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 Important new research was published in January 2016 about a fecal microbiota transplant (FMT) or "poop transplant". The research compared only one patient's gut microbes (thus a case study) to her fecal transplant donor's gut microbes, but it is important for looking at how gut microbes change long-term after a fecal microbiota transplant (poop transplant) and the actual length of time that it takes for the recipient's gut microbial community  to become like the donor's gut microbiome. The patient was quickly "cured" of a serious recurrent Clostridium difficile infection after one fecal micriobiota transplant (FMT) from her sister, but there were ongoing long-term changes in the patient's gut microbes for 4.5 years, at which point the microbes (bacteria and viruses) were like the donor's (at the phylum, class, and order levels), and with similar bacterial diversity. At this point the researchers said that "full engraftment" of microbes had occurred.

Until 7 months post-FMT, the  patient's microbial communities varied over time and showed little overall similarity to the donor, indicating "ongoing gut microbiota adaption" during the first seven months. But right after the transplant, the changes were enough for the patient to be immediately "cured" of her recurrent Clostridium difficile infection. The long-term results also suggested that phages (viruses) may play an important role in gut health. From Cold Spring Harbor Molecular Case Studies:

Long-term changes of bacterial and viral compositions in the intestine of a recovered Clostridium difficile patient after fecal microbiota transplantation

Fecal microbiota transplantation (FMT) is an effective treatment for recurrent Clostridium difficile infections (RCDIs). However, long-term effects on the patients’ gut microbiota and the role of viruses remain to be elucidated. Here, we characterized bacterial and viral microbiota in the feces of a cured RCDI patient at various time points until 4.5 yr post-FMT compared with the stool donor. Feces were subjected to DNA sequencing to characterize bacteria and double-stranded DNA (dsDNA) viruses including phages.

The patient's microbial communities varied over time and showed little overall similarity to the donor until 7 mo post-FMT, indicating ongoing gut microbiota adaption in this time period. After 4.5 yr, the patient's bacteria attained donor-like compositions at phylum, class, and order levels with similar bacterial diversity. Differences in the bacterial communities between donor and patient after 4.5 yr were seen at lower taxonomic levels.

C. difficile remained undetectable throughout the entire time span. This demonstrated sustainable donor feces engraftment and verified long-term therapeutic success of FMT on the molecular level. Full engraftment apparently required longer than previously acknowledged, suggesting the implementation of year-long patient follow-up periods into clinical practice. The identified dsDNA viruses were mainly Caudovirales phages. Unexpectedly, sequences related to giant algae–infecting Chlorella viruses were also detected. Our findings indicate that intestinal viruses may be implicated in the establishment of gut microbiota

FMT has shown impressive success rates of ∼90% against RCDIs and no severe adverse effects (Gough et al. 2011; Cammarota et al. 2014; O'Horo et al. 2014).... FMT led to increased donor-like intestinal bacterial diversities within 2 wk (van Nood et al. 2013).....Because viruses, especially phages, are the most abundant intestinal entities with the ability to influence microbial communities (Barr et al. 2013; Virgin 2014), they may well be relevant to C. difficile infection and the microbial changes following FMT.

Briefly, the female patient was 51 years old when admitted to the University Hospital of Zurich with her sixth episode of RCDI, suffering from severe diarrhea and weight loss.....Following FMT, the patient reported changes in bowel movements and intermittent obstipation, both of which ceased within 10 wk. Ever since, the patient has remained free of symptoms for almost 5 yr now.. 

The analysis of viral dsDNA sequences reported earlier revealed the presence of 22 viruses throughout samples D0, P1, P2, and P3 . In each sample, eight to 11 different viruses were identified, mainly belonging to the Caudovirales order (tailed dsDNA phages) that contains the viral families Myo-, Podo-, and Siphoviridae. Most viruses, 14 of 22, were identified uniquely in either sample. Three phages, the Erwinia phage vB_EamP-L1 (Podoviridae) and the two Bacteroides phages B124-14 and B40-8 (Siphoviridae), were consistently detected in all four samples and each contained phages of all three Caudovirales groups.

The bacterial composition of the donor was relatively stable and comparable at the time of FMT and 4.5 yr later (Fig. 1B), which is in accordance with the known temporal stability of adult intestinal microbiota (Zoetendal et al. 1998)....The patient's fecal microbiota underwent extensive compositional fluctuations and were dominated by Firmicutes up to 7 mo post-FMT, suggesting ongoing adaptation processes of donor microbiota in the patient's intestine that may also reflect changes in nutrition over the observation period. This is in accordance with our and other groups’ recent findings that showed high degrees of bacterial variation in RCDI patients up to 7 mo post-FMT (Broecker et al. 2013; Weingarden et al. 2015).

