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Faecalibacterium Prausnitzii

Stool Test
Your most direct read on whether your gut's most important anti-inflammatory bacteria are thriving or disappearing.
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Should you take a Faecalibacterium Prausnitzii test?

This test is most useful if any of these apply to you.

Living With IBD or Gut Inflammation
A direct read on the beneficial bacteria most consistently depleted in Crohn's, ulcerative colitis, and chronic gut inflammation.
Recovering From Antibiotics or C. diff
After antibiotics or recurrent infections, this shows whether your most important peacekeeping bacteria are bouncing back.
Managing Metabolic or Autoimmune Conditions
If you have diabetes, kidney disease, psoriasis, or chronic hives, this reveals the gut dysbiosis pattern that often runs alongside them.
Building a Longevity Baseline
Healthy and proactive? Gives an early window into gut ecology that complements standard metabolic and inflammation labs.

About Faecalibacterium Prausnitzii

If your gut feels off, your inflammation markers are creeping up, or you have a condition like Crohn's, ulcerative colitis, or recurrent gut symptoms, one of the most informative things you can know is whether your colon still has enough of its most important peacekeeping bacteria. F. prausnitzii (Faecalibacterium prausnitzii) is one of those peacekeepers, and a stool PCR test measures how much of it you have.

This bacterium normally makes up roughly 5 to 15% of all the microbes in your intestines and is one of the largest producers of a fuel called butyrate that feeds the cells lining your colon. When it drops, it signals that your gut ecosystem has shifted toward a state linked to inflammation, digestive disease, and several whole-body conditions.

What This Test Measures

Stool PCR (polymerase chain reaction, a lab technique that detects and counts specific DNA sequences) for F. prausnitzii looks at the bacterial DNA in your stool and uses primers (short DNA probes) that match a region of the bacterial 16S rRNA gene unique to this species. Results may be reported as relative abundance compared to total bacteria, as gene copies per gram of stool, or as log-scaled counts depending on the lab.

F. prausnitzii belongs to a bacterial group called Firmicutes and is closely related to the Clostridium leptum group. It is a strictly oxygen-sensitive organism that lives in the lower gut, sticks to the mucus layer along the colon wall, and produces short-chain fatty acids, especially butyrate, which is the preferred energy source for the cells lining your colon.

One caveat about the science: the genus Faecalibacterium has recently been reclassified into several distinct species (including F. prausnitzii, F. duncaniae, F. taiwanense, and F. longum). Many older studies measured the broader genus rather than the species alone, and newer work suggests F. prausnitzii in the strict sense may not always be the dominant Faecalibacterium species in every population. This is worth keeping in mind when interpreting how your number compares to published reference groups.

This is a research and exploratory marker rather than a standardized clinical test. There are no universally agreed cutpoints for normal or abnormal, and different labs report results in different units, so the number on your report is most useful when you are looking at the direction of change over time or comparing it against well-defined healthy reference groups.

Crohn's Disease and Ulcerative Colitis

The strongest signal for this biomarker is in inflammatory bowel disease (IBD). Across many human studies and meta-analyses, people with Crohn's disease and ulcerative colitis consistently show less F. prausnitzii in their stool than healthy people, and active disease shows even lower levels than disease in remission.

Who Was StudiedWhat Was ComparedWhat They Found
Adults with active IBD vs healthy adultsStool F. prausnitzii by qPCR (log-scaled counts per gram)Substantially lower in active IBD on a log scale
Crohn's patients vs healthy controls (meta-analysis)Stool or mucosal F. prausnitzii abundanceA large drop, with the average patient sitting well over a standard deviation below healthy controls
Ulcerative colitis patients vs healthy controls (meta-analysis)Stool or mucosal F. prausnitzii abundanceA meaningful drop, with the average patient sitting nearly one standard deviation below healthy controls

Source: Sokol et al. 2009; Zhao et al. 2023; Cao et al. 2014.

What this means for you: a lower than expected level is not, on its own, a diagnosis of IBD, but in someone with gut symptoms it is part of the picture pointing toward a chronically inflamed and dysbiotic colon. In ulcerative colitis, low levels have also been tied to a higher chance of relapsing within the next year and to more frequent flares, so the marker can help reflect how stable your remission is rather than just whether you are inflamed today.

Recurrent C. difficile Infection

In people with recurrent Clostridioides difficile infection (a stubborn gut infection often triggered by antibiotic use), F. prausnitzii is depleted before fecal microbiota transplant and rises significantly afterward, with the increase still present two to four months later. This reinforces the idea that bringing back this bacterium is part of how a healthy gut community is reestablished after antibiotic damage.

Colorectal Cancer

Across pooled stool studies of colorectal cancer, F. prausnitzii is part of the microbiome signature linked to disease, but the relationship is not as simple as higher equals safer. Specific strain-level subgroups have been associated with late-stage disease, while total levels can look broadly similar to healthy controls. As a screening test for colorectal cancer this marker is not validated; if you are due for colon cancer screening, that decision should be made on its own terms with your clinician.

