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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
Other Scientific Names
- Poxvirus avium
International Common Names
- English: avian pox; canarypox; fowlpox; juncopox; pigeonpox; psittacinepox; quailpox; sparrowpox; starlingpox; turkeypox
- Spanish: viruela aviar
- French: variole aviaire
Local Common Names
- Germany: Gefluegelpocken
- Portugal: bouba
- UK: avian diphtheria; bird pox; contagious epithelioma; poxvirus infection
OverviewTop of page
The avian poxviruses (genus Avipoxvirus) constitute a group of viruses in the subfamily Chordopoxvirinae, family Poxviridae (ICTV, 2009). Depending on the authority, there are as many as 13 recognized, more or less host specific, species. The archetype, and best studied species, is fowlpox virus (Tripathy, 1993). Avian pox was one of the earliest described diseases of birds due to its distinctive gross lesions and histopathology. In 1873, Bollinger described the pathology of avian pox and the characteristic inclusion bodies that bear his name. Decades later, Woodruff and Goodpasture cultured fowlpox virus on embryonic, chorioallantoic membrane and conclusively demonstrated that it was the causative agent of fowlpox disease (van Riper and Forrester, 2007).
Avian pox presents as two common forms: 1) dry or cutaneous pox affecting the exposed skin of the head and feet and 2) wet or diphtheritic pox affecting the mucous membranes of the mouth, esophagus and upper respiratory tract. A systemic or septicemic form may also occur in canaries and some wild passerines (van Riper and Forrester, 2007).
Avian poxviruses cause economically significant disease in chickens (fowlpox), domestic turkeys (turkeypox), farmed game birds (quailpox) and caged canaries (canarypox). Fowlpox causes significant economic loss worldwide through mortality (50-60%), decreased egg production or retarded growth in broilers, layers and breeding stock. Canarypox, perhaps the most lethal form of avian pox, can result in high losses over a short period in large commercial aviaries (Cumnningham, 1978; Tripathy and Reed, 2003).
Hosts/Species AffectedTop of page
It is thought that most birds are susceptible to some species or strains of Avipoxvirus. Avian pox has been reported in at least 280 species from at least 70 families (Bolte et al., 1999; van Riper and Forrester, 2007). Host specificity can be complicated with some species/strains specific for a single host species (e.g. Yellow-shafted flicker Colaptes auratus) while other strains (e.g. canarypox) might be infective for a number of different species across multiple families (Kirmse, 1969). There are some bird orders – Tinamiformes (Tinamous), Gaviiformes (Loons), Caprimulgiformes (Nightjars) and Coraciiformes (Kingfishers) – from which Avipoxvirus has never been reported and other orders – Anseriformes (Ducks & Geese), Falconiformes (Falcons & Hawks), Columbiformes (Pigeons & Doves) and Psittaciformes (Parrots) – from which Avipoxvirus has only recently been reported in wild birds (van Riper and Forrester, 2007). Avian species occurring in warm, moist habitats where arthropod vectors are abundant are most likely to be infected with Avipoxvirus. Where other environmental conditions are similar, domestic and captive species held at high densities are more likely to be infected with Avipoxvirus.
DistributionTop of page
Avian poxviruses occur worldwide except in the Arctic and some remote island locations (van Riper and Forrester, 2007; Shearn-Bochsler et al., 2008). There are fewer published reports from Africa and South America but this probably reflects limited research activity and not a natural distribution. In North America it appears to be more prevalent in the warmer and moister regions of the United States (van Riper and Forrester, 2007). Where it has been reported on remote oceanic islands, like the Hawaiian Islands, Galapagos Islands and Canary Islands, avian poxvirus behaves as an invasive species, spreading rapidly among susceptible species and causing higher mortality.
Distribution TableTop of page
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/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||Present||Winteroll et al., 1979|
|Azerbaijan||Present||1990||OIE Handistatus, 2005|
|Bahrain||Present||OIE Handistatus, 2005|
|Bhutan||Present||1996||OIE Handistatus, 2005|
|-Gansu||Present||Zhang et al., 1996|
|-Hong Kong||Present||OIE Handistatus, 2005|
|-Shaanxi||Present||Wang et al., 1996|
|-Shanxi||Present||Wang et al., 1996|
|Georgia (Republic of)||Present||1983||OIE Handistatus, 2005|
|India||Present||Mathur et al., 1972; Pandey and Mallick, 1974|
|-Andhra Pradesh||Present||Rao, 1965|
|Indonesia||Present||OIE Handistatus, 2005|
|Iran||Present||2000||OIE Handistatus, 2005|
|Iraq||Present||Al-Falluji et al., 1979; Al-Ani, 1986|
|Israel||Present||Perelman et al., 1988||In captive birds|
|Japan||Present||Kawashima, 1962; Sato et al., 1962; Horiuchi et al., 1965; Iwata et al., 1986; Tsai et al., 1997|
|Jordan||Present||OIE Handistatus, 2005|
|Korea, Republic of||Present||OIE Handistatus, 2005|
|Kuwait||Present||1996||OIE Handistatus, 2005|
|Lebanon||Present||2000||OIE Handistatus, 2005|
|Malaysia||Present||Ideris and Ibrahim, 1986; Karpinski and Clubb, 1986; Reed and Schrader, 1989|
|-Peninsular Malaysia||Present||OIE Handistatus, 2005|
|-Sabah||Present||1997||OIE Handistatus, 2005|
|-Sarawak||Present||OIE Handistatus, 2005|
|Myanmar||Present||OIE Handistatus, 2005|
|Nepal||Present||OIE Handistatus, 2005|
|Philippines||Present||OIE Handistatus, 2005|
|Saudi Arabia||Present||Cooper, 1969; Greenwood and Blakemore, 1973||In captive birds.|
|Singapore||Present||1989||OIE Handistatus, 2005|
|Sri Lanka||Present||OIE Handistatus, 2005|
|Taiwan||Present||OIE Handistatus, 2005|
|Thailand||Present||OIE Handistatus, 2005|
|United Arab Emirates||Present||Kiel, 1985; Samour and Cooper, 1993; Samour et al., 1996|
|Uzbekistan||Present||OIE Handistatus, 2005|
|Vietnam||Present||OIE Handistatus, 2005|
|Algeria||Present||1997||OIE Handistatus, 2005|
|Angola||Present||OIE Handistatus, 2005|
|Benin||Present||OIE Handistatus, 2005|
|Botswana||Present||OIE Handistatus, 2005|
|Burundi||Present||OIE Handistatus, 2005|
|Cameroon||Present||OIE Handistatus, 2005|
|Cape Verde||Present||OIE Handistatus, 2005|
|Côte d'Ivoire||Present||OIE Handistatus, 2005|
|Djibouti||Present||OIE Handistatus, 2005|
|Egypt||Present||1996||OIE Handistatus, 2005|
|Eritrea||Present||OIE Handistatus, 2005|
|Ethiopia||Present||2002||OIE Handistatus, 2005|
|Ghana||Present||OIE Handistatus, 2005|
|Kenya||Present||OIE Handistatus, 2005|
|Libya||Present||OIE Handistatus, 2005|
|Madagascar||Present||OIE Handistatus, 2005|
|Malawi||Present||OIE Handistatus, 2005|
|Morocco||Present||OIE Handistatus, 2005|
|Mozambique||Present||OIE Handistatus, 2005|
|Namibia||Present||OIE Handistatus, 2005|
|Nigeria||Present||OIE Handistatus, 2005|
|Sao Tome and Principe||Present||OIE Handistatus, 2005|
|South Africa||Present||Allwright et al., 1994; Stannard et al., 1998|
|-Canary Islands||Localised||Introduced||Invasive||Medina et al., 2004; Smits et al., 2005; Illera et al., 2008|
|Sudan||Present||OIE Handistatus, 2005|
|Tanzania||Present||OIE Handistatus, 2005|
|Togo||Present||OIE Handistatus, 2005|
|Tunisia||Present||2003||Loir and Ducloux, 1894; OIE Handistatus, 2005|
|Uganda||Present||OIE Handistatus, 2005|
|Zambia||Present||OIE Handistatus, 2005|
|Bermuda||Localised||Since 1958||Wingate et al., 1980|
|Canada||Present||Syverton and McTaggerty, 1944; Kuntze et al., 1968; Moffat, 1972; Cox, 1980; Mikaelian et al., 1996|
|-Ontario||Widespread||Not invasive||Karstad, 1965; Kirmse, 1966; Kirmse, 1967|
|-Quebec||Present||Mikaelian et al., 1997|
|Mexico||Present||GALLAGHER, 1916; Graham, 1978; Olmos et al., 1986|
|USA||Present||Baldwin, 1922; Emmel, 1930; BUMP et al., 1947; Locke et al., 1960; Goodpasture and Anderson, 1962; Minsky and Petrak, 1982|
|-Alaska||Present||Morton and Dieterich, 1979|
|-Arizona||Present||Blakenship et al., 1966|
|-California||Present||Power and Human, 1976; Hill and Bogue, 1977; Emanuelson et al., 1978; Harris et al., 1978; McDonald et al., 1981; Wheeldon et al., 1985|
|-Florida||Present||Simpson et al., 1975; Hitchner and Clubb, 1980; Jacobson et al., 1980; Akey et al., 1981; Deem et al., 1997|
|-Georgia||Present||Musselman, 1928; STODDARD, 1931; Wheeldon et al., 1985|
|-Hawaii||Widespread||Invasive||Henshaw, 1902; Locke et al., 1965; Warner, 1968; Jenkins et al., 1989; Sileo et al., 1990; Tripathy et al., 2000; van Riper et al., 2002; Atkinson et al., 2005; Jarvi et al., 2008|
|-Idaho||Localised||Docherty and Long, 1986||Boise, feeding station|
|-Illinois||Present||BRANDLY and DUNLAP, 1938; Labisky and Mann, 1961; Sharma et al., 1968|
|-Indiana||Present||Boosinger et al., 1982|
|-Kentucky||Present||Poonacha and Wilson, 1981||In captive birds|
|-Maryland||Present||IRONS, 1934; Herman et al., 1962; Montgomery et al., 1980|
|-Mississippi||Present||Goodpasture and Anderson, 1962|
|-Missouri||Present||Halliwell, 1972||In captive birds|
|-New Jersey||Localised||Worth, 1956||Princeton, banding station|
|-New York||Present||COULSTON and MANWELL, 1941; Leibovitz, 1969; Tangredi, 1974; Donnelly and Crane, 1984|
|-North Dakota||Present||Pearson et al., 1975; Wheeldon et al., 1985||In captive birds.|
|-Oklahoma||Present||Johnson and Castro, 1986||In captive birds|
|-Oregon||Present||Dickenson, 1967; Crawford et al., 1979; Crawford, 1986|
|-Pennsylvania||Widespread||Locke, 1961; Ratcliff, 1967; Petrak, 1982|
|-South Carolina||Present||STODDARD, 1931|
|-Tennessee||Present||Goodpasture and Anderson, 1962|
|-Texas||Widespread||Dubose, 1965; Clark et al., 1988; Wilson and Crawford, 1988; Docherty et al., 1991|
|-Washington||Present||Giddens et al., 1971; Landolt and Kocan, 1976; Fitzner et al., 1985; Garner, 1989|
Central America and Caribbean
|Barbados||Present||OIE Handistatus, 2005|
|British Virgin Islands||Present||1995||OIE Handistatus, 2005|
|Cayman Islands||Present||2000||OIE Handistatus, 2005|
|Cuba||Present||OIE Handistatus, 2005|
|Dominica||Present||OIE Handistatus, 2005|
|Dominican Republic||Present||OIE Handistatus, 2005|
|Guadeloupe||Present||1997||OIE Handistatus, 2005|
|Guatemala||Present||OIE Handistatus, 2005|
