Ching-Hsi Hsiao, Eugene Yu-Chuan Kang, Ya-Tung Liu, Hung-Chi Chen, Lung-Kun Yeh, David H K Ma, Kuo-Hsuan Hung, Yhu-Chering Huang
Ocular MRSA infections in Taiwan demonstrate longitudinal changes in clonal distribution, characterized by declining CC59 and increasing CC8, and a concurrent increase in fluoroquinolone-resistant CC8. This evolution may compromise fluoroquinolone-based empirical therapy, a cornerstone of first-line treatment for ocular infections, and highlights the importance of continued molecular surveillance.
BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of ocular infections, with evolving molecular epidemiology observed in systemic infections in Taiwan. However, longitudinal data on clonal distribution and antibiotic susceptibility in ocular MRSA isolates remain limited.
MATERIAL AND METHODS: Patients with culture-proven S. aureus ocular infection at Chang Gung Memorial Hospital between 2013 and 2022 were included. MRSA isolates were characterized by pulsed-field gel electrophoresis, multilocus sequence typing, and staphylococcal cassette chromosome mec typing, and Panton-Valentine leucocidin genes detection. Antibiotic susceptibility was examined using disk diffusion method and E-test. Temporal trends were analyzed using chi-square tests for trend.
RESULTS: A total of 154 MRSA ocular isolates were identified. The predominant clone complex (CC) was CC59 (80/154, 52.0%), followed by CC8 (30/154, 19.5%) and CC45 (25/154, 16.2%). Over the decade, CC59 declined while CC8 increased significantly (P = 0.005 and P = 0.002, respectively), paralleling nationwide systemic MRSA trends. CC8 isolates were more frequently associated with eyelid disorders than CC59 (50.0% vs 28.8%; P = 0.045). CC59 isolates remained highly susceptible to fluoroquinolones (> 95%), while CC8 demonstrated marked resistance (≤ 11% susceptible; P < 0.0001). All isolates were susceptible to vancomycin and teicoplanin.
CONCLUSIONS: Ocular MRSA infections in Taiwan demonstrate longitudinal changes in clonal distribution, characterized by declining CC59 and increasing CC8, and a concurrent increase in fluoroquinolone-resistant CC8. This evolution may compromise fluoroquinolone-based empirical therapy, a cornerstone of first-line treatment for ocular infections, and highlights the importance of continued molecular surveillance.