Journal of clinical pathology · 2010
In vitro susceptibility of Clostridium difficile to rifaximin and rifampin in 359 consecutive isolates at a university hospital in Houston, Texas.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Jiang Z-D, DuPont H L, La Rocco M, Garey K W
Аннотация
AIM: This was an in vitro study to analyse the susceptibility of Clostridium difficile isolates to rifampin and rifaximin.
METHODS: Stool samples from patients who had nosocomial diarrhoea and C difficile toxin B at a university hospital between August 2006 and December 2007 were cultured for C difficile. Susceptibility of C difficile isolates to rifaximin and rifampin was determined by agar dilution and E strips, respectively. C difficile isolates were analysed via PCR for genes encoding toxins A and B, for binary toxin (BT), and for partial deletions of the tcdC gene (tcdC-del).
RESULTS: Rifaximin exhibited high-level activity against 359 C difficile isolates, with MIC(50) <0.01 microg/ml and MIC(90) 0.25 microg/ml; rifampin had MIC(50) <0.002 microg/ml and MIC(90) 4 microg/ml. Among isolates analysed, 55 (15%) were positive for BT and tcdC-del. 28 (8% of 359) isolates were resistant to rifampin (> or = 32 microg/ml), of which 6 (2% of 359) were resistant to rifaximin and rifampin with MIC values > or = 32 microg/ml. 2 of the 28 isolates resistant to rifampin were A(+)/B(+)/BT(+)/tcdC-del(+), 5 were A(+)/B(+)/BT(-)/tcdC-del(+), 4 were A(+)/B(+)/BT(+)/tcdC-del(-), 13 were A(+)/B(+)/BT(-)/tcdC-del(-), and 4 had no detectable toxin genes. Of the 11 isolates resistant to rifaximin alone, 1 was A(+)/B(+)/BT(-)/tcdC-del(+), 2 were A(+)/B(+)/BT(+)/tcdC-del(-), 6 were A(+)/B(+)/BT(-)/tcdC-del(-), and 2 had no detectable toxin genes.
CONCLUSIONS: The study demonstrates that rifaximin has high-level activity against C difficile in vitro. Determination of resistance to rifampin by E strip did not predict rifaximin resistance.
METHODS: Stool samples from patients who had nosocomial diarrhoea and C difficile toxin B at a university hospital between August 2006 and December 2007 were cultured for C difficile. Susceptibility of C difficile isolates to rifaximin and rifampin was determined by agar dilution and E strips, respectively. C difficile isolates were analysed via PCR for genes encoding toxins A and B, for binary toxin (BT), and for partial deletions of the tcdC gene (tcdC-del).
RESULTS: Rifaximin exhibited high-level activity against 359 C difficile isolates, with MIC(50) <0.01 microg/ml and MIC(90) 0.25 microg/ml; rifampin had MIC(50) <0.002 microg/ml and MIC(90) 4 microg/ml. Among isolates analysed, 55 (15%) were positive for BT and tcdC-del. 28 (8% of 359) isolates were resistant to rifampin (> or = 32 microg/ml), of which 6 (2% of 359) were resistant to rifaximin and rifampin with MIC values > or = 32 microg/ml. 2 of the 28 isolates resistant to rifampin were A(+)/B(+)/BT(+)/tcdC-del(+), 5 were A(+)/B(+)/BT(-)/tcdC-del(+), 4 were A(+)/B(+)/BT(+)/tcdC-del(-), 13 were A(+)/B(+)/BT(-)/tcdC-del(-), and 4 had no detectable toxin genes. Of the 11 isolates resistant to rifaximin alone, 1 was A(+)/B(+)/BT(-)/tcdC-del(+), 2 were A(+)/B(+)/BT(+)/tcdC-del(-), 6 were A(+)/B(+)/BT(-)/tcdC-del(-), and 2 had no detectable toxin genes.
CONCLUSIONS: The study demonstrates that rifaximin has high-level activity against C difficile in vitro. Determination of resistance to rifampin by E strip did not predict rifaximin resistance.