|Honduras||Present||OIE Handistatus, 2005|
|Jamaica||Present||OIE Handistatus, 2005|
|Martinique||Present||OIE Handistatus, 2005|
|Nicaragua||Present||OIE Handistatus, 2005|
|Panama||Widespread||Kirmse and Loftin, 1969|
|Saint Vincent and the Grenadines||Present||OIE Handistatus, 2005|
|Trinidad and Tobago||Widespread||Since 1964||Invasive||Tikasingh et al., 1982|
|Argentina||Present||OIE Handistatus, 2005|
|Bolivia||Present||Hitchner and Clubb, 1980|
|Brazil||Present||Reis and Nobrega, 1937; OIE Handistatus, 2005|
|Chile||Present||Cubillos et al., 1979|
|Colombia||Present||OIE Handistatus, 2005|
|Ecuador||Present||Present based on regional distribution.|
|-Galapagos Islands||Present||Introduced||Invasive||Vargas, 1987; Curry and Grant, 1989; Thiel et al., 2005|
|Falkland Islands||Localised||Introduced||2004||Invasive||Munro, 2006||Port Stevens, New Island and Albemarle|
|Paraguay||Present||OIE Handistatus, 2005|
|Uruguay||Present||OIE Handistatus, 2005|
|Venezuela||Present||OIE Handistatus, 2005|
|Austria||Present||Loupal et al., 1985|
|Belarus||Present||OIE Handistatus, 2005|
|Croatia||Present||1996||OIE Handistatus, 2005|
|Cyprus||Present||OIE Handistatus, 2005|
|Czech Republic||Present||Rajchard and Rachac, 2001|
|Denmark||Present||Christiansen, 1949; OIE Handistatus, 2005|
|France||Present||Heusinger, 1844; Megnin, 1878; Curasson, 1946; OIE Handistatus, 2005|
|Germany||Present||Hartig and Frese, 1973; Kitzing, 1980; Kaleta and Marschall, 1982; Luthgen, 1983; Herbst and Krauss, 1989; Krone et al., 2004|
|Ireland||Present||OIE Handistatus, 2005|
|Italy||Present||Maggiora and Valenti, 1903; Rinaldi et al., 1972; Mani et al., 1990; Chiocco, 1992; Cerrone et al., 1999|
|Macedonia||Present||OIE Handistatus, 2005|
|Malta||Present||OIE Handistatus, 2005|
|Moldova||Present||1997||OIE Handistatus, 2005|
|Netherlands||Present||De Jong, 1912; Jansen, 1942; OIE Handistatus, 2005|
|Norway||Present||Holt and Krogsrud, 1973; Weli et al., 2004|
|Poland||Present||Landowska-Plazewska and Plazewski, 1968|
|Portugal||Present||2003||OIE Handistatus, 2005|
|-Madeira||Localised||Illera et al., 2008||On Porto Santo Island only|
|Romania||Present||Cociu et al., 1972|
|Russian Federation||Present||2002||OIE Handistatus, 2005|
|Slovakia||Present||1999||OIE Handistatus, 2005|
|Spain||Widespread||Vogelsang, 1938; Groth, 1963; Orós et al., 1997; Hernández et al., 2001; Buenestado et al., 2004|
|Switzerland||Present||Bouvier, 1946; Zangger and Muller, 1990|
|UK||Present||Miles and Stocker, 1948; JENNINGS, 1954; Edwards, 1955; Poulding, 1960; Pomeroy, 1962; Keymer and Blackmore, 1964; Green, 1969; Kear and Brown, 1976; Nuttall et al., 1985|
|Ukraine||Present||2002||OIE Handistatus, 2005|
|Australia||Present||BURNET and STANLEY, 1959; Harrigan et al., 1975; Chung and Spradbow, 1977; Wobeser, 1981; Annuar et al., 1983; Sutton and Fillipich, 1983; Raidal et al., 1996|
|French Polynesia||Present||OIE Handistatus, 2005|
|New Caledonia||Present||OIE Handistatus, 2005|
|New Zealand||Present||Westerskov, 1953; Quinn, 1971; Austin et al., 1973|
|Samoa||Present||2003||OIE Handistatus, 2005|
PathologyTop of page
Gross lesions are as described in the Disease Course section. Microscopically, Avipoxvirus infection of epithelial cells in the strata germinativum causes hyperplastic growth. Maturing cells become hypertrophic as large granular eosinophilic intracytoplasmic inclusions are formed. The inclusion body may occupy the entire cytoplasm resulting in necrosis of the cell. Intranuclear inclusions have also been observed in cutaneous lesions from various wild birds. The localized epithelial hyperplasia and hypertrophy or stacking up of infected cells forms the characteristic pock seen in cutaneous avian pox (Karstad, 1971; Cunningham, 1978; van Riper and Forrester 2007).
In acute, septicaemic pox of canaries (Serinus canaria), lesions may be found on the serous membranes, liver, and lungs. Liver degeneration and necrosis may occur. Oedema and hyperemia of the lungs results in fibrinous pneumonitis that leads to pneumonia. Tumours are common in the lungs of surviving, post-poxvirus canaries (Ritchie 1995; van Riper and Forrester, 2007). Similar lesions have been found in related finch species (Ritchie, 1995).
DiagnosisTop of page
Clinical Diagnosis and Lesions
A presumptive diagnosis can be made on the basis of gross lesions: proliferative wart-like growths on exposed body regions, typically the head, feet, and legs. Confirmation of Avipoxvirus can be made by histological examination of the lesions and identification of characteristic eosinophilic intracytoplasmic inclusions (Bollinger bodies). Electron microscopy can also be used to directly identify Avipoxvirus virions (Tripathy, 1993). In-field biopsies of lesions on live wild passerines must be considered an invasive procedure and should be conducted with caution. Presumptive diagnosis, based on gross lesions, may be highly accurate (>90%) (Riper et al., 2002) and provide a reasonable alternative to definitive diagnosis in field situations where invasive sampling procedures are unwarranted or more sophisticated methods are logistically infeasible.
