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The Enterococcus faecalis pathogenicity island (PAI) encodes known virulence traits and > 100 additional genes with unknown roles in enterococcal biology. Phage-related integration and excision genes, and direct repeats flanking the island, suggest it moves as an integrative conjugative element (ICE). However, transfer was observed not to require these genes. Transfer only occurred from donors possessing a pheromone responsive-type of conjugative plasmid, and was invariably accompanied by transfer of flanking donor chromosome sequences. Deletion of plasmid transfer functions, including the cis-acting origin of transfer (oriT), abolished movement. In addition to demonstrating PAI movement by a mechanism involving plasmid integration, we observed transfer of a selectable marker placed virtually anywhere on the chromosome. Transfer of this selectable marker was observed to be accompanied by chromosome-chromosome transfer of vancomycin resistance, MLST markers, and capsule genes as well. Plasmid mobilization therefore appears to be a major mechanism for horizontal gene transfer in the evolution of antibiotic resistant E. faecalis strains capable of causing human infection.

Multidrug-resistant enterococci are leading causes of hospital infection. The antibiotic-perturbed patient gut serves as a staging ground—small numbers of resistant hospital strains colonize and then, greatly amplify in the colon. Little is known of the colonization principles involved—whether hospital strains are competitive or noncompetitive with commensal enterococci or whether mobile elements comprising over 25% of the genome of the former impose significant fitness costs. We unexpectedly found that the prototype vancomycin-resistant Enterococcus faecalis strain V583 was actively killed by fecal organisms, and we traced that to pheromone production by commensal enterococci that trigger lethal mobile element cross-talk. This work highlights the importance of maintaining commensal enterococci in the gut of the hospitalized patient. Multidrug-resistant Enterococcus faecalis possess numerous mobile elements that encode virulence and antibiotic resistance traits as well as new metabolic pathways, often constituting over one-quarter of the genome. It was of interest to determine how this large accretion of mobile elements affects competitive growth in the gastrointestinal (GI) tract consortium. We unexpectedly observed that the prototype clinical isolate strain V583 was actively killed by GI tract flora, whereas commensal enterococci flourished. It was found that killing of V583 resulted from lethal cross-talk between accumulated mobile elements and that this cross-talk was induced by a heptapeptide pheromone produced by native E. faecalis present in the fecal consortium. These results highlight two important aspects of the evolution of multidrug-resistant enterococci: ( i ) the accretion of mobile elements in E. faecalis V583 renders it incompatible with commensal strains, and ( ii ) because of this incompatibility, multidrug-resistant strains sharing features found in V583 cannot coexist with commensal strains. The accumulation of mobile elements in hospital isolates of enterococci can include those that are inherently incompatible with native flora, highlighting the importance of maintaining commensal populations as means of preventing colonization and subsequent infection by multidrug-resistant strains.

The gastrointestinal (GI) tract is a dynamic environment and therefore the stability of the commensal community, or microbiota, is under constant challenge. Microscopic observations have revealed that the majority of bacteria present in the GI tract are not detected using standard culturing techniques, however with the application of culture-independent techniques it has been estimated that between 500 to 1000 bacterial species inhabit the human GI tract. Numerically predominant organisms in the microbiota belong to two eubacterial divisions, the Cytophaga-Flavobacterium-Bacteroides (CFB) and the Firmicutes, and fall into three main groups; Clostridium rRNA subcluster XIVa, Clostridium rRNA subcluster IV and Bacteroides. The prevalence and diversity of bacteria in different areas of the GI tract is influenced by the different conditions at these sites and thus the microbiota of the stomach and jejunum varies with that of the large intestine. Additionally, host genotype, age and diet have all been shown to affect microbial diversity in the GI tract. The distal intestine harbours the highest bacterial cell densities for any known ecosystem. Characterizing the species composition of the healthy microbiota may be a key step in identifying bacterial or associated physiological conditions that are present or absent in an unhealthy microbiota.

