- Host Animals
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
International Common Names
- English: avian diphtheria; canker; fowl pox; fowlpox, fowl pox; pox
- Spanish: viruela aviar
Local Common Names
- Italy: epitelioma dei polli
OverviewTop of page
Avipoxviruses infect a wide variety of birds, including domestic, wild and pet birds. All the avian poxviruses belong to the genus Avipoxvirus, within the subfamily Chordopoxvirinae of the family Poxviridae. Fowlpox virus is the type species of the genus Avipoxvirus. This genus also comprises the following species: turkeypox, canarypox, pigeonpox, quailpox, sparrowpox, starlingpox, juncopox and psittacinepox viruses. Other probable members of this genus are peacockpox, penguinpox, mynahpox and albatrosspox viruses. The term fowl pox initially included all pox virus infections of birds, but now it is often used to refer to the disease in commercial poultry, such as chickens and turkeys.
Fowl pox is a common and economically important disease of domestic birds and is distributed worldwide. It is slow spreading and characterized by the formation of proliferative lesions, scabs on the skin and diphtheric lesions in the upper regions of the respiratory and digestive tracts.
The first description of the occurrence of pox virus infection in birds appeared in Europe around 1850. Bollinger, in 1873 published his microscopic findings on pox virus-infected cells from chickens. Large, cytoplasmic, eosinophilic inclusions were observed, which are now known as Bollinger’s inclusion bodies. The first attempts to grow this virus in chicken embryos were made by Centanni in Italy in 1902 (Bolte et al., 1999).
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Accipitridae||Experimental settings, Wild host|
|Anatidae||Experimental settings, Wild host|
|Columba livia (pigeons)||Domesticated host|
|Columbiformes||Domesticated host, Experimental settings, Wild host|
|Falconiformes||Domesticated host, Wild host|
|Galliformes||Domesticated host, Experimental settings, Wild host||Poultry: All Stages|
|Gallus gallus domesticus (chickens)||Domesticated host, Experimental settings||Poultry: All Stages|
|Meleagris gallopavo (turkey)||Domesticated host||Poultry: All Stages|
|Passeriformes||Domesticated host, Experimental settings, Wild host|
|Phasianidae||Domesticated host, Experimental settings, Wild host|
|Psittaciformes||Domesticated host, Experimental settings, Wild host|
|Strigiformes||Experimental settings, Wild host|
Systems AffectedTop of page digestive diseases of poultry
respiratory diseases of poultry
skin and ocular diseases of poultry
DistributionTop of page
Avian pox viruses are distributed worldwide in domestic poultry and wild birds. Their incidence, however, is variable in different geographical regions because of:
- differences in climate (the incidence is more important in countries located in tropical areas), management and hygienic conditions
- presence of vectors
- practice of prophylactic immunization. In many developed countries, regular immunization of poultry flocks has virtually eliminated avian pox in commercial poultry,
In recent years, reports of pox virus infection in wild birds have increased (Bolte et al., 1999; Kreuder et al., 1999; Tripathy et al., 2000). This may be important because wild birds may serve as virus carriers and may transmit and/or maintain the infection in a commercial poultry flock.
