Talk:Vancomycin-resistant Staphylococcus aureus
From Wikipedia, the free encyclopedia
 |
Vancomycin-resistant Staphylococcus aureus is part of WikiProject Microbiology, which aims to improve Wikipedia's coverage of microbiology and microbiology-related topics. Please work to improve this article, or visit our project page to find other ways of helping. |
||
| Start | This article has been rated as start-Class on the assessment scale. |
||
| High | This article is on a subject of high-importance within microbiology. | ||
|
Article Grading: The article has been rated for quality and/or importance but has no comments yet. If appropriate, please review the article and then leave comments here to identify the strengths and weaknesses of the article and what work it will need. |
|||
 |
This article is within the scope of WikiProject Medicine. Please visit the project page for details or ask questions at the doctor's mess. |
| Start | This page has been rated as Start-Class on the quality assessment scale |
| Mid | This article has been rated as Mid-importance on the importance assessment scale |
[edit] How
How many cases globally to date?
THIRD PARAGRAPH, THIRD LINE DOWN: "deplete the vancomycin available to kill the..." end of sentence. Can someone complete please.
I deleted the paragraph about gylcopeptide resistance and beta-lactam resistance not co-existing in S. aureus because it is untrue. In Michigan, PA, and NY strains have been found that carry both the vanA resistance to glycopeptides as well as mecA resistance to beta-lactam antibiotics. In general this article is confusing and does not accurately explain the two distinic mechanisms of resistance to vancomycin that exist in S.aureus.
[edit] Highly relevant recent research
Michael M. Mwangi et al. (2007-05-21). "Tracking the in vivo evolution of multidrug resistance in Staphylococcus aureus by whole-genome sequencing" (fee required). Proc Natl Acad Sci U S A.. doi:. ISSN 1091-6490. PMID 17517606. Lay summary – Respectful Ignorance (2007-05-24). “The spread of multidrug-resistant Staphylococcus aureus (MRSA) strains in the clinical environment has begun to pose serious limits to treatment options. Yet virtually nothing is known about how resistance traits are acquired in vivo. Here, we apply the power of whole-genome sequencing to identify steps in the evolution of multidrug resistance in isogenic S. aureus isolates recovered periodically from the bloodstream of a patient undergoing chemotherapy with vancomycin and other antibiotics. After extensive therapy, the bacterium developed resistance, and treatment failed. Sequencing the first vancomycin susceptible isolate and the last vancomycin nonsusceptible isolate identified genome wide only 35 point mutations in 31 loci. These mutations appeared in a sequential order in isolates that were recovered at intermittent times during chemotherapy in parallel with increasing levels of resistance. The vancomycin nonsusceptible isolates also showed a 100-fold decrease in susceptibility to daptomycin, although this antibiotic was not used in the therapy. One of the mutated loci associated with decreasing vancomycin susceptibility (the vraR operon) was found to also carry mutations in six additional vancomycin nonsusceptible S. aureus isolates belonging to different genetic backgrounds and recovered from different geographic sites. As costs drop, whole-genome sequencing will become a useful tool in elucidating complex pathways of in vivo evolution in bacterial pathogens.”
I'm not quite sure how to describe it in the wikipedia article; this is a big step in understanding the mechanism and particularly the evolution of vancomycin resistance, but it doesn't reach any final conclusions. 71.41.210.146 16:23, 26 May 2007 (UTC)
