Friday · October 9, 2026
Emerging

Kids With Crohn’s Have Disrupted Gut Fungi Too, and It Lingers After Treatment

A new peer-reviewed study followed treatment-naive children with Crohn's disease from diagnosis through three months of treatment and found that while some gut bacteria bounce back, the gut fungi stay disrupted, and specific stool odor compounds track with the bacteria driving inflammation.

Kids With Crohn's Have Disrupted Gut Fungi Too, and It Lingers After Treatment

If your child has just been diagnosed with Crohn's disease, you've probably already heard that gut bacteria are part of the picture. A new study out of three UK pediatric gastroenterology centers adds a piece that gets far less attention: the gut's fungal community is disrupted too, and while some bacterial damage eases with treatment, the fungal disruption does not budge.

Key takeaways:

  • Researchers tracked 44 children newly diagnosed with Crohn's disease (before any treatment) against 44 matched non-IBD controls, sequencing both gut bacteria and gut fungi, plus stool odor chemistry.
  • After three months of treatment, some disease-associated bacteria eased back toward a healthier pattern, but the fungal (mycobiome) disruption did not meaningfully improve.
  • Specific stool odor compounds, phenol and propan-1-ol, tracked closely with a bacterium called Fusobacterium nucleatum, which was itself shown to produce those same compounds in the lab.

Pediatric Crohn's Disease Disrupts Both Gut Bacteria And Gut Fungi

The study, published in the journal Gut Microbiology, enrolled 44 children with newly diagnosed, treatment-naive Crohn's disease (CD, a chronic inflammatory bowel disease that causes inflammation anywhere along the digestive tract) and compared them with 44 non-IBD control children matched for age and sex. Using stool samples, the researchers sequenced both the bacterial community (via 16S rRNA gene sequencing) and the fungal community, or mycobiome (via 18S rRNA gene sequencing), and ran shotgun metagenomics on a subset of 36 samples for a deeper functional look. Bacterial diversity was lower in children with Crohn's than in controls, and the CD gut communities were also less similar to one another, what researchers call reduced homogeneity, a pattern also reported in adult IBD and sometimes called the Anna Karenina principle: healthy guts tend to resemble each other, while disrupted guts are each disrupted in their own way. The fungal community showed the same pattern of reduced homogeneity, even though overall fungal diversity did not differ much from controls.

Why This Matters For Families Managing A New Crohn's Diagnosis

For parents navigating a new Crohn's diagnosis, this study is a reminder that "gut health" in IBD is not just about bacteria. The researchers found that key bacteria linked to Crohn's, notably Fusobacterium and Aggregatibacter, were more abundant in children with the disease, while beneficial, fiber-fermenting bacteria like Roseburia were more common in the healthy controls. On the fungal side, a group called Clavispora-Candida was elevated in children with Crohn's. Because fungal disruption persisted even after bacterial improvement, families and clinicians managing pediatric Crohn's may want to know that a return to normal bowel symptoms or lab markers does not necessarily mean the whole gut ecosystem, fungi included, has recovered.

How Researchers Tracked The Gut Ecosystem From Diagnosis Through Treatment

This was a prospective study, meaning children were enrolled and followed forward in time rather than analyzed after the fact. All 44 Crohn's patients were sampled at diagnosis, before starting any treatment, and a subset of 16 patients provided a second stool sample three months later, after starting treatment; by that point, disease activity scores and calprotectin (a stool marker of gut inflammation) had dropped in every one of those 16 children, with half in remission and the rest showing partial improvement. The researchers went beyond simply counting which microbes were present, applying ecological modeling methods (originally developed to study wild plant and animal communities) to ask whether the gut community in Crohn's disease is shaped more by predictable, disease-driven pressures or by essentially random colonization events. They found that in children with Crohn's, over 70% of the community assembly process was attributable to these random, unpredictable events, compared to a more orderly, predictable pattern in healthy controls, evidence that the Crohn's gut is a less stable environment that lets opportunistic microbes take hold more easily.

The Bacteria Behind The Smell, And What It Might Mean For Faster Diagnosis

The study also measured volatile organic compounds (VOCs, the chemical compounds responsible for odor) in stool and found that two of them, phenol and propan-1-ol, correlated strongly with the abundance of Fusobacterium and with the Clavispora-Candida fungal group. To confirm this wasn't coincidental, the researchers grew Fusobacterium nucleatum (a specific Fusobacterium species already implicated in gut inflammation) in the lab and confirmed it produces both phenol and propan-1-ol itself. This builds on a separate pediatric IBD study of the same stool compounds, which found propan-1-ol and phenol levels track with IBD severity and fall with treatment, and on a systematic review of stool VOC testing for IBD that found fecal VOC panels can diagnose IBD with over 85% accuracy. Together, this raises the possibility that stool odor chemistry could eventually serve as a cheap, non-invasive way to flag which children have Fusobacterium-driven inflammation, though that application has not been tested here and remains a future direction rather than a current tool.

