Introduction: Solving the Clinical Problem of Vancomycin Resistance

Vancomycin was isolated by scientists at Eli Lilly and Company (Lilly) in the mid-1950s from a soil sample obtained in the interior jungle of Borneo. The organism producing vancomycin was identified as a Streptomyces species (now known as Streptomyces orientalis, subsequently renamed Amycolatopsis orientalis) [1]. Because of the rapid emergence of penicillin resistance in staphylococci, the drug, which has an outstanding spectrum of activity against Gram-positive cocci, including staphylococci, streptococci and enterococci, was rapidly approved by the United States Food and Drug Administration. Nonetheless, it was not widely used by clinicians, because it was perceived to have significant oto- and nephrotoxicity. As it turns out, much of this toxicity may have been due to impurities in the original preparations (dubbed “Mississippi mud” because of the brown-black color of the powder) [2]. Methicillin and the other antistaphylococcal penicillins were developed concomitantly and were much more widely used by clinicians, who considered them safer and at least equally efficacious drugs for staphylococcal infections.