Background: We used an ultrasensitive, quantitative single molecule array (Simoa) immunoassay to test whether concentrations of Clostridioides (formerly Clostridium) difficile toxins A and/or B in the stool of adult inpatients with C. difficile infection (CDI) were higher than in asymptomatic carriers of toxinogenic C. difficile. Methods: Patients enrolled as CDI-NAAT had clinically significant diarrhea and a positive nucleic acid amplification test (NAAT), per US guidelines, and received CDI treatment. Potential carriers had recently received antibiotics and did not have diarrhea; positive NAAT confirmed carriage. Baseline stool samples were tested by Simoa for toxin A and B. Results: Stool toxin concentrations in both CDI-NAAT (n = 122) and carrier-NAAT (n = 44) cohorts spanned 5 logs (0 pg/mL to >100000 pg/mL). Seventy-nine of 122 (65%) CDI-NAAT and 34 of 44 (77%) carrier-NAAT had toxin A + B concentration ≥20 pg/mL (clinical cutoff). Median toxin A, toxin B, toxin A + B, and NAAT cycle threshold (Ct) values in CDI-NAAT and carrier-NAAT cohorts were similar (toxin A, 50.6 vs 60.0 pg/mL, P = .958; toxin B, 89.5 vs 42.3 pg/mL, P = .788; toxin A + B, 197.2 vs 137.3 pg/mL, P = .766; Ct, 28.1 vs 28.6, P = .354). However, when CDI/carrier cohorts were limited to those with detectable toxin, respective medians were significantly different (A: 874.0 vs 129.7, P = .021; B: 1317.0 vs 81.7, P = .003, A + B, 4180.7 vs 349.6, P = .004; Ct, 25.8 vs 27.7, P = .015). Conclusions: Toxin concentration did not differentiate an individual with CDI from one with asymptomatic carriage. Median stool toxin concentrations in groups with CDI vs carriage differed, but only when groups were defined by detectable stool toxin (vs positive NAAT).
Background: We used an ultrasensitive, quantitative single molecule array (Simoa) immunoassay to test whether concentrations of Clostridioides (formerly Clostridium) difficile toxins A and/or B in the stool of adult inpatients with C. difficileinfection (CDI) were higher than in asymptomatic carriers of toxinogenic C. difficile. Methods:Patients enrolled as CDI-NAAT had clinically significant diarrhea and a positive nucleic acid amplification test (NAAT), per US guidelines, and received CDI treatment. Potential carriers had recently received antibiotics and did not have diarrhea; positive NAAT confirmed carriage. Baseline stool samples were tested by Simoa for toxin A and B. Results: Stool toxin concentrations in both CDI-NAAT (n = 122) and carrier-NAAT (n = 44) cohorts spanned 5 logs (0 pg/mL to >100000 pg/mL). Seventy-nine of 122 (65%) CDI-NAAT and 34 of 44 (77%) carrier-NAAT had toxin A + B concentration ≥20 pg/mL (clinical cutoff). Median toxin A, toxin B, toxin A + B, and NAAT cycle threshold (Ct) values in CDI-NAAT and carrier-NAAT cohorts were similar (toxin A, 50.6 vs 60.0 pg/mL, P = .958; toxin B, 89.5 vs 42.3 pg/mL, P = .788; toxin A + B, 197.2 vs 137.3 pg/mL, P = .766; Ct, 28.1 vs 28.6, P = .354). However, when CDI/carrier cohorts were limited to those with detectable toxin, respective medians were significantly different (A: 874.0 vs 129.7, P = .021; B: 1317.0 vs 81.7, P = .003, A + B, 4180.7 vs 349.6, P = .004; Ct, 25.8 vs 27.7, P = .015). Conclusions: Toxin concentration did not differentiate an individual with CDI from one with asymptomatic carriage. Median stool toxin concentrations in groups with CDI vs carriage differed, but only when groups were defined by detectable stool toxin (vs positive NAAT).
Authors: Dubert M Guerrero; Christina Chou; Lucy A Jury; Michelle M Nerandzic; Jennifer C Cadnum; Curtis J Donskey Journal: Clin Infect Dis Date: 2011-08-01 Impact factor: 9.079
Authors: Christina M Surawicz; Lawrence J Brandt; David G Binion; Ashwin N Ananthakrishnan; Scott R Curry; Peter H Gilligan; Lynne V McFarland; Mark Mellow; Brian S Zuckerbraun Journal: Am J Gastroenterol Date: 2013-02-26 Impact factor: 10.864
Authors: M J T Crobach; T Planche; C Eckert; F Barbut; E M Terveer; O M Dekkers; M H Wilcox; E J Kuijper Journal: Clin Microbiol Infect Date: 2016-07-25 Impact factor: 8.067
Authors: J Origüen; L Corbella; M Á Orellana; M Fernández-Ruiz; F López-Medrano; R San Juan; M Lizasoain; T Ruiz-Merlo; A Morales-Cartagena; G Maestro; P Parra; J Villa; R Delgado; J M Aguado Journal: Clin Microbiol Infect Date: 2017-08-12 Impact factor: 8.067
Authors: Michelle M Riggs; Ajay K Sethi; Trina F Zabarsky; Elizabeth C Eckstein; Robin L P Jump; Curtis J Donskey Journal: Clin Infect Dis Date: 2007-09-04 Impact factor: 9.079
Authors: Timothy D Planche; Kerrie A Davies; Pietro G Coen; John M Finney; Irene M Monahan; Kirsti A Morris; Lily O'Connor; Sarah J Oakley; Cassie F Pope; Mike W Wren; Nandini P Shetty; Derrick W Crook; Mark H Wilcox Journal: Lancet Infect Dis Date: 2013-09-03 Impact factor: 25.071
Authors: Jianling Xie; Gillian A M Tarr; Samina Ali; Linda Chui; Xiao-Li Pang; Bonita E Lee; Otto G Vanderkooi; Phillip I Tarr; Ran Zhuo; Brendon Parsons; Byron M Berenger; Kelly Kim; Stephen B Freedman Journal: J Clin Microbiol Date: 2019-05-24 Impact factor: 5.948
Authors: Marie L Landry; Jeffrey E Topal; Joel Estis; Phoebe Katzenbach; Niamh Nolan; Johanna Sandlund Journal: J Clin Microbiol Date: 2020-01-28 Impact factor: 5.948
Authors: Alice Y Guh; Kelly M Hatfield; Lisa G Winston; Brittany Martin; Helen Johnston; Geoffrey Brousseau; Monica M Farley; Lucy Wilson; Rebecca Perlmutter; Erin C Phipps; Ghinwa K Dumyati; Deborah Nelson; Trupti Hatwar; Marion A Kainer; Ashley L Paulick; Maria Karlsson; Dale N Gerding; L Clifford McDonald Journal: Clin Infect Dis Date: 2019-10-30 Impact factor: 9.079