Fowlpox is a slow-spreading viral infection of chickens and turkeys characterized by proliferative lesions in the skin that progress to thick scabs (cutaneous form) and by lesions in the upper GI and respiratory tracts (diphtheritic form). Virulent strains may cause lesions in the internal organs (systemic form). Fowlpox is seen worldwide.
Etiology and Epidemiology
The large DNA virus (an avipoxvirus in the Poxviridae family) is resistant and may survive in the environment for extended periods in dried scabs. Photolyase and A-type inclusion body protein genes in the genome of fowlpox virus appear to protect the virus from environmental insults. Field and vaccine strains have only minor differences in their genomic profiles, although the strains can be differentiated to some extent by restriction endonuclease analysis and immunoblotting. Recently, molecular analyses of vaccine and field strains of fowlpox viruses have shown some significant differences. The virus is present in large numbers in the lesions and is usually transmitted by contact through abrasions of the skin. Skin lesions (scabs) shed from recovering birds in poultry houses can become a source of aerosol infection. Mosquitoes and other biting insects may serve as mechanical vectors. Transmission within flocks is rapid when mosquitoes are plentiful. The disease tends to persist for extended periods in multiple-age poultry complexes because of slow spread of the virus and availability of susceptible birds.
The cutaneous form of fowlpox is characterized by nodular lesions on various parts of the unfeathered skin of chickens and on the head and upper neck of turkeys. Generalized lesions of feathered skin may also be seen. In some cases, lesions are limited chiefly to the feet and legs. The lesion is initially a raised, blanched, nodular area that enlarges, becomes yellowish, and progresses to a thick, dark scab. Multiple lesions usually develop and often coalesce. Lesions in various stages of development may be found on the same bird. Localization around the nostrils may cause nasal discharge. Cutaneous lesions on the eyelids may cause complete closure of one or both eyes. Only a few birds develop cutaneous lesions at one time. Lesions are prominent in some birds and may significantly decrease flock performance.
In the diphtheritic form of fowlpox, lesions develop on the mucous membranes of the mouth, esophagus, pharynx, larynx, and trachea (wetpox or fowl diphtheria). Occasionally, lesions are seen almost exclusively in one or more of these sites. Caseous patches firmly adherent to the mucosa of the larynx and mouth or proliferative masses may develop. Mouth lesions interfere with feeding. Tracheal lesions cause difficulty in respiration. Laryngeal and tracheal lesions in chickens must be differentiated from those of infectious laryngotracheitis (see Infectious Laryngotracheitis), which is caused by a herpesvirus. In cases of systemic infection caused by virulent fowlpox virus strains, lesions may be seen in internal organs. More than one form of the disease, ie, cutaneous, diphtheritic, and/or systemic, may be seen in a single bird.
Often, the course of the disease in a flock is protracted. Extensive infection in a layer flock results in decreased egg production. Cutaneous infections alone ordinarily cause low or moderate mortality, and these flocks generally return to normal production after recovery. Mortality is usually high in diphtheritic or systemic infections.
Cutaneous infections usually produce characteristic gross and microscopic lesions. When only small cutaneous lesions are present, it is often difficult to distinguish them from abrasions caused by fighting. Microscopic examination of affected tissues stained with H&E reveals eosinophilic cytoplasmic inclusion bodies. Cytoplasmic inclusions are also detectable by fluorescent antibody and immunohistochemical methods (using antibodies against fowlpox virus antigens). The elementary bodies in the inclusion bodies can be detected in smears from lesions stained by the Gimenez method. Viral particles with typical poxvirus morphology can be demonstrated by negative-staining electron microscopy as well as in ultrathin sections of the lesions. The virus can be isolated by inoculating chorioallantoic membrane of developing chicken embryos, susceptible birds, or cell cultures of avian origin. Chicken embryos (9–12 days old) from an SPF flock are the preferred and convenient host for virus isolation.
The genomic profiles of field isolates and vaccine strains of fowlpox virus can be compared by restriction fragment length polymorphism. This method is useful to compare closely related DNA genomes. However, because of the large size of the genome, minor differences are difficult to detect by this method. Detailed genetic analysis reveals differences between vaccine strains and field strains responsible for outbreaks of fowlpox in previously vaccinated chicken flocks. Whereas vaccine strains of fowlpox virus contain remnants of long terminal repeats of reticuloendotheliosis virus (REV), most field strains contain full-length REV in their genome.
Nucleic acid probes derived from cloned genomic fragments of fowlpox virus can also be used for diagnosis. This procedure is especially useful for differentiation of the diphtheritic form of fowlpox (involving the trachea) from infectious laryngotracheitis.
PCR can be used to amplify genomic DNA sequences of various sizes using specific primers. This procedure is useful when an extremely small amount of viral DNA is present in the sample. PCR has been used effectively to differentiate field and vaccine strains of the virus, whether full-length REV is present in those strains that are associated with outbreaks in vaccinated birds. DNA isolated from the formalin-fixed tissue sections of birds that are histologically positive for fowlpox can be used for PCR amplification of genomic fragments using specific primers. Because most outbreaks of fowlpox in previously vaccinated chickens are caused by strains with a genome that contains full-length REV, use of REV envelope-specific primers to determine the presence of full-length REV is helpful in such cases.
Two monoclonal antibodies that recognize different fowlpox virus antigens have been developed. These monoclonal antibodies are useful for strain differentiation by immunoblotting.
The complete nucleotide sequence of the fowlpox virus genome has been determined. It is useful in comparing the sequences of selected genes of other avian poxviruses.
Prevention and Treatment
Where fowlpox is prevalent, chickens and turkeys should be vaccinated with a live-embryo or cell-culture-propagated virus vaccine. The most widely used vaccines are attenuated fowlpox virus and pigeonpox virus isolates of high immunogenicity and low pathogenicity. In high-risk areas, vaccination with an attenuated vaccine of cell-culture origin in the first few weeks of life and revaccination at 12–16 wk is often sufficient. Health of birds, extent of exposure, and type of operation determine the timing of vaccinations. Because the infection spreads slowly, vaccination is often useful in limiting spread in affected flocks if administered when <20% of the birds have lesions. Passive immunity may interfere with multiplication of vaccine virus; progeny from recently vaccinated or recently infected flocks should be vaccinated only after passive immunity has declined. Vaccinated birds should be examined 1 wk later for swelling and scab formation (“take”) at the site of vaccination. Absence of “take” indicates lack of potency of vaccine, passive or acquired immunity, or improper vaccination. Revaccination with another serial lot of vaccine may be indicated.
Naturally infected or vaccinated birds develop humoral as well as cell-mediated immune responses. Humoral immune responses can be measured by ELISA or virus neutralization tests.
There is no zoonotic risk associated with fowlpox virus. Avian poxviruses cause a productive infection in avian species but a nonproductive infection in mammalian hosts. Consequently, avianpox viruses have been used as vectors for expression of genes from mammalian pathogens in the development of safe recombinant vaccines.
Last full review/revision July 2013 by Deoki N. Tripathy, DVM, MS, PhD, DACVM, DACPV