The bacterial amyloid curli is associated with urinary source bloodstream infection.
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.
Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America ; Center for Women's Infectious Diseases Research, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Chia
C
Hung
Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America ; Center for Women's Infectious Diseases Research, Washington University School of Medicine, St. Louis, Missouri, United States of America ; Department of Infectious Diseases, Bern University Hospital, Bern, Switzerland.
Jonas
J
Marschall
Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America ; Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Carey-Ann D
CA
Burnham
Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America ; Center for Women's Infectious Diseases Research, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Albert S
AS
Byun
Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America ; Center for Women's Infectious Diseases Research, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Jeffrey P
JP
Henderson
D000682:Amyloid / Q000032:analysis / Q000235:genetics*; D016470:Bacteremia / Q000097:blood / Q000150:complications* / Q000382:microbiology / Q000652:urine; D001426:Bacterial Proteins / Q000032:analysis / Q000235:genetics*; D004926:Escherichia coli / Q000235:genetics* / Q000302:isolation & purification / Q000472:pathogenicity; D004927:Escherichia coli Infections / Q000097:blood / Q000150:complications* / Q000382:microbiology / Q000652:urine; D015964:Gene Expression Regulation, Bacterial; D014644:Genetic Variation; D006801:Humans; D013696:Temperature; D014552:Urinary Tract Infections / Q000097:blood / Q000150:complications* / Q000382:microbiology / Q000652:urine
D000682:Amyloid; D001426:Bacterial Proteins; C077481:Crl protein, Bacteria