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.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Angola||Present||OIE Handistatus (2005)|
|Benin||Present||OIE Handistatus (2005)|
|Botswana||Present||OIE Handistatus (2005)|
|Burundi||Present||OIE Handistatus (2005)|
|Cabo Verde||Present||OIE Handistatus (2005)|
|Cameroon||Present||OIE Handistatus (2005)|
|Côte d'Ivoire||Present||OIE Handistatus (2005)|
|Djibouti||Present||OIE Handistatus (2005)|
|Eritrea||Present||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)|
|Mauritius||Absent, No presence record(s)||OIE Handistatus (2005)|
|Morocco||Present||OIE Handistatus (2005)|
|Mozambique||Present||OIE Handistatus (2005)|
|Namibia||Present||OIE Handistatus (2005)|
|Nigeria||Present||Sa'idu et al. (1994); Oladele et al. (1996); Halle et al. (1998); OIE Handistatus (2005)|
|São Tomé and Príncipe||Present||OIE Handistatus (2005)|
|Seychelles||Absent, No presence record(s)||OIE Handistatus (2005)|
|South Africa||Present||Allwright et al. (1994); Stannard et al. (1998); OIE Handistatus (2005)|
|Sudan||Present||El-nur-Abd-El-Rahman et al. (1999); OIE Handistatus (2005)|
|Tanzania||Present||OIE Handistatus (2005)|
|Togo||Present||OIE Handistatus (2005)|
|Tunisia||Present||2003||Loir and Ducloux (1894)|
|Uganda||Present||OIE Handistatus (2005)|
|Zambia||Present||OIE Handistatus (2005)|
|Afghanistan||Present||CABI (Undated a)|
|Bahrain||Present||Samour and Cooper (1993); OIE Handistatus (2005)|
|China||Present||Hu (1982); Xu et al. (1993); Zhang DeLing et al. (1996)|
|-Shaanxi||Present||Wang JingXu et al. (1996)|
|-Shanxi||Present||Wang JingXu et al. (1996)|
|Hong Kong||Present||OIE Handistatus (2005)|
|India||Present||Mathur et al. (1972); Pandey and Mallick (1974); OIE Handistatus (2005)|
|-Andhra Pradesh||Present||Rao (1965)|
|Indonesia||Present||OIE Handistatus (2005)|
|Iraq||Present||Al-Falluji et al. (1979); Tantawi et al. (1981); Al-Ani (1986); OIE Handistatus (2005)|
|Israel||Present||OIE Handistatus (2005)|
|Japan||Present||2003||Kawashima (1962); Sato et al. (1962); Iwata et al. (1986); Tsai et al. (1997)|
|Jordan||Present||OIE Handistatus (2005)|
|Kazakhstan||Absent, No presence record(s)||OIE Handistatus (2005)|
|Malaysia||Present||Ideris and Ibrahim (1986); Karpinski and Clubb (1986); Reed and Schrader (1989)|
|-Peninsular Malaysia||Present||OIE Handistatus (2005)|
|-Sarawak||Present||OIE Handistatus (2005)|
|Mongolia||Absent, No presence record(s)||OIE Handistatus (2005)|
|Myanmar||Present||OIE Handistatus (2005)|
|Nepal||Present||OIE Handistatus (2005)|
|Philippines||Present||OIE Handistatus (2005)|
|Saudi Arabia||Present||Ostrowski et al. (1995); Sami et al. (1995)|
|South Korea||Present||OIE Handistatus (2005)|
|Sri Lanka||Present||OIE Handistatus (2005)|
|Syria||Absent, No presence record(s)||OIE Handistatus (2005)|
|Taiwan||Present||OIE Handistatus (2005)|
|Tajikistan||Absent, No presence record(s)||OIE Handistatus (2005)|
|Thailand||Present||OIE Handistatus (2005)|
|United Arab Emirates||Present||Kiel (1985); Samour and Cooper (1993); OIE Handistatus (2005)|
|Vietnam||Present||OIE Handistatus (2005)|
|Andorra||Absent, No presence record(s)||OIE Handistatus (2005)|
|Austria||Absent, No presence record(s)||Loupal et al. (1985); OIE Handistatus (2005)|
|Belarus||Present||OIE Handistatus (2005)|
|Belgium||Absent, No presence record(s)||OIE Handistatus (2005)|
|Bosnia and Herzegovina||Absent, No presence record(s)||OIE Handistatus (2005)|
|Cyprus||Present||OIE Handistatus (2005)|
|Czechia||Present||OIE Handistatus (2005)|
|Denmark||Present||Christiansen (1949); OIE Handistatus (2005)|
|Estonia||Absent, No presence record(s)||OIE Handistatus (2005)|
|Finland||Absent, No presence record(s)||OIE Handistatus (2005)|
|France||Present||OIE Handistatus (2005)|
|Germany||Present||Seidel (1972); OIE Handistatus (2005)|
|Iceland||Absent, No presence record(s)||OIE Handistatus (2005)|
|Ireland||Present||OIE Handistatus (2005)|
|Isle of Man||Absent, No presence record(s)||OIE Handistatus (2005)|
|Italy||Present||Chiocco (1992); OIE Handistatus (2005)|
|Jersey||Absent, No presence record(s)||OIE Handistatus (2005)|
|Latvia||Absent, No presence record(s)||OIE Handistatus (2005)|
|Liechtenstein||Absent, No presence record(s)||OIE Handistatus (2005)|
