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a mixed population of inflammatory cells in the lamina propria 1983; Montgomery et al., 1985) or a diminished cellular immune
immediately surrounding crypts that included macrophages, response (Hill et al., 1989).
lymphocytes and heterophils. Increased numbers of intraepi-
thelial leucocytes were also present. In natural outbreaks, the Other orthoreovirus related disease problems in
initial microscopic lesions include cystic dilatation of the crypts chickens
of Lieberkuhn, necrosis of crypt epithelial cells, deposition of In addition to the major disease conditions associated with
cellular debris within the crypts, apparent loss of crypts in a high avian orthoreoviruses that are described above, there are many
proportion of birds in the first week (Smart et al., 1988; Reece other disease problems potentially connected with them. Avian
and Frazier, 1990), and vacuolar degeneration and sloughing of orthoreovirus has been associated with severe hepatic necrosis
enterocytes in the small intestine (Songserm et al., 2003). causing significant mortality in chickens (Mandelli et al., 1978;
Takase et al., 1984). Other lesions in birds associated with avian
Immunosuppression associated with orthoreoviruses included splenic haemorrhage, congestion,
orthoreovirus necrosis and lymphostromal cell hyperplasia (Hieronymus et al.,
Numerous authors have described the immunosuppressive 1983b), renal haemorrhage, and congestion and nephritis (Hiero-
activity of orthoreovirus on the avian immune system. Kerr and nymus et al., 1983b).
Olson (1969) noted lymphoid cell degeneration in the bursa of Avian orthoreoviruses were reported to be involved in out-
Fabricius of birds infected with a tenosynovitis producing avian breaks of high chick mortality associated with hydropericardium
orthoreovirus strain WVU 1675 as early as 7 days PI. Mont- (Bains et al., 1974; Spradbrow and Bains, 1974), pericarditis
gomery et al. (1985) demonstrated the ability of orthoreovirus (Mustaffa-Babjee et al., 1973), and myocarditis (Hieronymus et
to cause transient alterations in bursal and splenic weights, and al., 1983b; Davis et al., 2012). Histological examination in these
many authors have discussed reovirus-related bursal atrophy cases revealed focal to multifocal myocarditis with focal myofiber
(Page et al., 1982b; Montgomery et al., 1986a; Ni and Kemp, necrosis, and the inflammatory cell population was predomi-
1995), haemorrhages, congestion, and necrosis (Hieronymus nantly lymphocytes and histiocytes with scattered heterophils
et al., 1983b; Tang et al., 1987). Roessler and Rosenberger (Davis et al., 2012).
(1989) noted avian orthoreovirus infection causes cell damage Avian orthoreovirus infection in commercial laying flocks was
in vivo in several organs including bursa of Fabricius, thymus, shown to cause a 15–20% drop in egg production during the acute
and spleen which is characterized by lymphocyte depletion. phase of the disease (Schwartz et al., 1976). Avian orthoreovirus
However, Sharma et al. (1994) noted orthoreovirus does not infection in breeders caused reduced egg fertility and excessive
replicate in the thymus nor does it cause a detectable alteration culling due to lameness (Bradbury and Garuti, 1978). The low-
in peripheral T-cell subpopulations in chickens. Chenier et al. ered fertility was mainly associated with the male birds because
(2014) observed a generalized depletion of lymphocytes and painful legs reduced their desire to mate because their heavier
lymphocytolysis in lymphoid organs associated with orthoreo- weight meant they were more severely affected than their female
virus infection. counterparts (Bradbury and Garuti, 1978). Experimentally,
There was not unanimous agreement on the immunosup- Glass et al. (1973) and Bradbury and Garuti (1978) observed an
pressive ability of avian orthoreovirus as some considered them increased incidence of breast blisters in broilers vaccinated with
to be highly immunosuppressive (Montgomery et al., 1986a; avian orthoreovirus that caused downgrading of their breast meat
Sharma et al., 1994) whereas others considered their immuno- due to sternal bursitis. Economic losses caused by avian orthoreo-
suppressive effects to be relatively mild and transient (Cook and virus disease include those associated with poor feed conversion,
Springer, 1983; Springer et al., 1983; Montgomery et al., 1985; poor flock uniformity, reduced weight gain, unthriftiness, mortal-
Pertile et al., 1995) and probably associated with other factors ity, severe lameness, low egg production, and lowered egg fertility.
depressing the immune system such as transport and lack of food
(Meulemans et al., 1983). Immunosuppression results in a poor Avian orthoreoviruses in commercial poultry
response to vaccinations and predisposes the host to infection species other than chickens
with other pathogens, which might account for the diversity of
syndromes associated with avian orthoreoviruses (Montgomery Avian orthoreovirus disease in the domestic turkey
et al., 1986a). Many studies have shown that avian orthoreovirus (Meleagris gallopavo)
infections have enhanced the pathogenic effects of co-infecting Avian orthoreoviruses had been isolated from clinically normal as
pathogens such as CAV (McNeilly et al., 1995), IBDV (Springer well as apparently sick turkeys (Wooley and Gratzek, 1969; Ger-
et al., 1983), E. coli (Rosenberger et al., 1985), and coccidia showitz and Wooley, 1973; McFerran et al., 1976; França et al.,
(Ruff and Rosenberger, 1985). Kibenge et al. (1982a,b) noted 2010). The turkey was more resistant than the chicken to avian
chickens infected with orthoreovirus in the field had an increased orthoreovirus related disease problems (Glass et al., 1973; Afaleq
incidence of secondary bacterial infections with Staphylococcus and Jones, 1989, 1991). Clinical disease in domestic turkeys was
aureus. Therefore, avian orthoreovirus induced immunosuppres- reported to be consistent with orthoreovirus disease in chickens
sion in chickens has been documented to cause either a depressed and included viral arthritis/tenosynovitis (Page et al., 1982a; Mor
humoral immune response to other pathogens (Springer et al., et al., 2013; Sharafeldin et al., 2014), sudden death, infectious