Pediatric oncology and stem cell transplant patients with healthcare‐associated <i>Clostridium difficile</i> infection were already colonized on admission

Al‐Rawahi, Ghada N.; Alnajjar, Abeer A; McDonald, Rachel; Deyell, Rebecca J.; Golding, George R.; Brant, Rollin; Tilley, Peter; Thomas, Eva; Rassekh, Shahrad R.; O’Gorman, Aisling; Wong, Pauline; Turnham, Lucy; Dobson, Simon

doi:10.1002/pbc.27604

Cited by 17 publications

(21 citation statements)

References 22 publications

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“…The increased risk in recipients with a history of prior CDI may reflect increased C difficile colonization or absence of antibodies to the toxin. One study found that asymptomatic colonization with a toxigenic strain of C difficile on admission was predictive of subsequent CDI in pediatric oncology recipients, and almost all the isolates shared identical pulsed‐field gel electrophoresis patterns with the initial colonizing isolate . A retrospective study examining C difficile prophylaxis with oral vancomycin in adult allo‐HCT recipients found no cases of CDI in the 90 recipients who received prophylaxis while 20% of recipients who did not receive prophylaxis developed CDI .…”

Section: Discussionmentioning

confidence: 99%

“…One study found that asymptomatic colonization with a toxigenic strain of C difficile on admission was predictive of subsequent CDI in pediatric oncology recipients, and almost all the isolates shared identical pulsed-field gel electrophoresis patterns with the initial colonizing isolate. 32 A retrospective study examining C difficile prophylaxis with oral vancomycin in adult allo-HCT recipients found no cases of CDI in the 90 recipients who received prophylaxis while 20% of recipients who did not receive prophylaxis developed CDI. 33 Additional studies are needed before recommendations for screening and prevention strategies can be made for recipients with a history of CDI before transplant.…”

Section: Ta B L Ementioning

confidence: 99%

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A multicenter study to define the epidemiology and outcomes of Clostridioides difficile infection in pediatric hematopoietic cell and solid organ transplant recipients

Mayer

Maron

Dallas

et al. 2020

American Journal of Transplantation

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Hematopoietic cell transplant (HCT) and solid organ transplant (SOT) recipients are at increased risk for Clostridioides difficile infection (CDI). We conducted a multicenter retrospective study to describe the incidence of CDI in children transplanted between January 2010 and June 2013. Nested case-control substudies, matched 1:1 by transplant type, institution, patient age, and time of year (quartile) of transplant, identified CDI risk factors. Cohorts included 1496 HCT and 1090 SOT recipients.

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Section: Discussionmentioning

confidence: 99%

Section: Ta B L Ementioning

confidence: 99%

A multicenter study to define the epidemiology and outcomes of Clostridioides difficile infection in pediatric hematopoietic cell and solid organ transplant recipients

Mayer

Maron

Dallas

et al. 2020

American Journal of Transplantation

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“…Because of the ubiquity of C. difficile spores in the environment, focusing on ways to increase the resilience of the host to colonization is one important prevention strategy. However, modulation of host factors that influence virulence of C. difficile already present in the gut is also a key aspect of prevention, as CDI is often caused by C. difficile that is already residing in the gut before the onset of symptomatic CDI rather than acquisition of a new infection (3) .…”

Section: Discussionmentioning

confidence: 99%

“…As discussed above, a fiber-deficient diet has been shown to hinder clearance of C. difficile after challenge (15) . This is particularly relevant in a clinical context as recent studies of both pediatric and adult oncology patients have shown asymptomatic colonization rates with C. difficile of ∼30% and ∼10%, respectively (3, 31) . Further, in pediatric patients it was demonstrated that the vast majority of “hospital-acquired” CDI may be caused by a strain of C. difficile that is present at admission rather than a strain acquired during the patient stay (3) .…”

Section: Discussionmentioning

confidence: 99%

“…These prevention approaches treat CDI as a traditional communicable infection. However, recent data suggests that CDI is often caused by the activation of strains that were already carried in the gut prior to hospital admission and prior to the onset of symptoms rather than by acquisition of a hospital-resident strain (3) . Thus, determining strategies to reduce C. difficile carriage and attenuate CDI severity is critical.…”

Section: Introductionmentioning

confidence: 99%

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Dietary fat promotes antibiotic-induced Clostridioides difficile mortality in mice

