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Avian Pox

Avian Pox


Fowl pox is a slow-spreading viral infection of birds. The virus belongs to the genus Avipoxvirus, and is in the family Poxviridae. Clinically, fowl pox occurs in two forms. In the cutaneous or dry form, discrete nodular proliferative skin lesions occur in the nonfeathered parts of the body. In the diphtheritic or wet form, fibrino-necrotic and proliferative (canker) lesions form on the mucous membranes of the mouth, pharynx, esophagus, and trachea. Fowl pox is an economically important disease of commercial poultry because it is associated with a drop in egg production and may cause mortality.

Host Range

Many species of birds are susceptible to avian pox including domestic poultry (chickens and turkeys), pet birds, and more than 60 species of free-living birds, representing 20 families. Avian pox occurs in all age groups of birds. Avian pox does not represent a risk to human heath, however some mammalian species may be susceptible to the virus. In the distant past, the disease was mistakenly thought to be related to small pox or chicken pox in humans.


The avian pox virus is usually transmitted mechanically to pen-mates through skin abrasions. Humans can also inadvertently spread the virus through contact with infected poultry (via ocular infection) during vaccination regimens. Mosquitoes, other flying insects, and parasites can serve as mechanical vectors. In contaminated environments, the dried virus can also become aerosolized and gain entry into birds' mucous membranes and respiratory tracts.

The incubation time varies by species but is typically 4-10 days in chickens and turkeys. Morbidity in chickens and turkeys varies from a few birds to an entire flock, depending on virulence and control measures. The course of the disease may last approximately 2-8 weeks, during which time birds can lose weight and egg production may be retarded. Although mortality is typically low, it may be as high as 50% with virulent strains or if secondary infections complicate the disease.

Avian pox is distributed worldwide. Wild birds are a reservoir for this virus.

Clinical Signs

Clinical signs are somewhat variable depending on the host species, virulence of the virus strain, distribution of lesions, and other complicating factors. The disease onset is often gradual in poultry and usually goes undetected until skin lesions are obvious. Only a few birds develop lesions at one time. In chickens and turkeys, signs may vary with two overlapping forms of the disease:

Cutaneous (dry pox): Common form in most outbreaks. The dry form begins with a pimple or scab on nonfeathered areas of the skin such as the comb, wattles, eyelids, feet, and legs. Eventually, the infection may spread to other feathered areas of the body (especially in turkeys). Infected birds often have difficulty eating and reduced feed intake and weight loss is common. Other signs may include drop in egg production, facial swelling, blindness (caused by ocular and periocular involvement) and loss of vigor. Mortality is usually low in uncomplicated cases, unless secondary infections become a problem.

Diphtheritic (wet pox): The wet-mucous form produces diphtheritic, yellow canker lesions on oral mucous membranes, tongue, esophagus, or trachea. Lesions in the upper digestive and respiratory tract may result in inappetence and dyspnea, respectively. Other mild to severe respiratory signs may also occur. Lesions in the eye and nasal cavity lead to oculonasal discharges. Mortality often results from suffocation or starvation.

Avian pox is generally associated with a more chronic condition in turkeys than in chickens. Canary pox causes systemic infection with high mortality.

Post-mortem Lesions

Cutaneous (dry pox): this form is characterized by a local epithelial hyperplasia involving the epidermis and feather follicles. The nodules begin as small white foci, which rapidly increase in size and turn yellow. Within 5-6 days, papules develop and progress into vesicles. These vesicles may coalesce and turn grey to dark brown, with a rough wart-like texture. Within two weeks, the pox lesions develop inflammation and hemorrhage around their base. Over time, the lesions turn into scabs which eventually slough, often revealing a smooth scar.

Diphtheritic (wet pox): this form is characterized by the development of white opaque nodules on the mucous membranes of the digestive and respiratory tracts, such as the oral cavity, tongue, larynx, esophagus, trachea, and sinuses. These nodules enlarge and coalesce into yellow diptheritic membranes. On post-mortem examination, if these diptheritic membranes are removed, bleeding erosions will be found beneath the membranes. In some cases, birds may have a localized pox infection, with small nodules found on internal organs.

Birds may have a combination of both cutaneous pox lesions (typically involving the comb, wattles, and eye region) as well as diptheritic lesions in the digestive and respiratory tracts.

Differential Diagnosis

For the cutaneous form, bacterial dermatitis should be ruled out. Cutaneous lesions, caused by pantothenic acid or biotin deficiency in young chicks, or by T-2 toxin could be mistaken for pox lesions.

For the diptheritic form, when respiratory signs are present, rule outs must include diseases such as avian influenza and infectious bronchitis. The diphtheritic lesions may resemble signs of infectious laryngotracheitis. Histologic examination of poxvirus lesions will reveal epithelial hyperplasia with intracytoplasmic inclusion bodies; whereas, laryngotracheitis, caused by a herpesvirus, produces intranuclear inclusions. In doves and pigeons, diphtheritic pox lesions may be mistaken for lesions caused by Trichomonas gallinae, which is diagnosed by microscopic examination of smears or by culture.


A presumptive diagnosis can be made in the field based on characteristic skin lesions. The diagnosis should be confirmed by laboratory testing. Collect and submit cutaneous and diptheritic tissue lesions to the laboratory. Diagnosis is confirmed by the presence of cytoplasmic inclusions found on microscopic examination of affected tissue sections, stained with H & E (haematoxylin and eosin) stain. Inclusions are also detected by fluorescent antibody and immunoperoxidase methods. Viral particles, with typical poxvirus morphology, can be detected by electron microscopy. The virus can be isolated in the chorioallantoic membrane (CAM) of chicken embryos, susceptible birds, or avian cell cultures. Field viruses can be detected in the laboratory by polymerase chain reaction (PCR) and can be compared by restriction endonuclease digestion.

Prevention and Control

In the United States, pox has been a common problem for commercial poultry. The large DNA virus is highly resistant and can survive in dried scabs in the environment for months to years, infecting replacement birds.

Fowl pox and pigeon pox live virus vaccines are commonly used for immunization of chickens. Administration in laying birds is performed around four weeks of age, following by a boost one or two weeks before the onset of egg production. Broilers are only vaccinated at an early age in areas in which the disease is endemic. On average, immunity develops around two weeks post-vaccination.

Vaccination is commonly applied by the wing-web method and induces a mild form of the disease. The evidence of a "take" should be verified in the wing web seven to ten days after vaccination. A "take" is a swelling of the skin or a scab at the site where the vaccine was applied and is evidence of successful vaccination.

No treatment exists for birds infected with avian pox viruses.

Selected References

  1. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  2. Tripathy, D.N. and W.M. Reed. 2008. Pox. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  3. Tripathy, D.N. and W.M. Reed. 2008. Pox. In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  4. World Organization for Animal Health (OIE) website. 2008.

Thank you to the following individuals for reviewing these materials:

Richard Chin
Jaime Ruiz

Avian Influenza
Bacterial Dermatitis
Biotin Deficiency
Infectious Bronchitis
Infectious Laryngotracheitis
Pantothenic Acid Deficiency
Trichomonas gallinae