However, 4.5 yr post-FMT, the patient's bacteria have attained a donor-like composition at the phylum level, indicating full and stable engraftment of the donor's microbiota.....Of note, four of the five most prominent genera identified in both donor samples as well as the patient sample after 4.5 yr, Alistipes, Bacteroides, Dialister, and Faecalibacterium (Fig. 1D), are known constituents of healthy fecal microbiota (Claesson et al. 2011; Joossens et al. 2011). This further indicated that FMT led to healthy and sustainable microbiota in the patient.

One notable species detected in these three samples is Faecalibacterium prausnitzii (Fig. 1D). This species was also detected in the patient samples 6–7 mo post-FMT with abundances of <0.1% (data not shown). Faecalibacterium prausnitzii is recognized as one of the most important species of healthy individuals and normally constitutes >5% of the gut microbiota (Miquel et al. 2013). 

The fact that the patient's clinical symptoms, which included severe diarrhea in the absence of antibiotic treatment against C. difficile (Broecker et al. 2013), resolved promptly after FMT suggests that gut microbiota were able to exert normal metabolic functions even before full engraftment. This may be explained by the fact that the patient's bacterial diversity even during the highly variable time period up to 7 mo post-FMT was already in the range of the healthy donor. In agreement with the absence of symptoms until today, C. difficile bacteria were undetectable in the samples of the patient, similar to the donor who tested negative for C. difficile before FMT.....The finding that the patient's fecal microbiota attained a highly donor-like composition after 4.5 yr suggests that long-term follow-up should be implemented into clinical practice. 

The analysis of viral dsDNA sequences from a previous study revealed the presence of Caudovirales phages in all investigated samples of the donor and the patient. Caudovirales have been shown before to be the dominant viruses in the human intestine, followed by ssDNA phages of the Microviridae family that we were unable to detect with the metagenomic sequencing approach (Lepage et al. 2008; Norman et al. 2015). Three phages were identified in all of the analyzed samples of the donor and the patient. 

More research that supports that both more variety (diversity) of microbes and the actual mix of types of microbes are involved in a healthy gut microbiome. Healthy communities don't have just one important species of bacteria, but a mix of bacteria, and some mixes of bacteria work better than others in preventing infections. One can say that some mixes of bacteria are "protective" against infections. And once again, antibiotics screw up the microbial communities and cause imbalances. This study was done in mice looking at gut bacteria and Clostridium difficile (which kills about 14,000 Americans annually), but they are now continuing this research in humans. From Medical Xpress:

It takes a village... to ward off dangerous infections? New microbiome research suggests so

Like a collection of ragtag villagers fighting off an invading army, the mix of bacteria that live in our guts may band together to keep dangerous infections from taking hold, new research suggests. But some "villages" may succeed better than others at holding off the invasion, because of key differences in the kinds of bacteria that make up their feisty population, the team from the University of Michigan Medical School reports. The researchers even show it may be possible to predict which collections of gut bacteria will resist invasion the best—opening the door to new ways of aiding them in their fight.

Working in mice, the team studied one of the most dangerous gut infections around: Clostridium difficile, which kills more than 14,000 Americans a year. C-diff also sickens hundreds of thousands more, mostly hospital patients whose natural collection of gut bacteria—their gut microbiome—has been disturbed by antibiotics prescribed to protect them from other infections.

In a new paper published in the journal mBIO, the team reports the results from tests of seven groups of mice that were given different antibiotics, then were exposed to C-diff spores. The scientists used advanced genetic analysis to determine which bacteria survived the antibiotic challenge, and looked at what factors made it most likely that C-diff would succeed in its invasion.The team also developed a computer model that accurately predicted C-diff's success rate for other mice in the study, based solely on knowing what bacteria the mice had in their natural gut 'village'. The model succeeded 90 percent of the time.

"We know that individual humans all have different collections of gut bacteria, that your internal 'village' is different from mine. But research has mostly focused on studying one collection at a time," says Patrick D. Schloss, Ph.D., the U-M associate professor of microbiology and immunology who led the team. "By looking at many types of microbiomes at once, we were able to tease out a subset of bacterial communities that appear to resist C-diff colonization, and predict to what extent they could prevent an infection."

