Abstract
Burkholderia cepacia complex (Bcc) bacteria emerged as opportunistic pathogens in cystic fibrosis and immunocompromised patients. Their eradication is very difficult due to the high level of intrinsic resistance to clinically relevant antibiotics. Bcc bacteria have large and complex genomes, composed of two to four replicons, with variable numbers of insertion sequences. The complexity of Bcc genomes confers a high genomic plasticity to these bacteria, allowing their adaptation and survival to diverse habitats, including the human host. In this work, we review results from recent studies using omics approaches to elucidate in vivo adaptive strategies and virulence gene regulation expression of Bcc bacteria when infecting the human host or subject to conditions mimicking the stressful environment of the cystic fibrosis lung.
Highlights
The Burkholderia cepacia complex (Bcc) is a group of 20 closely-related bacterial species, with up to78% of their genes in common [1]
Bcc infections are especially feared by cystic fibrosis (CF) patients due to the intrinsic resistance of these bacteria to current antimicrobial agents and the cepacia syndrome, a fast and often lethal necrotizing pneumonia accompanied with septicemia developed by up to 20% of the infected patients [7,8]
A Quorum sensing (QS) system based on the fatty acid molecule cis-2-dodecenoic acid as the signaling molecule was identified for the first time in B. cenocepacia J2315 and was named Burkholderia diffusible signal factor (BDSF) [61]
Summary
The Burkholderia cepacia complex (Bcc) is a group of 20 closely-related bacterial species, with up to. Several studies have been performed aiming at the understanding of the strategies used by Bcc to survive and thrive in the CF host and how the bacterium adapts its gene expression program to survive the hostile environment that is the CF host. We review selected studies based on the comparative genomics and/or quantitative transcriptomics of Bcc isolates when infecting the CF host
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