Department of Microbiology and Immunology, Faculty of Pharmacy, Mansoura University, Mansoura, 35516, Egypt.
Ann Clin Microbiol Antimicrob. 2024 May 24;23(1):46. doi: 10.1186/s12941-024-00705-3.
Proteus mirabilis is an opportunistic pathogen that has been held responsible for numerous nosocomial and community-acquired infections which are difficult to be controlled because of its diverse antimicrobial resistance mechanisms.
Antimicrobial susceptibility patterns of P. mirabilis isolates collected from different clinical sources in Mansoura University Hospitals, Egypt was determined. Moreover, the underlying resistance mechanisms and genetic relatedness between isolates were investigated.
Antimicrobial susceptibility testing indicated elevated levels of resistance to different classes of antimicrobials among the tested P. mirabilis clinical isolates (n = 66). ERIC-PCR showed great diversity among the tested isolates. Six isolates (9.1%) were XDR while all the remaining isolates were MDR. ESBLs and AmpCs were detected in 57.6% and 21.2% of the isolates, respectively, where bla, bla, bla, bla and bla were detected. Carbapenemases and MBLs were detected in 10.6 and 9.1% of the isolates, respectively, where bla and bla genes were detected. Quinolone resistant isolates (75.8%) harbored acc(6')-Ib-cr, qnrD, qnrA, and qnrS genes. Resistance to aminoglycosides, trimethoprim-sulfamethoxazole and chloramphenicol exceeded 80%. Fosfomycin was the most active drug against the tested isolates as only 22.7% were resistant. Class I or II integrons were detected in 86.4% of the isolates. Among class I integron positive isolates, four different gene cassette arrays (dfrA17- aadA5, aadB-aadA2, aadA2-lnuF, and dfrA14-arr-3-bla-aadA15) and two gene cassettes (dfrA7 and aadA1) were detected. While class II integron positive isolates carried four different gene cassette arrays (dfrA1-sat1-aadA1, estXVr-sat2-aadA1, lnuF- dfrA1-aadA1, and dfrA1-sat2).
P. Mirabilis ability to acquire resistance determinants via integrons may be held responsible for the elevated rates of antimicrobial resistance and emergence of XDR or even PDR strains limiting the available therapeutic options for management of infections caused by those strains.
奇异变形杆菌是一种机会致病菌，由于其具有多种抗菌药物耐药机制，已被认为是导致许多医院内和社区获得性感染的病原体，这些感染难以控制。
从埃及曼苏拉大学医院不同临床来源的奇异变形杆菌分离株中检测抗菌药物敏感性模式。此外，还研究了分离株之间的潜在耐药机制和遗传相关性。
抗菌药物敏感性测试表明，测试的奇异变形杆菌临床分离株（n=66）对不同类别的抗菌药物表现出高水平的耐药性。ERIC-PCR 显示测试分离株之间存在很大的多样性。6 株（9.1%）为 XDR，而其余分离株均为 MDR。57.6%和 21.2%的分离株分别检测到 ESBLs 和 AmpCs，检测到 blaCTX-M-15、blaTEM-1、blaDHA-1、blaOXA-1 和 blaPER-1 基因。10.6%和 9.1%的分离株分别检测到碳青霉烯酶和 MBLs，检测到 blaNDM-1 和 blaVIM-1 基因。75.8%的喹诺酮耐药分离株携带 acc(6')-Ib-cr、qnrD、qnrA 和 qnrS 基因。对氨基糖苷类、磺胺甲恶唑-甲氧苄啶和氯霉素的耐药率均超过 80%。磷霉素是测试分离株最有效的药物，只有 22.7%的分离株耐药。86.4%的分离株检测到 I 类或 II 类整合子。在 I 类整合子阳性分离株中，检测到 4 种不同的基因盒阵列（dfrA17-aadA5、aadB-aadA2、aadA2-lnuF 和 dfrA14-arr-3-bla-aadA15）和 2 种基因盒（dfrA7 和 aadA1）。而 II 类整合子阳性分离株携带 4 种不同的基因盒阵列（dfrA1-sat1-aadA1、estXVr-sat2-aadA1、lnuF-dfrA1-aadA1 和 dfrA1-sat2）。
奇异变形杆菌通过整合子获得耐药决定因子的能力可能是导致其抗菌药物耐药率升高以及出现 XDR 甚至 PDR 菌株的原因，这限制了治疗这些菌株引起的感染的可用治疗选择。
