Bovine Adenovirus

Causative agent: bovine adenovirus
Rhinitis
May contribute to Enzootic pneumonia of calves

Virus info below references of diseases info

Animal Health and Production Compendium

Selected sections for: bovine adenoviruses infections Identity Pathogen/s Overview Distribution Distribution Table Hosts/Species Affected Host Animals Systems Affected List of Symptoms/Signs Epidemiology Zoonoses and Food Safety Pathology Diagnosis Disease Course Disease Treatment Prevention and Control References Images

Datasheet Type(s): Animal Disease Identity

Preferred Scientific Name bovine adenoviruses infections

International Common Names

English adenovirus infection in ruminants

Pathogen/s

bovine adenoviruses

Overview

Rowe et al. (1953) isolated a new virus from cultures of human adenoids. The currently accepted name, "adenovirus", was proposed for this group of viruses by Enders et al. (1956). The family Adenoviridae now comprises a well-defined group of viruses with wide distribution in nature. Adenovirus types are defined based on the species of origin of the virus and quantitative neutralization assays with antisera prepared in non-host species. The family Adenoviridae is currently divided into three genera, Mastadenovirus, Aviadenovirus, and Atadenovirus (Benkö et al., 2000). Klein et al. (1959) reported the first isolation of a bovine adenovirus (BAdV). Bovine adenoviruses have been isolated from healthy cattle, but more often, the isolations are associated with some form of clinical disease. The preponderance of isolations from cattle with clinical disease is because this is the type sample submitted to diagnostic laboratories. Most adenovirus infections in cattle involve either the respiratory or gastrointestinal tracts. In addition there have been reports of adenovirus associated with conjunctivitis, keratoconjunctivitis, and weak calf syndrome. Currently the International Committee on Taxonomy of Viruses recognizes 10 types in cattle (Benkö et al., 2000). Strain Rus is being evaluated as a potential new type (Zakharchuk et al., 1993). The table shows prototype strains and origin.

Serotype Strain Reference

BAdV-1 No. 10 Klein et al., 1959

BAdV-2 No. 19 Klein et al., 1960

BAdV-3 WBR 1 Darbyshire et al., 1965a

BAdV-4 THT/62 Bartha and Áldásy, 1966

BAdV-5 B4/65 Bartha and Áldásy, 1966

BAdV-6 671130 Rondhuis, 1968

BAdV-7 Fukuroi Inaba et al., 1968

BAdV-8 Misk/67 Bartha et al., 1970

(BAdV-9) Sofia 4/67 Guenov et al., 1970

BAdV-10 78-5371 Horner et al., 1989

(BAdV-11) Rus Zakharchuk et al., 1993 BAdVs were originally divided into two groups based on cultural and antigenic characteristics by Bartha (1969). Subgroup 1 contained BAdV 1, 2, and 3 with similarities to human and other mammalian adenoviruses. Subgroup 2 contained the atypical BAdV 4, 5, 6, 7, and 8 that could not replicate in kidney epithelial cells, produced noticeably different nuclear inclusion bodies, and lacked the common complement-fixing antigen found in members of the genus Mastadenovirus. Division was further supported after genomic analysis demonstrated marked differences in the two groups. The subgroup 1 BAdVs (BAdV-1 through -3 and -9) are members of the genus Mastadenovirus and the subgroup 2 BAdVs (BAdV-4 through -8) have been recently assigned to a proposed new Atadenovirus genus within the family Adenoviridae(Benkö and Harrach 1998; Benkö et al, 2000). BAdV 10 does not fit clearly into either genus (Maitz et al., 1998) but, based on genomic analysis, has been assigned to the genus Atadenovirus for now (Benkö et al., 2000).

Distribution Bovine adenoviruses are found worldwide as indicated by either serology or virus isolation. Antibodies to adenoviruses have been demonstrated in sera in virtually every cattle population tested. Serum-virus neutralization tests have been used to detect adenovirus type-specific antibodies, and complement fixation and agar gel immunodiffusion tests have been used to detect the adenovirus group-specific antibody in serological surveys.

