Prevalence and characterization of β-lactamase-producing bacteria in gingivitis among diabetic and non-diabetic patients: a comparative microbiological study

糖尿病患者和非糖尿病患者牙龈炎中产β-内酰胺酶细菌的流行情况和特征:一项比较微生物学研究

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Abstract

Background. Gingivitis is a reversible gingival inflammation that may progress to periodontitis if untreated. Diabetes mellitus alters the oral microbiota and weakens host defenses, increasing susceptibility to infection. Objectives. To investigate the prevalence and characterization of β-lactamase-producing bacteria isolated from gingival swabs of diabetic and non-diabetic patients with clinically confirmed gingivitis. Methods. Thirty-seven patients were enrolled (17 diabetics and 20 non-diabetics). Gingival swabs were cultured and identified by conventional microbiological and analytical profile index (API). Antimicrobial susceptibility was tested according to the Clinical and Laboratory Standards Institute 2023 guidelines. β-Lactamase activity was assessed using an iodometric colourimetric assay. Results. A total of 65 bacterial isolates were obtained from 37 gingivitis patients. Polymicrobial infections predominated in diabetics (82.4%) vs. non-diabetics (45.0%). Non-diabetics were mainly colonized by Streptococcus mutans (45.9%) and Staphylococcus aureus (40.5%), while diabetics harboured more Gram-negative species, particularly Pseudomonas aeruginosa (21.4%) and Enterobacteriaceae (46.4 % vs. 2.7 %). Overall, 67.7 % of isolates were β-lactamase producers. Resistance was highest to ampicillin (92.3%) and amoxicillin-clavulanate (84.6%), whereas ciprofloxacin (89.2%) and piperacillin-tazobactam (78.5%) retained the greatest activity. Conclusions. Diabetes is associated with increased microbial diversity, Gram-negative colonization, and a frequency of β-lactamase-producing bacteria in gingivitis. These findings highlight diabetes as a risk factor for resistant oral infections and underscore the need for antimicrobial stewardship, resistance surveillance and future molecular studies to clarify resistance mechanisms in high-risk groups.

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