ESBL colonization pressure was associated with individual risk of acquiring ESBL on the neonatal unit, suggesting that unit-level interventions targeting colonization rather than infection may have important direct and indirect benefits in units with high colonization pressure.
Key Findings
Results
ESBL-harboring bacteria were the most common resistant organisms detected in European neonatal units, found in 14.2% of stool samples with high unit-level variation.
205 of 1448 samples (14.2%) tested positive for ESBL-encoding genes
Study conducted across 24 tertiary neonatal units in 8 European countries (Estonia, Greece, Germany, Italy, Poland, Spain, Switzerland, and the United Kingdom)
Stool samples were collected and PCR results obtained in 1448 of 1847 infant surveys (78.4%)
High unit-level variation in ESBL prevalence was noted across the participating centers
Real-time quantitative PCR was used for sample analysis between January 2022 and June 2024
Results
Unit-level ESBL colonization pressure was associated with increased odds of individual infant ESBL acquisition across all survey intervals.
4-day interval: mean odds ratio (OR) 1.89; 95% credible interval (CrI) 1.22-2.94 per 10% increase in colonization pressure
7-day interval: OR 1.76; 95% CrI 1.26-2.63 per 10% increase in colonization pressure
14-day interval: OR 1.73; 95% CrI 1.15-2.52 per 10% increase in colonization pressure
Bayesian hierarchical logistic regression modeling was used to assess the association
The association was consistent in direction and magnitude across all three survey interval lengths
Results
16.9% of eligible infants became newly ESBL-colonized during the study observation period.
90 of 533 infants (16.9%) became ESBL-colonized during the study
The acquisition analysis included 829 samples from 533 infants hospitalized since birth who were either newly admitted or not colonized at the previous survey time point
Median gestational age of newly colonized infants was 34 (IQR 30-37) weeks
Median length of stay at survey time for newly colonized infants was 14 (IQR 5-32) days
Results
The study enrolled 943 infants contributing to 1847 infant-survey observations across 24 European tertiary neonatal units.
547 of 943 enrolled infants were male (58.0%)
Median gestational age was 34 (IQR 30-38) weeks
Median birth weight was 2130 (IQR 1254-3084) g
Infants could contribute to multiple surveys; all infants present on the neonatal unit at 8:00 am on the survey day were eligible
Surveys were conducted with 4-, 7-, and 14-day intervals over 4 survey rounds
Methods
The study design used repeated cross-sectional surveys with real-time quantitative PCR to measure colonization pressure and acquisition across multiple European neonatal units.
Part of the NeoIPC project, conducted January 2022 to June 2024
Four surveys per site with 4-, 7-, and 14-day intervals between surveys
Stool samples were analyzed using real-time quantitative PCR
24 tertiary neonatal units in 8 European countries participated
Colonization pressure was defined as the proportion of infants carrying resistant bacteria on a unit at the previous survey
Discussion
The authors conclude that unit-level interventions targeting colonization rather than infection may have important direct and indirect benefits in neonatal units with high colonization pressure.
The finding that colonization pressure drives acquisition risk supports a 'herd protection' rationale for decolonization strategies
High unit-level variation in ESBL prevalence suggests that colonization pressure differs substantially between neonatal units
The consistent association across all three survey intervals (4, 7, and 14 days) strengthens the causal inference
The authors frame this as informing the design and implementation of effective infection prevention and control (IPC) interventions
What This Means
This research suggests that when more babies in a neonatal unit carry drug-resistant bacteria called extended-spectrum beta-lactamase (ESBL) producers, individual babies on the same unit are significantly more likely to pick up these bacteria themselves. The study tracked nearly 1,000 premature and sick newborns across 24 hospital neonatal units in 8 European countries, collecting stool samples at multiple time points to see which babies acquired resistant bacteria and whether the proportion of already-colonized babies in the unit predicted that risk. About 1 in 7 stool samples tested positive for ESBL genes, and about 1 in 6 babies who were not initially colonized became colonized during their stay. For every 10% increase in the proportion of babies already carrying ESBL bacteria on the unit, an individual baby's odds of acquiring those bacteria increased by roughly 73–89%, depending on the time interval examined.
This research suggests that the risk of a baby picking up antibiotic-resistant bacteria is not just about that individual baby's own exposure or vulnerability, but is also strongly shaped by how many other babies around them are already colonized — a concept called 'colonization pressure.' This is similar to how the spread of any infectious agent in a community depends on how many people in that community are already carrying it. The finding held true consistently across different time windows (4, 7, and 14 days), lending confidence to the conclusion.
The practical implication is that infection control efforts in neonatal units may benefit from focusing not just on preventing serious infections in individual babies, but on reducing overall carriage of resistant bacteria across the whole unit. Reducing colonization pressure — through measures like decolonization, enhanced hygiene, or screening — could theoretically protect all babies on the unit, not just those directly treated. This research provides a scientific basis for designing unit-wide strategies to combat antibiotic-resistant bacteria in some of the most vulnerable hospital patients.
Cook A, Berkell M, van Werkhoven C, Sieswerda E, Smith D, Minotti C, et al.. (2026). Neonatal Unit Colonization Pressure and Acquisition of Extended-Spectrum β-Lactamase Gut Colonization.. JAMA network open. https://doi.org/10.1001/jamanetworkopen.2026.32644