Department of Genetic Engineering, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur-603203, Tamilnadu, India.
Recent Pat Biotechnol. 2022;16(4):329-354. doi: 10.2174/1872208316666220512121205.
Stenotrophomonas maltophilia is an opportunistic pathogen that results in nosocomial infections in immunocompromised individuals. These bacteria colonize on the surface of medical devices and therapeutic equipment like urinary catheters, endoscopes, and ventilators, causing respiratory and urinary tract infections. The low outer membrane permeability of multidrug-resistance efflux systems and the two chromosomally encoded β- lactamases present in S. maltophilia are challenging for arsenal control. The cell-associated and extracellular virulence factors in S. maltophilia are involved in colonization and biofilm formation on the host surfaces. The spread of antibiotic-resistant genes in the pathogenic S. maltophilia attributes to bacterial resistance against a wide range of antibiotics, including penicillin, quinolones, and carbapenems. So far, tetracycline derivatives, fluoroquinolones, and trimethoprim-sulfamethoxazole (TMP-SMX) are considered promising antibiotics against S. maltophilia. Due to the adaptive nature of the intrinsically resistant mechanism towards the number of antibiotics and its ability to acquire new resistance via mutation and horizontal gene transfer, it is quite tricky for medicinal contribution against S. maltophilia. The current review summarizes the literary data on pathogenicity, quorum sensing, biofilm formation, virulence factors, and antibiotic resistance of S. maltophilia.
嗜麦芽寡养单胞菌是一种机会致病菌，可导致免疫功能低下个体发生医院获得性感染。这些细菌定植在医疗设备和治疗设备的表面，如导尿管、内窥镜和呼吸机，引起呼吸道和尿路感染。多药耐药外排系统的低外膜通透性和嗜麦芽寡养单胞菌中存在的两种染色体编码的β-内酰胺酶，对控制 arsenal 构成挑战。嗜麦芽寡养单胞菌中细胞相关和细胞外毒力因子参与在宿主表面的定植和生物膜形成。致病性嗜麦芽寡养单胞菌中抗生素耐药基因的传播导致细菌对包括青霉素、喹诺酮类和碳青霉烯类在内的广泛抗生素产生耐药性。迄今为止，四环素衍生物、氟喹诺酮类和复方磺胺甲噁唑（TMP-SMX）被认为是对抗嗜麦芽寡养单胞菌有前途的抗生素。由于固有耐药机制对大量抗生素的适应性以及通过突变和水平基因转移获得新耐药性的能力，针对嗜麦芽寡养单胞菌的药物治疗相当棘手。本综述总结了嗜麦芽寡养单胞菌的致病性、群体感应、生物膜形成、毒力因子和抗生素耐药性的文献数据。
