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Heterogeneity of Clostridioides difficile asymptomatic colonization prevalence: a systematic review and meta-analysis

Gut Pathogens volume 17, Article number: 6 (2025) Cite this article

Abstract

Background

Asymptomatic carriers significantly influence the transmission dynamics of C. difficile. This study aimed to assess the prevalence of toxigenic C. difficile asymptomatic colonization (tCDAC) and investigate its heterogeneity across different populations. We searched MEDLINE, Web of Science, and Scopus for articles published between 2000 and 2023 on tCDAC. Studies including asymptomatic adults with laboratory-confirmed tCDAC were eligible. We performed a random-effects meta-analysis to estimate the pooled prevalence by clinical characteristics, settings, and geographic areas. In addition, we used outlier analyses and meta-regression to explore sources of prevalence variability.

Results

Fifty-one studies involving 39,447 patients were included. The tCDAC prevalence ranged from 0.5 to 51.5%. Among pooled estimates, a high prevalence was observed in patients with cystic fibrosis, outbreak settings, and cancer patients, whereas the lowest rates were found in healthy individuals and healthcare workers. Similar colonization rates were observed between admitted and hospitalized patients. Our meta-regression analysis revealed lower rates in healthy individuals and higher rates in cystic fibrosis patients and studies from North America. Additionally, compared with that among healthy individuals, the prevalence significantly increased by 15–47% among different populations and settings.

Conclusion

Our study revealed that tCDAC is a common phenomenon. We found high prevalence estimates that showed significant variability across populations. This heterogeneity could be partially explained by population characteristics and settings, supporting their role in the pathogenesis and burden of this disease. This highlights the need to identify high-risk groups to improve infection control strategies, decrease transmission dynamics, and better understand the natural history of this disease.

Introduction

Clostridioides difficile (CD) is an anaerobic, gram-positive, and spore-forming bacterium responsible for a broad clinical spectrum collectively referred to as Clostridioides difficile infection (CDI). Symptoms include acute episodes of diarrhea, fever, nausea, abdominal pain, and life-threatening complications such as colon perforation, toxic megacolon, and sepsis [1]. Despite its potential to cause symptomatic disease, C. difficile can also be present in the gut microbiota of asymptomatic carriers [2].

Asymptomatic carriers could play a significant role in the transmission dynamics of C. difficile. In this context, these individuals have the potential to serve as reservoirs of infection, contributing to disease endemicity and facilitating both community and nosocomial transmission. This is supported by evidence of bacterial shedding, environmental contamination among the colonized population, and genetic linkage between isolates from asymptomatic carriers and those associated with CDI-related diarrhea [3,4,5,6,7,8]. Additionally, the asymptomatic population poses a potential risk of progressing to symptomatic disease, which would directly exacerbate the burden of CDI in healthcare facilities and other settings [9].

Although estimating the burden of C. difficile asymptomatic colonization (CDAC) could be relevant for reducing and improving our understanding of C. difficile transmission dynamics, this has not been fully characterized. Current evidence reveals a wide range of colonization prevalence across different populations and settings [10, 11]. These heterogeneous estimates complicate the accurate assessment of the true burden of colonization, but they also present an opportunity to improve infection control strategies and enhance our understanding of the factors associated with colonization, helping to address important research gaps related to C. difficile [2].

In this work, we provide insights into C. difficile colonization by conducting a systematic review and meta-analysis to summarize and evaluate published data on toxigenic C. difficile colonization while also exploring heterogeneity and prevalence modifiers across different populations and settings.

Methods

Search strategy and study selection

We conducted a search via MEDLINE, Web of Science, and Scopus for articles published between January 2000 and December 2023. Since no universal definition for CDAC has been accepted, we included the following keywords to refer to this condition: (“Clostridioides difficile” OR “Clostridium difficile”) AND (asymptomatic OR colonization OR carrier) AND (prevalence). Languages were restricted to English, Spanish, and French. Additionally, manual screening of literature references from review articles was performed to retrieve articles that met the inclusion criteria.