Confirmation of Avipoxvirus can also be made by demonstration of characteristic pocks on inoculated chorioallantoic membranes of chicken embryos or cytopathic effects (CPE) on various avian cell cultures (e.g. chicken embryo dermis or duck embryo cells) (Tripathy, 1993). Immunofluorescence can be used to detect pox antigens in infected cells or suspect lesions (Tripathy, 1993). An enzyme-linked immunosorbent assay (ELISA) is currently the preferred serological test to detect a humoral response to fowlpox (Tripathy and Reed, 2003). Immunoblotting techniques have been employed to distinguish between fowlpox strains and pox species (Tripathy and Reed, 2003). Recently, genome-based probes and polymerase chain reaction (PCR) techniques have been used to identify Avipoxvirus in lesion tissue (Thiel et al., 2005; Tadese et al., 2008) and blood (Farias et al., 2010). These molecular techniques are particularly useful in making a differential diagnosis.
The diphtheritic lesions of avian pox may be confused with infectious laryngotracheitis or infection with Trichomonas gallinae, but differentiation can be made by histological examination of the lesions or amplification of pathogen-specific genomic fragments (Tripathy and Reed, 2003).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Other:Juvenile,Other:Adult Female,Other:Adult Male||Sign|
|Digestive Signs / Bloody stools, faeces, haematochezia||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Other:Juvenile,Other:Adult Female,Other:Adult Male||Sign|
|Digestive Signs / Difficulty in prehending or chewing food||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Other:Juvenile,Other:Adult Female,Other:Adult Male||Sign|
|Digestive Signs / Inability to open and / or close beak||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Diagnosis|
|Digestive Signs / Pharyngeal ulcers, vesicles, erosion, papules, sores pharynx||Diagnosis|
|Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears||Diagnosis|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Sign|
|General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass||Diagnosis|
|General Signs / Hindfoot swelling, mass rear foot, feet||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Lameness, stiffness, stilted gait in birds||Sign|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Diagnosis|
|General Signs / Oral cavity, tongue swelling, mass in mouth||Diagnosis|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Swelling of the comb, wattles in birds||Diagnosis|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Conjunctival, scleral, papules||Sign|
|Ophthalmology Signs / Corneal ulcer, erosion||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Obstruction of nasolacrimal duct||Sign|
|Reproductive Signs / Decreased, dropping, egg production||Poultry:Mature female,Other:Adult Female||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Diagnosis|
|Skin / Integumentary Signs / Nail, claw, hoof sloughing, separation||Sign|
|Skin / Integumentary Signs / Scarred skin||Sign|
|Skin / Integumentary Signs / Skin crusts, scabs||Sign|
|Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene||Sign|
|Skin / Integumentary Signs / Skin papules||Diagnosis|
|Skin / Integumentary Signs / Skin pustules||Diagnosis|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Poultry:All Stages,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male,Other:Juvenile,Other:Adult Female,Other:Adult Male||Diagnosis|
Disease CourseTop of page
Infection occurs when viral particles are exposed to live epithelial cells through injuries to the skin or mucous membranes of the upper digestive and respiratory tract (Cunningham, 1978; Tripathy, 1993). The virus penetrates the cell membrane within 1 hour of exposure and replication of viral DNA begins after 12 to 24 hours, reaching a maximum rate within 96 hours following exposure. Hyperplasia of host epithelium occurs between 36 and 72 hours after exposure. Inclusion bodies are present after 72 hours (Cunningham, 1978). At 72 hours, incomplete virions penetrate inclusion body vacuoles and acquire a membrane coat. Virions separate from epithelial cells during necrosis and desquamation. The incubation period is 4 to 10 days in domestic poultry and canaries (Serinus canaria) but can be prolonged to months in individual cases of wild birds (van Riper and Forrester, 2007).
Clinical disease is slow to develop and usually manifests in two forms. The more common form is dry or cutaneous pox, characterized by proliferative, warty lesions on the exposed skin of the feet, legs or head. The less common form is wet or diphtheritic pox, involving the mucous membranes of the upper digestive and respiratory tract. Cutaneous pox is usually a mild and self-limiting disease. In the first two weeks, lesions grow slowly, coalesce and, ultimately, become inflamed and hemorrhagic before they begin to heal. The course of mild cutaneous fowlpox usually lasts 3-4 weeks but can be extended if a particularly virulent strain in involved. Cutaneous pox in wild birds may be a protracted illness of several months (Kirmse, 1967). Proliferative cutaneous pox lesions in the area of the eyes and or mouth may cause blindness and often interferes with feeding. During this time, birds lose weight and, if the disease is extended in duration, may become emaciated and eventually die of starvation (Forrester and Spalding, 2003; van Riper and Forrester, 2007). Pox lesions may also provide a route of infection for bacteria and fungi (Karstad, 1971; van Riper and Forrester, 2007). Lesions on the feet often lead to the loss of digits (Riper et al., 2002).
Lesions of the diphtheritic form of avian pox occur on the mucous membranes of the mouth, trachea, and oesophagus and may be a single proliferative growth or a coalescence of lesions that form a necrotic, cheesy pseudomembrane (Tripathy, 1993). Lesions in the nasal passages, larynx, or trachea are often accompanied with labored breathing, gasping, and rales and may obstruct breathing leading to suffocation. Symptoms get progressively severe and mortalities occur by the second week of infection (Tripathy, 1993). A third form of avian pox, systemic or septicaemic pox, is seen in canaries and other highly susceptible species such as Hawaiian honeycreepers (Drepanidinae) (van Riper and Forrester, 2007). Laboured breathing is often the only clinical sign observable in afflicted canaries and is soon followed by death caused by pneumonia (Ritchie, 1995).