Distribution Table

Country Distribution Last Reported Origin First Reported Invasive References Notes ASIA Iran Present Afshar, 1969

Japan

-Honshu Widespread Inaba et al., 1968; Tanaka et al., 1968

Korea, Republic of Present Cho et al., 1985; Choi et al., 1982

Syria Present Giangaspero et al., 1992

Turkey Widespread Burgu & Akca, 1982; Burgu & Toker, 1985; YonguÇ et al., 1988; öztürk & Toker, 1988

AFRICA Congo Democratic Republic Present Eyanga et al., 1989

Egypt Present Hafez & Krauss, 1979

Morocco Present Mahin et al., 1985

Nigeria Present Obi & Taylor, 1984

Somalia Present Mani et al., 1978; Agrimi et al., 1982

Togo Present Espinasse et al., 1980

Zambia Present Ghirotti et al., 1991

Zimbabwe Present Baber & Candy, 1981

NORTH AMERICA Canada

-Ontario Present Bulmer et al., 1975; Thompson et al., 1981

-Quebec Present Key & Derbyshire, 1984; Richer et al., 1988

-Saskatchewan Present Orr, 1984

Mexico Present Suzan et al., 1983; Ramírez & Trigo, 1986

USA

-Alabama Present Rossi et al., 1973

-California Present Lehmkuhl et al., 1999; Bibrack & McKercher, 1971

-Idaho Present Stauber et al., 1976; Stauber et al., 1986

-Iowa Present Lehmkuhl et al., 1975; Lehmkuhl & Gough, 1977; Coria & Lehmkuhl, 1978; Coria & McClurkin, 1978

-Maryland Present Mohanty & Lillie, 1970

-Minnesota Present Reed et al., 1978; Baker et al., 1986a; Baker et al., 1986b

-Oregon Present Mattson, 1973; Mattson & Smith, 1977; Mattson et al., 1988

-Pennsylvania Present Welch & Dellers, 1973

-South Dakota Present Reed et al., 1978; Kirkbride, 1992

-Tennessee Present Lehmkuhl et al., 1998

-Washington Present Stauber et al., 1986

CENTRAL AMERICA Cuba Present Nunez & Castell, 1985

SOUTH AMERICA Argentina Present Carrillo et al., 1986

EUROPE Austria Present Coulibaly, 1990; Pernthaner et al., 1990; Peinhopf et al., 1996; Burki et al., 1978

Belgium Present Mammerickx et al., 1989

Bulgaria Widespread Haralambiev & Azev, 1969

Croatia Present Zupancic et al., 1984; Sabirovic et al., 1987; Sabirovic, 1988

Czechoslovakia (former) Present Novak, 1982; Krpata, 1978

Denmark Present Uttenthal et al., 1996; Tegtmeier et al., 1999

Finland Present Sihvonen & Tuomi, 1978

Germany Widespread Kretzschmar, 1973; Mayr et al., 1970

Hungary Widespread Bartha et al., 1984; Rusvai & Fodor, 1998; Endre, 1999; Bartha & Áldásy, 1966; Bartha et al., 1970

Ireland Present Timoney, 1971

Italy Widespread Cancellotti et al., 1976

Netherlands Present Opdenbosch et al., 1986; Rondhuis, 1968

Norway Present Saxegaard & Bratberg, 1971

Poland Widespread Buczek & Wrzolek-Lobocka, 1977; Majewska et al., 1978

Romania Present Istrate et al., 1983

Russian Federation

-Central Russia Present Frolov, 1984; Shichkina et al., 1971; Kis, 1977

-Southern Russia Present Zhumabaev et al., 1993; Dreizin et al., 1973

Switzerland Present Läuchli et al., 1990

United Kingdom Widespread Darbyshire et al., 1965b; Darbyshire et al., 1965a; Phillip & Sands, 1972

OCEANIA Australia

-Queensland Present Wilcox, 1969; Wilcox, 1970; Cole, 1970

New Zealand Present Thompson, 1977; Horner et al., 1980

Hosts/Species Affected Adenoviruses are generally confined to one host species or closely related species and are classified on the basis of species of origin and antigenic reactivity. Because bovine adenoviruses or closely related antigenic viruses have been isolated from a variety of other ruminant species (Belák and Palfi, 1974; Davies and Humphreys, 1977; Baber and Candy, 1981; Boros et al., 1985), the potential for infection across species exists among adenovirus isolates from ruminants.

