Epidemiology of Clostridium difficile Colonization in Newborns: Results Using a Bacteriophage and Bacteriocin Typing System

Bacon, Alfred E.; Fekety, Robert; Schaberg, Dennis R.; Faix, Roger G.

doi:10.1093/infdis/158.2.349

Cited by 53 publications

(36 citation statements)

References 18 publications

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“…This result is consistent with those of previous studies in European and North-American countries, where asymptomatic carriage rates in infants under 2 years of age were found to be high, varying from 24 to 75 % (Bacon et al, 1988;Brazier, 1998;Collignon et al, 1993;Matsuki et al, 2005;Rexach et al, 2006;Tullus et al, 1989;Yamamoto-Osaki et al, 1994). The great variability observed in carriage rates corresponds to the 0-1 year period, while at the age of 2 years, colonization is about 37-46 % regardless of the study (Collignon et al, 1993;Matsuki et al, 2005;Torres et al, 1984;Yamamoto-Osaki et al, 1994).…”

Section: Discussionsupporting

confidence: 93%

Prevalence and diversity of Clostridium difficile strains in infants

Rousseau

Lemée

Monnier

et al. 2011

Journal of Medical Microbiology

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During early infancy asymptomatic intestinal colonization by Clostridium difficile is frequent. To update information on infant colonization prevalence and to characterize infant strains, in terms of their virulence factors and their phylogenetic diversity, a prospective screening of C. difficile in the stools of infants 0 to 2 years old was conducted at Jean Verdier Hospital (Hô pital Jean Verdier) over an 18 month period. C. difficile was screened by toxigenic culture, and molecular characterization was performed by PCR-ribotyping and multilocus sequence typing (MLST). The overall C. difficile colonization prevalence was 33.7 % (99/294). The colonization rate by a toxigenic strain was 7.1 % (21/294). Community-acquired C. difficile accounted for 66.7 % (66/99) of cases. Molecular typing was performed on 90 isolates from Jean Verdier Hospital and 8 additional isolates from another hospital in Versailles (Centre Hospitalier de Versailles). Among these isolates, 23 were toxigenic (21 tcdA + /tcdB + and 2 tcdA " /tcdB + ). All the isolates were negative for the binary toxin genes. Seventeen PCR ribotypes (PRs) were identified, with five PRs accounting for 82.7 % (81/98) of the isolates. MLST generated 15 different sequence types (STs). The predominant genotype, PRJV11-ST38 (33.7 %), included only non-toxigenic strains. Toxigenic strains were distributed in eight genotypes. Neither PR027-ST3, nor PR078/126-ST49 were identified but some PRs/STs corresponded to well-known adult infectious strains. These results indicate that infants are widely colonized by non-toxigenic strains. However, toxigenic adult infectious strains circulate in asymptomatic infants even in the community; thus, infants may be a reservoir for adult infectious strains.

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Section: Discussionsupporting

confidence: 93%

Prevalence and diversity of Clostridium difficile strains in infants

Rousseau

Lemée

Monnier

et al. 2011

Journal of Medical Microbiology

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“…Leukocytosis is a common clinical feature in the severely ill patient, with leukocyte counts exceeding 15,000 cells per mm3 in 40 to 50% of patients (196,262 (34,35,73,118,153,178,228,252,258); however, other studies have reported acquisition rates of 0 to 6% (127,153,246,257). These differences in the acquisition rates of C. difficile in neonates and young children most likely represent varied degrees of environmental exposure in nurseries or transfer from the hands of hospital staff rather than disparities in the rate of maternal exposure (12). Prevalence of the carrier state has made it difficult to assess the relationship between C. difficile colonization and disease in this age group (57).…”

Section: Introductionmentioning

confidence: 99%

Clostridium difficile: clinical disease and diagnosis

1993

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Clostridium difficile is an opportunistic pathogen that causes a spectrum of disease ranging from antibiotic-associated diarrhea to pseudomembranous colitis. Although the disease was first described in 1893, the etiologic agent was not isolated and identified until 1978. Since clinical and pathological features of C. difficile-associated disease are not easily distinguished from those of other gastrointestinal diseases, including ulcerative colitis, chronic inflammatory bowel disease, and Crohn's disease, diagnostic methods have relied on either isolation and identification of the microorganism or direct detection of bacterial antigens or toxins in stool specimens. The current review focuses on the sensitivity, specificity, and practical use of several diagnostic tests, including methods for culture of the etiologic agent, cellular cytotoxicity assays, latex agglutination tests, enzyme immunoassay systems, counterimmunoelectrophoresis, fluorescent-antibody assays, and polymerase chain reactions.

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“…The high carriage rate in infancy has been ascribed to the low capacity of the infantile gut microbiota to suppress the growth of C. difficile. Colonization rates are increased in bottle-fed and caesarean section-delivered infants (14)(15)(16); in the latter case, carriage is probably dependent on delayed acquisition of suppressive anaerobes (17). A significant portion of C. difficile strains colonizing infants are toxin producers (13), but the vast majority of colonized infants have no overt symptoms.…”

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confidence: 99%

Toxin-Producing Clostridium difficile Strains as Long-Term Gut Colonizers in Healthy Infants

et al. 2014

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c Clostridium difficile is a colonizer of the human gut, and toxin-producing strains may cause diarrhea if the infectious burden is heavy. Infants are more frequently colonized than adults, but they rarely develop C. difficile disease. It is not known whether strains of C. difficile differ in the capacity to colonize and persist in the human gut microbiota. Here, we strain typed isolates of C. difficile that had colonized 42 healthy infants followed from birth to >12 months of age by using PCR ribotyping of the 16S-23S rRNA intergenic spacer region. The isolates were also characterized regarding carriage of the toxin genes tcdA, tcdB, and cdtA/B and the capacity to produce toxin B in vitro. Most strains (71%) were toxin producers, and 51% belonged to the 001 or 014 ribotypes, which often cause disease in adults. These ribotypes were significantly more likely than others to persist for >6 months in the infant micobiota, and they were isolated from 13/15 children carrying such long-term-colonizing strains. Ribotype 001 strains were often acquired in the first week of life and attained higher population counts than other C. difficile ribotypes in newborn infants' feces. Several toxin-negative ribotypes were identified, two of which (GI and GIII) were long-term colonizers, each found in one infant. Our results suggest that the toxin-producing C. difficile ribotypes 001 and 014 have special fitness in the infantile gut microbiota. Toxin-producing strains colonizing young children for long time periods may represent a reservoir for strains causing disease in adults.

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Epidemiology of Clostridium difficile Colonization in Newborns: Results Using a Bacteriophage and Bacteriocin Typing System

Cited by 53 publications

References 18 publications

Prevalence and diversity of Clostridium difficile strains in infants

Prevalence and diversity of Clostridium difficile strains in infants

Clostridium difficile: clinical disease and diagnosis

Toxin-Producing Clostridium difficile Strains as Long-Term Gut Colonizers in Healthy Infants

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