During avipox outbreaks, mortality can reach 80 to 100% in canaries and other finches. This is in contrast to a generally lower mortality seen in chicken and turkey [60] . Transmission of virus can occur through a break in the skin or, more commonly, when vectored by biting insect such as mosquitoes and mites [68] . Aerosols generated from infected birds, or the ingestion of contaminated food or water have also been implicated as a source of transmission [69] . The disease is most commonly characterized by cutaneous proliferative lesions consisting of epithelial hyperplasia of the epidermis that resulting in proliferative, wart-like projections. They are primarily confined to unfeathered parts of the body, such as legs, feet, eyelids and the base of the beak (Figure 4 ). Scars are usually visible after recovery and healing of skin lesions. The mortality in wild birds is usually low, depending on the number and size of the proliferative lesions. However, if infection occurs in feather-free areas of the skin, with secondary bacterial infection, mortality may be high. The other and less common form of APV infections is the diphtheritic or wet form [70] which occurs as fibrino-necrotic and proliferative lesions in the mucosa of the digestive and upper-respiratory tracts, and generally has a higher mortality than the cutaneous form [60] . In some instances, birds display both cutaneous and diphtheritic forms and in those cases, mortality rates are often higher compared to the cutaneous form alone. Despite the variety of hosts and virus strains, associated pathology remains the same in infected domestic birds, although clinical signs vary depending on the virulence of the virus, susceptibility of the host, distribution and type of lesions [60] . There exist a relationship between FWPV and the avian retrovirus, reticuloendotheliosis virus (REV) (see section on APVs and REV). However, the possible roles that simultaneous REV infection arising from the provirus integration into the FWPV genome might play in the expression FWPV during disease outbreak remain unresolved. It is well known that REV infection leads to immunosuppresion [71] in affected birds. Thus, it is plausible to suggest that the presence of REV in FWPV infection may exacerbate disease progression. In spite of the fact that some mammalian cell lines seems to be able to support the replication of APVs, there is no evidence that APVs have caused clinical disease in humans, in contrast to what is known for other poxviruses, such as several parapox and orthopoxviruses.