This review was carried out as recommended by the Meta-analyses of Observational Studies in Epidemiology Guidelines [12]. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist was used to report the findings [13]. This study was registered on the PROSPERO platform (ID CRD42021282347). Ethical approval was not required because this study retrieved data from previously published studies.

Screening process

Four authors independently reviewed the manuscripts in a two-step process. First, titles and abstracts were screened to identify eligible articles. The full text was subsequently evaluated independently by two investigators to identify those that fulfilled the following inclusion criteria: (a) studies included adults (> 18 years), (b) stool polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (EIA), toxigenic culture, or cell cytotoxicity assay were used for diagnosis, (c) they focused on asymptomatic colonization, (d) studies clearly identified the proportion of asymptomatic carriers of toxigenic strains, and (e) observational studies and clinical trials included at least ten subjects.

Toxigenic C. difficile asymptomatic carriers (tCDAC) were defined as those patients in whom toxigenic C. difficile was identified by stool PCR, enzyme-linked immunosorbent assay (EIA), toxigenic culture, or cell cytotoxicity assay. Given that bacterial toxins A and B are the primary virulence factors of C. difficile, non-toxigenic isolates were excluded from our prevalence estimates. Additionally, our analysis focused exclusively on the burden of colonization in asymptomatic carriers with no diarrhea, a population that is often neglected and excluded from infection control interventions [14].

Since we expected high heterogeneity among the populations, we described and classified studies based on their population and setting characteristics. For this purpose, we used clinical characteristics when studies explicitly restricted screening to select patients with certain comorbidities, including patients with cystic fibrosis, cancer, inflammatory bowel disease (IBD), cirrhosis, or those who had undergone kidney transplantation. The healthy population was treated as another category if studies explicitly mentioned it. Additionally, we formed another group that included individuals at occupational risk, such as healthcare workers.

The elderly population without identifiable comorbidities and residents of long-term care facilities (LTCFs) were classified into one group. In the healthcare context, studies were included in the intensive care unit (ICU) category if the surveillance was restricted to this hospital department. Studies that did not include a clearly differentiated population and could not be classified into the previous categories were grouped under the hospital setting category if surveillance was conducted during the hospital stay or under the hospital admission category if surveillance was performed upon hospital admission. Finally, we also differentiated those studies in which the screening was performed in the context of a hospital C. difficile outbreak.

Some studies evaluated the prevalence in two well-differentiated groups, and we treated them as two distinct cohorts. Thus, the number of cohorts included in our analysis was greater than the number of studies included. For example, one study might include a healthy group and a group with a specific comorbidity, which would be considered two independent cohorts within one manuscript. Finally, we also documented the year and region of publication to further describe the study characteristics.

Quality assessment and data collection

Two authors independently evaluated the relevance and quality of the data using the Joanna Briggs Institute Critical Appraisal Tool [15]. A third member of the research group adjudicated disagreements. To evaluate peer review concordance, the kappa coefficient was calculated for each peer review pair. Data from each included manuscript were extracted and summarized in a standardized database, which included the author, publication date, patient characteristics, comorbidities, and tCDAC prevalence.

Statistical analysis

We performed random-effects meta-analyses using the inverse variance weighting method to calculate the pooled prevalence. Additionally, the Freeman-Tukey double arcsine transformation was employed for the transformation of proportions, and the restricted maximum likelihood estimator was used for τ² estimation [16]. Confidence intervals were estimated with the Clopper–Pearson method. We assessed the presence of heterogeneity among the included studies using the Q statistic, which evaluates the weighted sum of squared differences between the individual study estimates and the pooled estimator. In the context of a random-effects meta-analysis, weights are adjusted to reflect both the within-study variance and the between-study variability (τ²). The I² statistic was subsequently calculated to quantify the proportion of total variability attributable to heterogeneity, where values of 25%, 50%, and 75% were considered low, moderate, and high heterogeneity, respectively [17].

