Background: Candida auris has emerged globally as a multidrug-resistant fungal pathogen responsible for healthcare-associated outbreaks and invasive infections. Whole-genome sequencing studies have demonstrated the existence of genetically distinct clades that differ in geographical distribution, antifungal resistance patterns, virulence traits, and outbreak potential. Objectives: This study aimed to evaluate the performance of the ClaID clade identification PCR system among clinical Candida auris isolates collected in İstanbul, Türkiye, and to investigate the clade-associated molecular profiles of circulating isolates. Methods: Forty-four clinical C. auris isolates were analysed using the auris universal sequence (AUS) assay and clade-specific sequence assays (CSS1–CSS5). PCR amplification results were interpreted according to the ClaID framework. Results: AUS amplification was detected in 41/44 isolates (93.2%). CSS1 amplification was observed in 39/44 isolates (88.6%), indicating a predominance of Clade I-associated molecular profiles within this regional İstanbul isolate collection. No amplification was detected using CSS2, CSS3, CSS4, or CSS5 assays. Three isolates were AUS-negative and five isolates did not yield CSS1 amplification despite repeated testing. Conclusions: The findings suggest that the majority of analyzed clinical isolates from İstanbul exhibited Clade I-associated molecular profiles rather than definitive WGS-confirmed clade assignments. This study provides one of the first field evaluations of the ClaID system in a Turkish clinical isolate collection and contributes regional molecular epidemiological data regarding PCR-based clade-associated profiles of C. auris in Türkiye.

Bacteriophage exposure can impose strong selective pressure on bacterial populations and may alter antimicrobial susceptibility beyond direct lytic effects. However, the persistence of such changes after the removal of phage pressure remains insufficiently characterized in clinical P. aeruginosa isolates. This study evaluated whether short-term exposure to the lytic bacteriophage KPP10 was associated with changes in antimicrobial susceptibility categories and whether these changes remained detectable after serial passage in phage-free medium. Five non-duplicate clinical P. aeruginosa isolates were exposed to KPP10 for 24 h at a multiplicity of infection of 10. Antimicrobial susceptibility testing was performed by disk diffusion at baseline, immediately after exposure (F24) and after four serial passages in phage-free medium. Categories were interpreted according to the EUCAST 2024 clinical breakpoints. Nine categorical susceptibility shifts were detected across six antibiotics: four toward increased susceptibility and five toward decreased susceptibility. Six shifts (66.7%) remained detectable after four serial passages, whereas three shifts (33.3%), involving ciprofloxacin, cefepime, and aztreonam in LBK20, reverted to their baseline categories. Eight of the nine shifts involved β-lactam antibiotics, and cefepime was the most frequently affected agent. These exploratory findings show that short-term KPP10 exposure was associated with isolate-specific and bidirectional changes in categorical antimicrobial susceptibility and support repeated susceptibility monitoring in future phage–antibiotic studies.