Host Animals

Animal name Context Bos indicus (zebu) Bos taurus (cattle) Domesticated host, Experimental settings Capra hircus (goats)

Ovis aries (sheep) Domesticated host, Experimental settings

Systems Affected

Digestive - Large Ruminants Digestive - Small Ruminants Multisystem - Large Ruminants Nervous - Large Ruminants Respiratory - Large Ruminants Respiratory - Small Ruminants

List of Symptoms/Signs

Sign Life Stages Type Digestive Signs Melena or occult blood in faeces, stools Sign [C] Anorexia, loss or decreased appetite, not nursing, off feed C1 ( All Stages ) Sign [C] Abdominal distention Sign [C] Dysphagia, difficulty swallowing C1 ( All Stages ) Sign Diarrhoea C1 ( All Stages ) Sign [C] Mucous, mucoid stools, faeces C1 ( All Stages ) Sign Bloody stools, faeces, haematochezia C1 ( All Stages ) Sign [C] General Signs Intraocular mass, swelling interior of eye C1 ( All Stages ) Sign Generalized weakness, paresis, paralysis C1 ( All Stages ) Sign [C] Reluctant to move, refusal to move C1 ( All Stages ) Sign Fever, pyrexia, hyperthermia C1 ( All Stages ) Sign [C] Lack of growth or weight gain, retarded, stunted growth C1 ( All Stages ) Sign Lymphadenopathy, swelling, mass or enlarged lymph nodes C1 ( All Stages ) Sign Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift C1 ( All Stages ) Sign Inability to stand, downer, prostration Sign [C] Dehydration Sign [C] Sudden death, found dead Sign [C] Nervous Signs Dullness, depression, lethargy, depressed, lethargic, listless C1 ( All Stages ) Sign [C] Ophthalmology Signs Lacrimation, tearing, serous ocular discharge, watery eyes C1 ( All Stages ) Sign Purulent discharge from eye C1 ( All Stages ) Sign Conjunctival, scleral, redness C1 ( All Stages ) Sign Pain/Discomfort Signs Pain, kidney, ureters, on palpation C1 ( All Stages ) Sign Pain, pharynx, larynx, trachea C1 ( All Stages ) Sign Pain, chest, thorax, ribs, sternum C1 ( All Stages ) Sign Reproductive Signs Vaginal or cervical ulcers, vesicles, erosions, tears, papules, pustules C3 ( Heifer ), C4 ( Cow ) Sign Abortion or weak newborns, stillbirth C4 ( Cow ) Sign Respiratory Signs Decreased, muffled, lung sounds, absent respiratory sounds C1 ( All Stages ) Sign Change in voice, vocal strength C1 ( All Stages ) Sign Dull areas on percussion of chest, thorax C1 ( All Stages ) Sign Haemoptysis coughing up blood C1 ( All Stages ) Sign Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring C1 ( All Stages ) Sign Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs C1 ( All Stages ) Sign Decreased respiratory rate C1 ( All Stages ) Sign Sneezing, sneeze C1 ( All Stages ) Sign Coughing, coughs C1 ( All Stages ) Sign [C] Mucoid nasal discharge, serous, watery C1 ( All Stages ) Sign [C] Dyspnea, difficult, open mouth breathing, grunt, gasping C1 ( All Stages ) Sign [C] Increased respiratory rate, polypnea, tachypnea, hyperpnea C1 ( All Stages ) Sign [C] Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules C1 ( All Stages ) Sign Purulent nasal discharge C1 ( All Stages ) Sign