We expected high heterogeneity in the calculated prevalence estimators. However, we were interested in evaluating the causes of variance in colonization prevalence; thus, additional analyses were performed to explore prevalence variability. We grouped the estimators by population characteristics and clinical settings and then conducted a sensitivity analysis by removing studies identified as outliers on the basis of the following criteria: (1) the lower bound of the confidence interval was above the upper bound of the pooled prevalence confidence interval, or (2) the upper bound of the confidence interval was below the lower bound of the pooled prevalence confidence interval [18].

Similarly, we explored the modifiers of prevalence using mixed effects univariate meta-regression models to assess the impact of study characteristics on the overall pooled prevalence from all included studies. Additionally, we conducted a sub-analysis using healthy individuals as the reference group to evaluate differences in prevalence between the groups. A p value < 0.05 was considered to indicate statistical significance. All analyses were performed in RStudio software (version 2024.04.2 + 764) using meta (version 7.0–0) and metafor (version 4.6-0) packages.

Results

We identified 1072 studies; 946 (88%) were duplicates or nonrelevant at screening; 124 (12%) were reviewed in full text, with 51 (41%) meeting the eligibility criteria for inclusion [3, 5, 8, 19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66]. However, we analyzed 62 cohorts, as 7 studies compared tCDAC prevalence between two well-distinguishable populations, and two included three distinct populations. The identification and selection process are described in Fig. 1. The kappa coefficients were 0.67 and 0.69 for the first and second pairs of reviewers, respectively.

Most of the manuscripts were point-prevalence studies that assessed colonization using a cross-sectional testing approach. Only 12 manuscripts (24%) included more than one test per participant, performed sequentially over time [3, 8, 24, 36, 37, 42, 54,55,56, 58, 60, 62]. However, the follow-up was inconsistent, ranging from weekly evaluations during hospitalization to repeated testing at discharge. Thus, the amount of transient vs. sustained colonization could not be determined.

Fig. 1
figure 1

Flowchart for inclusion in this systematic review. aNine studies reported tCDAC prevalence in two or three well-differentiated populations, resulting in a total of 62 cohorts included in the subsequent analyses

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In terms of geographic region, 19 (37%) studies were conducted in North America, 18 (35%) in Europe, 10 (20%) in Asia, 3 (6%) in Australia, and 1 (2%) in Africa. According to the publication years, only 2 (4%) manuscripts were published during the decade from 2000 to 2009. In contrast, 37 (72%) studies were published from 2010 to 2019, and 12 (24%) were reported from 2020 to 2023. The year with the highest number of published manuscripts was 2016, with 9 studies, followed by 2017, with 7 studies.

Based on individuals’ characteristics, six (12%) studies included patients with cancer (Study ID 39, 29, 42, 30.2, 35, 33), two (4%) included patients with cystic fibrosis (Study ID 5.2, 49), and one included patients with cirrhosis (2%) (Study ID 48), kidney transplant recipients (2%) (Study ID 46), or patients with IBD (2%) (Study ID 6.2). In the latter group, it is important to note that IBD symptoms could potentially overlap with and complicate the differentiation from CDI cases.

Five (10%) studies included healthy individuals (Study ID 3, 5, 20, 7, 6), including one with healthy pregnant women (Study ID 7.2). Regarding occupational risk, two (4%) studies involved healthcare workers (Study ID 20.2, 28). Details of the individual studies are provided in Table 1.