Multidrug-resistantEnterococcus faecalispossess numerous mobile elements that encode virulence and antibiotic resistance traits as well as new metabolic pathways, often constituting over one-quarter of the genome. It was of interest to determine how this large accretion of mobile elements affects competitive growth in the gastrointestinal (GI) tract consortium. We unexpectedly observed that the prototype clinical isolate strain V583 was actively killed by GI tract flora, whereas commensal enterococci flourished. It was found that killing of V583 resulted from lethal cross-talk between accumulated mobile elements and that this cross-talk was induced by a heptapeptide pheromone produced by nativeE. faecalispresent in the fecal consortium. These results highlight two important aspects of the evolution of multidrug-resistant enterococci: (i) the accretion of mobile elements inE. faecalisV583 renders it incompatible with commensal strains, and (ii) because of this incompatibility, multidrug-resistant strains sharing features found in V583 cannot coexist with commensal strains. The accumulation of mobile elements in hospital isolates of enterococci can include those that are inherently incompatible with native flora, highlighting the importance of maintaining commensal populations as means of preventing colonization and subsequent infection by multidrug-resistant strains.

Spread of antibiotic resistance among bacteria responsible for nosocomial and community-acquired infections urges for novel therapeutic or prophylactic targets and for innovative pathogen-specific antibacterial compounds. Major challenges are posed by opportunistic pathogens belonging to the low GC% Gram-positive bacteria. Among those, Enterococcus faecalis is a leading cause of hospital-acquired infections associated with life-threatening issues and increased hospital costs. To better understand the molecular properties of enterococci that may be required for virulence, and that may explain the emergence of these bacteria in nosocomial infections, we performed the first large-scale functional analysis of E. faecalis V583, the first vancomycin-resistant isolate from a human bloodstream infection. E. faecalis V583 is within the high-risk clonal complex 2 group, which comprises mostly isolates derived from hospital infections worldwide. We conducted broad-range screenings of candidate genes likely involved in host adaptation (e. g., colonization and/or virulence). For this purpose, a library was constructed of targeted insertion mutations in 177 genes encoding putative surface or stress-response factors. Individual mutants were subsequently tested for their i) resistance to oxidative stress, ii) antibiotic resistance, iii) resistance to opsonophagocytosis, iv) adherence to the human colon carcinoma Caco-2 epithelial cells and v) virulence in a surrogate insect model. Our results identified a number of factors that are involved in the interaction between enterococci and their host environments. Their predicted functions highlight the importance of cell envelope glycopolymers in E. faecalis host adaptation. This study provides a valuable genetic database for understanding the steps leading E. faecalis to opportunistic virulence.

Manson reviews \"Die Oregon-Frage: Amerikanische Expansions-politik und der Pazifische Nordwesten, 1814-1848 (The Oregon question: The Pacific Northwest in the American politics of expansion, 1814-1848)\" by Johannes Eue.

After Leonard became an atheist, he found guidance at St. Paul's and at Cambridge University through classical studies, particularly of Greek culture and its tradition of democracy and freedom. [...]Hebraism and Hellenism contributed to Leonard's \"moral and spiritual evolution\" (188). Leonard's political journey, his work for world peace through international government and the peaceful resolution of conflicts, and his work for a more equitable society that provided opportunities for all citizens, drew him into careers in politics and publishing. [...]Fabian Socialists Sidney and Beatrice Webb recruited Leonard to write a blueprint for international government for the Labour Party.

Janet Manson is an educational consultant and proud parent of five young adults. She is collecting case studies about character education -- how people learn about ethics and morals. If you have a true experience to share, fax it to her at (604) 533-2492. Please include a number where you can be reached.We'd like to hear your voice -- in about 550 words. Mail to Voices, Linda Bates, The Vancouver Sun, 2250 Granville St., Vancouver, B.C. V6H 3G2 or fax 732-2323. In the early morning hours of Jan. 1, my husband and I were driving to Vancouver. My throat was dry and there was a hard knot in the pit of my stomach. A phone call had precipitated this unplanned trip into the city. We picked up our son and my heart cried. His coat was all bloody and his bruised and battered head was neatly bandaged. This was no way to bring in the New Year.