BACKGROUND: Klebsiella oxytoca was recently shown to be the causative agent of antibiotic-associated hemorrhagic colitis. Because it is unclear whether K. oxytoca also causes nonhemorrhagic antibiotic-associated diarrhea, our study investigated a possible association between K. oxytoca and that disorder. METHODS: A total of 371 consecutive patients were recruited into 4 study groups: (1) group A+D+ (patients who received antibiotics and experienced diarrhea; n = 107), (2) group A+D- (patients who received antibiotics but did not experience diarrhea; np93), (3) group A-D+ (patients who experienced acute-onset diarrhea but did not receive antibiotics; n = 60), and (4) group A-D- (patients without diarrhea who did not receive antibiotics; n = 111). Stool samples were plated on MacConkey agar and K. oxytoca was identified using a standard test kit. Clostridium difficile was detected by a toxin A/B antigen test. K. oxytoca strains were tested for cytotoxicity with use of cell-culture assays. RESULTS: In 15 of 371 stool samples, K. oxytoca strains were isolated during the study period. There was no significant difference in the distribution of K. oxytoca among the 4 study groups. Six of the 15 strains were found to be toxin producing. Three of the toxin-producing strains caused antibiotic-associated hemorrhagic colitis. No case of nonhemorrhagic antibiotic-associated diarrhea due to toxin-producing K. oxytoca was detected. CONCLUSION: K. oxytoca is not the causative agent of nonhemorrhagic antibiotic-associated diarrhea. This is in contrast to the distinct clinical entity of antibiotic-associated hemorrhagic colitis. Testing for K. oxytoca is therefore only warranted for patients who experience bloody diarrhea during antibiotic therapy.
BACKGROUND:Klebsiella oxytoca was recently shown to be the causative agent of antibiotic-associated hemorrhagic colitis. Because it is unclear whether K. oxytoca also causes nonhemorrhagic antibiotic-associated diarrhea, our study investigated a possible association between K. oxytoca and that disorder. METHODS: A total of 371 consecutive patients were recruited into 4 study groups: (1) group A+D+ (patients who received antibiotics and experienced diarrhea; n = 107), (2) group A+D- (patients who received antibiotics but did not experience diarrhea; np93), (3) group A-D+ (patients who experienced acute-onset diarrhea but did not receive antibiotics; n = 60), and (4) group A-D- (patients without diarrhea who did not receive antibiotics; n = 111). Stool samples were plated on MacConkey agar and K. oxytoca was identified using a standard test kit. Clostridium difficile was detected by a toxin A/B antigen test. K. oxytoca strains were tested for cytotoxicity with use of cell-culture assays. RESULTS: In 15 of 371 stool samples, K. oxytoca strains were isolated during the study period. There was no significant difference in the distribution of K. oxytoca among the 4 study groups. Six of the 15 strains were found to be toxin producing. Three of the toxin-producing strains caused antibiotic-associated hemorrhagic colitis. No case of nonhemorrhagic antibiotic-associated diarrhea due to toxin-producing K. oxytoca was detected. CONCLUSION:K. oxytoca is not the causative agent of nonhemorrhagic antibiotic-associated diarrhea. This is in contrast to the distinct clinical entity of antibiotic-associated hemorrhagic colitis. Testing for K. oxytoca is therefore only warranted for patients who experience bloody diarrhea during antibiotic therapy.
Authors: Georg Schneditz; Jana Rentner; Sandro Roier; Jakob Pletz; Kathrin A T Herzog; Roland Bücker; Hanno Troeger; Stefan Schild; Hansjörg Weber; Rolf Breinbauer; Gregor Gorkiewicz; Christoph Högenauer; Ellen L Zechner Journal: Proc Natl Acad Sci U S A Date: 2014-08-25 Impact factor: 11.205
Authors: Laurie R Archbald-Pannone; Timothy L McMurry; Richard L Guerrant; Cirle A Warren Journal: Am J Infect Control Date: 2015-04-24 Impact factor: 2.918
Authors: Martina M Joainig; Gregor Gorkiewicz; Eva Leitner; Paul Weberhofer; Ines Zollner-Schwetz; Irmgard Lippe; Gebhard Feierl; Robert Krause; Thomas Hinterleitner; Ellen L Zechner; Christoph Högenauer Journal: J Clin Microbiol Date: 2010-01-06 Impact factor: 5.948