A49-02 Racing Against Resistance: Fulminant Septic Shock From Carbapenem-Resistant Acinetobacter Baumannii

Abstract Introduction Carbapenem-resistant Acinetobacter baumannii (CRAB) is an aggressive Gram-negative bacteria associated with ventilator-associated and hospital-acquired pneumonia in critically ill patients. Harboring plasmid-borne carbapenemases, CRAB rapidly spreads multidrug resistance and is recognized by the CDC and WHO as an urgent global threat. High-dose ampicillin-sulbactam remains first-line therapy, yet resistance mediated by OXA-type and Acinetobacter-derived cephalosporinase often renders this ineffective (Franzone et al., 2024). Sulbactam-durlobactam (Xacduro), a newly approved β-lactam/β-lactamase inhibitor, restores sulbactam’s intrinsic activity by blocking class D OXA enzymes — one of few targeted options against CRAB pneumonia. However, emerging reports have documented durlobactam resistance from metallo-β-lactamases and PBP3 mutations, underscoring the urgency of early antimicrobial selection (Pogue et al., 2025). Case Presentation A 60-year-old man with chronic obstructive pulmonary disease, heart failure with preserved ejection fraction, cryoglobulinemic vasculitis presented with acute hypoxic-hypercapnic respiratory failure. On arrival: blood pressure 81/62 mmHg, heart rate 120, lactate 6.2 mmol/L, pH 7.09, pCO2 61 mmHg, and dense right-lower-lobe consolidation on chest x-ray. He was intubated after failing BiPAP and required support with three pressors. Empiric meropenem and trimethoprim-sulfamethoxazole were started, then switched to ampicillin-sulbactam when A. baumannii was identified in blood and sputum. Despite therapy, lactate rose to 15 mmol/L, prompting continuous renal replacement therapy for refractory metabolic acidosis. Platelets fell from 235 to 5 × 109/L (presumed immune thrombocytopenia). CT chest showed persistent consolidation with tree-in-bud opacities. Infectious-disease consultants obtained sulbactam-durlobactam; six doses were given. Final susceptibilities showed resistance to carbapenems and ampicillin-sulbactam, with sensitivity only to aminoglycosides. The patient developed ventricular tachycardia and refractory shock and died after transition to comfort care. Discussion This case demonstrates the relentless course of CRAB pneumonia despite mechanism-directed therapy. Although aminoglycosides were active in vitro and may have transiently controlled bacteremia, they achieve subtherapeutic pulmonary concentrations, limiting source clearance. Durlobactam protects sulbactam from OXA-type enzyme degradation, restoring bactericidal activity and improving outcomes versus colistin (Kaye et al, 2023). Despite escalation, infection persisted, reflecting the narrow therapeutic window once shock and organ failure began. Lack of sulbactam-durlobactam susceptibility testing precluded confirmation of resistance, which may have contributed to failure. Conclusion CRAB pneumonia can cause fulminant lactic acidosis and multiorgan failure despite early recognition and advanced therapy. This case underscores the need for rapid diagnosis, prompt mechanism-based treatment, and realistic prognostication once futility develops. In community hospitals limited access to novel antimicrobials can delay definitive care. Streamlined regional drug-availability networks are vital to improve outcomes in multidrug-resistant infections. This abstract is funded by: None