Date Published: September 4, 2006
Publisher: BioMed Central
Author(s): Susanne Kabell, Kurt J Handberg, Magne Bisgaard.
This study aimed at investigating a potential effect caused by coccidia on the immune response to vaccine- and very virulent infectious bursal disase virus (vvIBDV) in SPF chickens.
Two groups of three weeks old SPF chickens were vaccinated prior to inoculation with coccidia and challenge with virulent IBDV, all within a period of eight days. Two control groups were similarly treated, except that challenge with field virus was omitted in one group while inoculation with coccidia was omitted in the other group. Clinical signs, lesions in the intestines caused by coccidia, lesions in the bursa of Fabricius caused by IBDV, IBDV-antibody titres, and virus detection by reverse transcription polymerase chain reaction (RT-PCR) were compared among the groups. Lymphoid tissues and swab samples were analysed by general RT-PCR, and positive results were identified by strain specific duplex (DPX) RT-PCR.
In the tripple-infected groups, vaccine strain IBDV was detected in spleen and thymus tissues, and no field virus was detected in bursa samples, contrary to the double-infected groups.
The results suggest an enhancing effect on the immune response caused by subclinical coccidiosis and vvIBDV acting in concert.
Gumboro disease, subsequently named infectious bursal disease (IBD) is a disease in young chickens caused by infectious bursal disease virus (IBDV), a double stranded, bi-segmented RNA virus . Two serotypes, 1 and 2, have been reported, serotype 1 being the only one pathogenic to the domestic chicken . Several serotype 1 strains of varying virulence have emerged, as reviewed by . So far definitive virulence markers have not been identified. IBDV targets the IgM positive B-lymphocytes in the bursa of Fabricius [4,5], transiently compromising the humoral as well as the cellular immune responses [6,7].
Although clinical symptoms were not observed, lesion scores and microscopy documented subclinical coccidiosis in groups 1, 3 and 4 two days after the chickens in groups 3 and 4 were challenged with field virus. From the same day, unprotected chickens would be expected to show clinical IBD symptoms . The presence of subclinical coccidiosis did not have a negative impact on the vaccination against IBD significant enough to provoke clinical symptoms, leaving the reasons for vaccine breaks observed under field conditions unexplained. The reasons why we did not observe an aggravating effect on the immune system favouring E. tenella as previously reported  could be differences in IBDV strains, differences in doses of sporulated coccidia (1500/150 000), or that our experimental inoculation with coccidia only resulted in a single life cycle in the host, probably due to the wire floor in the isolators. Different ages of the chickens also may have influenced the experiments.
In conclusion, coccidia did not seem to affect IBDV vaccination in chickens negatively. On the contrary, our results suggested an additive effect of concurrent stimulation of the immune system by subclinical coccidiosis and vvIBDV, enhancing the replication and distribution of the vaccine strain in chicken lymphoid tissues. Assuming that replication of and presence of vaccine virus in extra-bursal lymphoid tissues mediates improved protection, our experiment indicated that coccidia contributed to an improved immune response following IBDV vaccination. The perspectives of these conclusions might be a possibility of benefiting from an enhancing immunological effect of concurrent, controlled viral and parasitic infections. Further research into immunological consequences of complex infections in chickens is highly relevant.
The author(s) declare that they have no competing interests.
SK designed and carried out the experiments and drafted the manuscript