A brief review of medicine's war with Staphylococcus aureus during the past 4 decades reveals a remarkable sequence of survival through adaptation [1]. Although S. aureus was apparently defeated in the 1940s by penicillin (despite Sir Alexander Fleming's initial warning about eventual drug resistance from overuse and misuse [2]), a strain of S. aureus was rearmed within a decade with the resistance gene mecA, determinant of a unique penicillin-binding protein, PBP2A [3]. Carried in a unique molecular vector called the staphylococcal chromosomal cassette (SCCmec), the gene seems to have evolved from a domestic gene of the fully β-lactam-susceptible Staphylococcus sciuri, a colonizer of both wild and domestic animals [3]. Although the mortality associated with S. aureus infection decreased after the introduction of penicillinase-resistant methicillin, this resistant S. aureus clone spread extensively in hospitals for over 17 years as a single clonal type [4]. Then new clones with different genetic backgrounds that carry a variety of different SCCmec types (mainly I, II, and III) began to appear and to spread globally, resulting in the worldwide epidemic of nosocomial or health care—associated (HA) methicillin-resistant S. aureus (MRSA).
No takes yet. Share an insight, caveat, or question.
Tice et al. (2010) studied this question.
Synapse has enriched 5 related papers. Consider them for comparative context: