The Journal of antimicrobial chemotherapy · 2005
Colicins prevent colonization of urinary catheters.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПоддержка правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
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Trautner Barbara W, Hull Richard A, Darouiche Rabih O
Аннотация
OBJECTIVES: Natural microbial defence systems, such as bacteriocins, may be a novel means to prevent catheter-associated urinary tract infection. We investigated in vitro whether a colicin-expressing strain of Escherichia coli could prevent urinary catheter colonization by a colicin-susceptible, uropathgenic strain of E. coli.
METHODS: Segments of urinary catheter were inoculated with colicin-producing E. coli K-12 and then exposed to either colicin-susceptible E. coli (a uropathogenic clinical isolate) or colicin-resistant E. coli (derived from the susceptible clinical isolate). Catheters were then incubated overnight, rinsed and sonicated.
RESULTS: The presence of colicin-producing E. coli K-12 on the catheter surface completely prevented catheter colonization by colicin-susceptible E. coli but not by resistant E. coli. The colicin-susceptible strain but not the colicin-resistant strain also disappeared from broth cultures in the presence of colicin-producing E. coli K-12.
CONCLUSIONS: The observed inhibition of catheter colonization by the uropathogenic clinical isolate of E. coli can be attributed to the presence of a colicin-producing strain of E. coli on the catheter surface. Bacteriocin production by a non-pathogenic organism may have clinical applicability as a means to prevent catheter-associated urinary tract infection.
METHODS: Segments of urinary catheter were inoculated with colicin-producing E. coli K-12 and then exposed to either colicin-susceptible E. coli (a uropathogenic clinical isolate) or colicin-resistant E. coli (derived from the susceptible clinical isolate). Catheters were then incubated overnight, rinsed and sonicated.
RESULTS: The presence of colicin-producing E. coli K-12 on the catheter surface completely prevented catheter colonization by colicin-susceptible E. coli but not by resistant E. coli. The colicin-susceptible strain but not the colicin-resistant strain also disappeared from broth cultures in the presence of colicin-producing E. coli K-12.
CONCLUSIONS: The observed inhibition of catheter colonization by the uropathogenic clinical isolate of E. coli can be attributed to the presence of a colicin-producing strain of E. coli on the catheter surface. Bacteriocin production by a non-pathogenic organism may have clinical applicability as a means to prevent catheter-associated urinary tract infection.