Epidemiology

The respiratory and enteric tracts are the primary targets for adenovirus infection. Infection with adenovirus usually results in cell lysis and virus shedding, but some cells accumulate virus particles in the nucleus without lysis establishing persistent infections. Respiratory and faecal shedding usually last for about 10 days and, where the kidney is involved, virus can be excreted for over 10 weeks in urine (Aldásy et al., 1965). With persistent infection, lysis of fragile infected cells produces virus-shedding resulting in infection of susceptible animals that come in contact with the virus. Adenovirus infection is common in younger animals. Maternal antibodies provide protection from infection by homologous BAdV types. As specific maternal antibodies wane, calves can become infected if that particular adenovirus type is present in the calf’s environment. Depending on maternal antibody level, virus exposure can result in either a subclinical infection followed by an active antibody response or if the antibody level is high enough, virus replication can be prevented. The incidence of infection with a serotype appears to be high within a geographic area for a period of time and then may virtually disappear from a region when herd immunity reaches a certain level. Because of the number of adenovirus types and the lack of cross protection, newly introduced adenovirus types may emerge as the predominant infecting type.

Zoonoses and Food Safety Because adenoviruses are usually confined to one host species or closely related species, the zoonotic and food safety threat is very low. To date there are no documented cases of clinical disease in humans caused by bovine adenoviruses.

Pathology Gross lesions in cattle are limited primarily to the respiratory and gastrointestinal tracts and consist of atelectasis and consolidation of the lungs and erosions, ulcerations and haemorrhage in the intestinal tract. Bronchiolar, mediastinal, and mesenteric lymph nodes are usually enlarged. Depending on adenovirus serotype, either epithelial or epithelial and vascular endothelial cells are the primary targets for viral cytopathology. Microscopically the basic lesion is bronchiolitis with necrosis and sloughing early and hyperplasia later in the course of the infection. Amphophilic, intranuclear inclusions are seen in swollen cells in the respiratory epithelium and sloughed in the lumen. Where the gastrointestinal tract is involved, the basic lesions are fibrinonecrotic plaques overlying foci of haemorrhage and necrosis. Amphophilic intranuclear inclusions are seen in enterocytes as well as in vascular endothelial cells.

Diagnosis

Because adenoviruses can be isolated from apparently healthy cattle, isolation of adenoviruses from clinically sick calves does not necessarily mean that the isolated adenovirus type plays an aetiological role in the clinical disease. For adenovirus to be considered as the aetiologic agent in a particular disease, the antibody titre should be low at the onset of the infection and result in at least a four-fold increase in neutralizing antibodies to the virus type in question, either characteristic intranuclear inclusion bodies should be observed in tissues showing gross lesions or presence of viral antigen must be demonstrated by immunohistochemical methods, and finally, virus must be isolated from tissues showing gross lesions at the height of the clinical disease. Adenovirus infection can be diagnosed morphometrically, serologically, and by virus isolation. Rapid presumptive diagnosis can be made either by observation of characteristic virus morphology in intranuclear inclusions by transmission electron microscopy or by immunofluorescent or immunohistochemical labeling of adenovirus antigens in tissues with gross lesions. Serotype-specific diagnosis, while not important to the treatment of clinical disease, is important in the development of a database from which to evaluate the role of each viral serotype in disease production. For a serotype to be considered as the aetiologic agent in a clinical syndrome, it must be isolated from many cases with similar clinical syndromes and be capable of reproducing the disease experimentally. Because of the number of types of adenoviruses infecting cattle, virus isolation is necessary to definitively identify the virus. Virus can be isolated from nasal secretions, tracheal fluids, intestinal contents and tissue homogenates. Adenoviruses are best-propagated in homologous cell cultures. Low passage bovine fetal cornea, lung, and turbinate cell cultures, are preferred for virus isolation, because these cells will support replication of all known BAdV types. A permanent heteroploid embryonic calf thyroid cell culture has been developed that allows replication of all bovine adenoviruses although at a somewhat lower titre than those obtained on primary calf testicles (Benkö et al., 1989). Primary adenovirus isolation may require sub-passage of the cultures before viral-induced cytopathic effect appears. Serologic confirmation of adenovirus infection can be done by demonstrating the presence of adenovirus group-specific antigen by immunofluorescent, immunohistochemical, and complement fixation tests, and by enzyme-linked immunosorbent assay. Reciprocal cross-neutralization tests detect type-specific antigens and further distinguish serotypes. Caution must be exercised when interpreting serum-virus neutralization test results because of demonstrated cross neutralization both among and between adenoviruses isolated from different ruminant species. Molecular characterization of adenovirus using DNA hybridization, restriction endonuclease digestion patterns and polymerase chain reaction has been used for virus identification and classification (Benkö et al., 1988; Benkö et al., 1995; Matiz et al., 1998). Phylogenetic analysis based on the adenovirus protease, hexon and DNA polymerase gene nucleic acid sequences filed with GenBank should make it possible to precisely compare newly isolated adenovirus (Benkö et al., 2000).

