Garcia-Effron Guillermo, Park Steven, Perlin David S
Public Health Research Institute, New Jersey Medical School-UMDNJ, Newark, NJ 07103, USA.
Antimicrob Agents Chemother. 2009 Jan;53(1):112-22. doi: 10.1128/AAC.01162-08. Epub 2008 Oct 27.
A detailed kinetic characterization of echinocandin inhibition was performed for mutant 1,3-beta-d-glucan synthase enzymes from clinical isolates of Candida albicans with nine different FKS1 mutations resulting in high MICs. Among 14 mutant Fks1p enzymes studied, the kinetic parameters 50% inhibitory concentration and K(i) increased 50-fold to several thousandfold relative to those for the wild type. Enzymes with mutations at Ser645 (S645P, S645Y, and S645F) within hot spot 1 showed the most prominent decrease in sensitivity, while those with mutations at the N- and C-terminal ends of hot spot 1 generally retained greater sensitivity to all three drugs. Kinetic inhibitions by caspofungin, micafungin, and anidulafungin were comparable among the fks1 mutant enzymes, although absolute values did vary with specific mutations. Amino acid substitutions in Fks1p did not alter K(m) values, although some mutations decreased the V(max). Given the association of FKS1 mutations with clinical resistance, an evaluation of the kinetic parameters for the inhibition of mutant 1,3-beta-D-glucan synthase as a function of the MIC enabled an independent evaluation of the recently adopted susceptibility breakpoint for echinocandin drugs. Overall, a breakpoint MIC of >or=2 microg/ml for caspofungin captured nearly 100% of fks1 C. albicans strains when a kinetic inhibition rise threshold of <or=50-fold for the K(i) was used as a measure of susceptibility. A similar MIC breakpoint for micafungin and anidulafungin was less inclusive, and a projected MIC of >or=0.5 microg/ml was required for >95% coverage of clinical isolates. However, when MIC determinations were performed in the presence of 50% serum, all fks1 mutants showed MIC values of >or=2 microg/ml for the three echinocandin drugs. The 1,3-beta-D-glucan synthase kinetic inhibition data support the proposed susceptibility breakpoint for caspofungin in C. albicans, but a lower susceptibility breakpoint (<or=0.5 microg/ml) may be more appropriate for anidulafungin and micafungin. Overall, the data indicate that MIC testing with caspofungin may serve as a surrogate marker for resistance among the class of echinocandin drugs.
对来自白色念珠菌临床分离株的1,3-β-D-葡聚糖合酶突变体进行了棘白菌素抑制的详细动力学特征分析,这些突变体具有9种不同的FKS1突变,导致高最低抑菌浓度(MIC)。在研究的14种Fks1p突变酶中,50%抑制浓度和抑制常数(Ki)的动力学参数相对于野生型增加了50倍至数千倍。在热点1内Ser645处发生突变(S645P、S645Y和S645F)的酶敏感性下降最为显著,而在热点1的N端和C端发生突变的酶通常对所有三种药物保持较高的敏感性。尽管绝对数值因特定突变而有所不同,但卡泊芬净、米卡芬净和阿尼芬净的动力学抑制在fks1突变酶之间具有可比性。Fks1p中的氨基酸取代并未改变米氏常数(Km)值,尽管一些突变降低了最大反应速度(Vmax)。鉴于FKS1突变与临床耐药性的关联,对突变型1,3-β-D-葡聚糖合酶抑制的动力学参数作为MIC的函数进行评估,能够独立评估最近采用的棘白菌素类药物的敏感性断点。总体而言,当将Ki的动力学抑制上升阈值≤5倍作为敏感性衡量标准时,卡泊芬净≥2μg/ml的断点MIC捕获了近100%的fks1白色念珠菌菌株。米卡芬净和阿尼芬净的类似MIC断点包容性较差,对于>95%的临床分离株覆盖率,预计MIC≥0.5μg/ml。然而,当在50%血清存在下进行MIC测定时,所有fks1突变体对三种棘白菌素类药物的MIC值均≥2μg/ml。1,3-β-D-葡聚糖合酶动力学抑制数据支持了白色念珠菌中卡泊芬净的拟议敏感性断点,但较低的敏感性断点(≤0.5μg/ml)可能更适用于阿尼芬净和米卡芬净。总体而言,数据表明用卡泊芬净进行MIC检测可作为棘白菌素类药物耐药性的替代标志物。