Flavonifractor plautii
1. Classification
a. Higher order taxa
Bacteria; Firmicutes; Clostridia; Eubacteriales; Oscillospiraceae; Flavonifractor Include this section if your Wiki page focuses on a specific taxon/group of organisms
2. Description and significance
Flavonifractor plautii is a bacterium that normally resides within the human gastrointestinal tract. F. plautii occasionally acts as an opportunistic pathogen, primarily in immunocompromised individuals, leading to rare bloodstream infections and other serious conditions [3, 4, 5]. F. plautii is a member of the microbiome that exists within the human gut. Research has also linked F. plautii and its metabolites to cardiovascular benefits, such as protection against arterial stiffness and myocardial injury, suggesting therapeutic potential beyond the gut. While some metabolic activities of the bacterium like flavonoid degradation have been studied, there is still a lack of information about its mechanisms for pathogenesis and its potential implications for human health [6, 7]. This article provides an overview of its classification, biology, genome, metabolism, ecology, and role in health and disease.
3. Genome structure
The genome of Flavonifractor plautii is composed of a single circular chromosome 3,985,392 base pairs in length, with a guanine-cytosine (GC) content of 60.9%. Genome annotation has revealed 3,764 predicted protein-coding genes. The genome also encodes three ribosomal RNA (rRNA) operons and 63 transfer RNA (tRNA) genes necessary for protein synthesis [8]. Researchers have identified five primary antibiotic resistance genes. CatP was linked to chloramphenicol resistance. ErmB, providing resistance to macrolides and lincomamides. VanI, associated with glycopeptide resistance; ArnA associated with colistin resistance, and tet associated with tetracycline resistance [4]. Having resistance to specific antibiotics is relative to containing GC content greater than 50% since it allows prokaryotes like F. plautii to inherit greater DNA stability and enhanced repair efficiency [9]. Maintaining stability is significant in order for F. plautii to withstand the conditions within the environment of the human gut.
4. Cell structure
Morphologically, F. plautii is a non-motile, anaerobic, non-spore forming rod-shaped bacterium approximately 1-8 micrometers in length [10]. Although classified as Gram-positive due to the thick peptidoglycan layer in its cell wall, Gram-stain results can be variable due to its strict anaerobic nature and alterations to its cell wall after oxygen exposure [11]. The bacterium was shown to lack flagella and have a rough cell wall after analysis with scanning electron microscopy [10].
5. Metabolic processes
As a chemoorganotroph, one of the defining features of Flavonifractor plautii is its ability to degrade flavonoids by cleaving the C-ring structure as a carbon source[12]. Additionally, F. plautii produces metabolites, including short-chain fatty acids such as butyrate and propionate [7,12].
F. plautii is also able to ferment glucose, fructose, and ribose as a source of electrons [13]. It does not reduce nitrate or produce lecithinase, but it does show variable degrees of producing indole and hydrogen sulfide.
6. Ecology
Flavonifractor plautii thrives in the anaerobic, nutrient-rich environment of the human gut, specifically the large intestine [12,14]. Typically, F. plautii will colonize healthy adult guts, although its abundance varies with age and disease status. However, abundance increases within diets containing higher quantities of polyphenols, which flavonoids are the most significant type [12]. The optimal growth of F. plautii occurs at 37°C [14]. The absence of oxygen is crucial since exposure will inhibit growth and affects cell wall integrity, contributing to the variability in Gram staining [5]. Its distribution is closely linked to dietary flavonoid intake. Populations with diets rich in plant polyphenols tend to have higher detectable levels of F. plautii [5]. Understanding the ecological factors influencing F. plautii is essential to further examining its pathogenetic impact in the human body.
7. Pathology
Although F. plautii is typically a harmless component of intestinal microbiota, it has been occasionally associated with serious infections, particularly bloodstream infections (bacteremia) in immunocompromised individuals or those with impaired intestinal barriers [3, 5, 9, 10, 15, 16]. Reported cases include pleural effusion (fluid buildup in lungs) after kidney transplantation, peritonitis, and sepsis, likely resulting from bacterial translocation across the gut wall [5, 15]. Diagnosing these infections is difficult due to the bacterium’s slow growth, anaerobic nature, and inconsistent Gram staining results. New diagnostic tools such as MALDI-TOF mass spectrometry have improved detection. The number of reported infections of F. plautii appears to be increasing with the rising use of immunosuppressants in clinical practice, as F. plautii is mainly pathogenic in patients with compromised immune systems. [3, 5].
