Multi-drug-resistant Staphylococcus aureus and future chemotherapy

J Infect Chemother. 2014 Oct;20(10):593-601. doi: 10.1016/j.jiac.2014.08.001. Epub 2014 Aug 27.

Abstract

Staphylococcus (S.) aureus silently stays as our natural flora, and yet sometimes threatens our life as a tenacious pathogen. In addition to its ability to outwit our immune system, its multi-drug resistance phenotype makes it one of the most intractable pathogenic bacteria in the history of antibiotic chemotherapy. It conquered practically all the antibiotics that have been developed since 1940s. In 1961, the first MRSA was found among S. aureus clinical isolates. Then MRSA prevailed throughout the world as a multi-resistant hospital pathogen. In 1997, MRSA strain Mu50 with reduced susceptibility to vancomycin was isolated. Vancomycin-intermediate S. aureus (VISA), so named according to the CLSI criteria, was the product of adaptive mutation of S. aureus against vancomycin that had long been the last resort to MRSA infection. Here, we describe the genetic basis for the remarkable ability of S. aureus to acquire multi-antibiotic resistance, and propose a novel paradigm for future chemotherapy against the multi-resistant pathogens.

Keywords: MRSA; Reverse antibiotic (RA); SCCmec; mecA; rpoB; sVISA.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Anti-Bacterial Agents / therapeutic use*
  • Bacterial Proteins / genetics
  • DNA-Directed RNA Polymerases / genetics
  • Drug Resistance, Multiple, Bacterial / genetics*
  • Humans
  • Origin Recognition Complex / genetics
  • Penicillin-Binding Proteins
  • Phenotype
  • Staphylococcal Infections / drug therapy*
  • Staphylococcus aureus / drug effects
  • Staphylococcus aureus / genetics*

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • OriC chromosomal replication origin
  • Origin Recognition Complex
  • Penicillin-Binding Proteins
  • mecA protein, Staphylococcus aureus
  • DNA-Directed RNA Polymerases
  • RNA polymerase beta subunit