{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T08:13:28Z","timestamp":1788164008202,"version":"build-2803163510"},"reference-count":25,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T00:00:00Z","timestamp":1788134400000},"content-version":"vor","delay-in-days":242,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Scientifica"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>\n                      Resistance to macrolide, lincosamide, and streptogramin B (MLS\n                      <jats:sub>B<\/jats:sub>\n                      ) antibiotics in\n                      <jats:italic>Staphylococcus aureus<\/jats:italic>\n                      has emerged as a significant therapeutic challenge.\n                      <jats:italic>erm<\/jats:italic>\n                      gene\u2013encoded ribosomal methylation is expressed either constitutively or inducibly, causing resistance to erythromycin and clindamycin with possible induction of clindamycin resistance during therapy.\n                      <jats:italic>msrA<\/jats:italic>\n                      \u2010mediated active drug efflux confers resistance to macrolides and streptogramin B while preserving clindamycin susceptibility. This study aimed to determine the antimicrobial susceptibility pattern of\n                      <jats:italic>S. aureus<\/jats:italic>\n                      isolates and correlate between the phenotypic and genotypic patterns of clindamycin resistance.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      This cross\u2010sectional study was conducted from October 2022 to September 2023 at a tertiary care hospital laboratory. A total of 233 clinical isolates of\n                      <jats:italic>S. aureus<\/jats:italic>\n                      were included from exudate, blood, and bodily fluids. Antimicrobial susceptibility testing was performed using the Vitek 2 Compact system and interpreted according to CLSI 2022 and 2023 guidelines. Inducible clindamycin resistance was detected using the D\u2010test. Multiplex and uniplex PCR assays were performed for the detection of\n                      <jats:italic>ermA<\/jats:italic>\n                      ,\n                      <jats:italic>ermB<\/jats:italic>\n                      ,\n                      <jats:italic>ermC<\/jats:italic>\n                      , and\n                      <jats:italic>msrA<\/jats:italic>\n                      genes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Among 233\n                      <jats:italic>S. aureus<\/jats:italic>\n                      isolates, methicillin resistance was identified in 45.9% (107\/233) isolates. The prevalence of constitutive MLS\n                      <jats:sub>B<\/jats:sub>\n                      (cMLS\n                      <jats:sub>B<\/jats:sub>\n                      ), inducible MLS\n                      <jats:sub>B<\/jats:sub>\n                      (iMLS\n                      <jats:sub>B<\/jats:sub>\n                      ), and MS phenotypes was 23.17%, 12.01%, and 10.3%, respectively. Overall clindamycin resistance was observed in 38.6% (90\/233; 95% CI: 32.6%\u201345.0%). The\n                      <jats:italic>ermC<\/jats:italic>\n                      gene was detected in 30.47% (71\/233) isolates, while\n                      <jats:italic>msrA<\/jats:italic>\n                      was identified in 9.44% (22\/233), including 91.7% of isolates of the MS phenotype. Neither\n                      <jats:italic>ermA<\/jats:italic>\n                      nor\n                      <jats:italic>ermB<\/jats:italic>\n                      genes were detected. All isolates were susceptible to vancomycin, daptomycin, and tigecycline.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      <jats:italic>ermC<\/jats:italic>\n                      \u2010mediated MLS\n                      <jats:sub>B<\/jats:sub>\n                      resistance was present in 30.5% of isolates, with cMLS\n                      <jats:sub>B<\/jats:sub>\n                      (23.2%) being more common than iMLS\n                      <jats:sub>B<\/jats:sub>\n                      (12.0%). Routine D\u2010testing is essential to avoid clinical failure when using clindamycin for erythromycin\u2010resistant, clindamycin\u2010susceptible\n                      <jats:italic>S. aureus<\/jats:italic>\n                      . Also, 8 isolates were clindamycin resistant and susceptible to erythromycin, showcasing the diversity of the resistance profile of\n                      <jats:italic>S. aureus<\/jats:italic>\n                      toward MLS\n                      <jats:sub>B.<\/jats:sub>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/sci5\/8532158","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T07:14:07Z","timestamp":1788160447000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Detection and Genotypic Characterization of Clindamycin Resistance Among\n                    <i>Staphylococcus aureus<\/i>\n                    Clinical Isolates"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-5946-777X","authenticated-orcid":false,"given":"Raechal Sanjana","family":"Hans","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1425-0097","authenticated-orcid":false,"given":"Suchitra Shenoy","family":"M.","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,31]]},"reference":[{"key":"e_1_2_13_1_2","doi-asserted-by":"publisher","DOI":"10.1155\/2022\/1835603"},{"key":"e_1_2_13_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijid.2016.02.016"},{"key":"e_1_2_13_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.drup.2024.101147"},{"key":"e_1_2_13_4_2","doi-asserted-by":"publisher","DOI":"10.1186\/s12941-018-0291-8"},{"key":"e_1_2_13_5_2","doi-asserted-by":"publisher","DOI":"10.4103\/0974-2727.78558"},{"key":"e_1_2_13_6_2","doi-asserted-by":"publisher","DOI":"10.5812\/jjm.39274"},{"key":"e_1_2_13_7_2","volume-title":"Current Protocols in Molecular Biology","author":"Ausubel F. 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