Induction of Metronidazole and Clindamycin Resistance in Gardnerella vaginalis.

dc.contributor.advisorAfrica, Charlene
dc.contributor.advisorAbrantes, Pedro
dc.contributor.authorBelford, Robyn Beth
dc.date.accessioned2025-05-06T08:18:41Z
dc.date.available2025-05-06T08:18:41Z
dc.date.issued2023
dc.description.abstractBacterial vaginosis (BV) is known to be the most common polymicrobial vaginal disorder in females of childbearing age. It is characterised by a change in the healthy vaginal microbiome, from an environment dominated by hydrogen-producing lactobacilli, to the overgrowth of opportunistic pathogenic bacteria particularly Gardnerella vaginalis. G. vaginalis is a gram-variable pleomorphic bacterium which under normal conditions is considered to exhibit low virulence. G. vaginalis is the most common bacterial species isolated from patients with BV, and isolated in over 98% of BV cases. BV and other infections associated with G. vaginalis are typically treated with metronidazole or clindamycin. There has recently been an increase in recurrent BV infections and treatment failure. Antimicrobial resistance in bacteria has proven to lead to higher rates of adverse health outcomes. Understanding the susceptibility and resistance mechanisms of G. vaginalis is crucial in reducing the number of recurrent infections and treatment failures. Ten commercially acquired G. vaginalis type strains were tested in this study. The Kirby-Bauer and E-Test protocols were performed to determine the antibiotic susceptibility of selected strains and the minimum inhibitory concentrations (MIC) of metronidazole and clindamycin respectively. Clindamycin and metronidazole resistance were induced by culturing the G. vaginalis strains on 5% horse blood agar supplemented with increasing concentrations of the antibiotics. Following resistance induction, polymerase chain reaction (PCR) was performed to determine if nim and erm genes associated with metronidazole and clindamycin resistance were present. Sialidase activity was detected in three of the ten G. vaginalis type strains. Four of the type strains were resistant to metronidazole prior to antibiotic exposure. Following resistance induction, the metronidazole MIC increased from 12 μg/ml to >256 μg/ml. All ten strains were susceptible to clindamycin. The initial clindamycin MIC increased from 0,016 μg/ml to 0,38 μg/ml. No nim or erm genes were detected. BV recurrent infections occur in 70% of patients following antibiotic treatment. Due to the multifactorial nature of metronidazole and clindamycin resistance, healthcare workers need to formulate alternative treatment strategies for BV and G. vaginalis associated infections.
dc.identifier.urihttps://hdl.handle.net/10566/20356
dc.language.isoen
dc.publisherUniversity of the Western Cape
dc.subjectGardnerella vaginalis
dc.subjectBacterial vaginosis
dc.subjectMetronidazole
dc.subjectClindamycin
dc.subjectAntimicrobial resistance
dc.subjectAntibiotic susceptibility
dc.subjectSialidase
dc.subjectResistance genes
dc.subjectAntimicrobial resistance induction
dc.titleInduction of Metronidazole and Clindamycin Resistance in Gardnerella vaginalis.
dc.typeThesis

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