Schloss, who is a key member of the Medical School's Host Microbiome Initiative, notes that no one species of bacteria by itself protected against colonization. It was the mix that did it. And no one particular mix of specific bacteria was spectacularly better than others - several of the diverse "villages" resisted invasion.

Resistance was associated with members of the Porphyromonadaceae, Lachnospiraceae, Lactobacillus, Alistipes, and Turicibacter families of bacteria. Susceptibility to C. difficile, on the other hand, was associated with loss of these protective species and a rise in Escherichia or Streptococcus bacteria. "It's the community that matters, and antibiotics screw it up," Schloss explains. Being able to use advance genetic tools to detect the DNA of dozens of different bacteria species, and tell how common or rare each one is in a particular gut, made this research possible.  

It takes a village... to ward off dangerous infections? New microbiome research suggests soA Clostridium difficile cell.                                                      Credit: Centers for Disease Control and Prevention

Excerpts from an interesting article about microbes and some findings from 2014. From Wired:

9 Amazing and Gross Things Scientists Discovered About Microbes This Year

We can’t see them, but they are all around us. On us. In us. Our personal microbes—not to mention those in the environment around us—have us outnumbered by orders of magnitude, but scientists are only beginning to understand how they influence our health and other aspects of our lives. It’s an increasingly hot area of science, though, and this past year saw lots of interesting developments. Here are some of the highlights.

When you move, your microbes move with you

In a study published in Science in August, scientists cataloged the microbes of seven families, swabbing the hands, feet, and noses of each family member—including pets—for six weeks. They also collected samples from doorknobs, light switches, and other household surfaces. Each home had a distinct microbial community that came mostly from its human inhabitants, and the scientists could tell which home a person lived in just by matching microbial profiles. Three of the families moved during the study period, and it only took about a day for their microbes to settle in to the new place. As the journal’s editors put it: “When families moved, their microbiological ‘aura’ followed.”

Microbes could help solve crimes

Scientists made several findings this year that could potentially show up in court one day. One study found that the microbiome of human cadavers evolves in a predictable way, hinting at a new way to determine time of death. And earlier this month, researchers suggested that bacteria on pubic hair could be used to identify the perpetrators of sex crimes—especially useful when a rapist uses a condom to avoid leaving behind DNA evidence.

Your gut bacteria may be inherited

Exactly which bacteria choose to take up residence in your gut is determined, in part, by your genes, scientists reported this year after examining more than 1,000 fecal samples from 416 pairs of twins... One of the most heritable types was a family of bacteria called Christensenellaceae, which are more abundant in lean people than in obese people. 

Forget fecal transplants, poo pills may be just as effective

Clostridium difficile (pictured) is a nasty bacteria that wreaks havoc on the guts and kills 14,000 people a year in the US alone. Normally, other intestinal bacteria keep C. diff in check, but in the worst infections it starts to dominate. One effective but off putting treatment is a fecal transplant: taking a stool sample from a healthy person and transplanting it into the patient (in through the out door, so to speak). This year researchers developed a less cringe-inducing alternative. They created odorless frozen capsules that contained bacteria isolated from healthy stool samples. The poo pills successfully treated 18 of 20 patients with antibiotic-resistant C. diff infections, the team reported in JAMA in October.

Yeast evolved to lure fruit flies (not to make delicious beer)

There is crazy microbial diversity in cheese rinds

A tiny crumb of cheese rind contains about 10 billion microbial cells: bacteria and fungi that turn boring milk into something funky and delicious. Although cheesemakers have been manipulating them for centuries, not much is known about these microbes. This year scientists conducted the largest study yet on the microbial diversity of cheese, examining 137 cheeses from 10 countries.They found that microbial communities vary according to the style of cheese, but not so much according to where the cheese is made.

The microbiome could be a source of novel drugs

The bacteria that live on and in our bodies make countless molecules. Some of those molecules might make good drugs. 

We may need new branches on the tree of life for all the microbes

Life on Earth has traditionally been divided into three domains: Eukaryotes (plants, animals, and all other organisms that stash their DNA in a special compartment—the nucleus—inside their cells), Bacteria (our familiar one-celled friends and foes), and Archaea (single-celled organisms that are biochemically and genetically distinct from the other two groups). But do we really know that’s all there isWe do not, two scientists argued last month in Science. There may be entire domains of life that have eluded our methods of detection.

