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194 | Kibenge et al.

the Fahey and Crawley virus isolated from chickens can produce a 2013), femoral head fractures, and osteoporosis (van der Heide et
mild respiratory infection. Avian orthoreovirus has been isolated al., 1981). Elevated feed conversions and decreased body weights
from a laying flock concurrently infected with infectious bron- were constant clinical features of the syndrome, and there was a
chitis virus (McFerran et al., 1971). Hieronymus et al. (1983b) considerable amount of undigested feed in the faecal material,
noted some avian orthoreovirus infected birds had airsacculitis relating to decrease feed conversion efficiency and reduction of
and pulmonary congestion. profit (Page et al., 1982b). An enteric orthoreovirus strain causing
central nervous system signs in SPF chicks was reported (Van de
Enteric orthoreovirus diseases Zande and Kuhn, 2007).
Avian orthoreoviruses have frequently been isolated from chicks In the ‘helicopter disease’, the stunted 1-week-old chickens
with severe cloacal pasting (Dutta and Pomeroy, 1967; Desh- had 5–20% reduction in growth rates, exhibited paleness, and
mukh and Pomeroy, 1969a), from the enteric tract of chickens had clinical signs of lameness, poor feather development, and
with malabsorption (Page et al., 1982b; Hieronymus et al., broken feather shafts that led to the term ‘helicopter syndrome’
1983a; Kouwenhoven et al., 1988), from stunted, pale broilers (Kouwenhoven et al., 1978; Ruff, 1982).
with reduced digestion, depressed weight gain and feed conver- At necropsy, the most prominent lesions were proventriculitis
sion, and nutritional deficiencies (Giambrone et al., 1992), from and catarrhal enteritis (Page et al., 1982b) which consequently
broiler flocks with high mortality and signs of malabsorption (van impaired digestion of feed and could have resulted in decreased
Loon et al., 2001), from turkeys with depression, anorexia, 30% absorption of vitamin D, calcium and phosphorus, and vitamin E/
mortality (Simmons et al., 1972) or infectious enteritis (Ger- Se, leading to the deficiency of these vitamins and minerals (Brace-
showitz and Wooley, 1973), and from quails experiencing severe well and Wyeth, 1981; Page, 1983). Kouwenhoven et al. (1978a)
enteritis (Ritter et al., 1986; Guy et al., 1987). suggested that rachitis (rickets) was secondary to proventriculitis.
A collection of disease syndromes including stunted growth, Other lesions that were observed by Page et al. (1982b) included
elevated feed conversion ratios, poor feathering, leg weakness, myocarditis, bursal atrophy, and pancreatic atrophy.
and decreased weight gain was initially reported in chickens in the While the relationship between avian orthoreoviruses and
Netherlands (Kouwenhoven et al., 1978b) and later described in arthritis/tenosynovitis was well established, the causative
England (Bracewell and Wyeth, 1981), USA (Page et al., 1982b), role was less clear in RSS/MAS (van der Heide et al., 1981;
and Australia (Pass et al., 1982; Reece et al., 1984). Ultimately, Kouwenhoven et al., 1988), and Smart et al. (1988) suggested
it was identified as a complex syndrome affecting young broiler that it was a viral aetiology and the effects were greater in
chickens throughout the world (Page et al., 1982b; Ruff, 1982; birds subjected to stress, such as exposure to suboptimal tem-
Reece and Frazier, 1990). The name infectious stunting and perature within the first week of life. Orthoreovirus has been
runting syndrome was initially used to refer to this condition by most frequently isolated from affected birds and implicated as
Bracewell and Wyeth (1981). Other names that have been used the aetiology (Songserm et al., 2002). However, experimental
to refer to the same condition include infectious stunting syn- reproduction of the disease from isolated viruses is inconsist-
drome, runting-stunting syndrome (RSS) (McNulty et al., 1984), ent. Using infectivity trials with orthoreovirus, several authors
malabsorption syndrome (MAS) (Page et al., 1982b), infectious were able to reproduce some clinical signs and lesions of RSS/
proventriculitis, osteoporosis (Kouwenhoven et al., 1978a), MAS, but not all (van der Heide et al., 1981; Page et al., 1982b;
brittle bone disease, femoral head necrosis (van der Heide et al., Hieronymus et al., 1983a; van Loon et al., 2001), while others
1981), pale bird syndrome (van der Heide et al., 1981), wet litter were unable to produce any of the clinical or pathological fea-
syndrome, transient digestive system disorder (Clark et al., 1990), tures (McNulty et al., 1984; Guy et al., 1988). However, in a
malassimilation (Goodwin et al., 1993a), and ‘helicopter disease’ later study, the disease was experimentally reproduced by oral
of chicks (Kouwenhoven et al., 1978b). The transmissible nature or subcutaneous inoculation of day-old commercial broilers and
of the syndrome was noted in original descriptions (Kouwen- SPF chicks using enteric orthoreovirus strains (ERS), and the
hoven et al., 1978b) and the disease was identified as a problem authors subsequently postulated that ERS played a role in RSS/
primarily in broiler chickens rather than layer type birds (Reece MAS even though it is not considered the only cause (van Loon
and Frazier, 1990), affecting their growth principally in the first et al., 2001). RSS/MAS outbreaks are more common during
month of life (Rekik et al., 1991). cool weather and they can be exacerbated by cold stress (Reece
RSS/MAS is characterized by a high prevalence of birds and Frazier, 1990). Goodwin et al. (1993) described the histo-
with stunted growth, leg weakness, markedly decreased weight, pathology of small intestinal enteritis in chicks associated with
poor feed conversion, high condemnation rates at slaughter and intralesional orthoreovirus and supported the view that avian
retarded feathering at 2–5 weeks of age (Kouwenhoven et al., orthoreovirus can be intimately associated with enteritis. The
1978b; Bracewell and Wyeth, 1981; Page et al., 1982b, 1983), microscopic lesions consisted of mild villus atrophy and crypt
poor pigmentation of the shanks (Page, 1983), enlargement of the hypertrophy with mild to marked multifocal distension of crypts
proventriculus and a decrease in the size of the ventriculus (Page that were partly filled with exocytotic inflammatory cells and
et al., 1982b), diarrhoea (Vertommen et al., 1980; Page, 1983), sloughed degenerate and necrotic epithelial cells. Small eosino-
orange to yellowish mucus in the faeces (Clark et al., 1990), sig- philic cytoplasmic inclusion bodies were seen in some of the
nificant gross and microscopic pancreatic damage (Davis et al., degenerating epithelial cells. There were increased numbers of