Faecalibacterium prausnitzii

Faecalibacterium prausnitzii
Fusobacterium prausnitzii under scanning electron microscope.
Scientific classification Edit this classification
Domain: Bacteria
Kingdom: Bacillati
Phylum: Bacillota
Class: Clostridia
Order: Eubacteriales
Family: Oscillospiraceae
Genus: Faecalibacterium
Species:
F. prausnitzii
Binomial name
Faecalibacterium prausnitzii
(Hauduroy et al. 1937) Duncan et al. 2002
Synonyms

Bacteroides prausnitzii
Fusobacterium prausnitzii

Faecalibacterium prausnitzii is a non-spore-forming, non-motile, rod-shaped, anaerobic, Gram-positive bacteria species of the genus Faecalibacterium.[1][2][3][4] It is the single most abundant bacteria in the human gut and is the major butyric acid (butyrate)-producing species in the gut.[1][2][3][4]

Biology

Occurrence

F. prausnitzii is found in the human gut and is the most abundant single bacteria species in the human gut microbiota, making up approximately 5% of the total bacterial population in healthy adults.[1][2][3][4] However, F. prausnitzii can make up as much as 15% of the bacterial population in some people.[1][4] Many different strains of F. prausnitzii with varying properties are known and have been studied.[5][6][7][8] F. prausnitzii is ubiquitous in humans, detectable in over 85% of individuals.[4]

F. prausnitzii is an extremely oxygen-sensitive bacteria and is difficult to cultivate even under oxygen-free conditions.[1][2][4] However, advances have been made in the cultivation of F. prausnitzii.[1][3]

Metabolism

The end products of glucose fermentation by F. prausnitzii include acetate (acetic acid), formate, small amounts of D-lactate, and substantial amounts of butyrate (butyric acid).[1][2] It also consumes acetate and lactate and forms butyrate from them.[3][9][4] F. prausnitzii is strictly dependent on acetate and lactate produced by other bacteria such as Bifidobacterium, Bacteroides, and Akkermansia.[4] Salicylic acid is another product of F. prausnitzii.[2][3] F. prausnitzii is the most important butyrate-producing bacteria in the gut and colon.[2][1][10]

Butyrate is a short-chain fatty acid (SCFA) and has a large variety of biological effects.[1][11] It is an agonist of the FFAR2 (GPR43), FFAR3 (GPR41), and GPR109A and a histone deacetylase (HDAC) inhibitor of HDAC classes I and II.[11] It is known to activate the brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) signaling pathway via its HDAC inhibition and produce associated effects.[12][13] In addition to its mechanistic actions, butyrate is the preferred energy source for colonocytes, and has been found to provide approximately 70% of total energy needs for colonocytes in mice.[11][4] Butyrate plays a key role in gut homeostasis and has anti-inflammatory effects among others.[11]

Role in health and disease

F. prausnitzii abundance has been inversely associated with inflammatory bowel diseases such as Crohn's disease and ulcerative colitis.[2][1][11] It has also been inversely associated with colorectal cancer and other diseases.[2][3] In the 2020s, it was found that F. prausnitzii is depleted in people with systemic lupus erythematosus (SLE; "lupus"), and that its restoration could improve symptoms of the disease in animal models.[14][10][8] One possible mechanism for these apparent benefits is increased butyrate production and consequent anti-inflammatory effects.[15][16][17] Reduced Faecalibacterium prausnitzii abundance and butyrate production has been associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID and in the case of ME/CFS this has been assessed and found to correlate with fatigue severity as well.[18][19][20][21]

Influences

Prebiotics like fiber, such as fructooligosaccharides (FOS), galactooligosaccharides (GOS), and inulin among others, have been found to increase gut F. prausnitzii abundance.[3][22][23][4] Supplementation with 1-kestose, an FOS, for 10 weeks increased F. prausnitzii levels by 10-fold in healthy adults.[4][24] Similarly, 1-kestose increased cecal butyrate levels by 10-fold in rodents.[24][25] Inulin has also been found to increase Faecalibacterium abundance by about an order of magnitude in humans.[4][26][22] Maltobionic acid is a functional sugar and has been found to markedly increase F. prausnitzii abundance in humans.[4][27]

