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The Bacterial Amyloid Curli Is Associated with Urinary Source Bloodstream Infection
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Details:
  • Pubmed ID:
    24465838
  • Pubmed Central ID:
    PMC3896446
  • Funding:
    5K12HD001459-13/HD/NICHD NIH HHS/United States
    DK064540-09/DK/NIDDK NIH HHS/United States
    HD001459-09/HD/NICHD NIH HHS/United States
    KL2 TR000450/TR/NCATS NIH HHS/United States
    KL2RR024994/RR/NCRR NIH HHS/United States
    P50 DK064540/DK/NIDDK NIH HHS/United States
    U54 CK000162/CK/NCEZID CDC HHS/United States
    UL1 TR000448/TR/NCATS NIH HHS/United States
    UL1RR024992/RR/NCRR NIH HHS/United States
  • Document Type:
  • Collection(s):
  • Description:
    Urinary tract infections are the most common cause of E. coli bloodstream infections (BSI) but the mechanism of bloodstream invasion is poorly understood. Some clinical isolates have been observed to shield themselves with extracellular amyloid fibers called curli at physiologic temperature. We hypothesize that curli fiber assembly at 37 °C promotes bacteremic progression by urinary E. coli strains. Curli expression by cultured E. coli isolates from bacteriuric patients in the presence and absence of bacteremia were compared using Western blotting following amyloid fiber disruption with hexafluoroisopropanol. At 37 °C, urinary isolates from bacteremic patients were more likely to express curli than those from non-bacteremic patients [16/22 (73%) vs. 7/21 (33%); p = 0.01]. No significant difference in curli expression was observed at 30 °C [86% (19/22) vs. 76% (16/21); p = 0.5]. Isolates were clonally diverse between patients, indicating that this phenotype is distributed across multiple lineages. Most same-patient urine and blood isolates were highly related, consistent with direct invasion of urinary bacteria into the bloodstream. 37 °C curli expression was associated with bacteremic progression of urinary E. coli isolates in this population. These findings suggest new future diagnostic and virulence-targeting therapeutic approaches.