Field Trials to Test the Efficacy of Polyvalent Marek's Disease Vaccines in Broilers

Abstract

The efficacies of trivalent (Md11/75C + SB-1 + HVT), bivalent (SB-1 + HVT), and turkey herpesvirus (HVT) vaccines against Marek's disease (MD) were compared in commercial broiler flocks in four trials involving 11 farm locations and 486,300 chickens. In all four trials, chickens receiving polyvalent vaccines had lower leukosis (MD) condemnation rates than chickens vaccinated with HVT alone; when data were summarized for each vaccine type in each trial, condemnation rates for the bivalent- or trivalent-vaccinated groups were 56-96% (mean 78%) lower than those for HVT-vaccinated chickens. Polyvalent vaccination was clearly mor efficacious than HVT in 8 of 11 individual farms, although it did not always reduce leukosis condemnations to acceptable levels. Body weights of chickens vaccinated with polyvalent vaccines did not differ consistently from those vaccinated with HVT. Chickens inoculated with the trivalent vaccine had slightly lower overall leukosis condemnation rates (0.24%) than those inoculated with the bivalent vaccine (0.45%) in trials 1-3, where direct comparisons were made. Bivalent vaccines containing either 1,500 or 200 plaque-forming units of SB-1 virus were equally effective; thus, HVT may need to be supplemented with only small amounts of SB-1 to obtain the benefits of protective synergism. SB-1 virus did not appear to carry over from polyvalent-vaccinated flocks to subsequent HVT-vaccinated flocks in the same houses, even when old litter was used.

Revaccination with Marek's Disease Vaccines Induces Productive Infection and Superior Immunity

“…Unlike virulent MDV, which can effectively spread horizontally between weeks 3 and 5 after infection, resulting in infection of other chickens or reinfection (4,14), the horizontal transmission of avirulent strains is very poor or absent (24). Serotype 2 MDV and CVI988 spread horizontally 2 weeks after immunization (30,31), but neither attenuated MDV nor HVT does so (4,14), even though viral antigens can be detected for a limited period in the feather follicle epithelium of chickens infected with HVT (15,18,31,40). The CVI988 strain initially spread well by contact, but partial flock vaccination does not work in practice, as the spread of the vaccine strain was very poor and not rapid enough to precede infection with virulent strains from the field (1,29).…”

“…The CVI988 strain initially spread well by contact, but partial flock vaccination does not work in practice, as the spread of the vaccine strain was very poor and not rapid enough to precede infection with virulent strains from the field (1,29). By 2 weeks after vaccination, specific immunity to MD has been developed (31,33), which inhibits reinfection caused by limited cell-free vaccine viruses inhaled from dust or dander (8,26,40), resulting in the failure of the reinfection. This study demonstrated only one phase of productive infection in the chickens receiving a single vaccination and two phases of productive infection in revaccinated chickens within 7 weeks after immunization, suggesting that the productive infection caused by vaccine viruses shed from vaccinated chickens is not successful or that reactivation of latent viruses in PBLs does not occur; thus, there is no persistent antigen supply after vaccine viruses enter latency.…”

“…Because of the agedependent resistance to MD (11), the earlier that the induction of specific immunity is, the more protection against MD that there is. Early exposure to pathogenic MDV is undoubtedly one of the most important causes of excessive MD in vaccinated chickens, since up to 7 days is required to develop detectable immunity (40). Virus exposure in the field usually occurs very soon after the hatching or placement of chickens, and the shorter that the interval between vaccination and exposure to pathogenic MDV is, the poorer that the level of protection is (25).…”

Antiviral Activity of Lactoferrin and Ovotransferrin Derived Peptides Towards Herpesviridae

“…It was probably due to imperfect vaccination practices and, in some countries, wrong hygienic conditions that led to reservoirs of viruses in poultry houses (Bourne, 1996). In response to the increasing number of MD outbreaks in vaccinated flocks, in the 1980s, new vaccines based on the non-oncogenic serotype-2 MDV were introduced in bivalent www.intechopen.com combination with HVT Witter et al, 1984). The use of polyvalent vaccine provided a better protection against MDV challenge (Witter, 1992).…”

Identification of Virus-specific Polypeptides by Monoclonal Antibodies against Serotype 2 Marek's Disease Virus

“…Because vvMDV has emerged, improvement of the vaccines is urgently needed. Protection against vvMDV by inoculation of the combination of HVT and MDV2 strain SB1 has been demonstrated in laboratory experiments (Witter, 1982) and in field trials (Calnek et al, 1983;Witter et al, 1984). Further, Witter et al (1987) examined several vaccine candidates against vvMDV and demonstrated that some of the MDV2 isolates may be good vaccine candidates.…”