The short-chain triglyceride triacetin (glycerol triacetate) may also increase F. prausnitzii abundance by providing acetate.[28][3][9] Tributyrin (glycerol tributyrate) directly converts into butyrate and has additionally been found to increase butyrate-producing bacteria, though effect on F. prausnitzii specifically has not been reported.[29][30][31][32][33] Riboflavin (vitamin B2) can enhance F. prausnitzii survival and abundance.[4][34]

Existing probiotics do not contain F. prausnitzii, which is both due to viability problems as well as regulatory reasons, but some probiotics may nonetheless increase F. prausnitzii abundance via increased acetate and lactate production and hence bacterial cross-feeding.[3][8][4] In addition, facultative anaerobes like Bacillus coagulans can profoundly increase gut F. prausnitzii abundance in the elderly by depleting oxygen.[4][35] As of 2021, there has been very little research into the role of short chain fatty acid (SCFA)-producing bacteria and potential therapeutic benefits in inflammatory bowel disease.[36] However, F. prausnitzii supplementation is now being studied in clinical trials for certain indications.[3] There are challenges to F. prausnitzii manufacturing and administration due to its oxygen sensitivity among other issues.[3][4] The first clinical study of F. prausnitzii supplementation in humans, which was specifically for treatment of Crohn's disease, was published in 2026.[4][37]

Various medications have been found to increase or reverse depletion of F. prausnitzii concentrations, such as the antibiotic rifaximin, interferon α-2b, high-dose hydrocortisone, and the TNF inhibitor infliximab.[1][2][38] Another means of increasing F. prausnitzii abundance is fecal microbiota transplant (FMT).[3] Antibiotics such as amoxicillin and ciprofloxacin have been found to decrease Faecalibacterium species, whereas nitrofurantoin increased them.[3][39][40]

History

F. prausnitzii was discovered by C. Prausnitz in 1922.[3][4][41] It was initially classified as Bacteroides prausnitzii in 1937 by P. Hauduroy and colleagues.[3][42] Subsequently, the bacteria was reclassified as Fusobacterium prausnitzii in 1974.[3][1][43] In 1996 however, genetic analysis revealed that F. prausnitzii is only distantly related to Fusobacterium.[1] Later, a new genus called Faecalibacterium was proposed and the species was renamed to Faecalibacterium prausnitzii in 2002.[1][3][4] Relatedly, F. prausnitzii was the first member of Faecalibacterium to be discovered.[3] The first complete genome of F. prausnitzii was sequenced in 2010 in the frame of the Human Microbiome Project.[1] F. prausnitzii has received very little scientific attention until around the 2010s, probably in part due to its extreme oxygen sensitivity and cultivation difficulties.[1][2][3]

