Comparative genomic analyses shed light on the introduction routes of rice-pathogenic Burkholderia gladioli strains into Bangladesh.

backgroundThe gram-negative bacterium Burkholderia gladioli can cause diseases in a wide range of hosts, including humans and plants. In rice, it produces Bacterial Panicle Blight (BPB), an emerging disease that is threatening the production of this staple food worldwide. Recently, BPB has affected several rice fields in Bangladesh, and B. gladioli has been reported as the causative agent in one of these fields, raising questions about how the pathogen was introduced into the country. Understanding the introduction routes into Bangladesh and the pathogenicity mechanisms of B. gladioli is essential to develop sustainable management strategies to control BPB.

resultsTo investigate the origin of pathogenic B. gladioli strains and their introduction routes into Bangladesh, we sequenced the complete genomes of 19 strains isolated from symptomatic rice panicles from four major rice-growing districts of the country (Rangpur, Faridpur, Natore, and Mymensingh). A phylogenetic analysis encompassing all 320 publicly available B. gladioli genomes along with the 19 newly sequenced genomes suggested five independent introduction events into Bangladesh—four of which showed close phylogenetic links to clinical isolates from the USA—and no evidence of inter-district dissemination within the country. Many host transitions (35 human-to-plant and 1 plant-to-human) were inferred across the phylogeny, highlighting the pathogen’s versatile and cross-kingdom transmission dynamics. Analysis of the presence/absence patterns of 37 virulence-related genes across all 339 B. gladioli strains indicated that human-to-plant host transitions often coincided with loss of the tsr and motB genes—which are associated with bacterial motility—, suggesting convergent adaptive shifts in response to host switches.

conclusionOur findings shed light on the introduction pathways of pathogenic B. gladioli strains into Bangladesh and highlight specific virulence-related genes as potentially responsible for cross-kingdom host shifts.