Disease Course Adenoviruses infections are frequently inapparent, but may also result in self-limiting disease. Multiple attributes involving host, viral, and husbandry practices influence disease production. Host factors include age and immune status, viral factors include serotype and, possibly, strain of the infecting adenovirus, and husbandry factors include practices causing stress. Infections with currently recognized bovine adenovirus types are usually associated with either pneumonitis or pneumonitis with enteritis (pneumoenteritis). Pneumonitis is usually more prominent and consistent than is enteritis. Clinical disease produced by inoculation of calves with field isolates does not mimic that seen naturally, indicating that the clinical signs and lesions observed naturally result from other superimposed factors such as secondary bacteria and immunosuppression. Infection most frequently occurs in calves of 2 weeks to 4 months old but animals of any age can be infected. Colostral antibodies will only protect against the homologous adenovirus types, and infection can occur as antibody wanes. Under natural conditions, the incubation period is probably 5 to 10 days. The serological response to adenovirus infection develops about 7 days after the onset of illness and maximum titres are attained after 3 to 4 weeks. Adenovirus antibody titres decrease little over the life of the animal. Infection by heterologous adenovirus serotypes can result in an anamnestic response for any prior infecting adenoviruses. Fever (39.5 to 41.0°C) usually develops 3 to 5 days after infection, lasting for 2 to 5 days. Respiratory and enteric symptoms usually occur following the onset of the febrile response. Respiratory symptoms include serous excretions (purulent with secondary bacterial infections) from the nose and eyes. Coughing often occurs and can be elicited with exercise or by grasping the trachea. Rapid respiration, anorexia and listlessness are frequent clinical signs. Enteric symptoms may include excessive salivation and loose stools to profuse diarrhoea. With BAdV-10 infection, minimal clinical signs followed by sudden death within 12 to 48 h is common. The prominent clinical sign with BAdV-10 may be severe diarrhoea containing blood and fibrin clots. With uncomplicated infections, clinical improvement is seen after 7 to 9 days.

Disease Treatment When economically feasible, cattle can be treated to provide relief from clinical signs associated with adenoviral infection. Left untreated however, the uncomplicated clinical disease will run its course in seven to 10 days. Because secondary bacterial infections such as Mannheimia haemolytica, Pasteurella multocida and Haemophilus somnus are common in cattle, antibiotics are often used as part of the treatment. Where clinical signs are detected early and treated there are few long-term effects.