Table 1 Characteristics of identified studies evaluating toxigenic C. difficile colonization from 2000 to 2023
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Thirteen studies (25%) reported prevalence rates in the geriatric population or LTCFs (Study IDs: 50, 11, 40, 27.2, 24, 45, 12, 32, 8, 4, 2, 22.3, 16.2), and seven studies (14%) focused on the intensive care unit (Study IDs: 47, 26, 21, 23, 18, 22.2, 16.3). Manuscripts that did not represent one identifiable characteristic or comorbidity were classified as either hospitalized individuals if the screening was performed during the hospital stay (Study IDs: 36, 23.2, 25, 34, 22, 16) or as hospital admission if the screening occurred at admission or during the early period of hospitalization (Study IDs: 19, 27, 14, 41, 44, 30, 15, 43, 31, 38). In four (8%) manuscripts, patients could not be classified into the mentioned groups: two involved veterinarians or community individuals with close contact with small companion animals (Study IDs: 13, 9), one included community patients attending to their general practitioners (Study IDs: 1), and the other included patients presenting at the emergency departments of eight institutions (Study IDs: 10). Finally, in three (6%) manuscripts (Study IDs: 37, 17, 51), screening was conducted in the context of an outbreak.

Prevalence of asymptomatic colonization by toxigenic C. difficile

Among the 51 studies involving 39,447 patients, 2,091 C. difficile asymptomatic carriers were documented. The prevalence of C. difficile colonization varied widely across cohorts, ranging from 0.5 to 51%. Individual study prevalence rates and 95% confidence intervals for the included cohorts are depicted in Supplementary Fig. 1.

Our global meta-analysis estimated an overall prevalence of 7.6% (95% CI: 5.7–9.7%). However, a significant degree of heterogeneity was observed (I² = 96%, Q statistic = 1684, p < 0.001). Although this heterogeneity decreased, it remained high even after the sensitivity analysis for outliers (I² = 73%, Q statistic = 99, p < 0.001).

To address the heterogeneity in our estimation, we performed a subgroup analysis and conducted 9 separate meta-analyses based on population characteristics and settings. A complete description of the prevalence estimators and sensitivity outlier analyses is provided in Table 2. Forest plots for subgroup meta-analyses are presented in Supplementary Figs. 2–10.

Table 2 Toxigenic clostridioides difficile asymptomatic carrier pooled prevalence based on study level characteristics
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Among the pooled estimations, the populations with the highest tCDAC prevalences were patients with cystic fibrosis (31.1%; 95% CI: 22.6–40.4; I²= 0%), studies conducted during outbreaks (18.5%; 95% CI: 0.5–52.1; I²= 98%), and patients with cancer (12.1%; 95% CI: 10.5–13.9; I²= 10%). In contrast, healthy individuals (1.5%; 95% CI: 0.7–2.6, I²= 87%) and healthcare workers (4.9%; 95% CI: 0.2–9.7; I²= 53%) showed the lowest colonization rates. Additionally, patients with cirrhosis (19.8%; 95% CI: 16.5–23.3) and kidney transplant recipients (16.9%; 95% CI: 11.2–23.6) also exhibited high prevalence rates of colonization. However, these values were derived from individual studies.

With respect to the healthcare setting, we did not observe differences in prevalence rates among patients at admission (8.6%; 95% CI: 5.3–12.5; I²= 97%), in the ICU (6.6%; 95% CI: 3.5–10.6; I²= 92%), or in hospitalized individuals (7.6%; 95% CI: 4.3–11.6; I²= 92%). Although heterogeneity decreased in all estimates after the sensitivity outlier analysis, it remained high for most of them (Table 2).

Thirty-four (67%) manuscripts provided some information on prior antibiotic use in the tested populations. Among those with available data, prior antimicrobial exposure ranged from 13 to 96%, with particularly high levels observed in post-transplant patients [50, 54], patients with cystic fibrosis [33], and patients admitted to intensive care units [25].

Although antibiotic exposure information was available for most studies, its definition varied widely across manuscripts. Authors used timeframes ranging from one to six months to define prior antibiotic exposure. Moreover, some studies reported general antibiotic use without specifying types, while others detailed individual use of specific antibiotic classes. Additionally, some manuscripts did not stratify overall use by age or by the subpopulations evaluated, making it challenging to derive prior exposure for certain cohorts included in our review. Due to the lack of granularity, we were unable to explicitly include antibiotic exposure in our meta-regression model.

