Annals of Clinical Microbiology, The official Journal of the Korean Society of Clinical Microbiology
Kuenyoul Park, Heungsup Sung
Ann Clin Microbiol 2026 September, 29(3):10. Published on 22 June 2026.
Mycoplasma pneumoniae is a leading atypical cause of community-acquired pneumonia in children and adults, and the prevalence of resistance to macrolides, the recommended first-line agents, varies markedly by region. Since the fastidious growth of M. pneumoniae makes phenotypic antimicrobial susceptibility testing impractical for routine use, clinical microbiology laboratories have focused on 23S rRNA gene-targeted molecular detection. This mini-review examines the molecular mechanisms of macrolide resistance, laboratory detection strategies, global epidemiology, and clonal dynamics revealed by molecular typing. Macrolide resistance is primarily driven by point mutations in domain V of the 23S rRNA gene, with A2063G accounting for most mutations worldwide, and A2064G being reported less frequently. Resistance in Korea rose from 2.9% in 2003 to 87.2% in a 2015 pediatric cohort, with subsequent studies reporting persistently high rates of approximately 78-87%. Earlier molecular typing studies suggest that this high resistance burden has been associated, at least in part, with the expansion of sequence type (ST) 3 and ST14 lineages. In contrast, Japan and Taiwan showed sharp declines following reductions in macrolide prescribing and P1 genotype turnover. Following the COVID-19 pandemic, a strong resurgence centered in East Asia, the possible global dispersal of ST3 and ST14 to Australia, Iran, and Canada, and the impact of co-circulation with influenza H3N2 have been reported. Real-time polymerase chain reaction (PCR) with simultaneous detection of 23S rRNA gene mutations and targeted metagenomic sequencing are emerging as next-generation surveillance tools. In summary, clinical microbiology laboratories should integrate M. pneumoniae detection with 23S rRNA gene resistance mutation detection using molecular assays and strengthen typingbased surveillance, thereby responding actively to the changing dynamics in East Asia and contributing to antimicrobial stewardship.
Sunjoo Kim
Ann Clin Microbiol 2026 September, 29(3):11. Published on 14 September 2026.
Group A Streptococcus (GAS), or Streptococcus pyogenes, remains predictably susceptible to penicillin, whereas resistance to macrolides has become an important therapeutic and epidemiological concern. This narrative review summarizes the molecular mechanisms, epidemiology, clonal dissemination, and clinical implications of macrolide resistance in GAS. Macrolide resistance is mediated mainly by active efflux, commonly associated with mef genes and the M phenotype, and by ribosomal target-site methylation mediated by erm genes, which produces constitutive or inducible macrolide-lincosamide-streptogramin B resistance. Reported resistance rates vary markedly across geographic regions and study settings, from < 5% in some surveillance populations to > 90% in selected East Asian cohorts. However, direct comparisons are limited by differences in study period, patient population, infection type, and susceptibility testing methods. Molecular epidemiological and whole-genome sequencing studies indicate that both clonal expansion of successful emm lineages and horizontal transfer of resistance determinants carried by mobile genetic elements contribute to dissemination. Clinically, macrolide resistance may compromise treatment in patients requiring non-β-lactam therapy, while erm-mediated cross-resistance can limit the activity of clindamycin in invasive infections. Particular attention is required for inducible clindamycin resistance, which may be missed by routine susceptibility testing. GAS has not developed widespread clinically established penicillin resistance, although isolates with reduced in vitro β-lactam susceptibility associated with penicillin-binding protein alterations have been reported. Fluoroquinolone and tetracycline resistance remain less prominent but warrant continued surveillance. Integrated phenotypic and genomic surveillance, antimicrobial stewardship, and development of effective preventive strategies, including vaccines, are essential to monitor emerging resistant lineages and preserve therapeutic options.
Kwangjin Ahn, Young Uh
Ann Clin Microbiol 2026 September, 29(3):12. Published on 16 September 2026.