Antibiotic testing indicates that F. plautii commonly exhibits resistance to fluoroquinolones and tetracyclines but remains susceptible to vancomycin and metronidazole [4, 16]. Although F. plautii has pathogenicity mechanisms that are not well understood, infections appear to occur when host immunity is weakened or the gut barrier is impaired [16].
F. plautii produces metabolites, including short-chain fatty acids such as butyrate and propionate [7,12]. Since low levels of these metabolites have been linked to inflammatory bowel diseases and colorectal cancer, the production of short-chain fatty acids by F. plautii suggests that it can potentially play a protective role in maintaining a healthy gut and preventing disease [12].
The metabolite desaminotyrosine (DAT), produced by F. plautii, has demonstrated cardioprotective effects in animal models by showing cardioprotective effects against ischemia-reperfusion injury, a condition caused by oxygen deprivation and subsequent restoration in heart tissue. DAT reduced inflammation and oxidative stress after ischemia-reperfusion injury, suggesting therapeutic potential in cardiovascular disease prevention [6].
Phytosphingosine, another metabolite synthesized by F. plautii, is negatively correlated with phlegm-dampness constitution (PDC) score. Individuals with high PDC scores are at an increased risk of metabolic disorders, thus positioning F. plautii as an influential player in host-microbe interactions that affect health beyond the gut through phytosphingosine binding to hepatic peroxisome proliferator-activated receptor α, which activates its nuclear transcription activity and thereby regulates downstream gene expression [17].
8. Current Research
Recent studies have helped expand our understanding of F. plautii beyond its traditional role as a commensal bacterium. For example, a comprehensive gut microbiome analysis of colorectal cancer (CRC) patients in India found that the presence of F. plautii was positively associated with colorectal cancer. In addition to being abundant, F. plautii was also the most critical species setting colorectal cancer samples apart from healthy samples in Indian populations [12].
Animal and cellular models reveal that F. plautii metabolite desaminotyrosine (DAT) decreases risk of myocardial ischemia/reperfusion injury by reducing cardiac inflammation and oxidative damage, which suggests that gut microbiota manipulation could enhance cardiovascular health [6]. Another study identified cis-aconitic acid (CAA) as a metabolite that F. plautii produces to protect against arterial stiffness by inhibiting enzymes that break down extracellular matrix proteins and reducing inflammation in vascular tissues [7].
Sequencing analysis of infections caused by F. plautii is also currently of interest in order to understand what causes F. plautii to become pathogenic. It is hypothesized that broad-spectrum antibiotics can deteriorate the mucosal barrier in the digestive tract, which enables F. plautii to translocate from the gut to the bloodstream, causing infection [4, 18]. Alternative methods could involve descension from the intestinal tract to the urinary tract, resulting in a urinary tract infection that eventually leads to the bacterium spreading to the bloodstream, although the exact mechanism of action has not yet been fully understood [4].
References
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[2] Sayers, E. W., Cavanaugh, M., Clark, K., Ostell, J., Pruitt, K. D., & Karsch-Mizrachi, I. (2019). GenBank. Nucleic acids research, 47(D1), D94–D99. https://doi.org/10.1093/nar/gky989
[3] Berger, F. K., Schwab, N., Glanemann, M., Bohle, R. M., Gärtner, B., & Groesdonk, H. V. (2018). Flavonifractor (Eubacterium) plautii bloodstream infection following acute cholecystitis. IDCases, 14. https://doi.org/10.1016/j.idcr.2018.e00461
[4] Chen X, Bi, W., Ruan X., Jin L., & Zhang N. (2024) Genome sequencing analysis of a rare case of blood infection caused by Flavonifractor plautii. American Journal Case Report, 25:e943920. doi: 10.12659/AJCR.943920. PMID: 38881048; PMCID: PMC11196211.
