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to have originated in scaled reptiles (Squamata) and switched to 1975), but there are some minor differences at the genomic level
avian hosts relatively late (Farkas et al., 2008). (Jucker et al., 1996; Pitcovski et al., 1998; Davison and Harrach,
2011). A mild disease, named avian adenovirus splenomegaly
(AAS) is known for broiler breeders and the causative virus
Pathogenesis (AASV) is serologically indistinguishable from HEV (Domer-
muth et al., 1975, 1979, 1980, 1982). No reports are available on
Host range the genetic relatedness of these viruses. Birds of different orders
Fowl adenoviruses are ubiquitous in poultry, and have been can also be infected with HEV (Pierson and Fitzgerald, 2013).
detected and isolated from chickens, guinea fowls, turkeys,
pheasants, pigeons, budgerigars, geese and ducks (McFerran Entry, spread, tissue tropism
and Smyth, 2000; Hess, 2013). Broilers are the most susceptible Fowl adenoviruses are transmitted both horizontally and verti-
to FAdV infection, though outbreaks in layers have also been cally. The latter combined with concentrated breeder operations
described (Shah et al., 2017). FAdV-induced disease occurs and industry practices more likely contributed to the explosion
mainly in 2- to 4-week-old meat type chickens, with a median of IBH and HPS outbreaks worldwide from the beginning of
age of 21 days reported for Canada (Ojkic et al., 2008a). Cases in the century (Saifuddin et al., 1991; Toro et al., 2001; Grgić et al.,
younger and older birds have been also reported (McFerran and 2006). FAdVs may also be present in the semen, which is to be
Smyth, 2000). Virulent Chinese FAdV-4 isolates can cause high considered where artificial insemination is employed. Infections
mortality in ducks (Pan et al., 2017b,c). Experimental studies can remain latent in flocks at least for a generation (Fadly et al.,
have been conducted with different ages of chickens with varying 1980). Since the virus is present in all excretions including faeces,
routes of inoculations of FAdVs (Schachner et al., 2018). tracheal and nasal mucosa, the horizontal spread is also impor-
3
The virus isolated from goslings exhibiting inclusion body tant. Virus titre in the faeces can be as high as 4 × 10 PFU/ml
hepatitis and hydropericardium syndrome is different from (Deng et al., 2013). Contaminated fomites and personnel could
FAdVs and forms a new species, Goose aviadenovirus A, in the play a role in virus transmission. The natural route of infec-
genus Aviadenovirus (Ivanics et al., 2010; Kaján et al., 2012). tion is mainly oral through contact with contaminated faeces
While pigeons can be infected with fowl adenoviruses, distinct (Hess, 2013). Experimentally, however chickens can be infected
pigeon adenoviruses have also been described and named pigeon subcutaneously, intramuscularly, intraperitoneally, and ocularly;
adenovirus 1 (PiAdV-1) and pigeon adenovirus 2 (PiAdV-2) the route of inoculation combined with the age of the birds
(Marek et al., 2014a; Teske et al., 2017; Vereecken et al., 1998). (and viral dose) results in different pathological pictures (Erny
Type 2 adenovirosis, described for pigeons of all ages, character- et al., 1991; Mazaheri et al., 1998). Following initial replication
ized by hepatic necrosis (Vereecken et al., 1998) is caused by viraemia occurs and virus can be detected from 24 hours post-
PiAdV-1. A disease among young pigeons, type 1 adenovirosis infection (h.p.i.) in the blood and virus is delivered to different
was described in the seventies (McFerran et al., 1976), and an organs, bursa of Fabricius, oesophagus, trachea, spleen, proven-
emerging new disease, young pigeon disease syndrome (YPDS) triculus, bone marrow, thymus, and kidney; the main target
shows similarities to type 1 adenovirosis; and the aetiological organs are the pancreas and liver (Saifuddin and Wilks, 1991;
agent for YPDS is PiAdV-2 (Teske et al., 2017). Steer et al., 2015). The fibres are involved in cellular receptor(s)
Egg drop syndrome virus was first isolated from chickens, later binding and tissue tropism (Marek et al., 2012; Grgić et al.,
it was shown that the natural hosts for EDSV are domestic and 2014). After experimental oral infection with FAdV-8 high
wild ducks and geese. However, the infection of coots, grebes, genome copy numbers were detected in the liver and caecal
herring gulls, egrets, owls, storks, swans, and quails among others tonsil with a peak at 5–7 days post-inoculation (Grgić et al.,
has also been shown (Smyth, 2013). Both in ducks and chickens 2011). Virus could be shed in the faeces for a long period of
EDSV infection can cause rough, thin-shelled eggs and decreased time due its persistence in the caecal tonsil (Cook, 1983; Jones
egg productions (Gough et al., 1982; Bartha, 1984). Geese and and Georgiou, 1984; Grgić et al., 2011; Oliver-Ferrando et al.,
goslings can be experimentally infected with EDSV but no egg 2017). Avian adenoviruses are very stable and resistant to heat
production problems and only little clinical signs were observed and can persist in the environment for days (Monreal, 1992;
(Zsák et al., 1982). The causative agent of a severe respiratory McCracken and Adair, 1993).
outbreak in young goslings was identified as EDSV (Ivanics et The main source of infection for the classic form of EDS is
al., 2001). Chickens of all ages are susceptible to infection, and a vertical transmission of the virus from breeders through the
wide range of chicken breeds can be infected. Quail also exhibit embryonating eggs (McFerran et al., 1978). Horizontal transmis-
typical clinical features after infection with EDSV (Das and Prad- sion occurs when the in ovo infected chicks excrete the reactivated
han, 1992). virus later in the egg-laying period. The endemic form is associated
The natural host for HEV is turkey (Dhama et al., 2017; with infected egg-trays, egg-packing station (Smyth and Adair,
Pierson and Fitzgerald, 2013). Disease is normally seen between 1988; Kumar et al., 1992). The sporadic type of outbreaks occurs
6 and 11 weeks of age, when maternal antibodies decline (Fadly when EDSV spreads by infected droppings from domestic or wild
and Nazerian, 1989). Ring-necked pheasants can also be infected ducks, geese, wild waterfowls to hens; these outbreaks could lead
with HEV (Domermuth et al., 1979). Marble spleen disease virus to endemic infection (Gulka et al., 1984; Smyth, 2013). Virus rep-
(MSDV) is serologically identical to HEV (Domermuth et al., lication starts in the nasal mucosa and through viraemia the virus