In a new study, researchers modeled the transmission of Clostridioides difficile ( C. diff ) infections among patients in hospital cancer units. They found that most new infections were introduced by patients who were infected but not symptomatic at the time of admission, rather than by patients who were infected and symptomatic. The model provides a clearer picture of C. diff transmission events in oncology wards and could help inform protocols aimed at preventing future disease transmission in a highly susceptible population.
Cancer treatments, while increasingly effective, leave their recipients immunocompromised and at greater risk of contracting infection than the general population. Hospital-acquired infections can cause severe complications in cancer patients, and C. diff is one of the most common.
“Physicians have singled out antimicrobial resistance as a big issue for improvement in cancer patients,” says Cristina Lanzas, professor of infectious disease at North Carolina State University’s College of Veterinary Medicine and corresponding author of the research.
“The cancer treatments are improved, but the secondary infections patients get because they are so immunocompromised can be fatal. We decided to look at how C. diff infections were transmitted in oncology wards.”
Generally speaking, clinicians test patients for C. diff only when they have clinical signs; however, patients can also carry this pathogen in the gut without symptoms and may contribute to its transmission.
The researchers combined six months of active patient surveillance (testing patients for C. diff regardless of clinical signs) with a simulation model of every room, patient and staff connection on two cancer units. The data was provided by collaborators at Washington University School of Medicine.
“Testing data only provides a snapshot – are you positive or negative on a given day and time – but transmission events are invisible,” Lanzas says. “We developed models that traced potential transmission routes and then looked at each model’s ability to replicate actual infection data. Then we chose the model that aligned best with the data we had.”
According to the model, testing alone only captures 23% of patients carrying C. diff .
The modeling also revealed that patients with active C. diff infections were not the main source of new colonization. Rather, asymptomatic colonized (AC) patients – people who carry C. diff but don’t have clinical signs – were responsible for 92% of transmissions that resulted in new colonizations.
The researchers hope that their model could be applied to different pathogens to help clinicians and hospitals identify contact points where risks for infections are increased.
“The issue of people carrying pathogens without knowing about it is very common with all antimicrobial resistant pathogens – we can really be our own worst enemies,” Lanzas says. “But by modeling these events, we can make the invisible visible, and perhaps that can lead to new protocols for patients coming into these wards.”
The study appears in Infection Control and Hospital Epidemiology , was supported by the Centers for Disease Control (grants BAA #200-2018-02926 and U01CK000587), the National Science Foundation Graduate Research Fellowship Program (grant DGE-2137100) and received approximately 50% of its funding from the National Institutes for Health. Other NC State collaborators are Ph.D. candidate Savannah Curtis and postdoctoral researcher Sankalp Arya. Tiffany Hink, Kimberly Reske, Emily Struttmann, Zainab Hassan Iqbal, Candice Cass, Margaret Olsen, Carey-Ann Burnham, and Erik R. Dubberke from Washington University School of Medicine; Mary Lee of Vanderbilt University Medical Center; and Suzanne Lenhart from the University of Tennessee also contributed to the work.
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Note to editors: An abstract follows.
“Quantifying the contributions of asymptomatic and symptomatic colonized patients to Clostridioides difficile acquisition in oncological units”
DOI : 10.1017/ice.2026.10557
Authors: Savannah Curtis, Arya Sankalp, Cristina Lanzas, North Carolina State University; Mary Lee, Vanderbilt University Medical Center; Tiffany Hink, Kimberly Reske, Emily Struttman, Zainab Hassan Iqbal, Candice Cass, Margaret Olsen, Carey-Ann Burnham, Eric R. Dubberke, Washington University School of Medicine; Suzanne Lenhart, University of Tennessee
Published: Oct. 1, 2026 in Infection Control and Hospital Epidemiology
Abstract:
Objective
Leukemic and hematopoietic cell transplant patients have one of the highest incidences of C. difficile infection (CDI). While CDI patients are considered the primary source of transmission, asymptomatic colonized patients (AC) can progress to CDI or contribute to in-unit transmission. We aim to quantify the roles of CDI and AC patients in C. difficile importation and transmission within oncological units.
Design
Prospective cohort study
Setting
Two leukemia and HCT transplant units in a large tertiary care hospital in the US for a 6-month period.
Methods
We developed a stochastic, individual-based network model to simulate C. difficile acquisition and transmission. Data from cultures and nucleic acid amplification testing (NAAT) obtained at admission and weekly, and toxin enzyme immunoassay (EIA) tests used for CDI diagnosis were used to calibrate the model. Healthcare worker room assignments informed the network structure. Key parameters were estimated via particle filtering.
Results
The model reproduced observed weekly test counts and transmission pairs. Only 23% of new colonization events were observed via testing. AC patients were the primary source of new colonizations: 51% (range: 38-70%) were due to importation (of those, 87% were admitted as AC), and 49% (30-62%) were due to transmission (AC was the source in 92% of transmissions that resulted in new colonizations).
Conclusions
These findings reinforce the role of AC, particularly via admission importation, in sustaining C. difficile transmission in high-risk hospital settings. Infection control focused on CDI effectively reduced onward transmission, as indicated by CDI’s low contribution to new colonizations.
Infection Control and Hospital Epidemiology
Computational simulation/modeling
Not applicable
1-Oct-2026
Olsen reports consulting fees from Pfizer and Ferring International. Burnham reports honoraria and support for meetings from American Society for Microbiology and employee of Pattern Bioscience. Dubberke reports research funding from Theriva Biologics, Pfizer, AstraZeneca, and Vedanta Bioscience, and consulting fees from GlaxoSmithKline, Pfizer, AstraZeneca, Vedanta Bioscience, and Idorsia. All other authors report no potential conflicts.