Nosocomial
Return to Library
Research from SUNY Downstate Medical Center, Department of Medicine reveals new findings on pneumonia therapy
2009 JUL 27 - (NewsRx.com) -- A new study, 'Correlation of the expression of acrB and the regulatory genes marA, soxS and ramA with antimicrobial resistance in clinical isolates of Klebsiella pneumoniae endemic to New York City,' is now available. According to recent research from the United States, "Nosocomial isolates of Klebsiella pneumoniae resistant to all commonly used antimicrobial agents have emerged in many regions of the world. It is unknown if efflux systems contribute to the multidrug resistance phenotype." "The expression of genes encoding the efflux pump AcrAB and the global regulators MarA, SoxS and RamA were examined and correlated with antimicrobial resistance. Twenty isolates belonged to the two important clones representing KPC-possessing strains endemic to our region. Virtually all of these isolates had negligible or absent expression of the genes, and resistance to fluoroquinolones and aminoglycosides could be explained by alternative mechanisms. All of these isolates were susceptible to tigecycline. A group of 14 heterogeneous isolates was also examined. There was a correlation between expression of marA with expression of soxS. Only expression of soxS was significantly correlated with expression of acrB. With a background substitution in GyrA, increased expression of acrB and marA appeared to contribute to fluoroquinolone resistance in some isolates. A correlation was noted between expression of soxS and ramA (but not marA and acrB) and tigecycline MICs. Following in vitro exposure to tigecycline, resistance occurred in association with a marked increase in marA and acrB expression in isolates lacking expression of soxS and ramA. While laboratory-derived tigecycline resistance was associated with increased acrB expression, the variation in tigecycline MICs in clinical isolates was associated only with selected regulator genes," wrote S. Bratu and colleagues, SUNY Downstate Medical Center, Department of Medicine. The researchers concluded: "It appears that other mechanisms beyond activation of the acrAB system mediate tigecycline resistance." Bratu and colleagues published their study in the Journal of Antimicrobial Chemotherapy (Correlation of the expression of acrB and the regulatory genes marA, soxS and ramA with antimicrobial resistance in clinical isolates of Klebsiella pneumoniae endemic to New York City. Journal of Antimicrobial Chemotherapy, 2009;64(2):278-83). For additional information, contact S. Bratu, SUNY Downstate Medical Center, Dept. of Medicine, Brooklyn, NY USA.. Publisher contact information for the Journal of Antimicrobial Chemotherapy is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England. Keywords: United States, Brooklyn, Pneumonia Therapy, Anti-Infectives, Antibiotic, Antimicrobial Resistance, Antimicrobials, Chemotherapy, Drug Development, Drug Resistance, Drug Therapy, Drugs, Infectious Disease, Klebsiella pneumoniae, Nosocomial Infection, Pneumonia, Pulmonology, Therapy, Tigecycline, Treatment. This article was prepared by Anti-Infectives Week editors from staff and other reports. Copyright 2009, Anti-Infectives Week via NewsRx.com.
|
