Unveiling of genetic basis of resistance of S aureus to antibiotics

• Published in: The Lancet (British edition) 2001-04, Vol.357 (9264), p.1218-1219
• Main Authors: Ala'Aldeen, Dlawer AA, Grundmann, Hajo
• Format: Article
• Language: English
• Subjects: Antibiotic resistance; Antibiotics; Bacteria; Bacterial diseases; Biological and medical sciences; Drug resistance; Drug Resistance, Microbial - genetics; Genetics; Genome, Bacterial; Human bacterial diseases; Human populations; Infections; Infectious diseases; Medical research; Medical sciences; Minority & ethnic groups; Pathogens; Public health; Staphylococcal infections, streptococcal infections, pneumococcal infections; Staphylococcus aureus - genetics
• ISSN: 0140-6736; 1474-547X
• DOI: 10.1016/S0140-6736(00)04447-0

When Sir Alexander Ogston (1844-1929), a Scottish surgeon and amateur microbiologist, spotted what is now known as Staphylococcus aureus during microscopical examination of pus from the leg of a young man he wrote "My delight may be conceived when there were revealed to me beautiful tangles, tufts, and chains of round organisms in great numbers which stood out clear and distinct among the pus cells and debris".1 S aureus continues to evoke wonder. It is one of the most successful human pathogens. It is carried by about 30% of the healthy human population of all ethnic groups, its natural habitat being the anterior nares and the skin. Despite its predominantly benign lifestyle, S aureus has a formidable pathogenic potential. Carriers are at greater risk of developing clinical manifestations, and the highest burden of disease is among those aged 65 years or over. Before antibiotics became available, 80% of invasive bloodstream infections were invariably fatal,2 and now the most challenging public-health issue related to S aureus infections is the continuous dissemination of strains resistant to meticillin and other antibiotics. Glycopeptides (such as vancomycin and teicoplanin) became the mainstay of treatment of invasive diseases due to meticillin-resistant S aureus (MRSA) until the arrival of strains of reduced susceptibility to glycopeptides.3 A concern is that strains resistant to all antistaphylococcal agents may soon become prevalent.3-5 Underlying this concern is insufficient knowledge about the organism's genetic regulation and evolution or its interaction with the various hosts. The report in today's Lancet by Makoto Kuroda and colleagues of their analysis (panel) of two genome sequences, one of an MRSA strain (N315) and the other of a vancomycin-resistant strain (VRSA, Mu 50), is a major contribution to the understanding of the molecular evolution of antibiotic resistance of this important pathogen.