Abstract
Infectious bursal disease (IBD) is an acute, highly contagious and immunosuppressive poultry disease. IBD virus (IBDV) is the causative agent, which may lead to high morbidity and mortality rates in susceptible birds. IBDV-pathogenesis studies have focused mainly on primary lymphoid organs. It is not known if IBDV infection may modify the development of the gut associated lymphoid tissues (GALT) as well as the microbiota composition. The aim of the present study was to investigate the effects of IBDV-infection on the bursa of Fabricius (BF), caecal tonsils (CT) and caecum, and to determine the effects on the gut microbiota composition in the caecum. Commercial broiler chickens were inoculated with a very virulent (vv) strain of IBDV at 14 (Experiment 2) or 15 (Experiment 1) days post hatch (dph). Virus replication, lesion development, immune parameters including numbers of T and B lymphocytes, macrophages, as well as the gut microbiota composition were compared between groups. Rapid IBDV-replication was detected in the BF, CT and caecum. It was accompanied by histological lesions including an infiltration of heterophils. In addition a significant reduction in the total mucosal thickness of the caecum was observed in vvIBDV-infected birds compared to virus-free controls (P < 0.05). vvIBDV infection also led to an increase in T lymphocyte numbers and macrophages, as well as a decrease in the number of B lymphocytes in the lamina propria of the caecum, and in the caecal tonsils. Illumina sequencing analysis indicated that vvIBDV infection also induced changes in the abundance of Clostridium XIVa and Faecalibacterium over time. Overall, our results suggested that vvIBDV infection had a significant impact on the GALT and led to a modulation of gut microbiota composition, which may lead to a higher susceptibility of affected birds for pathogens invading through the gut.
Highlights
Infectious bursal disease virus (IBDV) is the causative agent of infectious bursal disease (IBD) [1]
Comparable results were observed in Experiment 2, with a significant decrease in bursa to body weight ratios (B/BW) at 21 dpi in comparison to the virus-free control (S2 Table, P < 0.05). vvIBDV infection induced an increase in anti-IBDV IgG-specific antibodies in both experiments
A significant upregulation was observed in both experiments with enzyme-linked immunosorbent assay (ELISA)-titers of log10 3.5 ± 0.2 at seven dpi in Experiment 1 and 3.2 ± 0.2 in Experiment 2 at 10 days post hatch compared to virus-free controls in Experiment 1 (2.4 ± 0.8) and 2 (1.6 ± 0.8), respectively (P < 0.05)
Summary
Infectious bursal disease virus (IBDV) is the causative agent of infectious bursal disease (IBD) [1]. IBDV influences GALT and microbiota composition did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section
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