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Miquel S, Martín R, Rossi O, Bermúdez-Humarán LG, Chatel JM, Sokol H, Thomas M, Wells JM, Langella P (June 2013). "Faecalibacterium prausnitzii and human intestinal health". Curr Opin Microbiol. 16 (3): 255–261. doi:10.1016/j.mib.2013.06.003. PMID 23831042.
  2. 1 2 3 4 5 6 7 8 9 10 11 Ferreira-Halder CV, Faria AV, Andrade SS (December 2017). "Action and function of Faecalibacterium prausnitzii in health and disease". Best Pract Res Clin Gastroenterol. 31 (6): 643–648. doi:10.1016/j.bpg.2017.09.011. PMID 29566907.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Martín R, Rios-Covian D, Huillet E, Auger S, Khazaal S, Bermúdez-Humarán LG, Sokol H, Chatel JM, Langella P (July 2023). "Faecalibacterium: a bacterial genus with promising human health applications". FEMS Microbiol Rev. 47 (4) fuad039. doi:10.1093/femsre/fuad039. PMC 10410495. PMID 37451743.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 Deng X, Sheng X, Yang C, Xiang Q, Meng L, Li Y, Yang J (November 2026). "Microecological modulation of Faecalibacterium spp.: Prebiotic-mediated cross-feeding networks". Microbiol Res. 312 128657. doi:10.1016/j.micres.2026.128657. PMID 42551227. An 8-week clinical trial demonstrated that daily supplementation with 5 g of 1-kestose (the lowest polymerisation component of FOS) yielded a tenfold increase in Faecalibacterium (commonly referred to as F. prausnitzii in traditional sequencing) abundance in healthy adults (Tochio et al., 2018). [...] Clinical evidence consistently demonstrates that inulin supplementation induces an order-ofmagnitude increase in Faecalibacterium abundance, an effect sustained regardless of intervention duration (Dewulf et al., 2013; Ramirez-Farias et al., 2009).
  5. ↑ Bai Z, Zhang N, Jin Y, Chen L, Mao Y, Sun L, Fang F, Liu Y, Han M, Li G (2022). "Comprehensive analysis of 84 Faecalibacterium prausnitzii strains uncovers their genetic diversity, functional characteristics, and potential risks". Front Cell Infect Microbiol. 12 919701. doi:10.3389/fcimb.2022.919701. PMC 9846645. PMID 36683686.
  6. ↑ Martín R, Miquel S, Benevides L, Bridonneau C, Robert V, Hudault S, Chain F, Berteau O, Azevedo V, Chatel JM, Sokol H, Bermúdez-Humarán LG, Thomas M, Langella P (2017). "Functional Characterization of Novel Faecalibacterium prausnitzii Strains Isolated from Healthy Volunteers: A Step Forward in the Use of F. prausnitzii as a Next-Generation Probiotic". Front Microbiol. 8 1226. Bibcode:2017FrMic...801226M. doi:10.3389/fmicb.2017.01226. PMC 5492426. PMID 28713353.
  7. ↑ Hu W, Gao W, Liu Z, Fang Z, Zhao J, Zhang H, Lu W, Chen W (January 2022). "Biodiversity and Physiological Characteristics of Novel Faecalibacterium prausnitzii Strains Isolated from Human Feces". Microorganisms. 10 (2): 297. doi:10.3390/microorganisms10020297. PMC 8876097. PMID 35208752.
  8. 1 2 3 Kowalick, Claire (24 June 2026). "First potential probiotic treatment for lupus identified at UT San Antonio". UT Health San Antonio. Retrieved 7 July 2026.
  9. 1 2 Miquel S, Martín R, Bridonneau C, Robert V, Sokol H, Bermúdez-Humarán LG, Thomas M, Langella P (2014). "Ecology and metabolism of the beneficial intestinal commensal bacterium Faecalibacterium prausnitzii". Gut Microbes. 5 (2): 146–151. doi:10.4161/gmic.27651. PMC 4063839. PMID 24637606. F. prausnitzii is an acetate consumer and butyrate producer, and it can also produce carbon dioxide, formate, and D-lactate, although none of the strains isolated to date produce hydrogen.1,53 In batch cultures, most of the carbon in the butyrate produced (around 85%) is derived from external acetate, with only 15% provided directly from glucose.54 [...] This is consistent with a putative symbiotic cooperation or cross feeding between F. prausnitzii and microbes generally recognized as beneficial, such as Bifidobacterium and Lactobacillus spp.45,46 For instance, Bifidobacteria are acetate producers in the gut, and one possible approach to increase the F. prausnitzii population is to feed Bifidobacteria, which then feed F. prausnitzii by producing acetate.
