ABSTRACT
Optimizing antimicrobial use should be viewed as a strategy to minimize the development and dissemination of resistant organisms in general, and as a complementary partner to infection control efforts. The methods for prevention and treatment of infection due to resistant organisms are hindered by the many complexities associated with “bug-drug-host” interactions that are not easily measured. This chapter discusses some of those complexities, the diversity of betalactamases found among organisms causing clinical infection that have limited the use of many cephalosporins, and collateral resistance issues contributing to some of their demises. Extended-spectrum beta-lactamases, first described in Germany, followed the introduction of cefotaxime to clinical use, and these enzymes are mutant plasmid-mediated derivatives of the basic and well-described TEM-1 and -2 as well as SHV-1 penicillinases. Cefazolin is a traditional workhorse cephalosporin that has the benefit of a narrow spectrum of activity, an inexpensive purchase price, and an every-8-hour dosing schedule.
