title: Multi-drug-resistant Staphylococcus aureus and future chemotherapy.
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.
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan. Electronic address: khiram06@juntendo.ac.jp.
authors.forename: K
authors.initials: K
authors.lastname: Hiramatsu
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Katayama
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Matsuo
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sasaki
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Morimoto
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Sekiguchi
authors.affiliation: Research Center for Infection Control Science, Juntendo University, 2-1-1 Hongo, Bunkyo-Ku, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Baba
mesh_terms: D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D001426:Bacterial Proteins / Q000235:genetics; D012321:DNA-Directed RNA Polymerases / Q000235:genetics; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics*; D006801:Humans; D051738:Origin Recognition Complex / Q000235:genetics; D046915:Penicillin-Binding Proteins; D010641:Phenotype; D013203:Staphylococcal Infections / Q000188:drug therapy*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000235:genetics*
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; C114650:OriC chromosomal replication origin; D051738:Origin Recognition Complex; D046915:Penicillin-Binding Proteins; C487789:mecA protein, Staphylococcus aureus; D012321:DNA-Directed RNA Polymerases; C105078:RNA polymerase beta subunit
keywords: MRSA; Reverse antibiotic (RA); SCCmec; mecA; rpoB; sVISA