Abstract
Over the past several decades, the overuse of antibiotics leads to the development of multidrug resistance in pathogens. Many bacteria can resist beta-lactam antibiotics by disrupting the beta-lactam ring of the drugs with -lactamase. To counter the effects of -lactamase, scientists have developed -lactamase inhibitors which protect beta-lactam antibiotic from degradation by irreversible binding with -lactamase. Beta-lactamase inhibitors do not exhibit strong antibacterial activity if given alone. Interestingly, it was noted recently that sulbactam, a -lactamase inhibitor, can inhibit growth of Acinetobacterium baumannii, a human opportunistic pathogen, although the mechanism remains not clear. To explore the antibacterial mechanism of sulbactam, this study first isolated sulbactam resistant strains (SRSs) of A. baumannii ATCC 19606, and then determined their minimal inhibitory concentration of sulbactam. These sulbactam-resistant strains grew slower and appeared longer. Comparison of sulbactam affinity to penicillin-binding proteins between ATCC 19606 and SRSs showed no difference. Introduction of pbp1a, pbp1b and pbp3 gene of Pseudomonas aeruginosa PAO1, a sulbactam resistant bacterium, into A. baumannii ATCC 19606 individually did not confer the recipient sulbactam resistance. Sequence analysis of pbp1a, pbp1b and pbp3 gene of A. baumannii ATCC 19606 and its SRSs also revealed no difference. It conclusion, this study is unable to identify a direct role of PBP1a, PBP1b and PBP3 in growth inhibition of A. baumannii by sulbactam.