Clinical Microbiology and Antimicrobial Chemotherapy. 2019; 21(4):340-351
To present the data on the main mechanism of molecular variation in P. aeruginosa causing chronic lung infection in patients with cystic fibrosis.
A total of 1800 throat swabs and sputum samples from cystic fibrosis patients were included in the study over the 10-year period. P. aeruginosa isolates were primarily identified by the biochemical method using the API 20NE test strips (bioMerieux, France). Antimicrobial susceptibility testing was performed by disc diffusion method. Genotyping was conducted by RAPD-PCR and MLST. Whole genome sequencing of three typical P. aeruginosa isolates was performed on an Ion PGM Torrent platform with Ion Sequencing Kit and 316v1 chips (Life Technologies Thermo Fisher, US) according to the manufacturer’s protocol. The RAST web application was used for initial annotation.
There were three main variants of the pathogen variability found: population heterogeneity, pathogen microevolution, and replacement by another genotype of the same species. The variation of the pathogen’s genome is due to the acquisition of mobile genetic elements (plasmids), mutations in the chromosomal genes responsible for antibiotic resistance, bacterial viability and survival during persistence in a host, and changes in the prophage regions of the pathogen.
Epidemiological significance of the molecular mechanisms of pathogen variation is primarily due to the ability of strains to form epidemiologically significant clone. This requires control measures aimed to limit emergence and distribution of such clones to be developed.