|Lithuania||Absent, No presence record(s)||OIE Handistatus (2005)|
|Malta||Present||OIE Handistatus (2005)|
|Netherlands||Present||OIE Handistatus (2005); CABI (Undated)|
|North Macedonia||Present||OIE Handistatus (2005)|
|Norway||Absent, No presence record(s)||Holt and Krogsrud (1973); OIE Handistatus (2005)|
|Poland||Absent, No presence record(s)||Landowska-Plazewska and Plazewski (1968); OIE Handistatus (2005)|
|Romania||Present||Cociu et al. (1972); OIE Handistatus (2005)|
|Serbia and Montenegro||Absent, No presence record(s)||OIE Handistatus (2005)|
|Slovenia||Absent, No presence record(s)||OIE Handistatus (2005)|
|Spain||Present||Vogelsang (1938); Groth (1963); Orós et al. (1997); OIE Handistatus (2005)|
|Sweden||Absent, No presence record(s)||Hulphers (1943); OIE Handistatus (2005)|
|United Kingdom||Present||Green (1969); OIE Handistatus (2005)|
|Barbados||Present||OIE Handistatus (2005)|
|Bermuda||Absent, No presence record(s)||Wingate et al. (1980); OIE Handistatus (2005)|
|Canada||Present||SYVERTON and COWAN (1944); Kuntze et al. (1968); Moffatt (1972); Cox (1980); OIE Handistatus (2005)|
|-Quebec||Present||CABI (Undated a)|
|Cuba||Present||Boado et al. (1992); OIE Handistatus (2005)|
|Curaçao||Absent, No presence record(s)||OIE Handistatus (2005)|
|Dominica||Present||OIE Handistatus (2005)|
|Dominican Republic||Present||OIE Handistatus (2005); CABI (Undated)|
|Guatemala||Present||OIE Handistatus (2005)|
|Haiti||Absent, No presence record(s)||OIE Handistatus (2005)|
|Honduras||Present||OIE Handistatus (2005)|
|Jamaica||Present||OIE Handistatus (2005)|
|Martinique||Present||OIE Handistatus (2005)|
|Mexico||Present||Graham (1978); OIE Handistatus (2005)|
|Nicaragua||Present||OIE Handistatus (2005)|
|Saint Kitts and Nevis||Absent, No presence record(s)||OIE Handistatus (2005)|
|Saint Vincent and the Grenadines||Present||OIE Handistatus (2005)|
|Trinidad and Tobago||Present||OIE Handistatus (2005)|
|United States||Present||OIE Handistatus (2005)|
|-Arizona||Present||Blakenship et al. (1966)|
|-California||Present||Morishita et al. (1998)|
|-Florida||Present||Deem et al. (1997); Kreuder et al. (1999)|
|-Georgia||Present||Wheeldon et al. (1985)|
|-Hawaii||Present||Locke et al. (1965)|
|-Idaho||Present||Docherty et al. (1991)|
|-Illinois||Present||Sharma et al. (1968)|
|-Indiana||Present||CABI (Undated)||Original citation: Boosinger TR et al. (1982)|
|-Kentucky||Present||Poonacha and Wilson (1981)|
|-Maryland||Present||Herman et al. (1962)|
|-New Jersey||Present||Worth (1956)|
|-New York||Present||Donnelly and Crane (1984)|
|-Oklahoma||Present||Johnson and Castro (1986)|
|-Oregon||Present||Crawford et al. (1979)|
|-Tennessee||Present||Goodpasture and Anderson (1962)|
|-Texas||Present||Clark et al. (1988)|
|Australia||Present||Raidal et al. (1996); OIE Handistatus (2005)|
|French Polynesia||Present||OIE Handistatus (2005)|
|New Caledonia||Present||OIE Handistatus (2005)|
|New Zealand||Present||Austin et al. (1973); OIE Handistatus (2005)|
|Vanuatu||Absent, No presence record(s)||OIE Handistatus (2005)|
|Argentina||Present||OIE Handistatus (2005)|
|Brazil||Present||2003||Fallavena et al. (1993); Back et al. (1995)|
|Chile||Present||Toro et al. (1997); OIE Handistatus (2005)|
|Colombia||Present||OIE Handistatus (2005)|
|Ecuador||Present||OIE Handistatus (2005)|
|Falkland Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|French Guiana||Absent, No presence record(s)||OIE Handistatus (2005)|
|Guyana||Absent, No presence record(s)||OIE Handistatus (2005)|
|Paraguay||Present||OIE Handistatus (2005)|
|Peru||Present||OIE Handistatus (2005)|
|Uruguay||Present||OIE Handistatus (2005)|
PathologyTop of page
In the cutaneous form of the disease, small papules or nodules are observed in non-feathered areas of the skin. This means the comb, wattles, corners of the mouth, angle of the beak, commisure of the mouth, ventral surface of the wings, the legs and the vent. Lesions may coalesce into large greyish, wart-like plaques. Removal of the lesions, if not completely dry, leaves a haemorrhagic, moist surface. Scabs or crusts finally drop off, leaving a scar. In turkeys and pigeons, cutaneous lesions may spread to the feathered areas of the body (see pictures) (Tripathy, 1993).