EpidemiologyTop of page
Since Avipoxvirus is resistant to desiccation and stable in most natural environments, virus may be mechanically transmitted by a number of different routes including biting arthropods, direct contact with contaminated surfaces or individuals, and ingestion/inhalation of infective food, water or dust in captive conditions (van Riper and Forrester, 2007). The virus cannot penetrate intact epidermis so some injury or laceration to the skin or mucous membrane is involved (Karstad, 1971; Tripathy, 1993).
While Avipoxvirus has a worldwide distribution and may occur throughout the year, disease is most prevalent in the warmer and moister regions and seasons. The seasonal peak in disease incidence often coincides with seasonal peaks in vector abundance suggesting that blood feeding by arthropods, particularly mosquitoes, is perhaps the most common route of transmission (Akey et al., 1981; van Riper and Forrester, 2007). Similarly, avian pox is more prevalent where mosquito populations are greatest (Forrester, 1991; Riper et al. 2002). The virus does not undergo replication in the vector but mosquitoes can remain infective for several weeks (DaMassa, 1966).
Along with vector abundance, host density and susceptibility are key factors influencing avian pox epizootiology (van Riper and Forrester, 2007). Outbreaks are most common and severe when domestic and wild bird densities are at their highest. High concentrations of birds occur in production and rehabilitation facilities as well as backyard feeding stations (Tripathy and Reed, 2003; Hansen, 1999). Under these conditions, transmission by direct contact with contaminated surfaces, aerosols, and other infected birds may become more significant than arthropod vectors.
Chickens, and presumably wild birds, are susceptible to avian pox at all ages. Among chickens the course of the disease lasts from 2 to 4 weeks (Cunningham, 1978). In unvaccinated chickens, mortality associated with cutaneous pox is negligible but wet pox may cause up to 50-60 % mortality (Beckman, 2007). Higher rates of mortality have been seen among captive pigeons, quail, and canaries (Serinus canaria) (Tripathy, 1993).
Individual cases of avian pox in wild birds are usually described as mild and self-limiting, but little is known about pox mortality in wild bird populations. Avian pox appeared to affect survivorship of fledgling Galapagos Mockingbirds (Nesomimus parvulus) in the Galapagos (Curry and Grant, 1989) and there is evidence that avian pox contributes to population declines of Elepaio (Chasiempis sandwichensis) in the Hawaiian Islands (VanderWerf, 2001; VanderWerf, 2009). Endemic birds of the Hawaiian Islands appear particularly susceptible to Avipoxvirus and experimental infections of Laysan Finch (Telespiza cantans) and Hawaii Amakihi (Hemignathus virens) have documented high rates of mortality (Warner, 1968; Riper et al., 2002).
ImpactTop of page
In chickens, cutaneous fowlpox seldom results in economically significant mortality; however, the diphtheritic form of fowlpox can cause up to 60% mortality in unvaccinated chickens. Cutaneous fowlpox can cause a transient drop in layer egg production, up to 15%, and reduces growth rate in young birds (Beckman, 2007). On a flock basis, outbreaks of fowlpox generally last 6-10 weeks resulting in significant economic loss in egg production. For domestic turkeys, the reduced weight gain in market birds has a larger impact (Cunningham, 1978). Septicaemic canarypox can have a great impact on individual commercial canary breeders due to the high incidence and mortality rates associated with this form of the disease (Ritchie, 1995).
Impact on Biodiversity
Although avian pox is typically an endemic, mild, and self-limiting disease among wild birds, epizootics among endemic birds on remote islands such as the Hawaiian Islands, (van Riper et al., 2004), Galapagos Archipelago (Vargas, 1987), Canary Islands (Smits et al., 2005) and Falkland Islands (Munro, 2006) are characterized by high morbidity and mortality.
Zoonoses and Food SafetyTop of page
Avian poxviruses are not known to be transmissible to humans (Cunningham, 1978; Tripathy and Reed, 2003). Poultry carcasses affected with generalized fowlpox lesions are condemned. Carcasses may be approved for consumption, if tissue affected by localized, cutaneous fowlpox lesions is removed in processing (Herenda and Franco, 1996).
Disease TreatmentTop of page
There are no drugs effective against Avipoxvirus (Tripathy and Reed, 2003). As supportive care, lesions can be washed with Lugol's solution of iodine, silver nitrate or saline solutions and treated with a topical antimicrobial agent. A broad spectrum oral antibiotic may be administered to prevent secondary bacterial infections (van Riper and Forrester 2007). Environmental temperature should be elevated (Cunningham 1978).
Prevention and ControlTop of page
Immunization and Vaccines
Vaccination is perhaps the best way to prevent poxvirus infections among domestic fowl and many pet trade species. A number of vaccines have been developed and are commonly used in poultry, pigeons, psittacines and canaries (Ritchie, 1995; Tripathy and Reed, 2003). Vaccines can be administered prophylactically or to contain an outbreak. Chickens can be initially vaccinated with an attenuated-live virus vaccine at four weeks and vaccinated again a month or two before egg production (Cunningham, 1978). Older chickens can be vaccinated annually one to two months before the appearance of mosquitoes (Tripathy and Reed, 2003). Psittacines should be vaccinated with inactivated psittacine poxvirus at quarantine stations and given a booster 2 – 8 weeks later. Canaries should be vaccinated at the time of fledging and annually just prior to the mosquito season (Ritchie, 1995).
Chicks can be vaccinated at hatching with attenuated fowl pox virus of tissue culture origin but this will not produce lasting immunity. If transmission is unlikely in the interim, initial vaccination could be postponed until after 4 weeks of age when a better and lasting immune response can be expected.
Vaccines are usually administered by wing-web injections or brushing on defeathered follicles (Cunningham, 1978). Birds should be healthy at the time of vaccination and all susceptible birds should be vaccinated at the same time. All vaccine vials and vaccination equipment should be thoroughly disinfected before disposal. A successful immunization (“take”) is made evident by a swelling at the injection site 7-10 days following vaccination. Immunity develops 10-14 days following vaccination (Tripathy and Reed, 2003). Commercial vaccines have not been used with wild bird populations.