Meta-regression to identify modifiers of tCDAC prevalence estimates

The subanalysis of specific populations, settings, or locations did not completely address study heterogeneity. Since each study had a combination of factors that could contribute to disease prevalence, we assessed whether meta-regression analysis could explain more of the heterogeneity in tCDAD prevalence (Table 3). Among all included populations, we found that the healthy population had a significantly lower colonization prevalence (coefficient: -0.17, 95% CI: -0.29; -0.06; p = 0.004), whereas those with cystic fibrosis had higher colonization rates (coefficient: 0.32, 95% CI: 0.11; 0.53; p = 0.003). Publications from North America reported significantly higher colonization rates (coefficient: 0.13, 95% CI: 0.06; 0.20; p < 0.001), whereas those published in Europe reported lower colonization rates (coefficient: -0.09, 95% CI: -0.16; -0.02; p = 0.013). We did not find differences in colonization rates based on publication date (coefficient: -0.005, 95% CI: -0.01; 0.005; p = 0.293).

Table 3 Meta-regression results relating study characteristics to asymptomatic carrier prevalence among all included studies
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Additionally, compared with the healthy group, certain populations or settings had a significantly greater disease burden. Those with the most pronounced differences were patients with cystic fibrosis (47%; 95% CI: 25–68%, p < 0.001), outbreak settings (30%; 95% CI: 13–48%, p < 0.001), and patients with cancer (23%; 95% CI: 9–37%, p = 0.001). Similarly, patients with cirrhosis (33%; 95% CI: 8–59%, p = 0.011) and those with kidney transplants (30%; 95% CI: 3–56%, p = 0.029) had significantly higher prevalence rates than healthy individuals. However, these prevalences were obtained from individual studies. No differences were found between healthy individuals and healthcare workers (11%; 95% CI: -9–32%, p = 0.272) or patients with inflammatory bowel disease (10%; 95% CI: -18–37%, p = 0.481). Additional population comparisons are presented in Table 4.

Table 4 Meta-regression comparing Clostridioides difficile asymptomatic carrier prevalence of specific populations versus healthy group
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Discussion

In this study, we performed a systematic review and meta-analysis to assess the prevalence of tCDAC and conducted meta-regression analyses to explore possible causes of prevalence heterogeneity among the published literature.

Other studies have been published regarding the prevalence of asymptomatic carriers. For example, Ziakas et al. and Zacharioudakis et al. reported, in their meta-analyses, a tCDAC pooled prevalence of 14.8% (95% CI: 7.6-24.0%) in long-term care facility residents and 8.1% (95% CI: 5.7-11.1%) for patients at hospital admission [10, 11]. Additionally, previous research focused on pediatric populations estimated a prevalence of 41% (95% CI: 32-50%) in children aged 6 to 12 months, which decreased to 12% (95% CI: 7-18%) among children aged 5 to 18 years [67].

Our study extends this work, as it is one of the few that examines tCDAC prevalence across different populations and settings. While our review estimated a prevalence similar to that previously reported for the adult population [10, 11], this estimate should be interpreted cautiously because of the significant heterogeneity observed across studies. This variability was expected, as specific population characteristics could influence susceptibility to colonization. Therefore, one of our primary objectives was to explore these differences through subgroup and meta-regression analyses to identify the sources of heterogeneity.

After our subgroup analysis, we identified variations in prevalence among different groups, particularly high prevalence rates among the oncologic population, patients with cystic fibrosis, the outbreak setting, and LTCF residents. Although other populations, such as cirrhosis patients and patients with kidney transplants, also presented high prevalence rates, these estimations were based on individual studies. As expected, the group with the lowest tCDAC prevalence was the healthy population. In the meta-regression analysis, we determined that patients with cystic fibrosis had prevalences that significantly differed from the overall prevalence estimate. In addition, when comparing subgroups with the healthy population, we found that the prevalence significantly increased by 15 to 47% among specific groups and settings (Table 4).

