Background Carbapenem-resistant Gram-negative bacilli are an increasing threat in diabetic foot ulcer (DFU) infections, limiting therapeutic options and worsening outcomes. However, data linking specific carbapenemase genes to clinical and metabolic factors remain limited. Objectives To isolate Gram-negative bacilli from deep tissue biopsies of DFUs, determine carbapenem susceptibility by minimum inhibitory concentration (MIC) testing, detect major carbapenemase genes by multiplex qPCR, and evaluate their association with glycemic control and Wagner grade. Methods This cross-sectional study included 150 patients with infected DFUs. Isolates recovered from tissue and other specimens were identified by standard microbiological methods, and carbapenem susceptibility was assessed by MIC testing. Multiplex qPCR was used to detect bla KPC, bla NDM, bla OXA-48, bla VIM, and bla IMP, and associations between resistance determinants and clinical variables were analyzed statistically. Results The mean patient age was 56.4 ± 9.8 years, with a male predominance (61.3%), and high-grade ulcers (Wagner III–V) were present in 54.7% of patients. Klebsiella pneumoniae predominated (60.0%), followed by Pseudomonas aeruginosa and Escherichia coli (each 14.7%). Resistance to meropenem and imipenem was high (77.3% and 75.3%, respectively), and carbapenemase production was detected in 84.0% of isolates. bla KPC (28.0%) and bla NDM (24.0%) were the most prevalent genes and were significantly associated with phenotypic carbapenemase production (P = 0.002 and P = 0.006, respectively). Carbapenemase producers showed significantly higher fasting glucose and HbA1c levels than non-producers (P < 0.001), with no significant association observed for Wagner grade (P = 0.570). Conclusions DFUs showed a high burden of carbapenemase-producing Gram-negative bacilli, driven mainly by bla KPC and bla NDM. Poor glycemic control was strongly associated with these resistant infections, underscoring the need for integrated metabolic management, molecular surveillance, and antimicrobial stewardship. These findings position glycemic control as a modifiable driver of antimicrobial resistance in DFUs.
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Othman et al. (2026) studied this question.
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