Alzayer Maha, Alkhulaifi Manal M, Alyami Ahmed, Aldosary Mohammed S, Alageel Abdulaziz, Garaween Ghada, Alsalloum Nada, Shibl Atef, Al-Hamad Arif M, Doumith Michel
Department of Microbiology and Immunology, College of Medicine, Alfaisal University, Riyadh, Saudi Arabia.
Department of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Infect Drug Resist. 2024 Aug 27;17:3715-3722. doi: 10.2147/IDR.S466726. eCollection 2024.
Published data on the molecular mechanisms underlying antimicrobial resistance in Group B (GBS) isolates from Saudi Arabia are lacking. Here, we aimed to determine the genetic basis of resistance to relevant antibiotics in a collection of GBS clinical isolates (n = 204) recovered from colonized adults or infected patients and expressing serotypes Ia, Ib, II, III, V, and VI. Initial susceptibility testing revealed resistance to tetracycline (76.47%, n = 156/204), erythromycin (36.76%, n = 75/204), clindamycin (25.49%, n = 52/204), levofloxacin (6.37%, n = 13/204), and gentamicin (2.45%, n = 5/204). Primers designed for the detection of known resistance determinants in GBS identified the presence of ), and/or genes at the origin of resistance to macrolides and/or clindamycin. Of these, and were associated with the cMLS (n = 46) and iMLS (n = 28) phenotypes, respectively, while was linked to the M phenotype (n = 1) and was present in isolates with the L phenotype (n = 8). Resistance to tetracycline was mainly mediated by alone (n = 112) or in combination with (n = 10); the remaining isolates carried (n = 29), (n = 2), or both (n = 3). Isolates resistant to gentamicin (n = 5) carried '', and those exhibiting resistance to levofloxacin (n = 13) had alterations in GyrA and/or ParC. Most isolates with the gene (93.24%, n = 69/74) also had the gene and were therefore resistant to erythromycin, clindamycin, and tetracycline. Overall, there were no clear associations between serotypes and resistance genotypes except for the presence of in serotype Ib isolates. Dissemination of antibiotic resistance genes across different serotypes represents a public health concern that requires further surveillance and appropriate antibiotic use in clinical practice.
关于沙特阿拉伯B组链球菌（GBS）分离株抗菌耐药性潜在分子机制的已发表数据尚缺。在此，我们旨在确定从定植成人或感染患者中分离出的一组GBS临床分离株（n = 204）中对相关抗生素耐药的遗传基础，这些分离株表达血清型Ia、Ib、II、III、V和VI。初始药敏试验显示对四环素耐药（76.47%，n = 156/204）、红霉素（36.76%，n = 75/204）、克林霉素（25.49%，n = 52/204）、左氧氟沙星（6.37%，n = 13/204）和庆大霉素（2.45%，n = 5/204）。为检测GBS中已知耐药决定因素而设计的引物确定了在对大环内酯类和/或克林霉素耐药的起源处存在 erm(B)、erm(A)、erm(TR)、msr(A)、mef(A) 和 lnu(A) 基因。其中，erm(B) 和 erm(A) 分别与cMLS（n = 46）和iMLS（n = 28）表型相关，而 erm(TR) 与M表型（n = 1）相关，lnu(A) 存在于具有L表型的分离株中（n = 8）。对四环素的耐药主要由 tet(M) 单独介导（n = 112）或与 tet(O) 联合介导（n = 10）；其余分离株携带 tet(S)（n = 29）、tet(K)（n = 2）或两者皆有（n = 3）。对庆大霉素耐药的分离株（n = 5）携带 ''aac(6')-aph(2''), 而对左氧氟沙星耐药的分离株（n = 13）在GyrA和/或ParC中有改变。大多数携带 erm(B) 基因的分离株（93.24%，n = 69/74）也有 erm(A) 基因，因此对红霉素、克林霉素和四环素耐药。总体而言，除了血清型Ib分离株中存在 lnu(A) 外血清型与耐药基因型之间没有明确关联。抗生素耐药基因在不同血清型之间的传播是一个公共卫生问题，需要在临床实践中进一步监测并合理使用抗生素。
