Galindo-Méndez Mario, Navarrete-Salazar Humberto, Baltazar-Jiménez Francisco, Muñoz-de la Paz Eduardo, Sánchez-Mawcinitt María Fernanda, Gómez-Pardo Alexis, Garza-González Elvira, Ponce-de-León-Garduño Luis Alfredo, Franco-Cendejas Rafael, Morfín-Otero Rayo, Rojas-Larios Fabián, Mena-Ramírez Juan Pablo, Morales-de-la-Peña Cecilia Teresita, García-Mendoza Lourdes, Choy-Chang Elena Victoria, Avilés-Benítez Laura Karina, López-Gutiérrez Eduardo, Canizales-Oviedo Jorge Luis, Barlandas-Rendón Nicolás Eric, Maldonado-Anicacio Joyarib Yanelli, Rosales-García Alina Aracely, Ostos-Cantú Heidy Leticia
Laboratorios Galindo SC, Department of Microbiology, Oaxaca 68000, Mexico.
School of Medicine, Universidad Anáhuac Oaxaca, San Raymundo Jalpan 71248, Mexico.
Antibiotics (Basel). 2022 Oct 9;11(10):1383. doi: 10.3390/antibiotics11101383.
Fosfomycin is currently a viable option against urinary tract infections, particularly against extended-spectrum β-lactamases (ESBL)-producing , due to its unique mechanism of action and its low resistance among bacteria. The objective of this study was to investigate two of the three most common mechanisms of resistance against this antibiotic among 350 ESBL-producing strains isolated from the urine of Mexican patients. The prevalence of fosfomycin resistance in our study was 10.9% (38/350). Of all resistant isolates analyzed, 23 (60.5%) were identified as -producing organisms, with 14 strains carrying and 9, . Additionally, 11 (28.9%) fosfomycin-resistant isolates presented resistance due to impaired antibiotic transport and 8 (21.0%) both mechanisms. No resistance mechanism investigated in the study was found on 12 strains. All 38 confirmed ESBL-producing isolates carried a subtype, 36 (94.5%) belonged to the O25b-ST131 clone, and all of them were able to transfer the fosfomycin resistance trait to recipient strains horizontally. This is the first study in Mexico demonstrating a plasmid-mediated fosfomycin resistance mechanism among clinical strains. Since our results suggest a strong association among and genes and ST131 clones in uropathogenic , plasmid-mediated fosfomycin resistance should be closely monitored.
由于其独特的作用机制和细菌中较低的耐药性，磷霉素目前是治疗尿路感染的一个可行选择，尤其是针对产超广谱β-内酰胺酶（ESBL）的细菌。本研究的目的是调查从墨西哥患者尿液中分离出的350株产ESBL菌株中对这种抗生素的三种最常见耐药机制中的两种。在我们的研究中，磷霉素耐药率为10.9%（38/350）。在所有分析的耐药菌株中，23株（60.5%）被鉴定为产ESBL的菌株，其中14株携带blaCTX-M-15基因，9株携带blaCTX-M-27基因。此外，11株（28.9%）磷霉素耐药菌株因抗生素转运受损而呈现耐药性，8株（21.0%）同时存在这两种机制。在12株菌株中未发现该研究中所调查的耐药机制。所有38株确诊的产ESBL菌株均携带blaCTX-M亚型，36株（94.5%）属于O25b-ST131克隆，并且所有这些菌株都能够将磷霉素耐药性状水平转移至受体菌株。这是墨西哥首次在临床分离菌株中证明质粒介导的磷霉素耐药机制的研究。由于我们的结果表明blaCTX-M基因和ST131克隆在尿路致病性大肠杆菌中存在密切关联，因此应密切监测质粒介导的磷霉素耐药性。