In the diphtheric form of the disease, white, opaque nodules may develop in the mucous membranes of the mouth, infraorbital sinuses, larynx, pharynx, trachea and oesophagus. Their coalescence results in yellowish, necrotic, cheesy pseudomembranes that leave a bleeding surface on removal. Often a solitary proliferative growth may be observed (Tripathy, 1993). In an unusual outbreak of pox virus infection in turkeys, proliferative lesions occurred in the oviduct, cloaca and skin surrounding the vent (Metz et al., 1985).
Microscopically, infection by any pox virus initially results in cell enlargement and proliferation. Epithelial cells show marked hyperplasia and ballooning degeneration with large eosinophilic intracytoplasmic A-type inclusion bodies, named Bollinger bodies (see pictures). The diphtheric lesions are characterized by oedema and hydropic degeneration of the epithelium of the larynx and trachea, and by the presence of intracytoplasmic inclusion bodies in the epithelial cells of these organs.
DiagnosisTop of page
Cutaneous and diphtheric lesions typical of avian pox infection may be confirmed by histopathology of the lesions or virus isolation. The cutaneous form must be differentiated from pantothenic acid or biotin deficiency in young chicks or from T-2 toxicosis. Diphtheric lesions associated with respiratory distress must be differentiated from infectious laryngotracheitis and vitamin A deficiency. In doves and pigeons, the diphtheric form may be mistaken for lesions caused by Trichomonas gallinae (Tripathy and Reed, 1997).
Observation of the inclusion bodies (Bollinger bodies) in the cell cytoplasm in a smear, stained with Wright’s stain or by the Gimenez method prepared from lesions is characteristic of pox virus infection. Protocol of this staining can be found at http://www.oie.int/eng/normes/mmanual/A_00121.htm. The method uses fuschin and malachite green, and can be used for both cutaneous and diphtheric lesions. The elementary bodies of fowl pox virus stain red and are either within intact structures of various sizes representing inclusion bodies, or scattered (approximately 0.2-0.3 micrometres).
Presence of characteristic lesions may also be observed in a tissue section prepared from a lesion processed by conventional histological methods. Electron microscopy may also be useful to demonstrate virus particles in lesions by negative staining or in ultra-thin sections. However, these methods do not provide a species diagnosis of the avipoxvirus involved in the lesion.
Viral isolation and identification
Avian pox viruses can be isolated by inoculating material from suspect lesions into susceptible birds, developing embryos or cell cultures from avian origin. Isolation is attempted from nodular or diphtheric lesions, which are removed with sterile scissors and forceps by cutting deep into the epithelial tissue. A suspension of this material is prepared in Hanks balanced salt solution or nutrient broth containing antibiotics and used for inoculation. The developing chicken embryo, 9 to 12 days, is the preferred host for viral isolation. Approximately 0.1 ml. of the tissue material is inoculated onto the CAM and the embryo is incubated at 37ºC. The embryo is examined to detect the presence of pock lesions in the CAM at 5 to 7 days post infection. White opaque pocks or a generalized thickening of the CAM is observed if the suspect material contains the pox virus. Histopathological examination of the CAM should be done to confirm the presence of intracytoplasmic inclusion bodies characteristic of pox virus infection. It has to be noted that some pox virus strains from wild birds do not grow in CAM and inoculation of susceptible birds is necessary to confirm the pathogenicity of the viral agent.
If susceptible birds are used for viral isolation, a homogenate of the lesion is applied by cutaneous scarification to the comb or any other unfeathered area of the skin. Susceptibility of the bird species is demonstrated by development of lesions at the site of inoculation.