  10. 1 2 Zhao N, Geng P, Jimenez D, Garcia AC, Six N, LaPlante CI, Perez AG, Silverman GJ, Morel L, Ge Y (April 2026). "Multiomics-guided discovery of protective microbiome signatures in lupus-prone mice treated with Faecalibacterium prausnitzii". Nat Commun. 17 (1) 5120. Bibcode:2026NatCo..17.5120Z. doi:10.1038/s41467-026-71718-z. PMC 13247269. PMID 41974712.
  11. 1 2 3 4 5 Mukhopadhya I, Louis P (October 2025). "Gut microbiota-derived short-chain fatty acids and their role in human health and disease". Nat Rev Microbiol. 23 (10): 635–651. doi:10.1038/s41579-025-01183-w. PMID 40360779.
  12. ↑ Korenblik V, Schilder NK, de Lange IG, Daams JG, Bockting CL, Brul S, Nieuwdorp M, Lok A, Korosi A (February 2026). "From gut to glee: Is butyrate a promising antidepressant? A systematic review and mechanistic insights". Brain Behav Immun. 132 106237. doi:10.1016/j.bbi.2025.106237. PMID 41429215.
  13. ↑ Kim HJ, Leeds P, Chuang DM (August 2009). "The HDAC inhibitor, sodium butyrate, stimulates neurogenesis in the ischemic brain". J Neurochem. 110 (4): 1226–1240. doi:10.1111/j.1471-4159.2009.06212.x. PMC 2726719. PMID 19549282.
  14. ↑ Xiao J, Duan L, Yang J, Deng Y, Pang S, Wang H, Yin X, Wang H, Qiu Y, Li X, Gong Y, Li H (2026). "The landscape of cellular immune alteration in systemic lupus erythematosus". Front Immunol. 17 1755310. doi:10.3389/fimmu.2026.1755310. PMC 13260079. PMID 42292405.
  15. ↑ Yao K, Xie Y, Wang J, Lin Y, Chen X, Zhou T (2023). "Gut microbiota: a newly identified environmental factor in systemic lupus erythematosus". Front Immunol. 14 1202850. doi:10.3389/fimmu.2023.1202850. PMC 10390700. PMID 37533870.
  16. ↑ Hua M, Luo J, Li P, Zhang Y, Zhang X, Wu Y, Dong H (2026). "The microbiota-systemic lupus erythematosus axis: mechanisms, diagnostics, and therapeutic frontiers". Front Immunol. 17 1782828. doi:10.3389/fimmu.2026.1782828. PMC 13153103. PMID 42112348.
  17. ↑ He H, Xu H, Xu J, Zhao H, Lin Q, Zhou Y, Nie Y (2020). "Sodium Butyrate Ameliorates Gut Microbiota Dysbiosis in Lupus-Like Mice". Front Nutr. 7 604283. doi:10.3389/fnut.2020.604283. PMC 7688247. PMID 33262998.
  18. ↑ Wang JH, Choi Y, Lee JS, Hwang SJ, Gu J, Son CG (March 2024). "Clinical evidence of the link between gut microbiome and myalgic encephalomyelitis/chronic fatigue syndrome: a retrospective review". Eur J Med Res. 29 (1) 148. doi:10.1186/s40001-024-01747-1. PMC 10908121. PMID 38429822. At the phylum level, ME/CFS patients showed a significant increase in Bacteroidetes, along with noticeable reductions in Firmicutes compared to healthy controls (P < 0.01, Fig. 3A). Interestingly, some potentially beneficial genera such as Bifidobacterium, Roseburia, and Faecalibacterium display a notable decrease in CFS patients compared to healthy controls (P < 0.05 or P < 0.01, Fig. 3C). [...] Conversely, some lactic acid bacteria and other beneficial species notably decreased in ME/CFS patients, such as Faecalibacterium prausnitzii, Bifidobacterium angulatum, Lactobacillus ruminis, Roseburia intestinalis etc. (Fig. 3C). [...] We also observed a decrease in butyrate-producing bacteria among ME/CFS patients, which has been confirmed by several studies involving genus/species like Ruminococcus, Faecalibacterium prausnitzii, and Eubacterium rectale [11, 13, 19, 42]. Moreover, the abundance of these species were negatively correlated with the severity of fatigue symptoms in ME/CFS patients [19].
