Species distribution and fluconazole susceptibility of Candida clinical isolates in a medical center in 2002
Jiun-Ling Wang, Shan-Chwen Chang, Po-Ren Hsueh, Yee-Chun Chen
Departments of Internal Medicine and Laboratory Medicine, National Taiwan University Hospital, Taipei, Taiwan, ROC
Received: August 5, 2003 Revised: September 9, 2003 Accepted: September 30, 2003
Fluconazole disk-diffusion susceptibility was evaluated in 230 blood isolates and 344 non-blood clinical isolates of Candida spp. collected in 2002 at National Taiwan University Hospital. Up to 93.5% of blood isolates were susceptible to fluconazole, 3% were susceptible dose-dependent, and 3.5% were resistant. The minimum inhibitory concentrations at which 50% of tested isolates were inhibited (MIC50) of fluconazole against Candida blood isolates were highest for Candida glabrata (5 µg/mL), followed by Candida tropicalis (2.4 μg/mL), Candida albicans (2.4 µg/mL), and Candida parapsilosis (0.41 µg/mL). C. glabrata had less fluconazole-susceptible strains (76.7%) than C. albicans (98.2%), C. tropicalis (98%) and C. parapsilosis (93.8%) [p< 0.05]. The proportions of fluconazole resistance in the non-blood isolates of C. albicans, C. glabrata and C. parapsilosis were similar to those of the blood isolates. However, the proportions of fluconazole resistance in the non-blood isolates of C. tropicalis surpassed those of the blood isolates (14.7% vs 2%, p<0.05). Comparison of species distribution of Candidablood isolates obtained in 2002 to those in 1981-2000 demonstrated that C. albicans remained the leading pathogen, and the proportion of C. albicans in blood isolates was lowest in 1996 (38%) and did not change significantly thereafter. However, the proportion of C. tropicalis increased from 14% during 1981-1993 to 22-23% during 1996-2002. Overall, the MIC50, MIC90 and the proportion of Candida blood isolates with fluconazole resistance remained stable during 1994-2002.
Candida, fluconazole, microbial drug resistance, microbial sensitivity tests
J Microbiol Immunol Infect 2004;37:236-241.