Without microbes, life as we know it would end

In December, two scientists posed a thought question in the journal PLOS Biology: What would happen in a world without microbes? ...Without nitrogen-fixing soil bacteria, crops would begin to fail. Decomposition would stop, waste would pile up, and the nutrient recycling that supports life as we know it would grind to a halt. “We predict complete societal collapse only within a year or so, linked to catastrophic failure of the food supply chain,” the researchers write. “Annihilation of most humans and nonmicroscopic life on the planet would follow a prolonged period of starvation, disease, unrest, civil war, anarchy, and global biogeochemical asphyxiation.”

Clostridium difficile

Clostridium difficile. Centers for Disease Control and Prevention

Natural ways that may help GERD symptoms without drugs : eating smaller portions, losing weight, not lying down for 2 hours after eating, and avoiding alcohol, cigarettes, and "trigger" foods.From Health Day News:

Could Popular Heartburn Drugs Upset Your 'Good' Gut Bugs?

Heartburn drugs such as Prilosec and Nexium may disrupt the makeup of bacteria in the digestive system, potentially boosting the risk of infections and other problems, a small new study suggests.

According to Harvard Medical School, billions of dollars are spent annually on antacid drugs in an attempt to combat heartburn, ulcers and gastroesophageal reflux disease, also known as GERD. Old standbys such as Maalox and Mylanta have been supplanted by more effective, more expensive drugs, including proton pump inhibitors. These include Prevacid (lansoprazole) and Protonix (pantoprazole) in addition to Prilosec (omeprazole) and Nexium (esomeprazole).

Long-term use of proton pump inhibitors has been linked to infection with a germ called Clostridium difficile, which causes severe diarrhea, he said. Researchers have also connected the medications to vitamin deficiencies, bone fractures and pneumonia, among other conditions.

In the new study, researchers sought to understand what happens to the trillions of germs in the digestive system when people take omeprazole, the generic name for the drug best known as Prilosec.Ten participants, aged 18 to 57, took 20 or 40 milligrams of the drug a day for 28 days. Researchers analyzed the study participants' stool samples to understand the germs in their guts.

"These microbes have evolved with us to participate in our normal development and metabolism, and perform certain functions that we would not be able to accomplish without their help," DiBaise said. Many scientists believe that people's risk of disease goes up when their normal germ makeup changes, he said.

The researchers found evidence that the medications disrupted the balance of bacteria in the digestive systems of the participants, and the changes lasted for at least a month after they discontinued the drug. It didn't seem to matter whether they took the higher or lower dose, DiBaise said.

DiBaise cautioned that the study doesn't prove that the drug causes users to become more vulnerable to C. difficile infections. However, it shows that the drug "creates a situation in the gut microbial environment that may increase an individual's susceptibility," he said.

What should users do for now? According to DiBaise, proton pump inhibitors are "the most effective medications to treat gastroesophageal reflux disease." If patients don't have the most severe symptoms, he said, other types of heartburn drugs might help. Also recommended: eating smaller portions, losing weight, not lying down for two hours after eating, and avoiding alcohol, cigarettes and "trigger" foods.

It is estimated that between 14,000 to 30,000 Americans die each year from Clostridium difficile infections. So finding a bacteria that could protect people from C. difficile is a big deal. However, it is only one bacteria, and sick people typically are depleted of a microbial community, not just one bacteria. From Science News:

Harmless bacterium edges out intestinal germ

Gut infections from the bacterium Clostridium difficile can be fought with a closely related but harmless microbe known as C. scindens. The friendly bacterium combats infection in mice by converting molecules produced in the liver into forms that inhibit C. difficile growth,researchers report October 22 in Nature.

C. scindens also appears to protect people from infection, the researchers found in a preliminary study in humans. The new findings could begin a path to the next generation of therapies using gut bacteria, says Alexander Khoruts, a gastroenterologist at the University of Minnesota in Minneapolis.

People who become infected with C. difficile typically have taken antibiotics, which wipe out the beneficial microbes in the gut, giving C. difficile a chance to take root. The infection can lead to cramps, diarrhea and even death. An estimated 500,000 to 1 million people get C. difficile infections each year in the United States. People with C. difficile receive more antibiotics to treat the infection or a fecal transplant to restore healthy microbes to the gut.

Several research groups have been trying to identify gut bacteria that are resilient in the face of C. difficile so that physicians can give patients those bacteria as a treatment, says Eric Pamer, an immunologist at Memorial Sloan Kettering Cancer Center. Single strains of bacteria such as C. scindens would offer significant advantages over fecal transplants: With a transplant, doctors screen the donated feces for pathogens that might sicken the recipient. But, Pamer says, “there are many things, viruses that have yet to be identified, that could be in a crude fecal product that might cause trouble.”  