  19. ↑ Annesley SJ, Missailidis D, Heng B, Josev EK, Armstrong CW (May 2024). "Unravelling shared mechanisms: insights from recent ME/CFS research to illuminate long COVID pathologies". Trends Mol Med. 30 (5): 443–458. doi:10.1016/j.molmed.2024.02.003. PMID 38443223. Butyrate-producing bacteria, including Faecalibacterium prausnitzii, were observed to be reduced alongside short-chain fatty acid levels in the gut of patients with ME/CFS [53], as were microbial butyrate synthesis and plasma butyrate levels in another study [54]. [...] Altered levels of butyrate-producing bacteria have been reported in LC as in ME/CFS. One study reported a decrease in F. prausnitzii and reported that the levels of it and other butyrate-producing bacteria produced the largest inverse correlations with LC disease status [57].
  20. ↑ Tabisz H, Kujawski S, Prylińska-Jaśkowiak M, Zalewski P, Słomko J (30 June 2025). "A systematic review of gut microbiota differences in ME/CFS and Long COVID patients". Medical Research Journal. 10 (2): 195–206.
  21. ↑ Guo C, Che X, Briese T, Ranjan A, Allicock O, Yates RA, Cheng A, March D, Hornig M, Komaroff AL, Levine S, Bateman L, Vernon SD, Klimas NG, Montoya JG, Peterson DL, Lipkin WI, Williams BL (February 2023). "Deficient butyrate-producing capacity in the gut microbiome is associated with bacterial network disturbances and fatigue symptoms in ME/CFS". Cell Host Microbe. 31 (2): 288–304.e8. doi:10.1016/j.chom.2023.01.004. PMC 10183837. PMID 36758522. Faecalibacterium prausnitzii and Eubacterium rectale, which are both recognized as abundant, health-promoting butyrate producers in the human gut, were reduced in ME/CFS. Functional metagenomics, qPCR, and metabolomics of fecal short-chain fatty acids confirmed a deficient microbial capacity for butyrate synthesis. [...] The abundance of Faecalibacterium prausnitzii was inversely associated with fatigue severity.
  22. 1 2 Ramirez-Farias C, Slezak K, Fuller Z, Duncan A, Holtrop G, Louis P (February 2009). "Effect of inulin on the human gut microbiota: stimulation of Bifidobacterium adolescentis and Faecalibacterium prausnitzii". Br J Nutr. 101 (4): 541–550. doi:10.1017/S0007114508019880. PMID 18590586.
  23. ↑ Verhoog S, Taneri PE, Roa Díaz ZM, Marques-Vidal P, Troup JP, Bally L, Franco OH, Glisic M, Muka T (July 2019). "Dietary Factors and Modulation of Bacteria Strains of Akkermansia muciniphila and Faecalibacterium prausnitzii: A Systematic Review". Nutrients. 11 (7): 1565. doi:10.3390/nu11071565. PMC 6683038. PMID 31336737.
  24. 1 2 Tochio T, Kadota Y, Tanaka T, Koga Y (September 2018). "1-Kestose, the Smallest Fructooligosaccharide Component, Which Efficiently Stimulates Faecalibacterium prausnitzii as Well as Bifidobacteria in Humans". Foods. 7 (9): 140. doi:10.3390/foods7090140. PMC 6164784. PMID 30200390.
  25. ↑ Tochio T, Kitaura Y, Nakamura S, Sugawa C, Takahashi M, Endo A, Shimomura Y (2016). "An Alteration in the Cecal Microbiota Composition by Feeding of 1-Kestose Results in a Marked Increase in the Cecal Butyrate Content in Rats". PLOS ONE. 11 (11) e0166850. Bibcode:2016PLoSO..1166850T. doi:10.1371/journal.pone.0166850. PMC 5115820. PMID 27861621.
  26. ↑ Dewulf EM, Cani PD, Claus SP, Fuentes S, Puylaert PG, Neyrinck AM, Bindels LB, de Vos WM, Gibson GR, Thissen JP, Delzenne NM (August 2013). "Insight into the prebiotic concept: lessons from an exploratory, double blind intervention study with inulin-type fructans in obese women". Gut. 62 (8): 1112–1121. doi:10.1136/gutjnl-2012-303304. PMC 3711491. PMID 23135760.
  27. ↑ Negishi H, Ichikawa A, Takahashi S, Kano H, Makino S (January 2025). "Targeted prebiotic application of gluconic acid-containing oligosaccharides promotes Faecalibacterium growth through microbial cross-feeding networks". ISME J. 19 (1) wraf027. doi:10.1093/ismejo/wraf027. PMC 11922316. PMID 39936592.
  28. ↑ Van den Abbeele P, Poppe J, Baudot A, Vu LD (September 2025). "Triacetin and a Mushroom Blend Restore Butyrate Production by IBS Microbiomes Ex Vivo, Thus Promoting Barrier Integrity". Int J Mol Sci. 26 (19): 9388. doi:10.3390/ijms26199388. PMC 12524982. PMID 41096656.
