Molecular Basis of Antimicrobial Resistance in Group B Clinical Isolates from Saudi Arabia.

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.