No abstract

A recent outbreak of multiresistant strains of Acinetobacter calcoaceticus biotype anitratus was observed mostly, but not exclusively, in the surgical intensive care unit in our hospital. Disk diffusion and microdilution susceptibility studies demonstrated resistance to imipenem, all aminoglycosides, and all individual beta-lactam antibiotics. Only ampicillin plus sulbactam, cefoperazone plus sulbactam, and polymyxin produced zone sizes and MICs in the susceptible ranges. Determination of MICs and MBCs demonstrated that sulbactam was the antimicrobial agent responsible for the killing of these organisms. Nine of 10 patients who were infected with imipenem-resistant Acinetobacter strains and received ampicillin plus sulbactam for > 3 days improved clinically, and in many cases organisms were eradicated from the site of isolation.

We have encountered clinical isolates of Acinetobacter baumannii which are resistant to all available antibiotics used in hospitals except for polymyxin B and the beta‐lactamase inhibitor, sulbactam. To investigate the mechanisms of this unique activity, affinities of sulbactam and other beta‐lactamase inhibitors for penicillin binding proteins were compared using imipenem‐resistant and imipenem‐sensitive isolates. The results of competition binding experiments indicate that all three beta‐lactamase inhibitors bound to imipenem‐susceptible Acinetobacter. Binding of sulbactam was greater than that of tazobactam and not detected with clavulanic acid to penicillin binding proteins of the imipenem‐resistant strain of Acinetobacter.