Limb Salvage in a Patient with a Massive Diabetic Foot Ulcer Infected with a Metalloß-Lactamase-Producing, Colistin-resistant Bacterium: A Case Report

The rise of Metallo-β-lactamase (MBL) producing Gram-negative bacilli in Diabetic Foot Ulcers (DFUs) presents a critical therapeutic challenge. MBLs hydrolyse nearly all β-lactam antibiotics, and the intrinsic resistance of organisms like Proteus species to colistin, a traditional last-resort agent, creates a “therapeutic dead-end”. A 67-year-old male presented with a massive, chronic DFU on the left foot measuring 15 cm × 15 cm with a depth of 6 mm. The wound was non responsive to prior empiric therapies and presented with significant purulent discharge over a stalled, necrotic wound bed. Clinical cultures identified a co-infection of Pseudomonas aeruginosa and Proteus mirabilis. Phenotypic testing via Modified Carbapenem Inactivation Method (mCIM) and EDTA-modified Carbapenem Inactivation Method (eCIM) confirmed MBL-mediated resistance. Additionally, Congo Red Agar (CRA) confirmed strong biofilm production. Targeted triple-drug synergy was initiated using Ceftazidime-Avibactam (CZA) and aztreonam to bypass MBL hydrolysis, supplemented with high-dose tigecycline to overcome intermediate susceptibility. This pharmacological approach was combined with aggressive serial surgical debridement to disrupt the biofilm matrix. Following infection eradication, the massive defect was reconstructed using a Split-Thickness Skin Graft (STSG). The 225 cm² defect achieved complete epithelialisation over three months, successfully averting major lower extremity amputation. This case demonstrates that limb salvage of massive, colistin-resistant, MBL-infected DFUs is achievable through a multidisciplinary approach combining precision laboratory diagnostics (mCIM/eCIM), synergistic antimicrobial therapy (CZA plus aztreonam), and aggressive surgical source control. The novelty lies in successfully navigating a therapeutic dead-end caused by intrinsic colistin resistance in a massive defect.