What Remains Unproven

This study shows correlations, not proof of cause and effect: it cannot say that Fusobacterium or the disrupted fungal community are causing Crohn's disease or its flares, only that they travel together with the disease. Most of the 16 children resampled after treatment received more than one type of therapy simultaneously, so the researchers could not tell which specific treatment was responsible for the partial bacterial recovery they observed. The deeper functional (shotgun metagenomics) analysis was run on just 14 Crohn's patients and 22 controls, a small enough group that findings there should be treated as preliminary until confirmed in larger studies. Recent mechanistic research on Fusobacterium nucleatum has begun to explain how it might actively drive gut inflammation, via specific immune-signaling pathways, but this pediatric study alone does not establish that pathway in children.

What Comes Next

The authors call for longitudinal studies that track children through disease relapse and remission, not just a single pre- and post-treatment snapshot, to determine how community assembly processes and the persistent fungal disruption behave over a longer course of the disease. No specific timeline or follow-up trial has been announced.

Common Questions

Does this mean fungi cause Crohn's disease in kids? No. The study found fungal disruption is present alongside Crohn's disease and does not resolve with treatment as some bacterial changes do, but it does not show that the fungi are causing the disease.

Can a stool smell test diagnose Crohn's disease? Not yet as a clinical tool. This study and a related pediatric study found that specific stool odor compounds correlate with Fusobacterium abundance and disease markers, which is a promising research signal but has not been validated as a diagnostic test in this study.

Why did the fungal disruption not improve with treatment when some bacteria did? The study does not establish why, only that it happened. The researchers note this is worth watching in future longitudinal research that follows children through relapse and remission rather than a single follow-up visit.

Were all children in the study on the same treatment? No. Most received more than one type of treatment at once, which is why the researchers could not determine which specific therapy drove the partial bacterial recovery seen at the 3-month follow-up.

Evidence Rating

EMERGING — 84/100

Caveats

  • Recruited across three UK paediatric gastroenterology centres but the treated, resampled follow-up group was small (n=16), and the shotgun-metagenomics subset was smaller still (14 Crohn’s patients, 22 controls)
  • Observational: the study shows correlations between bacteria, fungi, stool chemistry and disease, not proof that any of them cause Crohn’s disease or its flares
  • Most patients received more than one treatment simultaneously, so the study cannot isolate which specific therapy drove the partial microbiome recovery seen at 3 months

Prospective UK inception cohort of treatment-naive pediatric Crohn’s disease patients (n=44) vs matched non-IBD controls (n=44), with 16S/18S amplicon sequencing, shotgun metagenomics on a subset (n=36), and volatile organic compound (VOC) metabolomics. A follow-up subset (n=16) was resampled 3 months post-treatment. Bacterial diversity and community structure were disrupted in Crohn’s disease and partially normalized with treatment, while fungal community disruption persisted. Disease-associated bacterial taxa correlated with specific stool volatile compounds.

References

  1. Rachael Slater, Alessandra Frau, Salma Belnour, et al. (2026). Ecological mechanisms drive stool microbiome and mycobiome community assembly in paediatric Crohn’s disease. Gut Microbiology. https://doi.org/10.1016/j.gutmic.2026.100017
  2. Salma Belnour, Rachael Slater, Kukatharmini Tharmaratnam, et al. (2024). Faecal volatile organic compounds differ according to inflammatory bowel disease sub‐type, severity, and response to treatment in paediatric patients. United European Gastroenterology Journal. https://doi.org/10.1002/ueg2.12603
  3. Ashwin Krishnamoorthy, Subashini Chandrapalan, Marriam Ahmed, Ramesh P Arasaradnam (2023). The Diagnostic Utility of Volatile Organic Compounds in Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis. Journal of Crohn's and Colitis. https://doi.org/10.1093/ecco-jcc/jjad132
  4. Mingyuan Wang, Junjian Sun, Jiang Yu, et al. (2026). Fusobacterium nucleatum drives CD40-mediated dendritic cell activation and Th17/Treg imbalance to exacerbate intestinal inflammation in Crohn’s disease. Frontiers in Immunology. https://doi.org/10.3389/fimmu.2025.1712971