Some of the differences observed among particular subgroups could be influenced by the pathophysiology of the disease and specific exposures that condition different degrees of vulnerability to high colonization rates [48]. For example, patients with cystic fibrosis experience microbiome disturbances due to the high use of antibiotics, as well as pH and mucus disturbances in the gastrointestinal tract driven by cystic fibrosis transmembrane conductance regulator dysfunction [68, 69]. Patients with cancer are exposed to cytotoxic therapies that may alter the immunological response associated with colonization pathogenesis. In addition, both of these populations have a high prevalence of risk factors previously associated with C. difficile acquisition, such as prior hospitalizations (OR: 2.18; 95% CI: 1.86–2.56; p < 0.001), gastric acid suppression therapy (OR: 1.42; 95% CI: 1.17–1.73; p < 0.001), tube feeding (OR: 2.02; 95% CI: 1.06–3.85; p = 0.030), and steroid use (OR: 1.58; 95% CI: 1.14–2.17; p = 0.006) [70].

Antibiotic use plays a critical role in the pathophysiology of C. difficile and may contribute to high colonization rate [71]. In this review, although granular data regarding antimicrobial use was not widely available and the definitions of prior exposure were not standardized, overall antibiotic exposure was highly prevalent in some populations with high colonization rates, such as patients with cystic fibrosis [33] and post-transplant individuals with solid organ [50] or hematological malignancies [54]. This likely contributes to colonization susceptibility due to microbiome disruption caused by antimicrobial agents [71].

Older patients have a greater prevalence of comorbidities and more exposure to medical treatments, which could potentially increase the risk of tCDAC and CDI [72]. It is common for this population to live in LTCFs, which may confer higher CDAC risk because of close coexistence in communal housing settings [72, 73]. However, in addition to these examples, the synergistic interaction of multiple factors may be the reason for the higher colonization rates than any individual factor [7, 24].

Although HCWs are generally healthy, they are at increased risk of acquiring tCDAC due to occupational exposure. While the prevalence of colonization was greater among HCWs than among the healthy population, this difference was not statistically significant.

Colonization at admission did not differ from that observed in hospitalized patients and those in the ICU, which is relevant for several reasons. For example, asymptomatic carriers admitted to the hospital could play a significant role in transmission dynamics, potentially serving as reservoirs of infection and contributing to the endemic persistence of the pathogen within healthcare settings. These carriers could directly increase the CDI burden if they progress to symptomatic disease [74]. On the other hand, there is a risk of overdiagnosis, as colonized individuals may develop diarrhea from causes unrelated to CDI. In this context, relying solely on the presence of the bacteria to diagnose CDI could lead to unnecessary antibiotic use, which may negatively impact patients and contribute to antimicrobial resistance in healthcare environments [75].

Understanding the differences and conditions that contribute to varying levels of colonization burden could improve infection control interventions. Additionally, prospective follow-up of colonized individuals could provide valuable insights into the natural history of the disease, helping to identify patients at risk of progressing to symptomatic disease who may benefit from prophylactic treatment or decolonization strategies [2, 11, 76]. A more nuanced understanding of the epidemiology of asymptomatic carriers may also help resolve the controversy regarding the ability to distinguish between colonization and symptomatic C. difficile infection [2].

Although this work primarily focuses on the prevalence of asymptomatic carriers, a population that potentially facilitates C. difficile transmission dynamics within healthcare settings, we acknowledge that in non-healthcare contexts, such as the community, other C. difficile sources may also be relevant, including the burden of colonization in non-human reservoirs such as animals, food, and environment [77,78,79].