Husbandry Methods and Good Practice
Disease can be prevented by eliminating conditions that foster transmission. In production and captive settings, mosquitoes, other biting flies and mites should be effectively excluded from housing or be controlled by elimination of larval habitats and/or the appropriate use of pesticides (Karstad, 1971; van Riper and Forrester, 2007). Newly arrived and diseased birds should be quarantined until properly immunized or free of any sign of disease. Bird densities should be reduced whenever possible and poultry house dust should be controlled. Birds should be well fed and maintained in an appropriate environment to avoid stress (Cunningham, 1978). Biosecurity measures should be in place to prevent the movement of pox-contaminated equipment (Beckman 2007).
Among wild birds, avian pox may be prevented by discontinuing the practice of backyard feeding stations. Alternatively, bird feeders and bird baths should be routinely disinfected with a 5 – 10% bleach solution every two weeks (van Riper and Forrester, 2007). Eliminating man-made larval mosquito habitat should reduce local transmission. This is particularly important on remote islands, such as the Hawaiian Islands, where avian pox viruses and vectors are introduced species and endemic birds are highly susceptible (Riper et al. 2002; Atkinson et al. 2005).
Farm-Level and Local Control
Control of avian pox outbreaks in production and captive settings depends on similar actions to those needed for prevention. In addition, all surfaces, perches, feeders etc. should be disinfected with a strong disinfectant such as 10 % bleach solution or Virkon-S (Beckman, 2007). Diseased birds should be separated from uninfected birds and great care must be taken not to spread the virus directly. Birds can be vaccinated during an outbreak and this may significantly slow down the spread of disease. Finally, vector control is essential to stop an outbreak.
ReferencesTop of page
Akey BL; Nayar JK; Forrester DJ, 1981. Avian pox in Florida wild turkeys: Culex nigripalpus and Wyeomyia vanduzeei as experimental vectors. Journal of Wildlife Diseases, 17:597-599.
Aruch S; Atkinson CT; Savage AF; LaPointe DA, 2007. Prevalence and distribution of pox-like lesions, avian malaria, and mosquito vectors in Kipahulu Valley, Haleakala National Park, Hawai'i, USA. Journal of Wildlife Diseases, 43(4):567-575. http://www.wildlifedisease.org
Atkinson CT; Lease JK; Dusek RJ; Samuel MD, 2005. Prevalence of pox-like lesions and malaria in forest bird communities on Leeward Mauna Loa Volcano, Hawaii. Condor, 107(3):537-546. http://www.bioone.org/bioone/?request=get-abstract&issn=0010-5422&volume=107&issue=03&page=0537
Austin FJ; Bull PC; Chaudry MA, 1973. A poxvirus isolated from Silvereyes (Zosterops lat.) from Lower Hutt, New Zealand. Journal of Wildlife Diseases, 9:111-114.
Bataille A; Cunningham AA; Cedeño V; Patiño L; Constantinou A; Kramer LD; Goodman SJ, 2009. Natural colonization and adaptation of a mosquito species in Galapagos and its implications for disease threats to endemic wildlife. Proceedings of the National Academy of Sciences of the United States of America, 106(25):10230-10235. http://www.pnas.org/
Bollinger O, 1873. Ueber Menschen- und Thierpocken, ueber den Ursprung der Kuhpocken und Ueber intrauterine Vaccination ([English title not available]). 1021-1060. [Volkmann's Sammlung klinischer Vortraege 116.]
Bolte AL; Meurer J; Kaleta EF, 1999. Avian host spectrum of avipoxviruses. Avian Pathology, 28(5):415-432; 5 pp. of ref.
Boosinger TR; Winterfield WR; Feldman DS; Dhillon AS, 1982. Psittiacine pox virus: virus isolation and identification, transmission and cross-challenge studies in parrots and chickens. Avian Diseases, 26:437-444.
Bouvier G, 1946. Observations on the diseases of game, of some wild animals and of fish (1942-1945). (Observations sur les maladies du gibier, de quelques animaux sauvages et des poissones (1942-1945).) Schweizerisches Archive Tierheilkunde, 88:268-274.
Buenestado F; Gortazar C; Millan J; Hofle U; Villafurte R, 2004. Descriptive study of an avian pox outbreak in wild red-legged partridges (Alcetoris rufa) in Spain. Epidemiology and Infection, 132:369-374.
BURNET FM; STANLEY WM, 1959. The viruses: biochemical, biological and biophysical properties. Vol. III. Animal viruses [ed. by BURNET, F. M.\STANLEY, W. M.]. New York (& London) : Academic Press., xvii + 428 pp.
Cerrone A; Blasone M; Piccirillo A; Mariani F; Menna LF, 1999. Clinical findings observed in some ostrich-farms in Campania during the period 1997-1998. (L'allevamento dello struzzo in Campania: casi clinici osservati nel biennio 1997-98.) In: Selezione Veterinaria, No. 8/9. 653-661.
Cociu M; Wagner G; Micu N; Tuschak E; Mihaescu G, 1972. Avian pox in a bustard (Otis tarda). (Gefluegelpocken bei einer trappe (Otis tarda).) In: Diseases of Zoo Animals, 14th International Symposium, Wroclaw, Poland. 81-83.
Crawford JA; Oates RM, 1979. Avian pox in California quail from Oregon. Journal of Wildlife Diseases, 15:447-449.
Cunningham CH, 1978. Avian pox. In: Diseases of poultry (7th Edition) [ed. by Hofstad, M. S. \Calnek, B. W. \Helmboldt, C. F. \Reid, W. M. \Yoder Jr, H. W.]. Ames, Iowa: Iowa State University Press, 597-609.
Docherty DE; Long RIR; Flickinger EL; Locke LN, 1991. Isolation of poxvirus from debilitating cutaneous lesions on four immature grackles (Quiscalus sp.). Avian Diseases, 35(1):244-247; 7 ref.