Cell cultures are not usually employed for initial isolation of avian pox viruses. Chicken embryo fibroblasts, chicken embryo dermis and kidney cells and duck embryo fibroblasts may be used to propagate the virus. Viral infection in chicken fibroblasts causes cell rounding followed by cell degeneration and necrosis, by 4 to 6 days post infection. Adaptation of the virus to the host system is sometimes necessary, since not all strains produce cytopathic effects on initial inoculation (Tripathy and Reed, 1997; Tripathy, 1993).
Serological methods have been mainly used to characterize antigenically the relationship among avian pox viruses, but are not generally practical as routine diagnostic tests.
After virus/serum interaction the residual activity may be assayed in embryonating chicken eggs or cell cultures. Only some selected strains of the virus have plaque-forming ability in chicken embryo cells. Neutralizing antibodies develop within 1-2 weeks of infection.
Agar gel immunodiffusion
Precipitating antibodies can be detected by reacting sera against partially purified viral antigens, which are prepared by sonification and homogenization of infected lesion material or infected CAMs. The partial purification of the antigen is done by sonification and homogenization with 50% volume of a fluorocarbon such as Genetron 113(Allied Chemicals). The suspension is centrifuged and the supernatant aqueous layer is rehomogenized with fluorocarbon. The supernatant from this is collected and used as the antigen. Gel-diffusion medium is made with 1% agar, 8% sodium chloride and 0.01% thiomersol. Precipitation lines develop 24-48 hours after incubation of the antigen with the antibody to homologous or closely related strains. The test is less sensitive than the ELISA or the passive haemagglutination test.
Tanned sheep or horse red cells are sensitized with a partially purified fowlpox viral antigen. The antigen is prepared from infected CAMs by treatment with fluorocarbon as above. PHA is more sensitive than AGID. The test will give cross-reactions among avian pox viruses.
Enzyme-linked immunosorbent assay
ELISAs have been developed to detect humoral antibodies to fowlpox virus. They are capable of detecting antibodies at 7 days post infection.
Restriction endonuclease analysis has been used to compare the genomes of different avian pox viruses and is useful for comparison of field isolates and vaccine strains of fowlpox virus. In addition, cloned genomic fragments of fowlpox virus can be use effectively as nucleic acid probes for diagnosis of fowlpox virus infection (Tripathy and Reed, 1997). A polymerase chain reaction technique that amplifies a region within the gene coding the 4b-core-protein of fowlpox virus has been developed recently (Lee and Lee, 1997).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Poultry:All Stages||Sign|
|Digestive Signs / Difficulty in prehending or chewing food||Poultry:All Stages||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Poultry:All Stages||Sign|
|Digestive Signs / Esophageal obstruction||Poultry:All Stages||Sign|
|Digestive Signs / Hepatosplenomegaly, splenomegaly, hepatomegaly||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Poultry:All Stages||Diagnosis|
|Digestive Signs / Pharyngeal ulcers, vesicles, erosion, papules, sores pharynx||Poultry:All Stages||Diagnosis|
|General Signs / Dehydration||Poultry:All Stages||Sign|
|General Signs / Discomfort, restlessness in birds||Poultry:All Stages||Sign|
|General Signs / Exercise intolerance, tires easily||Poultry:All Stages||Sign|
|General Signs / Hindfoot swelling, mass rear foot, feet||Poultry:All Stages||Diagnosis|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Poultry:All Stages||Diagnosis|
|General Signs / Increased mortality in flocks of birds||Poultry:All Stages||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Poultry:All Stages||Sign|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Poultry:All Stages||Diagnosis|
|General Signs / Oral cavity, tongue swelling, mass in mouth||Poultry:All Stages||Diagnosis|
|General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass||Poultry:All Stages||Diagnosis|
|General Signs / Reluctant to move, refusal to move||Sign|
|General Signs / Swelling mass oviducts||Poultry:All Stages||Diagnosis|
|General Signs / Swelling of the comb, wattles in birds||Poultry:All Stages||Diagnosis|
|General Signs / Swelling of the limbs, legs, foot, feet, in birds||Sign|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Poultry:All Stages||Diagnosis|
|General Signs / Swelling, mass, prolapse, cloaca||Poultry:All Stages||Diagnosis|
|General Signs / Swelling, mass, wing||Poultry:All Stages||Diagnosis|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Poultry:All Stages||Sign|
|General Signs / Weight loss||Poultry:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Poultry:All Stages||Sign|
|Reproductive Signs / Decreased, dropping, egg production||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Poultry:All Stages||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Poultry:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Poultry:All Stages||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Poultry:All Stages||Sign|
|Skin / Integumentary Signs / Hyperkeratosis, thick skin||Sign|
|Skin / Integumentary Signs / Skin crusts, scabs||Poultry:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin papules||Poultry:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin plaque||Poultry:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin pustules||Sign|
|Skin / Integumentary Signs / Skin scales, flakes, peeling||Sign|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Poultry:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Sign|
Disease CourseTop of page
Infection with avipoxviruses usually resultsin one of two forms:
- Cutaneous or dry form: characterized by the development of discrete nodular proliferative skin lesions in the non-feathered areas of the body.