Pamer and his team gave mice antibiotics to deplete beneficial microbes but not wipe them out completely. The researchers then fed the mice C. difficile spores and identified microbes that appeared in mice with lower amounts of C. difficile in their guts. C. scindens was the clear victor. It is harmless and present in most people, but in very low numbers.

The researchers also examined the microbial populations of 24 patients undergoing stem cell transplants. Those patients had lowered microbial diversity after receiving combinations of antibiotics, radiation and chemotherapy. The patients who didn’t develop C. difficile after the transplant were more likely to have C. scindens in their guts.

The researchers also investigated how C. scindens combats C. difficileC. difficile begins growing after it is exposed to certain molecules secreted in bile after a meal. However, another form of the molecule inhibits C. difficile growth. C. scindens transforms the molecule from one form to the other, boosting resistance to C. difficile.  

An opinion piece from Dr. David Johnson, Prof. of Medicine and Chief of Gastroenterology at Eastern Medical School in Norfolk, Virginia but an interesting one that points out the limitations of current probiotic knowledge and that we shouldn't blindly take probiotics (with only a few bacteria strains) after antibiotic use thinking that they're all good, all the time. I'm including this article to show what many medical professionals think about probiotic use and why.

He discusses 2 large studies, but unfortunately both studies only looked at hospitalized patients - and the large PLACIDE study looked at over-65 year old patients. And in the second large study he discusses the benefits of the antibiotic metronidazole.

I agree with his need for caution and the need for more large studies, but I wish he had discussed children, people NOT hospitalized, people who just had a round of antibiotics without life threatening complications, and not dismissed small studies. Hospitalized vs non-hospitalized people are very, very different groups. Small studies are finding benefits of various bacteria, but yes, the research is in its infancy, especially what are "normal microbial communities" in the gut and in other parts of the body. He does not discuss fecal transplants of entire microbial communities for C. difficile and their over 90% success rate. Dr. S. Lynch has theorized that some bacteria act as "keystone species" that could help repopulate a biome after an insult (such as antibiotics). From Medscape:

Probiotics: Help or Harm in Antibiotic-Associated Diarrhea?

Today I want to discuss the issue of probiotics, and whether probiotics are doing an element of benefit or an element of harm. With access to over-the-counter products, use of probiotics has dramatically increased. Physicians recommend probiotics routinely to patients when they are taking antibiotics to prevent antibiotic-associated diarrhea. I would like to take a time-out and reevaluate what we are doing for these patients.

Not infrequently, antibiotics are associated with Clostridium difficile infections, which occur in up to one third of patients with antibiotic-associated diarrhea.

In 2012, highly publicized meta-analyses were published in JAMA [1] and Annals of Internal Medicine. [2]These studies, and a Cochrane review,[3] suggest that not only can probiotics prevent or diminish antibiotic-associated diarrhea, but probiotics may also be helpful in avoiding C difficile infection.

Enter the most recent study, which is called the PLACIDE study, from the United Kingdom[4] It involved 5 hospitals, 68 different medical and surgical units, and more than 17,000 patients aged 65 years or older. All patients were hospitalized and taking an antibiotic.

These patients were randomly assigned, if they met eligibility criteria, to receive either a microbial preparation (which is the term they used for "probiotic") or an identical placebo. The microbial preparation had 2 strains of Lactobacillus and 2 strains of bifidobacteria, which patients received for 21 days.... Even with evaluation for intention to treat, there was no difference in the outcomes for C difficile infection or antibiotic-associated diarrhea between the microbial preparation (probiotic) and placebo group. Of interest, there was an increase in flatus in the microbial preparation group, and patients with C difficile diarrhea who received the microbial preparation reported a 3-fold increase in bloating

Although intended to restore good health, we are seeing a dysbiosis. We have disrupted the microflora in the gut, and are trying to jam it back with strains of bacteria that we think are good bacteria, and it may not be the correct answer. We don't know the right answer. When you alter the microflora, you change some of the metabolism of carbohydrates, bile salts, and complex sugars. We are not clear whether jamming the gut with another strain of bacteria is going to be of benefit.

I want to posit an element of potential harm, and not rush in to recommend probiotics routinely in patients to whom you prescribe antibiotics. I would also caution you not to use probiotics in patients in the intensive care unit, or in any patient with an indwelling prosthesis, particularly an intravascular prosthesis. 