Farias MEM; LaPointe DA; Atkinson CT; Czerwonka C; Shrestha R; Jarvi SI, 2010. Taqman real-time PCR detects Avipoxvirus DNA in blood of Hawaìi 'Amakihi (Hemignathus virens). PLoS ONE, No.May:e10745. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0010745
Foster JT, 2009. The history and impact of introduced birds. In: Conservation biology of Hawaiian forest birds: Implications for island avifauna [ed. by Pratt, T. K. \Atkinson, C. T. \Banko, P. C. \Jacobi, J. D. \Woodworth, B. L.]. New Haven, Connecticut, USA: Yale University Press, 312-330.
Garner MM, 1989. Bumblefoot associated with poxvirus in a wild golden eagle (Aquila chrysaetos). Companion Animal Practice, 19(10):17-20; 12 ref.
Giddens WE Jr; Swango LJ; Henderson JD Jr; Lewis RA; Farner DS; Carlos A; Dolowy WC, 1971. Canary pox in sparrows and canaries (Fringillidae) and in weavers (Ploceidae). Pathology and host specificity of the virus. Veterinary Pathology, 8(No.3):260-280.
Goodpasture EW; Anderson K, 1962. Isolation of wild avian pox virus including both cytoplasmic and nuclear inclusions. American Journal of Pathology, 40:437-453.
Graham CLG, 1978. Poxvirus infection in a spectacled amaon parrot (Amazona albifrons). Avian Diseases, 22:340-343.
Hansen WR, 1999. Avian pox. In: Field manual of wildlife diseases: General field procedures and diseases of birds [ed. by Friend, M. \Franson, J. C. \Ciganovich, E. A.]. 163-169. [US Geological Survey, Biological Resources Division. Information and Technology Report 1999-001.]
Harrigan KE; Barker IK; Studdert MJ, 1975. Poxvirus infection in the white-backed magpie (Gymnorhina hypoleuca) and pox-like conditions in other birds in Australia. Journal of Wildlife Diseases, 11(No.3):343-347.
Herbst W; Krauss H, 1989. Isolation of a poxvirus from a sparrow (Passer domesticus). Journal of Veterinary Medicine, B (Infectious Diseases, Immunology, Food Hygiene, Veterinary Public Health), 36(6):477-479.
Hitchner SB; Clubb SL, 1980. Relationship between poxvirus of parrots and of other birds. In: Proceedings of 29th Western Poultry Disease Conference, Acapulco, Mexico, 22-25 April 1980 [ed. by D.A. McMartin]. Davis, California, USA: Cooperative Extension, University., 149-151.
Holt G; Krogsrud J, 1973. Pox in wild birds. Acta Veterinaria Scandinavia, 14:201-203.
Ideris A; Ibrahim AL, 1986. Poxvirus infection in turkeys. Kajian Veterinar, 18(1):85-87; 5 ref.
Illera JC; Emerson BC; Richardson DS, 2008. Genetic characterization, distribution and prevalence of avian pox and avian malaria in the Berthelot's pipit (Anthus berthelotii) in Macaronesia. Parasitology Research, 103(6):1435-1443. http://www.springerlink.com/content/n721h0532vn6525l/?p=0620fa7014bb4857a3a4dbaace4a28fc&pi=27
Jarvi SI; Triglia D; Giannoulis A; Farias M; Bianchi K; Atkinson CT, 2008. Diversity, origins and virulence of Avipoxviruses in Hawaiian forest birds. Conservation Genetics, 9(2):339-348. http://springerlink.metapress.com/link.asp?id=105709
Jenkins CD; Temple SA; Riper C van; Hansen WR, 1989. Disease-related aspects of conserving the endangered Hawaiian Crow. In: Disease and threatened birds. Proceedings of a Symposium held at the XIX World Conference of the International Council for Bird Preservation, June 1986, Queens University, Kingston, Ontario, Canada. Cambridge, UK: International Council for Bird Preservation, 77-87.
Krone O; Essbauer S; Wibbelt G; Isa G; Rudolph M; Gough RE, 2004. Avipoxvirus infection in peregrine falcons (Falco peregrinus) from a reintroduction programme in Germany. Veterinary Record, 154(4):110-113.
Kuntze A; Schroder HD; Ippen R, 1968. Avian pox in Broad-winged Hawks (Buteo platypterus). (Geflugelpocken bei Breitschwingenbussarden (Buteo platypterus).) In: Diseases of Zoo Animals, 10th International Symposium, Salzburg, Austria. 161-163.
Landowska-Plazewska E; Plazewski L, 1968. Outbreak of avian pox in Humboldt Penguins in Warsaw Zoo. (Ausbruch von vogelpocken bei Humboldttpinguinen im Warschauer Zoo.) In: Diseases of Zoo Animals, 10th International Symposium, Salzburg, Austria. 159.
Mani P; Fabiani O; Bellini S; Fontanellli M, 1990. [English title not available]. (Caratteristiche di crescita, morfologico-struttural i ed antigeniche di uno stipite di avipoxvirus isolato dalla stama (Perdix perdix).) Zootecnica International:147-152.
Mathur BBL; Verma KC; Agarwal K; Kumar S, 1972. Serological survey for the detection of certain common respiratory infections in migratory birds: a note. Indian Journal of Animal Science, 42:144-145.
Mikaelian I; Gauthier F; Fitzgerald G; Higgins R; Claveau R; Martineau D, 1997. Primary causes of death in wild birds of Québec. (Causes primaires de décès des oiseaux de la faune au Québec.) Médecin Vétérinaire du Québec, 27(3):94-102.
Munro G, 2006. Outbreak of Avian Pox Virus in Gentoo Penguins in the Falklands, February 2006. Sandy, UK: Falklands Conservation. http://www.falklandsconservation.com/wildlife/penguins/AvianPox2006Report.pdf
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
Olmos PR; Martinez BL; Lopez JE; Martinez LP, 1986. [English title not available]. (Patogenicidad y antigenidad de un aislamiento sospechoso de viruela de los loror (Amazona stivae), en gallinas.) Veterinario Mexico, 17:104-109.