Streptococcus agalactiae (group B Streptococcus, GBS) remains a major pathogen in neonatal and adult invasive diseases, while maternal colonization continues to shape prevention strategies for early-onset disease. This narrative review examines how changes in capsular serotypes, sequence types (STs), clonal complexes (CCs), and antimicrobial resistance (AMR) determinants are reshaping the molecular epidemiology of GBS, with emphasis on South Korea and comparisons across East Asia. Conventional serotyping and multilocus sequence typing remain useful for lineage definition, whereas whole-genome sequencing increasingly enables integrated assessment of serotype, clonal background, virulence factors, and resistance determinants. Major lineages show distinct epidemiologic and resistance trajectories. Serotype III/CC17 remains strongly associated with neonatal invasive disease and has acquired multidrug resistance in some settings through mobile genetic elements. In South Korea, serotype III/CC19 has shifted from ST19 toward ST335, accompanied by increasing fluoroquinolone resistance driven by alterations in gyrA and parC. Serotype Ib/CC12 has emerged as a high-risk lineage in parts of East Asia, although resistance phenotypes vary geographically and differ substantially across STs or populations. Serotype VIII/CC1, particularly ST2, has expanded in South Korea while generally retaining lower resistance to several non-beta-lactam agents. Across Korean studies, apparent temporal AMR changes warrant caution because they may reflect heterogeneity in population composition, sample collection and laboratory examination. Continued genomic surveillance with standardized susceptibility testing and comparable sampling helps distinguish true clonal evolution from surveillance artifacts. The resulting evidence landscape should inform intrapartum prophylaxis, empirical therapy, and antimicrobial stewardship for neonates, pregnant women, and adults with invasive GBS disease.
Banseok Kim, Young Ah Kim
Ann Clin Microbiol 2026 September, 29(3):13. Published on 20 September 2026.
Background: Early identification of high-risk patients for severe Clostridioides difficile infection (CDI) is critical for timely intervention. This study evaluated antecedent factors associated with severe CDI while minimizing potential circular reasoning and reverse causality from post-diagnostic clinical course variables.
Methods: In this 10-year retrospective cohort study (2014–2023) at National Health Insurance Service Ilsan Hospital, a Korean referral hospital, 908 consecutive adult inpatients with confirmed toxigenic CDI were enrolled. The patients were categorized as having severe (n = 485) or non-severe (n = 423) CDI according to guideline criteria. Intermediate post-infection events, including intensive care unit admission and total hospital stay, were strictly excluded from predictor models. Univariate screening and multivariable logistic regression were performed using R.
Results: Among 908 patients (median age 78.0 years; 48.6% male), 485 (53.4%) developed severe CDI, which was associated with higher in-hospital mortality than non-severe CDI (26.4% vs. 8.0%, P < 0.001). After multivariable adjustment, independent baseline risk factors for severe CDI were history of prior recurrent CDI (adjusted odds ratio [aOR], 2.77; 95% confidence interval [CI], 1.14–6.77; P = 0.025), prior exposure to β-lactamase inhibitor combinations (aOR, 1.71; 95% CI, 1.25–2.35; P < 0.001), narrow-spectrum cephalosporins (aOR, 2.00; 95% CI, 1.14–3.51; P = 0.016), teicoplanin (aOR, 1.86; 95% CI, 1.08–3.20; P = 0.024), and chronic renal disease (aOR, 1.49; 95% CI, 1.06–2.11; P = 0.022).
Conclusion: A history of recurrent CDI, chronic renal disease, and antecedent exposures to 乒-lactamase inhibitor combinations, narrow-spectrum cephalosporins, and teicoplanin were independently associated with severe CDI, potentially facilitating early risk stratification.
Eun-Young Kim, Su Man Kim, Si Hyun Kim, Jeong Hwan Shin
Ann Clin Microbiol 2026 September, 29(3):14. Published on 20 September 2026.
Background: Monophasic Salmonella enterica serovar Typhimurium variants, particularly the serotype I 4,[5],12:i:-, have globally emerged as important foodborne pathogens associated with multidrug resistance. However, their molecular epidemiology and clonal distribution in South Korea remain unclear. This study investigated the distribution, clonal characteristics, and antimicrobial resistance profiles of S. Typhimurium variants circulating in South Korea.
Methods: In total, 173 S. Typhimurium variant strains were collected from 18 university hospitals between 2019 and 2020. Isolates were identified and serotyped according to the Kauffmann〝White scheme. Gene patterns were determined based on seven phase 1 and 2 flagellar antigen-associated genes. Antimicrobial susceptibility was examined using broth microdilution.
Results: The monophasic variant I 4,[5],12:i:- (n = 131) was the most prevalent, followed by I 4,[5],12:i:1,2 (n = 38) and I 4,[5],12:-:- (n = 4). Gene patterns dominant among monophasic isolates included P5 (n = 72), P8 (n = 29), and P9 (n = 28). The P5 pattern corresponded to the typical Spanish clone. Monophasic variants showed higher resistance rates to ampicillin and third-generation cephalosporins than those of other variants, with higher cephalosporin resistance observed in P8 than in P5.
Conclusion: Among the isolates included in this study, the monophasic variant I 4,[5],12:i:- was more frequently identified than typical S. Typhimurium. Most I 4,[5],12:i:- isolates showed gene patterns previously associated with the Spanish clone and high rates of antimicrobial resistance. Overall, these findings highlight the need for continued surveillance of I 4,[5],12:i:- and its antimicrobial resistance patterns.
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