Tim Du

Publications (3)9.76 Total impact

• Article: Emergence of Clostridium difficile NAP1 in Latin America.

  Carlos Quesada-Gómez, César Rodríguez, María del Mar Gamboa-Coronado, Evelyn Rodríguez-Cavallini, Tim Du, Michael R Mulvey, Manuel Villalobos-Zúñiga, Ricardo Boza-Cordero
  [show abstract] [hide abstract]
  ABSTRACT: The NAP1 and NAP2 strains of Clostridium difficile have been linked to nosocomial outbreaks of antibiotic-associated diarrhea (AAD) and pseudo-membranous colitis in North American and European countries (4, 5)....
  Journal of clinical microbiology 11/2009; 48(2):669-70. · 4.16 Impact Factor
• Source

  Available from: Michael Richard Mulvey

  Article: VanG-type vancomycin-resistant Enterococcus faecalis strains isolated in Canada.

  David A Boyd, Tim Du, Romeo Hizon, Brynn Kaplen, Travis Murphy, Shaun Tyler, Shirley Brown, Frances Jamieson, Karl Weiss, Michael R Mulvey
  [show abstract] [hide abstract]
  ABSTRACT: Enterococcus faecalis G1-0247 (vancomycin MIC, 16 microg/ml) was found to harbor a vanG operon 99% identical to the vanG operon in E. faecalis BM4518. E. faecalis N03-0233 (vancomycin MIC, 16 microg/ml) was found to harbor a novel vanG operon, vanG2, on an element in a different chromosomal location than the vanG-harboring elements in G1-0247 and BM4518.
  Antimicrobial Agents and Chemotherapy 07/2006; 50(6):2217-21. · 4.84 Impact Factor
• Article: Translocation of Clostridium difficile toxin B across polarized Caco-2 cell monolayers is enhanced by toxin A.

  Tim Du, Michelle J Alfa
  [show abstract] [hide abstract]
  ABSTRACT: Clostridium difficile is the etiological agent of antibiotic-associated diarrhea; the most common form of nosocomial infectious diarrhea. The basis for the shock-like systemic symptoms observed in severe cases of this infection are not known. It is hypothesized that the invasion of C difficile toxins A and/or B from the gut mucosa may contribute to these symptoms.A polarized tissue culture model employing Caco-2 cells grown on transwell inserts was established to study the translocation of purified C difficile toxins A and B. C difficile toxins were (125)I labelled and inoculated onto confluent polarized Caco-2 cell monolayers to study translocation dynamics. Electrical resistance measurements were used to monitor monolayer confluence and tight junction integrity. Samples were taken from the apical and basal sides of the insert, as well as the insert itself, and tested using the human foreskin fibroblasts cell cytotoxicity assay to monitor partitioning of the radiolabelled toxins. Toxin A produced a 50% reduction in electrical resistance in 3 h whereas the same concentration of toxin B required at least 7 h to achieve the same effect. Both toxins A and B were able to translocate across confluent monolayers of Caco-2 cells. The combination of toxin A and B together was synergistic with respect to promoting the translocation of toxin B. Although the addition of toxin A resulted in a 100% increase in the amount of toxin B able to translocate, no increases in toxin A translocation were observed. These findings suggest a model of pathogenesis in which C difficile toxin A facilitates the translocation of toxin B from the gut into submucosal areas where it may play a role in inflammatory damage.
  The Canadian journal of infectious diseases = Journal canadien des maladies infectieuses 04/2004; 15(2):83-8. · 0.76 Impact Factor