Type 2 Diabetes and Metabolic Disease

Adults with type 2 diabetes have lower stool F. prausnitzii than people without diabetes in multiple studies. In one analysis of kidney transplant recipients, those who went on to develop new-onset diabetes after transplantation had substantially lower stool levels of F. prausnitzii than those who did not. The marker is associated with diabetes-relevant biology, although it has not been shown to drive risk on its own in humans.

Kidney Disease

In a study of chronic kidney disease, F. prausnitzii was significantly lower in patients than in controls, and its abundance was inversely related to two markers that go up when kidneys are failing: CRP (C-reactive protein, a marker of inflammation) and cystatin C (a kidney filtration marker). Lower gut levels tracked with worse kidney biology and more inflammation.

Allergic Asthma, Chronic Hives, and Other Inflammatory Conditions

Children with allergic asthma have lower stool F. prausnitzii than healthy children. Adults with chronic urticaria (long-running hives) and people with psoriasis also show stool depletion comparable to what is seen in IBD. None of these are diagnostic uses, but they show that low F. prausnitzii reflects a broader inflammatory tilt that can show up across very different organ systems.

ME/CFS and Fatigue

In people with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), F. prausnitzii is reduced and its abundance is inversely associated with fatigue severity. Fecal short-chain fatty acid data in the same study confirmed that the gut had a real deficit in butyrate-making capacity, which fits with the biology of this bacterium.

Reconciling a Counterintuitive Finding

Not every study shows the pattern of lower being worse. In one cohort of newly diagnosed pediatric Crohn's disease, F. prausnitzii was higher in the inflamed mucosa than in controls. The way to reconcile this with the larger body of evidence is to treat this biomarker as a context-dependent indicator of gut ecology, not a clean good number or bad number. Subspecies matter (different phylogroups behave differently), the compartment matters (stool versus mucosal biopsy can disagree), and disease stage matters. A single reading interpreted in isolation can mislead; trajectory and context interpret it well.

Tracking Your Trend

A single F. prausnitzii reading is the weakest way to use this test. Your gut microbiome shifts with diet, illness, travel, medications, and stress, and the lab assay can produce different absolute numbers depending on method and reporting unit. The far more useful read is your trend over time.

A reasonable cadence: a baseline test, a follow-up at three to six months if you are making targeted changes to your gut health or starting therapy for a known gut condition, then at least annually. If you are using this marker to track response to an intervention that has been shown to raise F. prausnitzii in human studies (such as certain prebiotic fibers), retest after roughly three months of consistent use to see whether the direction of your number actually moved.

When Results Can Be Misleading

  • Recent antibiotics: even short courses of common antibiotics like amoxicillin or ciprofloxacin can lower F. prausnitzii within days, and effects can last weeks. A low result soon after an antibiotic course often reflects the drug, not your baseline gut.
  • Acute illness, hospitalization, or recent surgery: hospitalized COVID-19 patients showed F. prausnitzii depletion that inversely tracked with disease severity, and after gastric bypass surgery this was one of the species that fell at three months. Wait until you have recovered and stabilized before drawing conclusions.
  • Heavy endurance exercise in the past day or two: after an ultramarathon, average F. prausnitzii fell substantially in runners (from about 2.9% to 1.6%), with one runner showing an 85.7% drop. Short, intense exertion can transiently shift the number.
  • Big diet changes in the days before testing: a short, calorie- and protein-restricted diet altered F. prausnitzii in healthy adults, with the change reversing once normal eating resumed. Try to test during a representative week of eating, not during a crash diet or refeed.

Stool Versus Mucosal Levels

F. prausnitzii lives both in the stool stream and attached to the mucus layer along your colon wall. A stool sample is far more practical than a biopsy, but the two do not always agree at the individual level. In a study comparing stool and colon biopsies, fecal F. prausnitzii counts were higher than mucosal counts, and stool did not reliably predict mucosal levels person by person. Your number is a real biological signal from your gut, but treat it as a window onto your microbiome ecology rather than a perfect snapshot of what is happening on the bowel wall.

Decision Pathway for an Unexpected Result

If your F. prausnitzii is much lower than expected, the next step is not panic and not a single retest. It is to look at the full context: your symptoms, your inflammatory markers, your medications, your recent diet, and whether you have known gut disease.

  • With gut symptoms and a low result: consider pairing with fecal calprotectin (a marker of intestinal inflammation), CRP, and a complete blood count, and discuss with a gastroenterologist whether further workup for IBD is warranted. F. prausnitzii is not diagnostic on its own.
  • No gut symptoms but a known systemic condition: in people with type 2 diabetes, chronic kidney disease, psoriasis, or chronic urticaria, a low result is consistent with the dysbiosis seen in those conditions and is best discussed with the clinician managing the underlying disease.
  • Recent antibiotic exposure or acute illness: retest in two to three months once you are stable and off antibiotics. A persistently low result then is more meaningful.
  • Healthy, asymptomatic, and curious: there is no evidence in humans that aggressively chasing a higher F. prausnitzii number in someone without disease changes long-term outcomes. Track the trend, optimize the inputs known to support gut health, and pair the marker with broader stool and metabolic panels rather than treating it as a single target.

