Institute of Specific Prophylaxis and Tropical Medicine, Centre for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria; Institute of Medical Microbiology and Hospital Hygiene, University Clinic of Heinrich Heine University, Düsseldorf, Germany.
Institute of Specific Prophylaxis and Tropical Medicine, Centre for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
J Glob Antimicrob Resist. 2018 Sep;14:169-175. doi: 10.1016/j.jgar.2018.04.003. Epub 2018 Apr 13.
Mycoplasma hominis, a genetically heterogeneous, cell-wall-less bacterium, is able to live in symbiosis with the protozoan parasite Trichomonas vaginalis. Whilst the impact of this symbiosis on T. vaginalis has been investigated to a certain extent, less light has been shed on the influence on M. hominis.
An in vitro minimum inhibitory concentration (MIC) study of the antimicrobial susceptibility of three clinical M. hominis isolates (V475, AKH136 and MhSS10) to clindamycin, moxifloxacin, ciprofloxacin and gentamicin was performed in dependence on symbiosis with T. vaginalis strain IR78.
Passaging of M. hominis through T. vaginalis led to an increase in MICs to all drugs investigated in M. hominis V475 and M. hominis MhSS10 (apart from gentamicin). Shifts from intermediate to resistant (MhSS10 for ciprofloxacin) and from susceptible to intermediate-resistant (V475 for gentamicin; P=0.015) were observed. Moreover, initial susceptibility of V475 to moxifloxacin (MIC=1.35μg/mL) was statistically significantly reduced (MIC=2.5μg/mL) following T. vaginalis passage concomitantly with mutations in the quinolone resistance-determining regions (QRDRs) of gyrA (S153L) and parC (E195G and K144R). In contrast, the susceptibility of M. hominis isolate AKH136 to all drugs investigated increased after passaging.
These findings suggest that symbiosis with T. vaginalis has an enhancing effect on selected antimicrobial resistances of distinct M. hominis isolates.
人型支原体是一种遗传上具有异质性、无细胞壁的细菌，能够与原生动物寄生虫阴道毛滴虫共生。虽然这种共生关系对阴道毛滴虫的影响已经在一定程度上得到了研究，但对人型支原体的影响却知之甚少。
在体外进行了最小抑菌浓度（MIC）研究，以评估三种临床分离的人型支原体（V475、AKH136 和 MhSS10）在与阴道毛滴虫株 IR78 共生的情况下对克林霉素、莫西沙星、环丙沙星和庆大霉素的抗菌敏感性。
将人型支原体通过阴道毛滴虫传代，导致人型支原体 V475 和 MhSS10 对所有研究药物的 MIC 值均增加（除庆大霉素外）。观察到从中介到耐药（MhSS10 对环丙沙星）和从敏感到中介耐药（V475 对庆大霉素；P=0.015）的转变。此外，V475 对莫西沙星（MIC=1.35μg/mL）的初始敏感性在与阴道毛滴虫共传代后统计学上显著降低（MIC=2.5μg/mL），同时在 gyrA（S153L）和 parC（E195G 和 K144R）的喹诺酮耐药决定区（QRDR）中出现突变。相比之下，AKH136 对所有研究药物的敏感性在传代后均增加。
这些发现表明，与人型支原体共生对特定人型支原体分离株的某些抗菌耐药性具有增强作用。
