Pathogenic bacteria distribution and antibiotic resistance analysis of diabetic foot infections based on the Wagner classification

Objective To provide a reference for the clinical selection of antimicrobial agents in treating diabetic foot infections (DFI) by analyzing the distribution and antibiotic resistance of pathogens in wound secretions of DFI. Methods A retrospective analysis was conducted on the distribution of pathogenic bacteria and their antibiotic resistance in patients with DFI diagnosed in the Endocrinology Department of Zhongda Hospital Southeast University, from January 2020 to March 2024, based on the Wagner classification (ulcer, soft tissue infection, ischemic necrosis, osteomyelitis, and gangrene). Results A total of 504 DFI patients were included, and 610 strains of pathogens were isolated. Among them, 358 strains (58.7%) were Gram-positive bacteria (G+), 243 strains (39.8%) were Gram-negative bacteria (G-), and 9 strains (1.5%) were fungi. In terms of Wagner classification, 197 strains were from Wagner grade 2 (G+ 69.6%, G- 28.4%), 179 strains from Wagner grade 3 (G+ 60.3%, G- 38.6%), 214 strains from Wagner grade 4 (G+ 46.7%, G- 51.9%), and 20 strains from Wagner grade 5 (G+ 65.0%, G- 35.0%). There were significant statistical differences in the pathogen distribution between Wagner grade 4 and grades 2/3 (P＜0.05). Staphylococcus aureus and Staphylococcus haemolyticus were highly sensitive to vancomycin, teicoplanin, nitrofurantoin, linezolid, tigecycline, and daptomycin (P＞90%). Enterococcus faecalis and Streptococcus species were highly sensitive to penicillin, vancomycin, linezolid and ampicillin. Escherichia coli, Klebsiella pneumoniae, and Proteus mirabilis showed high sensitivity (＞90%) to piperacillin-tazobactam, cefoperazone-sulbactam, meropenem, and amikacin. Pseudomonas aeruginosa had high sensitivity (＞90%) to tobramycin and amikacin. Conclusion As the severity of DFI progresses (from ulcer to soft tissue infection, ischemic necrosis, osteomyelitis and gangrene), the dominant pathogens shifts from G+ to G-, and the antibiotic resistance rate increases.