Fecal Transplant: What You Introduce and What You Change

Aziz koleilat

Published on: 2019-02-28


Fecal microbiota transplantation is an old procedure that has recently become popular again. It has shown a clear and good effect in the treatment resistant of C. difficile infection, and an effect on the composition of the microbiota by introducing microbes of the donner, what microbes and how long it stays.


Microbial flora; Bacteriophages; Virome, Bacterial microbiome


Fecal transplant of fecal microbiota transplant (FMT) is the transfer of microbial flora from a healthy human to another unhealthy human [1]. It is an old method used by the Chinese hundred years ago. It was also used during the First World War to treat diarrhea and dysentery. Lately the Europeans rediscovered it and tried to experiment it on several gastrointestinal diseases [2, 3]. Humans depend on symbiotic microbes living within them. The human microbiome has trillions of microscopic life forms living in it. The body is with symbiotic relationship with them since it provides them a place to live and they help the body stay alive. They aid in supporting the body health. They participate in digesting food and provide many kinds of protective mechanisms for the body [4]. They interact with each other and with the gastrointestinal mucosa as well as with the gut mucosal immune system. They consist of bacteria, viruses or fungi [4,5]. The most dominant divisions are the Fermicutes, Bacteriods, Actinobacteria and Proteobacteria [6].
The microbiota has various functions in the human body. It asists in recycling the fermented non-digested carbohydrates and changes them into short chain fatty acids that serve as nutrition for the colonocytes. It also has other functions such as micronutrient and vitamins synthesis, toxin’s elimination, gut development maturation and fortification of gut barrier against invaders [7]. Any disruption of the physiological composition of the microbiota will lead to what is called dysbiosis. Dysbiosis is the unbalance between helpful and harmful microbial flora. The consequence is resistant pathogenic bacteria (Pathobiont) [8]. Dysbiosis could cause irritable bowel syndrome, inflammatory bowel disease, autoimmunity, metabolic diseases as obesity, diabetes, and gestational diabetes, autism, cancer, neurological conditions including Parkinson’s disease, as well as suppression of the control system for making hormones (The Hypothalamic-Pituitary-Adrenal-Thyroid-Gonadal Axis or Gut-Brain Axis) [8]. Hence, fecal microbiota transplantation could restore theimbalance and prevent harmful consequences in the recipient who harbors an altered colonic microbiome [1]. The rationale of using FMT to treat diseases has been validated by its successful use in treating recurrent Clostridium difficile infection (CDI) [9,10]. The hypothesis behind fecal microbiota transplant is based on bacterial interference by using harmless bacteria to replace pathogens and restoration of missing components of the flora including Firmicutes and Bacteroidetes [11,12]. The restored colon microbial community could inhibit C. difficile by multiple mechanisms depending on the microbiota composition and the recipient’s genotype such as by competition for nutrients, direct suppression by antimicrobial peptides, bile-acid mediated inhibition of spore germination and vegetative growth, activation of immune-mediated colonization resistance, decreasing bacteria with genes resistant antibiotics, triggering mucosal immune responses, or rapid production of anti-inflammatory mediators that could counteract pro-inflammatory cytokines [12,13]. CDI was characterized by a high abundance of Caudovirales bacteriophages and a low Caudovirales diversity, richness and evenness compared with healthy household controls. Donor-derived Caudovirales taxa occupied a larger fraction of the enteric virome in CDI subjects who responded to FMT compared with those who did not. FMT was associated with alterations in the enteric virome and bacterial microbiome, while vancomycin treatment was associated with alterations of the bacterial microbiome only [14]. The effects of bacteria on CDI or on animal model traits such as obesity and toxin tolerance appear to occur in light of a limited understanding of the complex composition and nature of feces [15,16].
Several components are included in FMT. Changes observed in the recipient's biology are routinely attributed to bacterial cells in the donor feces (~10 per gram of human wet stool). In addition to viable bacteria (small fraction of total fecal matter), other components include: colonocytes (~10 per gram of wet stool), archaea (~10 per gram of wet stool), viruses (~10 per gram of wet stool), fungi (~10 per gram of wet stool), protists, and metabolites[17]. Thus, bacteria transferred within the fecal material, whether viable or not, are not the only player from the donor feces that affects the recipient's biology. Through bacterial targeting, phage therapy can potentially eliminate virulent bacteria in a diseased gut and allow commensal bacterial to re flourish. Colonocytes from the donor prevent bacterial translocation into internal tissues and organs and result in repair of superficial colon damage. Metabolites can feed the colonocyte barrier and intestinal bacteria. These metabolites can alleviate inflammation and mucosal damage [16]. However, although high concentrations of intestinal archaea and certain fungi are correlated to intestinal and autoimmune diseases, still their effect is not fully known. Nevertheless, individual components of fecal matter can yield health benefits and may work synergistically to restore homeostasis and resolve dysbiosis.