  29. ↑ Yu J, Li W, Xu Y, Tang J (June 2026). "Gut microbiota-derived short-chain fatty acids (SCFAs): immunomodulatory effects and therapeutic potential in infections". Clin Microbiol Rev e00368-25: e0036825. doi:10.1128/cmr.00368-25. PMID 42267834.
  30. ↑ Heidor R, Ortega JF, de Conti A, Ong TP, Moreno FS (December 2012). "Anticarcinogenic actions of tributyrin, a butyric acid prodrug". Curr Drug Targets. 13 (14): 1720–1729. doi:10.2174/138945012804545443. PMID 23140283.
  31. ↑ Duysburgh C, Verstrepen L, Van Meulebroek L, Marzorati M (2025). "Tributyrin (CoreBiome®) enhances butyrate levels and modulates the gut microbiota, barrier function, and immune response in vitro". Front Nutr. 12 1712993. doi:10.3389/fnut.2025.1712993. PMC 12746503. PMID 41473189.
  32. ↑ Dosz, Edward; Conley, Devin; Lelah, Michael (2025). "A Novel Butyrate Generator Helps Modulate the Gut-Brain Axis: A Randomized Double-Blind Placebo-Controlled Clinical Study". Nutrition and Dietary Supplements. 17: 127–143. doi:10.2147/NDS.S565532. ISSN 1179-1489.
  33. ↑ Yang N, Lan T, Han Y, Zhao H, Wang C, Xu Z, Chen Z, Tao M, Li H, Song Y, Ma X (2023). "Tributyrin alleviates gut microbiota dysbiosis to repair intestinal damage in antibiotic-treated mice". PLOS ONE. 18 (7) e0289364. Bibcode:2023PLoSO..1889364Y. doi:10.1371/journal.pone.0289364. PMC 10389721. PMID 37523400.
  34. ↑ Liu L, Sadaghian Sadabad M, Gabarrini G, Lisotto P, von Martels JZ, Wardill HR, Dijkstra G, Steinert RE, Harmsen HJ (February 2023). "Riboflavin Supplementation Promotes Butyrate Production in the Absence of Gross Compositional Changes in the Gut Microbiota". Antioxid Redox Signal. 38 (4–6): 282–297. doi:10.1089/ars.2022.0033. PMC 9986023. PMID 35943883.
  35. ↑ Nyangale EP, Farmer S, Cash HA, Keller D, Chernoff D, Gibson GR (July 2015). "Bacillus coagulans GBI-30, 6086 Modulates Faecalibacterium prausnitzii in Older Men and Women". J Nutr. 145 (7): 1446–1452. doi:10.3945/jn.114.199802. PMID 25948780.
  36. ↑ Deleu S, Machiels K, Raes J, Verbeke K, Vermeire S (April 2021). "Short chain fatty acids and its producing organisms: An overlooked therapy for IBD?". eBioMedicine. 66 103293. doi:10.1016/j.ebiom.2021.103293. PMC 8047503. PMID 33813134.
  37. ↑ Guarino-Vignon P, Louis E, Pham HP, Orianne G, Tkacz E, Brot L, Mazzetti E, Sedda D, Ruffié P, Rolhion N, D'Haens G, Hadida B, Langella P, Sokol H (April 2026). "Faecalibacterium prausnitzii EXL01 for the Maintenance of Steroid-induced Clinical Response or Remission in Patients with Crohn's Disease: a first in human trial". Nat Commun. 17 (1) 5823. Bibcode:2026NatCo..17.5823G. doi:10.1038/s41467-026-72375-y. PMC 13332046. PMID 42049742.
  38. ↑ Ponziani FR, Zocco MA, D'Aversa F, Pompili M, Gasbarrini A (July 2017). "Eubiotic properties of rifaximin: Disruption of the traditional concepts in gut microbiota modulation". World J Gastroenterol. 23 (25): 4491–4499. doi:10.3748/wjg.v23.i25.4491. PMC 5504364. PMID 28740337.
  39. ↑ Stewardson AJ, Gaïa N, François P, Malhotra-Kumar S, Delémont C, Martinez de Tejada B, Schrenzel J, Harbarth S, Lazarevic V (April 2015). "Collateral damage from oral ciprofloxacin versus nitrofurantoin in outpatients with urinary tract infections: a culture-free analysis of gut microbiota". Clin Microbiol Infect. 21 (4): 344.e1–11. doi:10.1016/j.cmi.2014.11.016. PMID 25658522.
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  43. ↑ Cato, E. P.; Salmon, C. W.; Moore, W. E. C. (1 April 1974). "Fusobacterium prausnitzii (Hauduroy et al.) Moore and Holdeman: Emended Description and Designation of Neotype Strain". International Journal of Systematic Bacteriology. 24 (2): 225–229. doi:10.1099/00207713-24-2-225. ISSN 0020-7713. Retrieved 7 July 2026.
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