- Diphtheric, pharyngeal or wet form: consisting of fibrinonecrotizing lesions in the mucous membranes of the mouth, oesophagus and upper respiratory tract.
Sporadically, other forms associated with pox virus infection have been reported: a mixed form, characterized by both, cutaneous and diphtheric lesions, a tumorous form and a per-acute form, associated with sudden death (Bolte et al., 1999).
Both cutaneous and diphtheric forms have a relatively acute course. In the cutaneous form, experimental intradermal inoculation resulted in primary lesions (papules) by day 5 and 6 post infection. In the diphtheric form, respiratory signs were observed 7 days after intralaryngeal inoculation and mortality began at 10 days post infection, reaching 45% of the animals (Tripathy, 1993). Incubation period of the naturally occurring disease varies from 4 to 10 days in chickens, turkeys and pigeons and is about 4 days in canaries. The course of the natural disease may be approximately 3 to 4 weeks (Tripathy and Reed, 1997).
Clinical signs in naturally infected birds vary depending on the virulence of the virus, susceptibility of the host, distribution and type of lesions in an infected bird and other complicating factors (Tripathy and Reed, 1997). Lesions on one or both eyelids, in the cutaneous form, may lead to partial or complete closure of the eyes and the birds may be unable to reach the water and feed. In the diphtheric form, with affects on the oral mucosa, difficulty in feeding and drinking may occur and the birds become anorexic, lose weight, and eventually die. Lesions in the respiratory passages may cause gasping, rales and laboured breathing, leading to respiratory distress and death due to suffocation. Transient drop in egg production in layers has also been associated with pox virus infection (Tripathy, 1993).
The disease spreads slowly, and morbidity and mortality are related to the susceptibility of the flock, virulence of the virus strain, environmental and physical stresses, concentration of the birds and the presence of other infections in the flock. Mortality is negligible in the mild cutaneous form of the disease, if infection does not involve the eyes or mucous membranes. The mortality rates of the diphtheric and mixed forms of the disease are higher than in the cutaneous form, however the mortality also depends on the action of the predisposing factors already mentioned. In highly susceptible flocks, a virulent virus strain may result in morbidity and mortality rates as high as 50%. High mortality has been observed in pigeons, quails and canaries. Of all pox virus infections, canarypox is the most lethal and frequently leads to the death of all infected canaries (Tripathy and Reed, 1997).
Infection occurs when cutaneous injuries on the feet, comb, other parts of the body or on the mucous membranes of the mouth or upper respiratory tract are exposed to virus-contaminated material. A breach in the skin or mucous membranes is required for the entry of the virus. Infection may be transmitted from bird to bird by direct contact, especially under crowded conditions where minor abrasions can occur as a result of fighting and pecking. Since the virus may survive in dried scabs for prolonged time, aerosols generated by feathers and dried scabs provide the conditions for both cutaneous and respiratory infections. Insects mechanically carrying the virus may deposit it in the eye. The virus may reach the laryngeal area via the lachrymal duct. Cells of the mucosa of the upper respiratory tract and mouth appear to be highly susceptible to the virus as initiation of the infection may occur in the absence of apparent trauma or injury. Local multiplication results in the development of lesions at the site of virus entry. Some authors have reported that, after intradermal or intratracheal inoculation, viraemia occurs and the virus may be localized in different organs (lung, liver, spleen, kidney and brain) at variable periods between 6 and 12 days post infection. Other authors have only detected viraemia if the birds are infected intravenously, but not when the inoculation route is intradermal (Tripathy, 1993).
