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Diagnosis for susceptible birds. The virus is resistant and survives under
normal environmental conditions in which other viruses may
Gross pathology not survive. For example, in a study, a poxvirus infection in newly
Nodular skin lesions resulting from epithelial hyperplasia introduced ostriches was related to contaminated premises where
involving the epidermis and underlying feather follicles first turkeys raised earlier had shown evidence of poxvirus infection
appear as small white foci and then rapidly increase in size and (Shivaprasad et al., 2002). Antigenic, genetic and biological
become yellow. A few primary lesions appear by the fourth day characterization of the virus isolated from the cutaneous lesions
after infection. Papules are formed by the fifth or sixth day. This in ostriches by Western blotting, restriction fragment length poly-
is followed by the vesicular stage, with formation of extensive morphism of genomic DNA, pathogenesis, and cross-protection
thick lesions (Minbay and Kreier, 1973). Adjoining lesions may studies in chickens revealed its similarity to FWPV. Further, sus-
coalesce and become rough and grey or dark brown. After about ceptible chickens immunized with the virus were protected when
2 weeks or sometimes sooner, lesions have areas of inflammation challenged with a virulent strain of FWPV.
at the base and become haemorrhagic. Formation of a scab, which In some cases, avian pox virus infection may be characterized by
may last for another 1–2 weeks, ends with desquamation of the cutaneous, diphtheritic, systemic and oncogenic manifestations
degenerated epithelial layer. If the scab is removed early in its (Tsai et al., 1997), while in others the infection may be localized
development, there is a moist, seropurulent exudate underneath and characterized by the presence of small, pale, firm nodules in
covering a haemorrhagic granulating surface. When the scab some internal organs. For example, in a natural pox virus infection
drops off naturally, a smooth scar may be present; in mild cases, in Galapagos doves (Nesopelia g. galapagoensis), small (1–6 mm),
there may be no noticeable scar. Attenuated vaccine viruses pro- pale, firm nodules in the lungs (Mete et al., 2001) were character-
duce localized lesions, which are mild in comparison to the severe ized by lobulated and non-lobulated nodular foci, located mainly
ones due to pathogenic strains. The secondary lesions produced in the airways, originating from primary and secondary bronchi.
by pathogenic strains may persist for several weeks. Similarly, in a 3-month-old fledgling Andean condor no lesions
In the diphtheritic form, slightly elevated, white opaque nod- were found on the entire skin. However, the oral cavity, oesopha-
ules or yellowish patches develop on the mucous membranes of gus, and crop had multifocal raised yellow plaques. Most internal
mouth, oesophagus, tongue, or upper trachea. Nodules rapidly organs including heart, lungs, liver, kidney, small intestine, pan-
increase in size and often coalesce to become a yellow, cheesy, creas, and spleen had single to multiple soft white nodules ranging
necrotic, pseudodiphtheritic, or diphtheritic membrane. If the in size from 0.2–0.8 cm in diameter (Kim et al., 2003).
membranes are removed, they leave bleeding erosions. The
inflammatory process may extend into sinuses, particularly the Microscopic pathology
infraorbital sinus (resulting in swelling) and also into the pharynx Avian pox viruses cause cellular hyperplasia of affected tissues in
and larynx (resulting in respiratory disturbances) and oesopha- both cutaneous and diphtheritic lesions (Figs. 13.6B and 13.7).
gus. It is not uncommon to find cutaneous as well as diphtheritic In this regard genomic analysis of fowlpox virus shows presence
lesions in the same bird. In canarypox virus infection, gross lesions of a gene encoding a protein similar to epidermal growth factor
may include thickened eyelids and small nodules on the skin of (EGF). Although this gene is not essential for virus replication, it
the head and neck, enlarged thymus, mild to severe consolidation may influence virulence, stimulate cell proliferation, and contrib-
of the lungs, and exudates in the sinuses and trachea (Shivaprasad ute to the hyperplasia observed in infected tissues. Hyperplasia
et al., 2009).
Whether in chickens, turkeys or other birds, variations in clini-
cal picture may be observed from as mild to severe disease leading
to significant mortality. In a mild poxvirus outbreak in turkeys,
Hess et al. (2011) reported cutaneous lesions and only 20 birds
were affected in a total of 11,680 birds. Mortality rates in turkeys
in cutaneous form of disease are usually low. The first indication
of pox in turkeys is appearance of minute yellowish eruptions on
the dewlap, snood, and other head parts. They are soft and easily
removed in this pustular stage, leaving an inflamed area covered
with a sticky serous exudate. The corners of the mouth, eyelids,
and oral membranes are commonly affected. Lesions enlarge
and become covered with a dry scab or a yellow-red or brown
wart-like mass. In young poults, the head, legs, and feet may be
completely covered with lesions, which may even spread to the
feathered parts of the body. In an unusual outbreak of pox virus
in breeding turkeys, proliferative lesions occurred in the oviduct,
cloaca, and skin surrounding the vent.
Avian pox viruses persist for long time in dried scabs shed Figure 13.7 Cutaneous pox lesion showing eosinophilic
cytoplasmic inclusion bodies (Bollinger bodies) (Courtesy of Dr
from the recovering birds can become a source of infection Oscar Fletcher).