What This Test Cannot Tell You

Stool F. prausnitzii does not distinguish between an active IBD flare and an infectious colitis on its own (both show depletion). It does not measure how metabolically active the bacterium is, only how much DNA is present. It does not capture which subspecies you have, even though phylogroup composition appears to carry diagnostic information in research settings. And there is no validated threshold to start or change therapy based on this number alone.

What Moves This Biomarker

Evidence-backed interventions that affect your Faecalibacterium Prausnitzii level

↓ Decrease
Take broad-spectrum antibiotics like amoxicillin or ciprofloxacin
Antibiotics can sharply lower F. prausnitzii in your stool, often within days of starting treatment. Amoxicillin and ciprofloxacin treatment have both been shown to reduce Faecalibacterium abundance in human studies, and low baseline F. prausnitzii was predictive of who would develop antibiotic-associated diarrhea after a short amoxicillin-clavulanate course. The drop reflects collateral damage to your gut ecosystem, not a benefit.
MedicationStrong Evidence
↑ Increase
Receive a fecal microbiota transplant for recurrent C. difficile infection
Fecal microbiota transplant (FMT, transferring stool bacteria from a healthy donor into a patient's gut) significantly raised stool F. prausnitzii in people with recurrent C. difficile infection, with the increase visible early after treatment and still present 2 to 4 months later. Pre-FMT levels were much lower than donor levels, and the rise paralleled clinical recovery from the infection.
MedicationStrong Evidence
↓ Decrease
Undergo Roux-en-Y gastric bypass surgery
Three months after gastric bypass surgery in obese adults, F. prausnitzii was among the species that decreased in relative abundance. Earlier work also linked this species to lower inflammation in obesity and diabetes, so the post-surgery drop is part of a broader microbiome remodeling that occurs after this procedure. The decrease is undesirable on its own but is one piece of a larger metabolic change that the surgery deliberately induces.
LifestyleStrong Evidence
↑ Increase
Eat prebiotic fibers like inulin, fructo-oligosaccharides, or raffinose-type fibers
Across human trials reviewed in a systematic review, prebiotic interventions were the most studied dietary lever for F. prausnitzii, with most studies reporting an increase, a smaller number reporting a decrease, and several reporting no change. The direction of effect favors a real rise in F. prausnitzii when you regularly feed your gut with fermentable fibers, although results vary by fiber type and individual.
DietModerate Evidence
↓ Decrease
Take antiretroviral therapy for HIV
Both NNRTI-based and ritonavir-boosted protease inhibitor regimens were associated with depletion of F. prausnitzii-related bacteria in the stool compared to HIV-negative controls. The depletion correlated with markers of intestinal barrier dysfunction. Lower F. prausnitzii here reflects an impact of the medication on the gut ecosystem, not a sign the therapy is failing, so the change is neutral in clinical meaning but worth knowing about.
MedicationModerate Evidence
↕ Up & Down
Take metformin for blood sugar control
Evidence on how metformin moves F. prausnitzii is mixed. Some reviews and studies report declines in people taking metformin, while a prospective cohort of treatment-naive type 2 diabetics found Faecalibacterium in a cluster of genera that continued to increase during metformin treatment, and other randomized work found no specific decrease in Faecalibacterium. The marker can shift in either direction on metformin, and the change does not reliably indicate whether the drug is helping or hurting you.
MedicationModest Evidence

Frequently Asked Questions

Panels containing Faecalibacterium Prausnitzii

Faecalibacterium Prausnitzii is included in these pre-built panels.

References

28 studies
  1. Sokol H, Seksik P, Furet J, Firmesse O, Nion-larmurier I, Beaugerie L, Cosnes J, Corthier G, Marteau P, Dore JInflammatory Bowel Diseases2009
  2. Zhao H, Xu H, Chen S, He J, Zhou Y, Nie YJournal of Gastroenterology and Hepatology2023
  3. Hansen R, Russell RK, Reiff C, Louis P, Mcintosh F, Berry S, Mukhopadhya I, Bisset M, Barclay AR, Bishop J, Flynn DM, Mcgrogan P, Loganathan S, Mahdi G, Flint HJ, El-omar EM, Hold GLThe American Journal of Gastroenterology2012
  4. Machiels K, Joossens M, Sabino J, De Preter V, Arijs I, Eeckhaut V, Ballet V, Claes K, Van Immerseel F, Verbeke K, Ferrante M, Verhaegen J, Rutgeerts P, Vermeire SGut2013