The investigated chicken flocks showed generalized weakness, depression, droopy appearance, pale comb and wattles, stunting, growth retardation, and high mortalities. The packed cell volumes measured were markedly reduced (average PCV was between 17% and 22%). Necropsy findings of the sampled chickens revealed watery blood, yellow fatty bone marrow, markedly atrophied thymus glands, atrophied bursa of
Fabricius, and enlarged livers and spleens. The clinical signs, postmortem lesions, and PCV values agreed with the findings of (Yuasa et al., 1979,
Taniguchi et al., 1982 & 1983, Aly 2001) and (Pope
1991, Ramadan et al., 1998) who stated that a case of hematocrit value below 27% with yellowish changes in bone marrow and thymic atrophy …show more content…
Bird 's age was intended to exceed the age of 3 weeks to exclude maternally derived immunity that persists for about 3 weeks. The overall findings of the study proved that CAV is widely distributed among chicken flocks where 84.72% of the tested serum samples reacted positive at different localities of Sharkia governorate, Egypt. (Zaki and El-Sanousi,
1994) reported that in Egypt, the incidence of CAV antibodies in serum samples collected from broiler breeder, layer, and day old broiler flocks was 70%,
(Amin et al., 1998) stated that it was 97.4% among 21 native and foreign grandparent, parent, and broiler flocks in 8 provinces, (Sabry et al., 1998) recorded that 1916 tested serum samples from 118 flocks of different breeds and ages in different governorates showed a high degree of positivity for CAV antibodies in both imported and locally produced broiler parent, broiler, and layer flocks, while (Islam
2003) reported that CAV seroprevalence was 74.6% and 67.3% in commercial broiler and broiler breeder flocks respectively in Sharkia province. In …show more content…
In addition,
(Hussein et al., 2002) reported some bursal changes with various degrees of atrophy in the lymphoid follicles with scattered necrotic foci, which were probably attributed to secondary infections. These findings similar to (Goryo et al., 1987, Smyth et al.,
1993) that proved immunosuppressive effect of the virus may be attributed directly to its destructive effect of hematopoietic and lymphopoietic tissues leading to impaired immune response. Moreover
(Adair et al., 1991) stated that CAV infection causes severe defects in splenic T-lymphocyte functions in form of decreased responsiveness to phytohemagglutinin, concanavalin A and fall in interleukin production. Macrophage concentration and functions are also severely reduced after in vivo or in vitro exposure to the virus such as interleukin-l
(IL-1) production, Fc receptor expression, phagocytosis and bactericidal activity (Cloud et al.,
1992; McConnell et al., 1993a & b). The adverse effects of the virus on lymphocyte and macrophage functions have substantial negative effects on immune response leading to enhancement of the concurrent infection with other pathogens