I have a relative who has gone through a few different courses of antibiotics to combat a Clostridium difficile infection, with limited success. As I understand it, the initial antibiotic course for an unrelated infection wiped out normal biota and allowed the C. difficile to get established.

However, what I'm not understanding is how fecal transplant can be effective? The C. difficile is already established, is the biota being transplanted enough to be able to suppress/supplant the already established infection?


It seems to be unclear and likely some kind of combination of several factors.

The paper Fecal microbiota transplantation in relapsing Clostridium difficile infection mentions two theories as to why it works (and works very well):

  1. The introduction of bacteria able to compete with C. difficile rebalances the fecal microbiota - under normal circumstances, CD is outcompeted by other bacteria (not always enough to vanish, it can be found in about 1 in 30 healthy people, but enough to not be problematic), and it can only thrive after the use of antibiotics. A FMT reintroduces its competitors
  2. The introduction of the 'new' bacteria leads to an immune response that helps eradicating C. difficile

The first mechanism is what I found mentioned in a few other sources as well, for example on OpenBiome:

Though the mechanism has yet to be determined, it is believed that FMT works by repopulating the patient’s microbiome with diverse microorganisms that competitively exclude C. difficile

Another hypothesis is that the acid composition in the feces is significantly altered and inhibits growth of CD, see Changes in Colonic Bile Acid Composition following Fecal Microbiota Transplantation Are Sufficient to Control Clostridium difficile Germination and Growth.


As an updating addendum to YviDe's answer:

While still very far from being completely understood fecal matter transplants are more than just the commensal bacteria that are beneficial to gut health and able to "just outcompete" Clostridium difficile (CD).

Humans are not only human dna-derived cells and many many bacteria. One part often overlooked is that the human microbiome is also populated with a an abundance of viruses that are surprisingly beneficial for the host's health.

Healthy subjects may be hosts to viruses that not only eat away the food of CD or produce substances that are a bit harmful to CD's metabolism. A healthy gut contains some viruses called bacteriophages that actively seek and destroy CD.

Bacteriophage transfer during faecal microbiota transplantation in Clostridium difficile infection is associated with treatment outcome:

Results: Subjects with CDI demonstrated a significantly higher abundance of bacteriophage Caudovirales and a lower Caudovirales diversity, richness and evenness compared with healthy household controls. Significant correlations were observed between bacterial families Proteobacteria, Actinobacteria and Caudovirales taxa in CDI. FMT treatment resulted in a significant decrease in the abundance of Caudovirales in CDI. Cure after FMT was observed when donor-derived Caudovirales contigs occupied a larger fraction of the enteric virome in the recipients (p=0.024). In treatment responders, FMT was associated with alterations in the virome and the bacterial microbiome, while vancomycin treatment led to alterations in the bacterial community alone.

Conclusions: In a preliminary study, CDI is characterised by enteric virome dysbiosis. Treatment response in FMT was associated with a high colonisation level of donor-derived Caudovirales taxa in the recipient. Caudovirales bacteriophages may play a role in the efficacy of FMT in CDI.

Discussion: Faecal microbiota transplantation (FMT) is highly effective for the treatment of recurrent Clostridium difficile infection (CDI).

Studies have shown bacterial colonisation after FMT, but data on viral alterations in CDI and the association between viral colonisation and treatment outcome are largely unknown.

CDI was characterised 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 significantly 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.

Recipients infused with donor faeces consisting of a higher richness of Caudovirales than that of recipient were all cured with FMT. CDI subjects who had restoration of bacteria community only were found to have disease recurrence.

The restoration of virome community is as important as that of bacterial microbiome in FMT.

Donor selection based on virome characteristics should be considered in FMT practice.

This means that the explanation models given in the first answer are not wrong, but likely incomplete.

Further links:

Bacteriophage and bacteriocin typing scheme for Clostridium difficile.
Prevention of Clostridium difficile -induced ileocecitis with Bacteriophage(Hamster model)
Molecular Characterization of a Clostridium difficile Bacteriophage and Its Cloned Biologically Active Endolysin
Genomic Organization and Molecular Characterization of Clostridium difficile Bacteriophage ΦCD119


As you pointed out, your bowl contains many many types of bacteria, the biodome. They live in harmony, balanced. No bacteria can overwhelm the other. These are commensal bacteria. https://en.wikipedia.org/wiki/Commensalism

If, through whatever reason like antibiotics, some bacteria are wiped out then sometimes there is no way to restore the balans. A fecal transplant can reintroduce the missing bacteria, which then take back their place and reduce the c. difficile colony to a size where it is useful instead of harmful.


  • 1
    Your answer explains the basics of fecal transplants but doesn't answer the OP's specific question. How is it that the transplanted bacteria can overcome an established c. diff. colony?
    – Carey Gregory
    Mar 23 '16 at 14:56
  • @carey i'm quite sure this is all whats happening. C difficile is normally overgrown with other competing bacteria so c difficile can't dominate. When those other bacteria are killed c difficile takes there place. The reintroduced bacteria just grow and compete with c difficile again.
    – Nicow
    Mar 23 '16 at 15:27
  • Well, but how? Why would a larger, well-established colony not be able to dominate a smaller number of newcomers? (And, BTW, I'm not one of the downvoters.)
    – Carey Gregory
    Mar 23 '16 at 19:10
  • Hmm, I think what might make it clearer why this can happen would be to point out that CD is not actually all that well-adapted to the human gut - it's mainly found in soil and only in 1 out of every 30 healthy humans (probably a combination of other bacteria outcompeting it and the human immune system killing it?) Under normal circumstances, it doesn't stand a very good chance in the human gut. It's not actually part of that balanced commensalism you mention.
    – YviDe
    Mar 23 '16 at 19:22
  • 1
    No, they're not the same. Your answer simply states that FMT works and you provide links to support that (however, wikipedia is a poor source). You don't delve into the why or how FMT works, and that's the gist of the question. The other answer does delve into those aspects.
    – Carey Gregory
    Mar 23 '16 at 23:34

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