There are indications that avian pox viruses may persist as latent infections in some flocks and that some species of wild birds may serve as latent pox virus carriers (Tripathy, 1993).
EpidemiologyTop of page
Most avian species are susceptible to avipoxviruses. Of the approximately 9000 birds species, about 232 species of birds, have been reported to acquire a natural pox virus infection and to have developed various forms of pox (Bolte et al., 1999). In both wild and commercial birds, the infection can occur in susceptible birds of any age, sex and breed.
Pox virus infection occurs through mechanical transmission of the virus to the injured or lacerated skin of the host. Mechanical transmission of fowl pox virus from infected toms to turkey hens, through artificial insemination has also been reported (Metz et al., 1985).
Insects serve as mechanical vectors of the virus. Eleven species of Diptera, specifically of the genus Culex and Aedes, have been found to be vectors of avian pox viruses (Akey et al., 1981). Mosquitoes have been shown to be capable of infecting a number of different birds after a single feeding on a bird infected with avian pox virus. The mite, Dermanyssus gallinae, has also been implicated in the spread of fowlpox virus (Shirinov et al., 1972). Infected mealworms Alphatobius diaperinus are also capable of retaining the fowlpox virus for a maximum of 6 days and elimination of this virus from the mealworm occurs through the excrement and this can be a source of contamination of the poultry environment (Casas et al., 1976). More recently, stick fast fleas have also been associated with fowl pox in chickens (Gustafson et al., 1997).
Impact: EconomicTop of page
No published data is available about treatment costs and economic losses due to pox virus infection, but it is known that, in domestic poultry, fowlpox and turkeypox infections cause economically important diseases. In domestic poultry flocks, avian pox can be a significant economic problem since, apart from mortality, it may cause a transient drop in egg production in layers and retarded growth in young birds (Tripathy, 1993).
Zoonoses and Food SafetyTop of page
The infectivity of avian poxviruses is limited to avian species and are not of public health significance. The human disease called chicken pox is not related to poultry or avipoxviruses.
Disease TreatmentTop of page
There are no specific treatments for avipox virus infections.
Prevention and ControlTop of page
Vaccination can be implemented in areas where the disease is endemic or where the disease has been diagnosed previously.
There are two types of live attenuated virus vaccines that are commercially available, these are fowlpox and pigeonpox vaccines. These vaccines can be of chicken embryo origin, prepared from infected CAM, or of tissue culture origin, usually prepared from chicken embryo fibroblast cultures. These vaccines should contain a minimum concentration of 105 EID50/ml. The chicken embryo origin vaccines are capable of producing serious disease in a flock if used improperly. Fowl pox and pigeon pox vaccines may be applied by the wing-web method to 4-week-old chickens and to pullets about 1-2 months before egg production starts. These vaccines may also be used to revaccinate chickens held for a second year of egg production. Turkeys are vaccinated by the thigh-stick method, usually when 2 to 3 months old. Pigeons are vaccinated by wing-web stick or feather-follicle methods. Vaccines of tissue culture origin can be administered as early as 1 day of age. These vaccines are considered to be genetically stable and protect immunocompetent birds for approximately 1 year (Tripathy, 1993).
Live attenuated vaccines from canarypox, quailpox and turkeypox viruses have also been developed and are commercially available in some countries.
Vaccination may produce a mild form of the disease. All birds within a house should be vaccinated on the same day. An important point is that if pox appears in a flock, as it spreads slowly, non-affected birds should be vaccinated. The positive vaccination response is indicated by the development of ‘takes’, which appear 5 to 10 days after vaccination and consists of swelling of the skin or a scab formation at the site of inoculation. Immunity develops 10 days after vaccination. Passively acquired immunity should be taken into account when vaccinating progeny from flocks, which either had experienced recent natural infection or had been vaccinated a short time ago (Tripathy, 1993).
Vaccination is usually carried out during spring or summer in areas where the disease occurs during fall and winter. In tropical climates, vaccination may be done at any time, because the disease may occur throughout the year (Tripathy, 1993).
As has been said previously, the pox virus has been used as a viral vector to create recombinant vaccines capable of expressing genes of several poultry and mammalian pathogens (Cardona et al., 1999; Elahi et al., 1999; Liu et al., 1999).
ReferencesTop of page
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