Previous studies have emphasized the high prevalence of toxigenic C. difficile in livestock, particularly in poultry (0-100%), pigs (0–96%), horses (4–33%), cattle (2–22%), sheep (0–18%), and goats (0–10%), as well as in companion animals such as cats (4–16%) and dogs (0-100%) [79]. Similarly, despite variability, spores have been detected in seafood (49–75%), meat (0–6%), and vegetables (3–5%) [79]. Interestingly, a significant number of ribotypes identified in these sources correspond to those observed in humans [77, 79].

In the environment, a collection of 7,857 samples from 10 countries across the Americas, Europe, and Asia documented a global prevalence of C. difficile as high as 25%, with small variation among healthcare (23%), non-healthcare (23%), and outdoor spaces (25%) [78]. The ribotypes identified in these settings were largely similar, highlighting potential uniformity in how C. difficile spreads in these environments [78].

Our study has several limitations. Some prevalence estimates included a wide range of diverse populations, which may have introduced bias. Additionally, most studies have relied on cross-sectional samples from single hospitals or locations over relatively short time frames, which may not accurately reflect the natural spatial‒temporal variation in colonization. Moreover, asymptomatic status was assessed at a single point in time, meaning that progression to symptomatic disease was not considered. As a result, it is possible that we did not identify long-term colonized individuals, and some of them may have been in the incubation period of the disease, potentially being identified later as symptomatic cases. However, the lack of follow-up data does not modify the potential role of colonized individuals in transmission dynamics. While this limitation affects estimates of the duration of infectiousness, it does not alter their potential capacity to shed bacteria during the testing period.

Conclusion

C. difficile asymptomatic colonization is a common phenomenon. In this study, we found that the prevalence of asymptomatic colonization by toxigenic C. difficile varied substantially among different populations. This heterogeneity could be partially explained by population characteristics and settings, supporting the significant role that individual and environmental characteristics play in the pathogenesis of this disease. Identifying groups with high colonization rates is crucial for several reasons, including a better understanding of C. difficile transmission dynamics, the natural history of the disease, and the improved implementation of infection control strategies.

Data availability

Data availability statement: All data are available from the cited literature.

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Acknowledgements

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Funding

This study was supported by the Centers for Disease Control and Prevention [U01CK000590] as part of the Modeling Infectious Diseases in Healthcare Network & NIH NIGMS [R35GM147702].

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  1. Francis I Proctor Foundation, University of California San Francisco, 490 Illinois St, San Francisco, CA, 94158, USA

    Daniel De-la-Rosa-Martínez & Seth Blumberg

  2. Department of Infectious Diseases, Instituto Nacional de Cancerología, Mexico City, Mexico

    Rodrigo Villaseñor-Echavarri, Diana Vilar-Compte, Virna Mosqueda-Larrauri & Paola Zinser-Peniche

  3. Department of Medicine, University of California San Francisco, San Francisco, CA, USA

    Seth Blumberg

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Contributions

Conceptualization: DDM, RVE, DVC. Formal analysis: DDM, RVE, DVC, SB, Methodology: DDM, RVE, DVC. Investigation: DDM, DVC, VML, PZP, SB. Software: DDM & RVE. Visualization: DDM, RVE, VML, PZP. Funding Acquisition: SB. Supervision: DDM, DVC, SB. Writing - Initial Draft: DDM, DVC, VML, PZP, SB. Writing – Review & Editing: DDM, DVC, VML, PZP, SB. DDM: Daniel De-la-Rosa-Martínez, RVE: Rodrigo Villaseñor-Echavarri, DVC: Diana Vilar-Compte, VML: Virna Mosqueda-Larrauri, PZP: Paola Zinser-Peniche, SB: Seth Blumberg.

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De-la-Rosa-Martínez, D., Villaseñor-Echavarri, R., Vilar-Compte, D. et al. Heterogeneity of Clostridioides difficile asymptomatic colonization prevalence: a systematic review and meta-analysis. Gut Pathog 17, 6 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s13099-024-00674-0

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Gut Pathogens

ISSN: 1757-4749