That is one of the conclusions reached by scientists at The Institute for Genomic Research (TIGR), which sequenced and analyzed the complete genome of E. faecalis V583, a strain of the opportunistic pathogen that is resistant to the antibiotic vancomycin. That strain was first isolated at a St. Louis hospital in 1987.
The results of this work, supported by the National Institute of Allergy and Infectious Diseases (NIAID), are published in a paper in this weeks issue of Science.
Ian Paulsen, Ph.D., the TIGR researcher who is the first author of the Science paper, says the genome analysis found that mobile elements small segments of DNA that can jump between organisms or their chromosomes appear to play an important role in helping the bacterium quickly develop drug resistance.
The TIGR analysis found that nearly a third of the E. faecalis genome which encompasses more than 3.2 million DNA base pairs consists of mobile or foreign DNA Thats an unusually high percentage of mobile elements in a microbial genome, said Paulsen.
Those mobile elements include three plasmids in the bacterium and multiple remnants of phage, plasmids, and other mobile elements, including transposons and a pathogenicity island located on its single chromosome. Scientists identified two sites in the genome that are related to vancomycin resistance or tolerance.
One of those sites, Paulsen said, appears to be a newly-identified vancomycin resistance transposon, carrying vanB resistance genes. A transposon is a mobile element that can jump from one part of a chromosome to another, or from a chromosome in one organism to that of another organism sometimes carrying along genes that encode for drug-resistance. In the case o
Contact: Robert Koenig
The Institute for Genomic Research