Furugaito Michiko, Arai Yuko, Uzawa Yutaka, Kamisako Toshinori, Ogura Kohei, Okamoto Shigefumi, Kikuchi Ken
Department of Clinical Laboratory and Biomedical Sciences, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan.
Department of Clinical Laboratory, Kindai University Hospital, Osakasayama, Osaka 589-8511, Japan.
Antibiotics (Basel). 2023 Oct 14;12(10):1538. doi: 10.3390/antibiotics12101538.
is a catalase-negative, facultative anaerobic, Gram-positive coccus that is commensal in humans but can become opportunistic and cause severe infectious diseases, such as infective endocarditis. Few studies have tested the antimicrobial susceptibility of . We tested its antimicrobial susceptibility to 27 drugs and defined the resistant genes using PCR in 58 strains, including 52 clinical isolates and six type strains. The type strains and clinical isolates included 22 , 18 (GH) group (genetically indistinguishable from and ), 13 , three , and two . No strain was resistant to beta-lactams and vancomycin. In total, 6/22 (27.3%) strains were erythromycin- and clindamycin-resistant -positive, whereas 5/18 (27.8%) in the GH group, 6/13 (46.2%) , and 1/3 (33.3%) of the strains were erythromycin-non-susceptible - or -positive and clindamycin-susceptible. The MIC of minocycline and the ratios of -positive strains varied across the different species-: 2 µg/mL and 27.3% (6/22); GH group: 8 µg/mL and 22.2% (4/18); : 8 µg/mL and 53.8% (7/13), respectively. Levofloxacin resistance was significantly higher in (8/13 61.5%) than in (2/22 9.1%). Levofloxacin resistance was associated with a substitution at serine 83 for leucine, phenylalanine, or tyrosine in GyrA. The mechanisms of resistance to erythromycin and clindamycin differed across species. In addition, the rate of susceptibility to levofloxacin differed across sp., and the quinolone resistance mechanism was caused by mutations in GyrA alone.
是一种过氧化氢酶阴性、兼性厌氧、革兰氏阳性球菌，在人类中属于共生菌，但可成为机会致病菌并引发严重感染性疾病，如感染性心内膜炎。很少有研究检测过其抗菌药敏性。我们检测了58株菌株（包括52株临床分离株和6株模式菌株）对27种药物的抗菌药敏性，并通过聚合酶链反应（PCR）确定了耐药基因。模式菌株和临床分离株包括22株[具体菌种1]、18株[具体菌种2]（GH组，在基因上与[具体菌种1]和[具体菌种3]无法区分）、13株[具体菌种3]、3株[具体菌种4]和2株[具体菌种5]。没有菌株对β-内酰胺类药物和万古霉素耐药。总体而言，22株[具体菌种1]菌株中有6株（27.3%）对红霉素和克林霉素耐药且[具体菌种1]呈阳性，而GH组中18株中有5株（27.8%）、13株[具体菌种3]中有6株（46.2%）以及3株[具体菌种4]中有1株（33.3%）对红霉素不敏感且[具体菌种1]或[具体菌种3]呈阳性但对克林霉素敏感。米诺环素的最低抑菌浓度（MIC）以及[具体菌种1]呈阳性的菌株比例在不同菌种间有所不同：[具体菌种1]：2μg/mL和27.3%（6/22）；GH组：8μg/mL和22.2%（4/18）；[具体菌种3]：8μg/mL和53.8%（7/13）。左氧氟沙星耐药率在[具体菌种3]中（8/13，61.5%）显著高于[具体菌种1]（（2/22，9.1%）。左氧氟沙星耐药与GyrA中丝氨酸83被亮氨酸、苯丙氨酸或酪氨酸取代有关。不同[具体菌种]对红霉素和克林霉素的耐药机制不同。此外，不同[具体菌种]对左氧氟沙星的敏感率也不同，喹诺酮类耐药机制仅由GyrA中的突变引起。