Hazleton

Martin

Arnolds

et al. 2019

Preprint

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One Sentence Summary: High dietary fat promoted mortality in a mouse model of antibiotic-17 induced C. difficile infection and low dietary fiber caused higher microbiome disturbance upon 18 broad-spectum antibiotic exposure, suggesting that diets low in fat and high in fiber may protect 19 against C. difficile pathogenesis.Abstract: Clostridoides difficile infection (CDI) is a leading cause of hospital-acquired diarrhea 22 and there has been a steady increase in the number of new infections, emphasizing the 23 importance of novel prevention strategies. Use of broad-spectrum antibiotics and disruption of 24 the intestinal microbiome is one of the most important risk factors of CDI. We used a murine 25 model of antibiotic-induced CDI to investigate the relative contributions of high dietary fat and 26 low dietary fiber on disease pathogenesis. We found that high fat, but not low fiber resulted in 27 increased mortality from CDI (HR 4.95) and increased levels of C. difficile toxin production 28 compared to a regular low-fat/high-fiber mouse diet even though we did not observe a significant 29 change in C. difficile carriage. The high-fat diet also increased levels of primary bile acids 30 known to be germination factors for C. difficile spores. Mice fed low-fat/low-fiber diets did not 31 show increased CDI pathogenesis, but did have a larger antibiotic-induced gut microbiome 32 disturbance compared to mice fed a high-fiber diet, characterized by a greater decrease in alpha 33 diversity. This microbiome disturbance was associated with a loss of secondary bile acids and 34 short chain fatty acids, which are both microbial metabolic products previously shown to protect 35 against CDI. These data suggest that a low-fiber diet contributes to antibiotic-induced dysbiosis, 36 while a high-fat diet promotes CDI pathogenesis. These findings indicate that dietary 37 interventions that increase fiber and decrease fat may be an effective prevention strategy for 38 individuals at high risk of CDI. 39 40 41Clostridoides difficile infection (CDI) is an important cause of morbidity and mortality, 42 with 500,000 cases every year causing 30,000 deaths per year in the US alone (1). Alarmingly, 43 there has been a steady increase in the number of new infections in spite of prevention efforts in 44 hospitals that have focused largely on increased sanitation and antibiotic stewardship (2). These 45 prevention approaches treat CDI as a traditional communicable infection. However, recent data 46 suggests that CDI is often caused by the activation of strains that were already carried in the gut 47 prior to hospital admission and prior to the onset of symptoms rather than by acquisition of a 48 hospital-resident strain (3). Thus, determining strategies to reduce C. difficile carriage and 49 attenuate CDI severity is critical. 50A complex gut microbiome has been shown to be protective against CDI (4). Broad 51 spectrum antibiotic usage, such as clindamycin, beta-lactams, and fluoroquinolones (5, 6) 52 increase risk of CDI as d...

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Prevalence of Detection of Clostridioides difficile Among Asymptomatic Children

et al. 2021

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IMPORTANCE Detection of Clostridioides difficile has frequently been described in asymptomatic infants and children, but accurate estimates across the age spectrum are unavailable. OBJECTIVE To assess the prevalence of C difficile detection among asymptomatic children across the age spectrum. DATA SOURCES This systematic review and meta-analysis included a search of the Cochrane Central Register of Controlled Trials, MEDLINE, Embase, CINAHL, Scopus, and Web of Science for articles published from January 1, 1990, to December 31, 2020. Search terms included Clostridium difficile, Peptoclostridium difficile, Clostridioides difficile, CDF OR CDI OR c diff OR c difficile, Clostridium infections OR cd positive diarrhea OR cd positive diarrhea OR Clostridium difficile OR Peptoclostridium difficile OR pseudomembranous colitis OR pseudomembranous enterocolitis, enterocolitis, and pseudomembranous. These were combined with the following terms: bacterial colonization and colonization OR colonized OR colonizing OR epidemiology OR prevalence OR seroprevalence. STUDY SELECTION Studies were screened independently by 2 authors. Studies were included if they reported testing for C difficile among asymptomatic children (ie, children without diarrhea) younger than 18 years.DATA EXTRACTION AND SYNTHESIS Data were extracted independently and in duplicate by 2 reviewers. Preferred Reporting Items for a Systematic Review and Meta-analysis (PRISMA) guidelines were used. Data were pooled using a random-effects model. MAIN OUTCOMES AND MEASURESThe primary outcome was prevalence of C difficile detection among asymptomatic children. Secondary outcomes included prevalence of toxigenic vs nontoxigenic strains of C difficile and prevalence of C difficile detection stratified by geographic region, income status, testing method, and year of testing. RESULTS A total of 95 studies with 19 186 participants were included. Rates of detection of toxigenic or nontoxigenic C difficile were greatest among infants aged 6 to 12 months (41%; 95% CI, 32%-50%) and decreased to 12% (95% CI, 7%-18%) among children aged 5 to 18 years. The prevalence of toxigenic C difficile colonization was lower, peaking at 14% (95% CI, 8%-21%) among infants aged 6 to 12 months and decreasing to 6% (95% CI, 2%-11%) among children older than 5 years. Although prevalence differed by geographic region (ie, North and South America vs Europe: β, −0.151, P = .001; North and South America vs Western Pacific: β, 0.136, P = .007), there was no difference by testing method (ie, culture vs polymerase chain reaction: β, 0.069, P = .052; culture vs enzyme immunoassay: β, −0.178, P = .051), income class (low-middle income vs high income: β, −0.144, P = .23; upper-middle vs high income: β, −0.020,

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Pediatric oncology and stem cell transplant patients with healthcare‐associated Clostridium difficile infection were already colonized on admission

Cited by 17 publications

References 22 publications

A multicenter study to define the epidemiology and outcomes of Clostridioides difficile infection in pediatric hematopoietic cell and solid organ transplant recipients

A multicenter study to define the epidemiology and outcomes of Clostridioides difficile infection in pediatric hematopoietic cell and solid organ transplant recipients

Dietary fat promotes antibiotic-induced Clostridioides difficile mortality in mice

Prevalence of Detection of Clostridioides difficile Among Asymptomatic Children

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