More studies continue to be published extolling the benefits of bacteriotherapy/fecal therapy. I expect at some point, the “yuck” factor which accompanies this will dissipate due to its incredible 90% success rate and the inability of antibiotics to offer any solution that can even come close to this. Some people are calling it “poop therapy” or “poo-poo therapy” but whatever it’s called, nothing offers relief from what has now become the most commonly acquired infectious agent, Clostridium difficile (C. diff). With a six-fold increase in the death rate due to C. diff, its time to get serious about the benefits of poo.


In a new study out today, researchers used mice to identify a combination six naturally occurring bacteria that eradicate a highly contagious form of Clostridium difficile, an infectious bacterium associated with many hospital deaths. Three of the six bacteria have not been described before. This work may have significant implications for future control and treatment approaches.

The researchers found that this strain of C. difficile, known as O27, establishes a persistent, prolonged contagious period, known as supershedding that is very difficult to treat with antibiotics. These contagious ‘supershedders’ release highly resistant spores for a prolonged period that are very difficult to eradicate from the environment. Similar scenarios are likely in hospitals.

C. difficile can cause bloating, diarrhea, abdominal pain and is a contributing factor to over 2,000 deaths in the UK in 2011. It lives naturally in the body of some people where other bacteria in the gut suppress its numbers and prevent it from spreading. If a person has been treated with a broad-spectrum antibiotic such as clindamycin, our bodies’ natural bacteria can be destroyed and the gut can become overrun by C. difficile. The aggressive strain of C. diff analysed in this study has been responsible for epidemics in Europe, North America and Australia.

“We treated mice infected with this persistent form of C. diff with a range of antibiotics but they consistently relapsed to a high level of shedding or contagiousness,” says Dr Trevor Lawley, first author from the Wellcome Trust Sanger Institute. “We then attempted treating the mice using faecal transplantation, homogenized faeces from a healthy mouse. This quickly and effectively supressed the disease and supershedding state with no reoccurrence in the vast majority of cases.”

This epidemic caused by C. diff is refractory to antibiotic treatment but can be supressed by faecal transplantation, resolving symptoms of disease and contagiousness.”

The team wanted to take this research one step further and isolate the precise bacteria that supressed C. diff. and restored microbial balance of the gut. They cultured a large number of bacteria naturally found in the gut of mice, all from one of four main groups of bacteria found in mammals. They tested many combinations of these bacteria, until they isolated a cocktail of six that worked best to suppress the infection.

The mixture of six bacterial species effectively and reproducibly suppressed the C. difficile supershedder state in mice, restoring the healthy bacterial diversity of the gut,” says Professor Harry Flint, senior author from the University of Aberdeen.

The team then sequenced the genomes of the six bacteria and compared their genetic family tree to more precisely define them. Based on this analysis, the team found that the mixture of six bacteria contained three that have been previously described and three novel species. This mix is genetically diverse and comes from all four main groups of bacteria found in mammals.

These results illustrate the effectiveness of displacing C. diff and the supershedder microbiota with a defined mix of bacteria, naturally found in the gut.

“Our results open the way to reduce the over-use of antibiotic treatment and harness the potential of naturally occurring microbial communities to treat C. difficile infection and transmission, and potentially other diseases associated with microbial imbalances,” explains Professor Gordon Dougan, senior author from the Wellcome Trust Sanger Institute. “Faecal transplantation is viewed as an alternative treatment but it is not widely used because of the risk of introducing harmful pathogens as well as general patient aversion. This model encapsulates some of the features of faecal therapy and acts as a basis to develop standardized treatment mixture.”

From the original article found at –

Antibiotic treatment of hospitalized patients is the major risk factor for C. difficile colonization and disease that are characterized by a toxin-mediated neutrophil response and a spectrum of outcomes from asymptomatic carriage, severe diarrhea, fulminant pseudomembranous colitis, toxic megacolon and occasionally death.”

“Recurrent C. difficile disease in humans is associated with a general reduction in intestinal bacterial diversity. We therefore hypothesized that the persistent supershedder state in mice caused by C. difficile 027/BI-7 is linked to alterations in the structure of the co-inhabiting bacterial community.”

“Short chain fatty acids (SCFA) are the end products of bacterial fermentation in the intestines and serve as important nutrients for the host. Imbalances in SCFA levels, particularly butyrate and acetate, have been associated with chronic intestinal diseases…Thus, we demonstrate that epidemic C. difficile 027/BI-7 maintains intestinal dysbiosis in mice after clindamycin treatment that is characterized by a simplified intestinal bacterial community, the presence of opportunistic bacteria and markedly altered SCFA production.”

Fecal transplantation, the administration of homogenized feces from a healthy donor, is a promising alternative therapy for recurrent C. difficile disease in humans, so we therefore tested the ability of bacteriotherapy to suppress the C. difficile supershedding state. Remarkably, a single treatment via oral gavage of C. difficile 027/BI-7 supershedding mice with homogenized feces from a healthy donor rapidly suppressed C. difficile shedding levels to below the detection limit within 5–7 days and, in contrast to vancomycin therapy, this lasted for months.

Further, fecal transplantation was consistently associated with a resolution of intestinal pathology and a reduction in the expression of proinflammatory genes. Therefore, intestinal dysbiosis caused by epidemic C. difficile is refractory to (caused by) vancomycin therapy but can be suppressed with feces of a healthy individual leading to resolution of disease and contagiousness.

Antibiotic perturbation of the intestinal microbiota is one of the major risk factors for C. difficile colonization and disease. We show that in the absence of C. difficile infection clindamycin treatment initially reduces the complexity of the murine microbiota before the diversity recovers to a level comparable to the original community by 2–3 weeks post-treatment. The majority of studies in humans and mice have also shown that the diversity of the microbiota is initially diminished by a variety of antibiotic treatments before the microbiota diversity re-establishes. However, there is variability in diversity recovery time and this is likely due to differences in the initial microbiota composition, the host’s genetics/immune system status, the spectrum and dose of the antibiotic used and the presence of bacteria in local environment that can potentially re-colonize the host.

Intestinal homeostasis is characterized by lack of pathology and a diverse, stable microbiota that produces SCFA via fermentation. Antibiotic perturbation kills susceptible bacteria resulting in a simplified community structure (and reduced SCFA production) and a loss of colonization resistance. In the absence of opportunistic infection, the microbiota generally rebounds in diversity and SCFA production to re-establish homeostasis and colonization resistance. However, exposure to C. difficile after antibiotic perturbation can lead to persistent dysbiosis that is characterized by a pathogenic microbial community, reduced SCFA and pathology. Bacteriotherapy disrupts dysbiosis leading to the clearance of C. difficile and re-establishment of intestinal homeostasis.

After antibiotic treatment there is a transient period where colonization resistance is reduced and the host is very susceptible to infection by such pathogens as C. difficile or S.Typhimurium.


For a healthier body and balanced intestinal flora, go to Dr. McCombs Candida Plan.


Additional studies: