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avian adenoviruses infections

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Datasheet

avian adenoviruses infections

Summary

  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • avian adenoviruses infections
  • Pathogens
  • Aviadenovirus
  • avian adenoviruses
  • pheasent adenovirus
  • Overview

  • Adenoviruses have been shown to be widespread throughout avian species in all parts of the world (

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Pictures

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PictureTitleCaptionCopyright
Eggs from birds infected with EDS, showing loss of pigment, cracked eggs, shell-less eggs and thin shelled eggs.
TitleEggs from EDS infected birds
CaptionEggs from birds infected with EDS, showing loss of pigment, cracked eggs, shell-less eggs and thin shelled eggs.
CopyrightBrian Adair
Eggs from birds infected with EDS, showing loss of pigment, cracked eggs, shell-less eggs and thin shelled eggs.
Eggs from EDS infected birdsEggs from birds infected with EDS, showing loss of pigment, cracked eggs, shell-less eggs and thin shelled eggs.Brian Adair
Fowl adenovirus intranuclear inclusions in nucleus of infected cells, each surrounded by a clear halo (haematoxlyin and eosin stain).
TitleIntranuclear inclusions
CaptionFowl adenovirus intranuclear inclusions in nucleus of infected cells, each surrounded by a clear halo (haematoxlyin and eosin stain).
CopyrightBrian Adair
Fowl adenovirus intranuclear inclusions in nucleus of infected cells, each surrounded by a clear halo (haematoxlyin and eosin stain).
Intranuclear inclusionsFowl adenovirus intranuclear inclusions in nucleus of infected cells, each surrounded by a clear halo (haematoxlyin and eosin stain).Brian Adair
Fowl adenovirus intranuclear inclusions in infected cells rendered by immunofluorescent staining.
TitleIntranuclear inclusions
CaptionFowl adenovirus intranuclear inclusions in infected cells rendered by immunofluorescent staining.
CopyrightBrian Adair
Fowl adenovirus intranuclear inclusions in infected cells rendered by immunofluorescent staining.
Intranuclear inclusionsFowl adenovirus intranuclear inclusions in infected cells rendered by immunofluorescent staining.Brian Adair

Identity

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Preferred Scientific Name

  • avian adenoviruses infections

International Common Names

  • English: adenoviral, adenovirus, respiratory disease in goslings, egg drop syndrome virus; adenovirus enteritis in birds, hemorrhagic enteritis; adenovirus-associated hemorrhagic disease in guinea fowl; egg drop syndrome; egg drop syndrome, adenovirus, of laying hens; haemorrhagic enteritis; hemorrhagic enteritis of turkeys; hydropericardium hepatopathy syndrome in broilers and pigeons- exotic; hydropericardium syndrome; inclusion body hepatitis; inclusion body hepatitis, adenovirus, in birds; marble spleen disease of pheasants

Pathogen/s

Top of page Aviadenovirus
avian adenoviruses
pheasent adenovirus

Overview

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Adenoviruses have been shown to be widespread throughout avian species in all parts of the world (McCracken and Adair, 1993). Many adenoviruses have been isolated from healthy as well as diseased birds and from uninfected cell cultures, and un-inoculated eggs (McCracken and Adair, 1993). Serological studies have demonstrated that antibodies are widespread in healthy poultry throughout the world, with the incidence of infection in poultry flocks approaching 100% in most countries. The viruses can be transmitted vertically through the egg, as well as laterally, and transmission by vectors has not been demonstrated. Some viruses are associated with important disease conditions such as quail bronchitis (QB), egg drop syndrome (EDS), haemorrhagic enteritis (HE), inclusion body hepatitis (IBH). Others have been associated with disease of the respiratory, nervous, reproductive and skeletal system, however experimental studies have generally resulted in no or only mild disease signs, suggesting that they are unlikely to be the primary agents involved (McFerran and Adair, 1977).

The genus Aviadenovirus is currently one of 2 genera in the Family Adenoviridae, and contains most of the characterised adenoviruses isolated from chickens, turkeys and geese. These viruses are often referred to as subgroup 1 avian adenoviruses in the literature (McFerran, 1997a; McFerran, 1997b). However, 2 of the most important adenoviruses causing significant disease in avian species (EDS virus and HE virus), show substantial differences at the molecular level from the Aviadenoviruses, and are currently unassigned members of the Adenovirus family (Benko et al., 2000). It seems likely that new genera will be created to accommodate them and that HE virus, along with marble spleen disease (MSD) virus of pheasants, and avian adenovirus group 2 splenomegally (AAS) of chickens, will form a separate genus for which the name Siadenovirus has been proposed, to reflect one of their unique genome characteristics, namely the presence of a gene coding for sialidase (Davison and Harrach, in press). EDS virus, along with certain ruminant adenoviruses, as well as a marsupial virus with similar genome characteristics, will be classified in a separate genus with the proposed name of Atadenovirus, which reflects their high AT content (Benko et al., 2000). Currently HE virus and the related MSD virus of pheasants, and AAS virus of chickens, are referred to in the literature as subgroup 2 avian adenoviruses, while EDS virus is referred to as subgroup 3 (McFerran, 1997a). These designations are also used in this datasheet.

Host Animals

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Animal nameContextLife stageSystem
Anas (ducks)Domesticated host, Wild hostPoultry: All Stages
Anser (geese)Domesticated host, Wild hostPoultry: All Stages
Anser anser (geese)
Anser cygnoides
Columba livia (pigeons)
Coturnix coturnix
Coturnix japonica (Japanese quail)
Gallus gallus domesticus (chickens)Domesticated hostPoultry: All Stages
MeleagrisDomesticated hostPoultry: All Stages
Meleagris gallopavo (turkey)
Numida meleagris (guineafowl)
Phasianus (pheasants)Domesticated host, Wild hostPoultry: All Stages
Phasianus colchicus (common pheasant)Domesticated host, Wild host

Systems Affected

Top of page blood and circulatory system diseases of poultry
digestive diseases of poultry
multisystemic diseases of poultry

Distribution

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Adenoviruses are widely distributed in avian species throughout the world. The incidence of infection appears to be high and approaches 100% in poultry flocks in most countries.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

ChinaPresentPresent based on regional distribution.
-LiaoningWidespreadZhu et al., 1987
IndiaWidespreadMaiti and Sarkar, 1997a; Maiti and Sarkar, 1997b; Oberoi et al., 1996
-HaryanaWidespreadKharole et al., 1991
-Indian PunjabWidespreadGrewal et al., 1981; Singh and Grewal, 1985
-KarnatakaWidespreadUmakantha, 1991
-Tamil NaduWidespreadBalachandran et al., 1993
-Uttar PradeshWidespreadShrivastava, 1990; Jadhao et al., 1997
-West BengalWidespreadBhattacharyya et al., 1983
IranWidespreadAl-Sheikhly and Mutalib, 1979
IraqWidespreadAbdul-Aziz and Al-Attar, 1991
IsraelWidespreadMeroz et al., 1977; Abdul-Aziz and Al-Attar, 1991
JapanWidespreadKawamura et al., 1963; Kawamura et al., 1964; Abdul-Aziz and Al-Attar, 1991
MalaysiaWidespreadDevi and Sam, 1983; Abdul-Aziz and Al-Attar, 1991
PakistanWidespreadAnjum, 1990; Afzal et al., 1991
TurkeyWidespreadGirgan, 1982

Africa

EgyptWidespreadMousa et al., 1984; Azab et al., 1992
South AfricaWidespreadBragg et al., 1991

North America

CanadaWidespreadHowell et al., 1970
-AlbertaWidespreadBrigden and Riddell, 1975
-QuebecWidespreadDi et al., 1974
MexicoWidespreadLotsy et al., 1976; Antillon Rionda, 1980
USAWidespreadFadly and Winterfield, 1973; Calnek and Cowen, 1975

Central America and Caribbean

CubaWidespreadMenéndez et al., 1983
Dominican RepublicWidespreadJoseph, 1990

South America

ArgentinaWidespreadMenendez, 1975
ChileWidespreadCubillos et al., 1986; Hidalgo et al., 1994; Toro et al., 1999
ColombiaWidespreadMorales et al., 1984

Europe

AustriaWidespreadKohler and Hromatka-Vasicek, 1974
BulgariaWidespreadKharalampiev et al., 1984
Czech RepublicWidespreadCada et al., 1975; Cerník, 1985
GreeceWidespreadVeimos et al., 1975
HungaryWidespreadPalya et al., 1977
ItalyWidespreadMandelli et al., 1976; Capua et al., 1995
NetherlandsWidespreadAkkermans, 1985
PolandWidespreadKarpinska and Samorek-Salamonowicz, 1981
RomaniaWidespreadBaba et al., 1977; Cotofan and Paul, 1979
UKWidespreadMcFerran et al., 1972; McDougall and Peters, 1974; McCracken et al., 1976; McFerran et al., 1977

Oceania

AustraliaPresentPresent based on regional distribution.
-VictoriaWidespreadKefford et al., 1980; Reece et al., 1987; Erny et al., 1991
New ZealandWidespreadGreen et al., 1976; Bains and Watson, 1977; Saifuddin and Wilks, 1992

Pathology

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Subgroup 1


Natural adenovirus infection of chickens or turkeys is often sub-clinical or accompanied by only mild clinical signs. Where clinical disease is present with adenovirus involvement, other agents are frequently involved (McCracken and Adair, 1993). Gross lesions of quail bronchitis (QB) are confined largely to the respiratory tract, with excess of mucus which may be haemorrhagic, often present in the bronchi and trachea (Reed and Jack, 1997). Nasal ocular discharge may be a feature. Basophilic, intranuclear inclusions are common in the tracheal epithelium. Inflammation and consolidation of the lungs particularly around the bronchial hilus are seen and the bronchi contain inflammatory exudates as in the trachea. Multifocal, pale, pinpoint lesions may also be present in the liver, with changes also in the spleen (Reed and Jack, 1997). In cases of inclusion body hepatitis (IBH) the main lesions are seen in the liver, which is generally enlarged, friable and pale yellow-brown in colour. Haemorrhages may be present on the liver surface, and are also, less frequently, seen in leg and breast muscle. Histological examination of the liver indicates a diffuse, generalised hepatic necrosis, with intranuclear inclusions in the hepatocytes (McFerran and Adair, 1977). In most field cases the inclusions are described as eosinophilic, surrounded by a halo, but basophilic bodies have also been described (McCracken and Adair, 1993).


Subgroup 2


Post mortem examination of turkey poults which have died during field outbreaks of haemorrhagic enteritis (HE), generally show distended intestines which may be dark red to black in colour, and which are filled with dark red bloody contents (Pierson and Domermuth, 1997). Enlargement of the spleen is a characteristic feature, and spleens may also be friable and mottled on gross examination. The lungs may also be congested and liver enlargement may be present. Histological examination of the spleen shows hyperplasia of the white pulp, with formation of large irregular islands, containing large numbers of intranuclear inclusions in lymphoreticular cells (Pierson and Domermuth, 1997). The infected cells appear to be principally B lymphoblasts. Proliferation of the white pulp is followed by necrosis and lymphoid depletion, and lymphoid depletion has also been noted in the thymus and bursa of Fabricius. The lesions in the gut are characterised by severe congestion of the intestinal mucosa, degeneration of the villous epithelium, and haemorrhage in villous tips (Pierson and Domermuth, 1997). Intranuclear inclusions and splenic lesions similar to those seen in cases of haemorrhagic enteritis virus (HEV) are also seen in cases of marble spleen disease (MSD) and avian adenovirus group 2 splenomegaly (AASV), although the gut lesions are less pronounced. In these cases the vascular damage resulting in oedema and congestion is more frequently seen in the respiratory tract (Pierson and Domermuth, 1997).


Subgroup 3


The disease in laying hens is characterised by the production of abnormal eggs, by a fall in egg production or by a failure to attain peak production. The disease appears in hens between the commencement of lay and 36 weeks of age, and can persist for up to 10 weeks (McCracken and Adair, 1993). Following infection with egg drop syndrome (EDS) virus, the first signs are normally seen after 7-9 days, with loss of eggshell pigment. This is followed by the appearance of thin-shelled, soft-shelled or shell-less eggs. Within 1-3 weeks, normal egg quality is restored, irrespective of the overall egg production. Oedema of the uterine mucosa and exudate in the lumen have been described following natural and experimental infection (McCracken and Adair, 1993). Histological studies on field cases of EDS indicated atrophy of uterine glandular tissue and oedema and infiltration with lymphocytes and plasma cells in the uterine villi (Eck et al., 1978). In experimentally infected birds, histological lesions in infundibulum, isthmus, magnum, uterus and vagina were described with the major changes seen in the pouch shell gland of the uterus (Taniguchi et al., 1981). Intranuclear inclusion bodies were observed in all regions of the oviduct, but were common in epithelial cells of the pouch shell gland (Taniguchi et al., 1981; Yamaguchi et al., 1981).

Diagnosis

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Subgroup 1


The main sites of virus replication appear to be the respiratory tract and the gut, and the best specimens for isolation of virus are therefore faeces and pharynx, as well as affected organs such as livers in suspect cases of inclusion body hepatitis (IBH) (McFerran 1998). Histopathological examination may show intranuclear inclusions in affected organs or tissues but are not specifically diagnostic of adenovirus infection. The most sensitive cell cultures for culture of fowl adenovirus are chick embryo liver or chick kidney cells. Chick embryo fibroblasts and tracheal organ cultures are less sensitive and not all strains grow in embryonated eggs. Eggs and chicks for preparation of cell cultures need to be carefully tested since latent avian adenoviruses have frequently been isolated from uninoculated cell cultures (McFerran, 1998). Specimens should be incubated for 14 days. Following development of cytopathic effects (CPE), adenovirus is easily recognisable by direct electron microscopy. Infected cultures may also be stained using fluorescent-labelled adenovirus antisera. Allocation to individual species requires typing by serum neutralisation test using standard antisera prepared and standardised to each virus species (McFerran, 1998).

The most commonly used test for detecting adenovirus antigens is the double immunodiffusion (or gel precipitin) test (McFerran, 1998). The test is rapid, inexpensive, and simple to perform and detects antibodies to the group reactive antigen which is shared by all subgroup 1 adenovirus serotypes. Antigen for the test may be prepared from homogenated chorioallantoic membranes harvested from embryonated eggs, 72 h after infection with an egg adapted subgroup 1 strain of virus such as CELO, or from infected cell cultures after development of complete CPE, as described in detail by McFerran (1998). Control antisera can be prepared by experimental infection of chickens, and the test has been widely used in field studies. Indirect immunofluorescence, using adenovirus-infected cell cultures grown and fixed in microtitre plate wells or coverslips, and ELISA tests have also been used for detection of adenovirus antibodies (McFerran, 1998).


Subgroup 2


Haemorrhagic enteritis (HE) in turkeys is suspected in birds with depression, pallour, bloody diarrhoea, prostration and death. The anterior small intestine may contain dark red or black contents (Pierson et al., 1998). Gastrointestinal involvement is not a feature of marble spleen disease (MSD) in pheasants, in which signs of disease include depression, weakness, nasal discharge, dyspnoea and death. Enlarged and mottled spleens are highly indicative of infection. Histopathological examination of spleen tissues from HE in turkeys or MSD in pheasants reveals distinctive microscopic changes, namely lymphoid hyperplasia and necrosis within the white pulp and intranuclear inclusions in lymphocytes and macrophages (Pierson et al., 1998). Propagation of the virus in cell culture is difficult. The viruses do not grow in conventional cell cultures such as are used for cultivation of subgroup 1 viruses (above), although HE virus has been grown in MDTC RP19 cells, which is a turkey lymphoblastoid B-cell line derived from a Marek's disease virus-induced tumour (Nazerian and Fadly, 1982). The viruses of HE and MSD are serologically identical, and the most widely used test for detection of virus or virus antigen is the immunodiffusion (or gel precipitin) test. Spleen from infected birds contains very large amounts of virus and virus antigen, and antigen for immunodiffusion tests can be prepared from enlarged spleens from field cases of HE or MSD, or from spleens from experimentally infected birds (Pierson et al., 1998). Spleen tissue may be disrupted by forcing through a syringe after removal of the capsule, followed by dilution in phosphate buffered saline (ph 7.4) (Pierson et al., 1998). Positive control antisera for immunodiffusion can be collected from experimentally infected birds, 4 weeks after inoculation. Operation of the test is performed by placing unknown test spleen material and known positive control antigen in alternating wells, with both placed opposite to wells containing positive HEV antiserum as described by Pierson et al., (1998).


Subgroup 3


Production of eggs with loss of pigment is often the first sign of egg drop syndrome (EDS) virus infection and is followed by production of soft-shelled, shell-less, thin-shelled or cracked eggs (McCracken and Adair, 1993). Duck cell cultures, chicken embryonic liver or chick kidney cells can be used for virus isolation, and up to 5 passages in culture may be required for isolation. EDS virus is unusual in that it haemagglutinates chicken and duck erythrocytes, but not mammalian erythrocytes, and therefore supernatants from inoculated cultures may be tested for haemagglutination (McFerran, 1998). Confirmation of the presence of virus can be achieved by examination of culture supernates by electron microscopy. EDS virus particles show typical adenovirus size (70-80 nm diameter) and icosahedral morphology, although the individual capsomeres may be difficult to resolve in some preparations. Staining of tissue sections of infundibulum or pouch shell gland from affected birds, using immunocytochemistry may be useful to show virus antigen in the cells. Because the virus haemagglutinates chicken and duck erythrocytes, haemagglutination-inhibition (HI) test can be used to detect and titrate EDS virus antibodies from infected chickens, and is appropriate for use in field laboratories. The supernates from virus infected cell cultures, or from inoculated duck eggs, can be used as a source of haemagglutinin (McFerran, 1998). Antisera are normally diluted 1/10 with PBS, then titrated in serial dilutions in microtitre plates. EDS haemagglutinin (HA) diluted to contain 4 HA units, is added to each serum dilution, allowed to react for 15 min and the erythrocytes are then added. Endpoints are read after settling of the control erythrocytes (McFerran, 1998). Immunodiffusion to detect EDS antibodies is less useful due to a partial cross-reaction with subgroup 1 adenoviruses (Adair et al., 1979).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Abnormal colour of stool in birds, white, green, yellow faeces Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Bloody stools, faeces, haematochezia Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Dark colour stools, faeces Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Diarrhoea Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Fecal incontinence Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Diagnosis
Digestive Signs / Melena or occult blood in faeces, stools Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Mucous, mucoid stools, faeces Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Digestive Signs / Unusual or foul odor, stools, faeces Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
General Signs / Ataxia, incoordination, staggering, falling Poultry:Day-old chick,Poultry:Young poultry Sign
General Signs / Cyanosis, blue skin or membranes Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel Sign
General Signs / Dehydration Sign
General Signs / Discomfort, restlessness in birds Poultry:Day-old chick,Poultry:Young poultry Sign
General Signs / Exercise intolerance, tires easily Poultry:Day-old chick,Poultry:Young poultry Sign
General Signs / Fever, pyrexia, hyperthermia Poultry:Day-old chick,Poultry:Young poultry Sign
General Signs / Haemorrhage of any body part or clotting failure, bleeding Poultry:Young poultry Sign
General Signs / Icterus, jaundice Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Increased mortality in flocks of birds Sign
General Signs / Lack of growth or weight gain, retarded, stunted growth Poultry:All Stages Sign
General Signs / Pale comb and or wattles in birds Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel Sign
General Signs / Pale mucous membranes or skin, anemia Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel Sign
General Signs / Reluctant to move, refusal to move Poultry:Day-old chick,Poultry:Young poultry Sign
General Signs / Sudden death, found dead Sign
General Signs / Sudden death, found dead Sign
General Signs / Sudden death, found dead Sign
General Signs / Sudden death, found dead Sign
General Signs / Trembling, shivering, fasciculations, chilling Poultry:Day-old chick,Poultry:Young poultry Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel Sign
General Signs / Weight loss Poultry:Young poultry,Poultry:Mature female Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female Sign
Nervous Signs / Tremor Sign
Reproductive Signs / Decreased hatchability of eggs Poultry:Mature female Sign
Reproductive Signs / Decreased in size, small ovary, ovaries Poultry:Mature female Sign
Reproductive Signs / Decreased size, small, uterus, cervix Poultry:Mature female Sign
Reproductive Signs / Decreased, dropping, egg production Sign
Reproductive Signs / Defective, misshapen, soft, rough, absent egg shell Poultry:Mature female Diagnosis
Reproductive Signs / Flabby egg yolk, thin albumin Poultry:Mature female Diagnosis
Reproductive Signs / Soft, thin egg shell Poultry:Mature female Diagnosis
Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Coughing, coughs Poultry:Young poultry,Poultry:Mature female Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Poultry:Young poultry Sign
Respiratory Signs / Purulent nasal discharge Poultry:Young poultry Sign
Respiratory Signs / Sneezing, sneeze Pigs:Growing-finishing pig,Pigs:Gilt Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Sign
Skin / Integumentary Signs / Ruffled, ruffling of the feathers Sign
Skin / Integumentary Signs / Soiling of the feathers, vent feathers Sign

Disease Course

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Subgroup 1 viruses


Subgroup 1 adenoviruses have been shown to be widespread in apparently healthy birds, and have also been associated with a number of disease conditions affecting the respiratory, digestive, nervous, reproductive and skeletal systems although in most cases, evidence of a primary role in the pathogenesis is lacking (McFerran and Adair, 1977). Adenoviruses have frequently been isolated from cases of respiratory disease in several avian species (McFerran, 1997b), often in association with other agents, however, in general, experimental infections have produced no or only mild clinical signs of respiratory disease. An exception to this is the severe respiratory disease in bobwhite quail (Colinus virginianus), known as quail bronchitis (QB). The causal agent, QB virus is serologically related to chicken embryo lethal orphan (CELO) virus and other serotype 1 fowl adenovirus strains and the disease has been reproduced by experimental infection of quails (Reed and Jack, 1997). The first signs of disease include increased mortality, with decreased feed consumption, ruffled feathers, rales, coughing, and depression (Reed and Jack, 1997). The severity of the disease depends on the age of the birds and is most severe in birds under 3 weeks of age. Inclusion body hepatitis (IBH) is recognised in poultry flocks throughout the world. It is normally seen in broilers between 5 and 7 weeks of age but has also been recognised in laying fowl (McCracken and Adair, 1993). Adenoviruses from several different serotypes have been associated with IBH (McFerran, 1997b; McCracken et al., 1976), however, several isolates from severe outbreaks in New Zealand were classed as group E viruses on restriction enzyme analysis (Erny et al., 1991). The disease has been reproduced by experimental inoculation of young chickens, and concurrent infectious bursal disease virus or chicken anaemia virus infection may contribute to the pathogenicity of some adenoviruses in producing IBH (McFerran, 1997b; Toro et al., 2000). The disease is characterised by suddenly increased mortality, depression with ruffled feathers, often followed by sudden death within 48 h. Mortality may reach 10-30% (McFerran, 1997b). Subgroup 1 adenoviruses have also been associated with egg production problems or poor shell quality, poor food conversion and growth rates, and with hydropericardium syndrome (McFerran 1997b), although experimental infection with isolates has not produced evidence of a causal relationship.


Subgroup 2 adenoviruses


These viruses cause significant disease in turkeys, chickens and pheasants. The adenoviruses involved are serologically indistinguishable from each other but show substantial differences from the subgroup 1 and 3 adenoviruses both genomically and antigenically (Pierson and Domermuth, 1997). Haemorrhagic enteritis (HE) is an economically important, acute disease of turkeys characterised by haemorrhagic diarrhoea, splenomegally and death. In field outbreaks, almost all birds are infected as indicated by development of antibodies, and mortality may reach over 60% although up to 15% is more typical. Marble spleen disease (MSD) affects pheasants causing an acute respiratory disease characterised by depression, weakness, dyspnoea, and eventually death due to asphyxia. Mortalities may reach 5-20%, but is generally lower. AAS of chickens is an acute disease characterized by pulmonary congestion and oedema, with enlargement of the spleen. Mortalities of up to 9% have been reported (Pierson and Domermuth, 1997). Following oral inoculation, viral replication seems to take place in B cells within the gut associated lymphoid tissue, and this is followed by a viraemia and subsequent infection of B lymphoblasts in the spleen and other lymphoid tissues. The subsequent necrosis and inflammatory response gives rise to vascular damage resulting in haemorrhage and oedema in infected tissues and organs (Pierson and Domermuth, 1997).


Subgroup 3 adenoviruses


Egg drop syndrome virus (EDS) virus causes economically important disease in laying hens, however evidence indicates that the natural hosts for the virus are probably ducks and geese (McFerran, 1997c). Following experimental infection by the oral route the virus replicates in the nasal mucosa and this is followed by a viraemia and virus replication in lymphoid tissues throughout the body (Smyth et al., 1988, McFerran 1997c). Virus antigen in large amounts was demonstrated in the oviduct and pouch shell gland which appear to be important target tissues for the virus, and the ensuing damage results in production of abnormally shelled eggs (Smyth et al., 1988; Taniguchi et al., 1981; Yamaguchi et al., 1981).

Epidemiology

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Subgroup 1


Vertical transmission through the egg appears to be common, as indicated by the reported frequency of isolation of adenoviruses from embryonated eggs, and from cell cultures derived from them (McFerran and Adair, 1977). The major site of virus replication in young birds appears to be the gut, and excretion of virus in the faeces is probably the major vehicle of lateral transmission. As maternal antibody levels decline in the young birds, virus replication and excretion increases. In broilers, peak excretion was reported between 4 and 6 weeks of age (McFerran, 1981), while in layer replacements, it was maximal between 5 and 9 weeks of age (Yates et al., 1976). Airborne spread is probably not an efficient means of transmission (McFerran and Adair, 1977), and transmission by vectors has not been demonstrated. Many adenovirus species appear to circulate on a given farm at any one time (Yates et al., 1976; Khanna, 1965), and several species have been isolated from one bird (Cowen et al., 1978). High neutralising antibody levels to one adenovirus species do not appear to reduce excretion of other species (McFerran, 1997b). Latency is a feature of adenovirus infection, and reactivation of virus may occur throughout life, influenced by a number of factors such as infection with other agents, crowding or immunosuppression. In particular, a second peak of virus excretion has been noted at around peak egg production, presumably due to physiological stresses during this period. This is likely to ensure maximum egg transmission to the subsequent generation of birds (McFerran, 1997b). The viruses also replicate in the trachea and upper respiratory tract, however airborne transmission is relatively inefficient (Cook, 1974), although it may be important over short distances.


Subgroup 2


Haemorrhagic enteritis is also spread to susceptible turkey poults through direct contact with infected faeces (Gross and Moore, 1967), and the virus has been isolated from infected litter (Pierson and Domermuth, 1997). However unlike the subgroup 1 viruses, there is no evidence for egg transmission.


Subgroup 3


Three types of spread have been recognised with egg drop syndrome (EDS) adenovirus (McCracken and Adair, 1993; McFerran, 1997c). 1) Vertical spread through the embryonated egg is of major importance in establishing infection in progeny flocks. The incidence of infection in embryos is probably low, and infected chicks do not excrete virus or develop antibodies until egg production is greater than 50% (McCracken and Adair, 1993; McFerran 1997c). 2) Lateral spread from excreted virus and from contaminated eggs then occurs, leading to contamination of cages, food, litter, egg trays, transport and packing stations, with subsequent spread within and between poultry houses, and infection of other flocks. Transmission by needles or blades used for vaccination or bleeding of viraemic birds may also be a factor in spread of the virus. 3) Contamination of water supplies by wild ducks, geese or other waterfowl carrying the virus may also be important in some areas. This type of spread is probably sporadic but could lead to foci of infection in poultry flocks becoming established, and subsequently amplified (McCracken and Adair, 1993; McFerran, 1997c).

Impact: Economic

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Outbreaks of IBH in recent years in Australia, New Zealand, and North and South America have been associated with high mortalities, although estimates of losses are not available. In Pakistan, outbreaks of hydropericardium syndrome (Angara disease) has caused major devastation to the poultry industry. EDS virus has not been identified in chickens in the USA., but has caused major losses to the poultry industries in most European countries, Africa, Australia and the Far East (McFerran, 1997c). Estimates of losses due to haemorrhagic enteritis (HE) virus infection are not complete, however, estimates within the USA before development of a vaccine were estimated to be in excess of US $3 million per year (Pierson and Domermuth, 1997).

Zoonoses and Food Safety

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Most avian adenoviruses are highly species specific and there is no evidence of infection in humans.

Disease Treatment

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There is no specific treatment for most adenovirus-associated diseases. Haemorrhagic enteritis (HE), however, has been successfully treated by inoculation of convalescent antiserum obtained from healthy flocks at slaughter. This may also be effective for marble spleen disease (MSD) of pheasants (Pierson and Domermuth, 1997).

Prevention and Control

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The value of attempted eradication is questionable since the viruses are highly resistant to inactivation, making inactivation in poultry houses difficult, and are efficiently spread by vertical transmission through the egg. Welfare improvements such as improved temperature control of poultry houses, adequate ventilation and adequate space per bird may be considered to reduce stress, optimise immunocompetence and reduce the efficiency of spread. Control of specific viruses shown to be primary agents in certain disease syndromes (e.g. inclusion body hepatitis, IBH), by vaccination is more realistic. Control of hydropericardium syndrome in Pakistan using inactivated liver homogenates from affected birds, has been shown to be effective (Afzal and Ahmad, 1990). Transportation of infected litter or faeces from flock to flock is a common mode of transmission of haemorrhagic enteritis virus (HEV) and this should be avoided. Control of HE by vaccination has been successfully applied and 2 forms of live vaccine, given by means of the drinking water are in widespread use in the USA. (Pierson and Domermuth, 1997). An oil-adjuvanted vaccine is available for control of EDS (McFerran, 1997c). Birds are vaccinated between 14 and 16 weeks of age, before coming into lay, and properly vaccinated birds are protected against the disease.

References

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