Prevention and Control Maternal antibodies provide protection against homologous virus type, thus it is important for calves to get colostrum to provide early protection from adenoviruses that might be in the calve’s environment. As calves loose maternal antibodies, they develop post-infection immunity to the prevalent adenovirus types in their environment. Husbandry conditions where calves are weaned at a young age (stressed) and mixed with calves with varying immune status and unknown adenovirus carrier status should be avoided when possible. Calves weaned at 5 to 6 months of age generally have a decreased susceptibility to adenovirus-induced disease. Both modified live and inactivated adenovirus vaccines have been developed and evaluated for use in cattle (Bartha, 1967; Tribe et al., 1969; Bartha, 1974; Bartha, 1975; Haralambiev, 1975; Khristov et al., 1976; Baczynski et al., 1977; Morzaria et al., 1979; Bergamaschi et al., 1981; Becker et al., 1982; Litvinov et al., 1983; Zygraich and Delforge, 1983; Mattson et al., 1987; Pavlov et al., 1987; Wrzolek-Lobocka, 1988b; Belousova, 1989; Nurgaziev and Belousova, 1989; Wrzolek-Lobocka et al., 1990; Deptula et al., 1991; Belousova et al., 1993). It has been difficult to attenuate live vaccines to the point where clinical disease is no longer produced following vaccination. ß-propriolactone- or formalin-inactivated adenoviruses however, elicit excellent antibody response providing immunity to homologous adenovirus. The value of subunit vaccines for bovine adenoviruses has not been fully evaluated (York and Thorsen, 1992). Where vaccines are available for prevailing bovine adenovirus serotypes, they should be administered when maternal antibodies have waned, but 2 to 3 weeks before calves from different places are assembled under stressful conditions. Bovine adenovirus vaccines are available in Europe and Japan, but there are no commercial adenovirus vaccines available in the USA. Most vaccines are formulated in combination with other agents. Two to 4 doses of vaccine administered subcutaneously or intramuscularly are recommended to provide proper protection. Vaccination has not eliminated infection entirely, but has resulted in the reduction in disease incidence and treatment costs.

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Images

Picture Title Caption Copyright

	Pathology 	Lung from an animal experimentally infected with an adenovirus with large red areas of consolidation in the middle and caudal lobes. 	NADC, ARS-USDA 
	Histopathology 	Histopathology observed in a calf with a natural adenovirus infection. Note the intranuclear inclusions in a blood vessel epithelial cell (A) and in the epithelial cells of the bronchiole (B). 	NADC, ARS-USDA

Date of report: 03/04/2011

Animal Health and Production Compendium

Selected sections for: bovine adenoviruses Identity Taxonomic Tree Disease/s Table Distribution Table Pathogen Characteristics Host Animals References Images

Datasheet Type(s): Pathogen Identity

Preferred Scientific Name bovine adenoviruses

Other Scientific Names bovine adenovirus serotype 1-10 Benkö et al., 2000

International Common Names

English acronym BAdV

English bovine adenovirus serotype 1, bovine adenovirus serotype 10, bovine adenovirus serotype 3, bovine adenovirus serotype 4, 5, 6, 7, 8

Taxonomic Tree

Domain: Virus Group: "dsDNA viruses" Group: "DNA viruses" Order: Caudovirales Family: Adenoviridae Genus: Mastadenovirus Species: bovine adenoviruses

Disease/s Table

bovine adenoviruses infections

Distribution Table

Country Distribution Last Reported Origin First Reported Invasive References Notes ASIA Turkey CAB Abstracts data mining CAB ABSTRACTS Data Mining 2001 NORTH AMERICA USA CAB Abstracts data mining CAB ABSTRACTS Data Mining 2001 EUROPE United Kingdom CAB Abstracts data mining CAB ABSTRACTS Data Mining 2001

Pathogen Characteristics Adenoviruses are intermediate-sized (70-90 nm), unenveloped, icosahedral virions with equi-angular triangular faces with each triangle containing six subunits (capsomeres) per side. Virions have 252 capsomeres, 240 non-vertex (hexon) capsomeres and 12 vertex (penton) capsomeres. The genome consists of linear double-stranded DNA ranging in size from 28 to 38 kilobase pairs. Adenoviruses are resistant to lipid solvents, some are resistant to acid treatment and sensitive to heat treatment. Adenoviruses in cultures are stable at room temperature (20°C) for days, refrigerator temperatures (4°C) for months, and frozen (-85°C) for years.