Rapid and accurate detection of tuberculosis (TB) drug resistance is critical for the successful treatment and control of TB. Here, we investigated resistance to anti-TB drugs and genetic variations in 215 drug-resistant Mycobacterium tuberculosis isolates in Korea. Genetic variations were observed in rpoB Ser531Leu, katG Ser315Thr, and gyrA Asp94Gly; however, the minimum inhibitory concentrations varied, which can be attributed to other resistance mechanisms. Examination of genetic relatedness among drug-resistant isolates revealed that the cluster size of resistant bacteria was less than six strains, suggesting no evidence of a large-scale epidemic caused by a specific strain. However, rpoC mutants of the rifampicin-resistant isolates were composed of five types of clusters, suggesting that these compensatory mutations advance propagation. In the present study, more than 90% of the resistance mechanisms to major anti-TB drugs were identified, and the effect of each mutation on drug resistance was estimated. With the clinical application of recent next-generation sequencing-based susceptibility testing, the present study is expected to improve the clinical utilization of genotype-based drug susceptibility testing for the diagnosis and treatment of patients with drug-resistant TB.

Background/Objectives: Methicillin-resistant Staphylococcus aureus (MRSA) is a major causative pathogen in Republic of Korea. While numerous variants exist, the long-term evolutionary history of indigenous lineages remains unclear. Therefore, this study aimed to reconstruct the high-resolution population structure of Korean MRSA. Methods: A total of 191 MRSA clinical isolates collected between 1999 and 2025 were obtained from four Korean biobanks. Whole-genome sequencing was conducted and international MRSA genomes from the National Center for Bioinformatics were used as a control group. A genome-wide association study, including single-nucleotide polymorphism (SNP)-based phylogenomic analysis, principal component analysis (PCA), and ADMIXTURE, was performed for distribution analysis. A time-scale epidemiological analysis was conducted using SNP-based phylogenetic data. Additional profiling was performed via core genome multilocus sequence typing (cgMLST) for comparison with the SNP-based phylogenomic results. Finally, antimicrobial resistance and virulence factor genes were annotated using the ResFinder and VirulenceFinder databases. Results: Phylogenetic analysis identified five major clades: 1 (ST5), 2 (ST6), 3 (ST72), 4 (ST1/ST188), and 5 (ST8/ST239/ST254). Time-scaled analysis estimated that these major clades began to diverge in the early 20th century (e.g., Clade 1 around 1918). Notably, Korean ST5 isolates formed a sublineage distinct from North American strains, characterized by unique AMR profiles and divergence in the 1960s. ST72 formed an independent clade that was phylogenetically closer to clade 4 (ST1/ST188) than to the canonical CC8 group (clade 5). Furthermore, the ST1 isolates showed a temporal split into an older lineage and a recent sublineage, with expanded AMR pro-files. Conclusions: By integrating time-scale phylogenetics with cgMLST, we elucidated the evolutionary history and transmission dynamics of Korean MRSA.

김현규, 정혜란, 김지은, 박영준. Public Health Weekly Report 2025;18:119-35. https://doi.org/10.56786/PHWR.2025.18.11suppl.9

Clinical isolates of Mycobacterium tuberculosis M64 strain from South Korea lack the katG gene, which is associated with isoniazid resistance. Herein, we report the whole genome sequence of M. tuberculosis M64, with genomic coverage of 2,791× and a genome size of 4,353,699 bp.

The genome of Coxiella burnetii KZQ2, isolated from clinical patients in Korea, is 2.04 MB long. Multispacer types were ST77, and phylogenetic tree analysis showed that KZQ2 is closely related to the CbuK_Q154 chronic strain isolated from human endocarditis patients in the USA.

Du-Gyeong Han, Ji-A Jeong, Sung-Kyoung Lee, Seong-Han Kim, and Se-Mi Jeon. Microbiol. Biotechnol. Lett. 2024;52:211-4. https://doi.org/10.48022/mbl.2403.03005