[5] Orlando, G., Pisani, F., Mastrantonio, P., Bonanni, L., Di Cocco, P., D’Angelo, M., Tabilio, A., & Famulari, A. (2008). Eubacterium plautii infection in a kidney transplant recipient: A noteworthy case of pleural effusion and fever. Clinical Transplantation, 22(4). https://doi.org/10.1111/j.1399-0012.2008.00805.x
[6] Du, H., Liu, X., Shen, J., Yuan, H., Zhang, H., Xi, G., Li, Y., Wang, Y., Zhang, J., Yang, C., Xu, P., Wang, J., Wang, F., Liu, S., Zhou, Y., Gu, Q., Lu, J., Wei, T., Gao, Z., . . . Song, M. (2025). Flavonifractor Plautii or its metabolite desaminotyrosine as prophylactic agents for alleviating myocardial ischemia/reperfusion injury. Advanced Science, 12(21), 2417827. https://doi.org/10.1002/advs.202417827
[7] Luo, S., Xia, M., Fan, J., Han, Y., Ye, B., Cheng, K., Liu, L., Zhu, S., & Zhao, Y. (2022, December 28). Flavonifractor Plautii protects against elevated arterial stiffness | circulation research. Circulation Research. https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.122.321975
[8] Tourlousse, D. M., Sakamoto, M., Miura, T., Narita, K., Ohashi, A., Uchino, Y., Yamazoe, A., Kameyama, K., Terauchi, J., Ohkuma, M., Kawasaki, H., & Sekiguchi, Y. (2020). Complete genome sequence of Flavonifractor plautii JCM 32125T. Microbiology Resource Announcements, 9(17), e00135-20. https://doi.org/10.1128/MRA.00135-20
[9] Weissman, J. L., Fagan, W. F., & Johnson, P. L. F. (2019). Linking high GC content to the repair of double strand breaks in prokaryotic genomes. PLoS Genetics, 15(11), e1008493. https://doi.org/10.1371/journal.pgen.1008493
[10] Mikami, A., Ogita, T., Namai, F., Shigemori, S., Sato, T., & Shimosato, T. (2021). Oral Administration of Flavonifractor plautii, a bacteria increased with green tea consumption, promotes recovery from acute colitis in mice via suppression of IL-17. Frontiers in Nutrition, 7, 610946. https://doi.org/10.3389/fnut.2020.610946
[11] Zamora Diaz, D., & Llanes Somellera, S. (2025). Flavonifractor plautii: A rare cause of anaerobic bacteremia. Cureus, 17(6), e86478. https://doi.org/10.7759/cureus.86478
[12] Gupta, A., Dhakan, D. B., Maji, A., Saxena, R., V.P.P.K., Mahajan, S., Pulikkan, J., Kurian, J., Gomez, A. M., Scaria, J., Amato, K. R., Sharma, A. K., & Sharma, V. K. (2019). Association of Flavonifractor Plautii, a flavonoid-degrading bacterium, with the gut microbiome of colorectal cancer patients in India. mSystems, 4(6). https://doi.org/10.1128/msystems.00438-19
[13] Carlier, J. P., Bedora-Faure, M., K'ouas, G., Alauzet, C., & Mory, F. (2010). Proposal to unify Clostridium orbiscindens Winter et al. 1991 and Eubacterium plautii (Séguin 1928) Hofstad and Aasjord 1982, with description of Flavonifractor plautii gen. nov., comb. nov., and reassignment of Bacteroides capillosus to Pseudoflavonifractor capillosus gen. nov., comb. nov. International journal of systematic and evolutionary microbiology, 60(Pt 3), 585–590. https://doi.org/10.1099/ijs.0.016725-0
[14] German collection of microorganisms and cell cultures gmbh. (n.d.). Flavonifractor plautii. DMDZ. Retrieved November 14, 2025, from https://webshop.dsmz.de/en/bacteria/Flavonifractor-plautii.html
[15] Osada, Y., Oka, K., Iguchi, M., Morioka, H., Iwata, K.-I., Ohara, M., Shimaoka, N., Sawada, T., & Yagi, T. (2025). Flavonifractor Plautii bacteremia following bacterial translocation from the gut: A case report and literature review. Journal of Infection and Chemotherapy, 31(3). https://doi.org/10.1016/j.jiac.2024.12.021
[16] U.S. National Library of Medicine. (n.d.). Taxonomy browser: Flavonifractor Plautii. National Center for Biotechnology Information. https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?command=show&mode=node&id=292800&lvl=
[17] Li, L., Li, T., Liang, X., Zhu, L., Fang, Y., Dong, L., & Zheng, Y. (2025). A decrease in Flavonifractor plautii and its product, phytosphingosine, predisposes individuals with phlegm-dampness constitution to metabolic disorders. Cell discovery, 11(1), 25.
[18] Saito, S., Baba, S., Nikai, H., Fujisawa, R., & Fujiwara, T. (2024). Flavonifractor Plautii bacteremia with generalized peritonitis: A case report and literature review. Cureus, 16(7). https://doi.org/10.7759/cureus.63890
Edited by Eliza Asante, Mikayla Gargani, Sasiru Pathiranage, Victoria Zhou, Darian Ventura, students of Jennifer Bhatnagar
for [http://www.bu.edu/academics/cas/courses/cas-bi-311/ BI 311 General
Microbiology], 2025, Boston University.
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