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Maha Alzayer,1 Manal M Alkhulaifi,2 Ahmed Alyami,3 Mohammed S Aldosary,3 Abdulaziz Alageel,3 Ghada Garaween,1 Nada Alsalloum,1 Atef Shibl,1 Arif M Al-Hamad,4 Michel Doumith5 1Department of Microbiology and Immunology, College of Medicine, Alfaisal University, Riyadh, Saudi Arabia; 2Department of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia; 3Pathology and Clinical Laboratory, Medicine Administration, King Fahad Medical City, Riyadh, Saudi Arabia; 4Division of Clinical Microbiology, Pathology and Laboratory Medicine, Qatif Central Hospital, Qatif, Saudi Arabia; 5Infectious Diseases Research Department, King Abdullah International Medical Research Center, Riyadh, Saudi ArabiaCorrespondence: Maha Alzayer, College of Medicine, Microbiology Department, Al Faisal University, PO Box 50927, Riyadh, 11533, Saudi Arabia, Email maha.alzayer180@gmail.com; maalzayer@alfaisal.eduAbstract: Published data on the molecular mechanisms underlying antimicrobial resistance in Group B Streptococcus (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 erm(A), erm(B), mef(A), and/or lsa(C) genes at the origin of resistance to macrolides and/or clindamycin. Of these, erm(B) and erm(A) were associated with the cMLSB (n = 46) and iMLSB (n = 28) phenotypes, respectively, while mef(A) was linked to the M phenotype (n = 1) and lsa(C) was present in isolates with the L phenotype (n = 8). Resistance to tetracycline was mainly mediated by tet(M) alone (n = 112) or in combination with tet(O) (n = 10); the remaining isolates carried tet(O) (n = 29), tet(L) (n = 2), or both (n = 3). Isolates resistant to gentamicin (n = 5) carried aac(6′)-Ie-aph(2′)-Ia, and those exhibiting resistance to levofloxacin (n = 13) had alterations in GyrA and/or ParC. Most isolates with the erm gene (93.24%, n = 69/74) also had the tet 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 erm(B) 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.Keywords: antibiotic resistance, gene resistance, macrolides, levofloxacin, gentamicin, Group B Streptococcus (GBS) |
