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faecal contamination is a primary source of contact infection would be able to result in the infection of a large flock over time
(Jones and Onunkwo, 1978; Macdonald et al., 1978). However, (Menendez et al., 1975). Al-Muffarej et al. (1996) showed that
Roessler (1987) demonstrated that one day old chickens were the egg transmission rate of trypsin-sensitive orthoreovirus was
more susceptible to orthoreoviruses introduced via the respira- lower than that of trypsin-resistant strains.
tory route than the oral route. Survival of avian orthoreoviruses Several avian viruses including orthoreoviruses, influenza A
on the surfaces within poultry houses, on the feathers of birds, viruses, West Nile virus, infectious bursal disease virus, and avian
and on poultry feed may play an important part in the trans- paramyxoviruses have been recovered from domestic poultry
mission of infection between batches of birds in a farm (Savage and from wild birds (Meulemans et al., 1983; Adair et al., 1987;
and Jones, 2003). This demonstrates that avian orthoreoviruses Kasanga et al., 2008) confirming the potential role of wild birds in
are ubiquitous in commercial chicken flocks and chickens are the epizootiology of many significant avian viral diseases affecting
regularly exposed to the virus in the environment, especially commercial poultry. Most of the avian orthoreoviruses are species
from the litter (al Afaleq and Jones, 1994). The virus survived specific, but at least some can cause cross-infections among spe-
more than 10 days on the egg shell surface when faeces were cies. Some isolates from turkeys, ducks, and a wedge-tailed eagle
present (Savage and Jones, 2003). Therefore, external egg shell were infectious to chickens, and an isolate from Common Eiders
surface contamination is another potential source of transmis- was infectious to Mallards (Jones and Guneratne, 1984; Nerses-
sion of orthoreoviruses. Additionally, stable orthoreovirus can sian et al., 1986; Hollmén et al., 2002). According to Vasserman
function as an incubator contaminant or a part of the brooder et al. (2004), it is possible that the virus changes over the period
house dust (Johnson, 1972) to initiate outbreaks. In a closed (antigenic variation) so that it can become capable of infecting
flock orthoreovirus may transmit laterally from a small nucleus other species as well.
of chicks infected congenitally (Jones and Onunkwo, 1978). Many orthoreoviruses do not cause disease or clinical signs in
Orthoreovirus may persist for long periods in the caecal tonsils their natural hosts (Hollmén and Docherty, 2007), and since wild
and hock joints, particularly in those birds infected at young age birds are potential reservoirs or carriers of viral diseases (Hlinak
(Jones and Guneratne, 1984), which implicates asymptomatic et al., 2006), they are assumed to represent a risk for the trans-
carriers as sources of orthoreovirus infection in domestic birds. mission of avian infectious diseases to commercial poultry. Bird
Rosenberger and Olson (1997) noted that persistently infected to bird contact, aerosols and contaminated feed or water could
birds may shed the virus even when circulating antibodies are be potential routes of transmission of viruses from wild birds
present. Al Afaleq et al. (1997) suggested that, for short periods, to domestic poultry (Hlinak et al., 2006). Wild birds that enter
wild mice can transmit avian orthoreoviruses between chicken poultry houses could carry pathogenic viruses directly into the
flocks contributing to the spread of infection. poultry flocks. Wild bird species living near poultry barns could
Vertical transmission or egg transmission of orthoreovirus contaminate areas near barns permitting viruses to be carried into
in chickens was first demonstrated by Deshmukh and Pomeroy the poultry barns by farm employees, equipment, pets, rodents,
(1969) and subsequently by Menendez et al. (1975) and Giam- and/or insects (Burns et al., 2012). Avian orthoreovirus survives
brone et al. (1991) following inoculation of breeder chickens. for at least 10 weeks in drinking water with little loss of infectivity
Menendez et al. (1975) isolated orthoreovirus from the repro- (Savage and Jones, 2003). Therefore, the drinking water system of
ductive tract of the challenged pullets. Infected chicks have a poultry house, once contaminated, could remain a source of sig-
been hatched from infected hens and experimentally infected nificant infection for many weeks, because the faecal oral route is
eggs (Menendez et al., 1975a). Egg transmission can be sus- the most common natural route of infection for orthoreoviruses
pected based on finding infection in isolated flocks (Glass et al., (Jones and Onunkwo, 1978). As a result of the factors mentioned
1973). Giambrone et al. (1991) showed that breeding chickens above, biosecurity, including practices aimed at decreasing wild
infected with orthoreovirus shed the virus for 28 days, but for bird activity near commercial poultry operations, is extremely
egg transmission to continue in a flock the virus infection would important. A study on wild bird activity on poultry farms in
have to be persistent in adult birds. Orthoreovirus infection is southwestern Ontario and the Fraser Valley of British Columbia,
reported to persist in some tissues for many months after infec- the largest poultry producing areas in Canada, identified the
tion (Olson and Kerr, 1967), and the reproductive tract in American crow as one of the 10 wild bird species most frequently
particular is a noted site of persistent infection (Menendez et observed at the poultry facilities, and as a result, was considered a
al., 1975). According to Menendez et al. (1975), egg transmis- species with the potential to transmit pathogens into commercial
sion of orthoreovirus occurred even after an antibody response poultry operations (Burns et al., 2012). However, there is cur-
was elicited and intestinal shedding had subsided in the parent rently little known about the role of wild bird orthoreoviruses
birds. The egg transmission rate in commercial chickens was as pathogens in the commercial poultry industry (Hollmén and
generally lower (Menendez et al., 1975). Jones and El-Taher Docherty, 2007).
(1985) demonstrated that the natural egg transmission rate Some livestock diseases have ‘spilled over’ to wildlife and then
could be underestimated if sampling was done at the 1-day-old ‘spilled back’ to livestock (Rhyan and Spraker, 2010). Establishing
stage because the virus takes a few days post hatch to multiply poultry farms in areas used by native avian species and increasing
in certain organs. However, the egg transmission rate is of little poultry production raises risk of poultry pathogen spillover into
relevance when large numbers of chicks are hatched together in indigenous wildlife populations, particularly through practices
the present-day poultry hatcheries because a single infected chick such as using contaminated poultry litter on agricultural fields as