Fecal transplant so far is promising. Further knowledge about all other components of the donor feces and long-term outcomes of management is needed to improve its effectiveness.


To Miss Lubna Sino Research department MUGH for review and corrections.


  1. Vindigni SM, Surawicz CM. Fecal microbiota transplantation. Gastroenterol Clin North Am. 2017; 46: 171-185.
  2. Zhang F, Luo W, Shi Y, Fan Z, Ji G. Should we standardize the 1,700-year-old fecal microbiota transplantation? Am J Gastroenterol. 2012; 107: 1755-1756.
  3. Lewin RA. More on merde. Perspect Biol Med. 2001; 44: 594-607.
  4. Michail S, Klonoff A. Review of fecal transplant in childhood gastrointestinal disorders. Ann Pediatr Child Health. 2015; 3: 1043.
  5. Lederberg J, McCray AT. Ome Sweet ’Omics-a genealogical treasury of words. Scientist. 2001; 15: 8.
  6. Tremaroli V, Bäckhed F. Functional interactions between the gut microbiota and host metabolism. Nature. 2012; 489: 242-249.
  7. Rowland I, Gibson G, Heinken A, Scott K, Swann J, Thiele I, Tuohy K, et al. Gut microbiota functions: metabolism of nutrients and other food components. Eur J Nutr. 2018; 57: 1-24.
  8. Carding S, Verbeke K, Vipond DT, Corfe BM, Owen LJ. Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015; 26: 26191.
  9. Malikowski T, Khanna S, Pardi DS. Fecal microbiota transplantation for gastrointestinal disorders. Curr Opin Gastroenterol. 2017; 33: 8-13.
  10. Choi HH, Cho YS. Fecal microbiota transplantation: current applications, effectiveness, and future perspectives. Clin Endosc. 2016; 49: 257-265.
  11. Grehan MJ, Borody TJ, Leis SM, Campbell J, Mitchell H, Wettstein A, et al. Durable alteration of the colonic microbiota by the administration of donor fecal flora. J Clin Gastroenterol. 2010; 44: 551-561.
  12. Khoruts A, Dicksved J, Jansson J, Sadowsky MJ. Changes in the composition of the human fecalmicrobiome after bacteriotherapy for recurrent Clostridium difficile associated diarrhoea. J Clin Gastroenterol. 2010; 44: 354-360.
  13. Pamer EG. Fecal microbiota transplantation: effectiveness, complexities, and lingering concerns. Mucosal Immunol. 2014; 7: 210-214.
  14. Zuo T, Wong SH, Lam k, Lui R, Cheung K, Tang W, et al. BacteriophageTransfer during Fecal Microbiota Transplantation is Associated with Treatment Response in Clostridium Difficile Infection. Gastroenterol. 2017; 152: 140-141.
  15. Kohl KD, Stengel A, Dearing MD. Inoculation of tannin?degrading bacteria into novel hosts increases performance on tannin?rich diets. Environ Microbiol. 2016; 18: 1720-1729.
  16. Den Besten G, Van Eunen K, Groen AK, Venema K, Reijngoud DJ, Bakker BM,et al. The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. J Lipid Res. 2013; 54: 2325-2340.

Bojanova DP, Bordenstein SR. Fecal transplants: what is being transferred?. PLoS Biol. 2016; 14: 1002503.