Orós J; Rodríguez F; Rodríguez JL; Bravo C; Fernández A, 1997. Debilitating cutaneous poxvirus infection in a Hodgson's grandala (Grandala coelicolor). Avian Diseases, 41(2):481-483; 10 ref.
Pandey KD; Mallick BB, 1974. Studies on pox infection in turkeys. Indian Veterinary Journal, 51:33-35.
Rinaldi A; Mahnel H; Nardelli L; Mandelli GC; Cervio G; Valeri A, 1972. [Characterization of a quail pox virus.]. (Charakterisierung eines Wachtelpockenvirus.) Zentralblatt fur Veterinarmedizin, 19B(Heft 3):199-212.
Sharma VK; Simon J; Hanson LE, 1968. Histologic study of tissue reaction in canaries, chicken embryos infected with a pox agent. Avian Diseases, 12:594-606.
Shearn-Bochsler V; Green DE; Converse KA; Docherty DE; Thiel T; Geisz HN; Fraser WR; Patterson-Fraser DL, 2008. Cutaneous and diphtheritic avian poxvirus infection in a nestling southern giant petrel (Macronectes giganteus) from Antarctica. Polar Biology, 31:569-573.
Smits JE; Tella JL; Carrete M; Serrano D; López G, 2005. An epizootic of avian pox in endemic short-toed larks (Calandrella rufescens) and Berthelot's pipits (Anthus berthelotti) in the Canary Islands, Spain. Veterinary Pathology, 42(1):59-65.
Tadese T; Fitzgerald S; Reed WM, 2008. Detection and differentiation of re-emerging fowlpox virus (FWPV) strains carrying integrated reticuloendotheliosis virus (FWPV-REV) by real-time PCR. Veterinary Microbiology, 127(1/2):39-49. http://www.sciencedirect.com/science/journal/03781135
Thiel T; Whiteman NK; Tirapé A; Baquero MI; Cedeño V; Walsh T; Uzcátegui GJ; Parker PG, 2005. Characterization of canarypox-like viruses infecting endemic birds in the Galápagos Islands. Journal of Wildlife Diseases, 41(2):342-353.
Tikasingh ES; Worth CB; Spence L; Aitken THG, 1982. Avian pox in birds in Trinidad. Journal of Wildlife Diseases, 18:133-139.
Tripathy DN; Reed WN, 2003. Pox. In: Diseases of poultry 11 Edition [ed. by Saif, Y. M. \Barnes, H. J. \Glisson, J. R. \Fadly, A. M. \McDougald, L. R.]. Ames, Iowa, USA: Iowa State University Press, 253-269.
Tsai SS; Chang TC; Yang SF; Chi YC; Cher RS; Chien MS; Itakura C, 1997. Unusual lesions associated with avian poxvirus infection in rosy-faced love birds (Agapornis roseicollis). Avian Pathology, 26(1):75-82; 14 ref.
Wang JingXu; Zhang GuoXiang; Liu ChangFu; Tian XiaoDi; Liu XiaoHong; Ma YingZhan, 1996. Current status and control policy of avian diseases in Shaanxi. Chinese Journal of Veterinary Science and Technology, 26(5):13-16.
Wheeldon EB; Sedgwick CJ; Schulz TA, 1985. Epornitic of avian pox in a raptor rehabilitation center. Journal of the American Veterinary Medical Association, 187(11):1202-1204; 5 ref.
Whiteman NK; Goodman SJ; Sinclair BJ; Walsh T; Cunningham AA; Kramer LD; Parker PG, 2005. Establishment of the avian disease vector Culex quinquefasciatus Say, 1823 (Diptera: Culicidae) on the Galápagos Islands, Ecuador. Ibis (London), 147(4):844-847. http://www.blackwell-synergy.com/servlet/useragent?func=showIssues&code=ibi
Wikelski M; Foufopoulos J; Vargas H; Snell H, 2004. Galapagos birds and disease: Invasive pathogens as threats for island species. Ecology and Society, 9(1):5. http://www.ecologyandsociety.org/vol9/iss1/art5
Winteroll G; Mousa S; Akrae M, 1979. Avipoxvirus isolated from Psittacidae and falcon. Detailed characterization. (Pockenisolate aus Psittaciden und Falken -Nahere Charakterisierung.) In: Krankheiten der Vogel. Tagung der Fachgruppe Geflugelkrankheiten (der DVG), 7-8. Marz 1979 in Munchen. Giessen-Lahn, German Federal Republic. 117-125.
Zhang DeLing; Jia JunYuan; Chen FuWang; Wei WanRen; Zhang ChengHu; Wu LianHua, 1996. Serological investigation of 16 infectious diseases in rare birds in the Lanzhou area. Chinese Journal of Veterinary Medicine, 22(6):22.
OrganizationsTop of page
UK: Falklands Conservation, 1 Princes Avenue, London N3 2DA, http://www.falklandsconservation.com/
USA: USDA-APHIS-NVSL: UDSA Animal and Plant Health Inspection Service, National Veterinary Services Laboratory, PO Box 844, Ames, IA 50010, http://www.aphis.usda.gov/animal_health/lab_info_services/
USA: USGS-NWHC - National Wildlife Health Center, 6006 Schroeder Road Madison, Wisconsin 53711, http://www.nwhc.usgs.gov/
USA: USGS-PIERC: Pacific Island Ecosystems Research Center, Kilauea Field Station, PO Box 44, Hawaii National Park Hawaii, http://biology.usgs.gov/pierc/
Galapagos Islands: Charles Darwin Research Station (CDRS), run by the Charles Darwin Foundaton, Puerto Ayora, Isla Santa Cruz, Galapagos, http://www.darwinfoundation.org/english/pages/index.php
ContributorsTop of page
21/07/10 Original text by:
Dennis LaPointe, US Geological Survey, Hawaii, USA
Distribution MapsTop of page
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