Wilcox, 1983; Takase et al., 1984), and the severity
the joint tissues by day 4 PI. of the disease is influenced by the strain of virus (Glass et al., 1973;
The incubation period of avian orthoreovirus disease differs Jones and Kibenge, 1984) or the viral heterogeneity (Gouvea and
depending upon the virus pathotype, age of host, and route of Schnitzer, 1982b) and the dose (Kibenge and Wilcox, 1983).
exposure (van der Heide, 1977; Robertson and Wilcox, 1986). The most virulent strains can kill almost all infected one-day old
Incubation period was approximately 4 days for footpad inocula- chicks (Gouvea and Schnitzer, 1982). The route of viral exposure
tion, 1–30 days for intravenous inoculations, and approximately influences severity of the disease (Glass et al., 1973; Sahu et al.,
13 days for contact exposure (Olson, 1959). Footpad inoculation 1979) and the incubation period. Montgomery et al. (1986)
resulted in more severe disease and slower growth rates than the noted chicks were more susceptible to orthoreovirus infection via
oral route of inoculation (Jones and Kibenge, 1984). the respiratory route than the oral route. Olson and Khan (1972)
Many factors affect the pathogenicity and influence the out- showed that Fahey-Crawley virus can induce inflammatory
come of avian orthoreovirus infection in chickens (Kibenge and lesions in tendons and metatarsal synovium of chickens infected
Wilcox, 1983). Viral factors include the virulence of the strain via respiratory route.
(Gouvea and Schnitzer, 1982b; Jones and Guneratne, 1984), the The severity of avian orthoreovirus disease is influenced by the
dose (Gouvea and Schnitzer, 1982b), the route of infection and breed of bird (Glass et al., 1973; Jones and Kibenge, 1984). Teno-
the tissue tropism. Host factors include the breed (Jones and synovitis caused by avian orthoreovirus was primarily associated
Kibenge, 1984), the age at infection (Jones and Georgiou, 1984), with broiler chickens (Jones and Onunkwo, 1978), but less so
and the immune status of the affected individual. Other factors with layers as reported by Schwartz et al. (1976) who observed a
include the diet (Cook et al., 1984a,b) and co-infecting pathogens. tenosynovitis outbreak in adult commercial white leghorn layers.
There is an age-linked susceptibility of chickens to avian Heavy breeds were considerably more susceptible to arthrotropic
orthoreovirus (Kerr and Olson, 1964; Jones and Georgiou, orthoreovirus than lighter breeds (Jones and Kibenge, 1984).
1984). Young chicks immediately after hatching were more The greater susceptibility of broilers to tenosynovitis may be due
susceptible to infection, had more severe lesions related to the to their greater weight and rapid growth rate, resulting in physical
infection, and higher mortality rates from the infection than older changes to the load-bearing tendons of the leg and predisposing
birds (Subramanyam and Pomeroy, 1960; Mustaffa-Babjee et them to the infection (Kibenge and Wilcox, 1983). It has been
al., 1973; Jones and Georgiou, 1984; Roessler and Rosenberger, shown that broiler tendons have lower tensile strength and a more
1989). The mortality caused by avian orthoreovirus was higher open fibrous connective tissue structure than those of lighter
in 1- to 7-day-old chickens than in those 2 weeks or older, and breeds of chickens, causing an increased susceptibility to infec-
the surviving 1- to 7-day-old birds frequently developed a per- tious agents (Walsum, 1977).
sistent virus infection (Toivanen, 1987). Both pathogenic and Many reoviruses are subclinical (Montgomery et al., 1985),
attenuated orthoreovirus were distributed more widely in tissue and infections caused by other aetiological agents may activate