Another article stating that the future is feces in treating a number of diseases. From Pacific Standard:

Medicine’s Dirty Secret: Fecal Transplants Are the Next Big Thing in Health Care

POO IS A DECIDEDLY IMPERFECT delivery vehicle for a medical therapy. It’s messy. It stinks. It’s inconsistent, not to mention a regulatory nightmare. But it can be incredibly potent. A classic study of nine healthy British volunteers found that bacteria accounted for more than half of the mass of their fecal solids. That astonishing concentration of microorganisms, both living and dead, makes sense when you consider that the microbial colonists inhabiting our gastrointestinal tract outnumber our own cells roughly three to one, on recent estimates.

In the ideal conditions of the human gut, a thriving ecosystem of 1,000 or more bacterial species that rivals the complexity of a rainforest has co-evolved with us. This microscopic jungle is constantly adapting in response to our diet, antibiotic use and other environmental influences. As the science has progressed, researchers are now comparing the entire collection of microbial inhabitants of the human gut, our microbiome, to a “hidden metabolic organ.” Scientists have linked disruptions to this organ, a condition known as dysbiosis, to everything from inflammatory bowel disease and high blood pressure to diabetes and obesity.

Viewed in this light, a fecal microbiota transplant is nothing more than an attempt to reseed an intestinal tract, often after antibiotics have killed off the native flora that might have kept invasive species at bay. No other medical therapy can claim such a high cure rate for the infection widely known as C. diff.

Some doctors have likened the recoveries of desperately ill patients to those seen with anti-HIV protease inhibitors in the mid-1990s. After the Mayo Clinic in Scottsdale, Arizona, performed its first fecal microbiota transplant in 2011, a patient who had been bed-ridden for weeks left the hospital 24 hours later. And in 2013, researchers in the Netherlands halted a landmark C. diff. clinical trial early for ethical reasons when they saw that the overall cure rate of 94 percent with donor feces had far outpaced the 31 percent cured with the antibiotic vancomycin.

Yet few other interventions elicit such disgust, revulsion, and ridicule. Chronicling a potential advance by a team of Canadian scientists, one newspaper account warned readers: “Hold your nose and don’t spit out your coffee.” In 2013, the founder of a patient advocacy blog called The Power of Poop wrote an open letter to 13 gastroenterology associations detailing the story of a Kentucky man who contracted an acute case of C. diff. Despite his family’s pleas, his doctor dismissed the idea of a fecal transplant as “quackery.” The man died the next day.

Although most providers haven’t published their overall success rates, their self-reported results are surprisingly similar, and consistent with what published reports there are. Khoruts says he has achieved a success rate of about 90 percent after one infusion, 99 percent after two. “In medicine, it’s pretty startling to have therapy that’s that effective for the most refractory patients with that condition,” he says. Colleen Kelly, a gastroenterologist with the Women’s Medicine Collaborative in Providence, Rhode Island, has performed the procedure on 130 patients with recurrent C. diff., with a success rate of about 95 percent. Most of the transplants have taken after just one attempt.

For a relatively simple bacterial infection, Petrof says, the potential remedy may be fairly straightforward. “With recurrent C. diff. what you’ve done is you’ve basically torched the forest,” she says. Nearly everything has been killed off by the antibiotics, leaving very low bacterial diversity. “So the C. diff. can just take root and grow.” Adding back almost any other flora—the equivalent of planting seedlings in the dirt—could help the ecosystem keep interloping pathogens at bay.

For more complicated conditions, though, a simple fecal transplant may not be enough, at least with donors from the Western world. One hypothesis suggests that people in lower-income countries might harbor more diverse bacterial populations in their guts than those who have grown up in a more sterile, antibiotic-rich environment. And in fact, a 2012 study found that residents of Venezuela’s Amazonas state and rural Malawi had markedly more diverse gut microbiomes than people living in three U.S. metropolitan areas. Scientists have already raised the idea that a rise in allergies and autoimmunity in industrialized nations may derive from a kind of collective defect of reduced microbial diversity.

“We cannot find people who’ve never been on antibiotics,” Khoruts says of his donors. For complex autoimmune diseases such as ulcerative colitis, fecal transplants may offer only a partial solution. And with some data suggesting that susceptibility may be linked in part to past antibiotic exposure, perhaps no Western donor can provide the microbes needed to fully reseed the gut.

What then? Khoruts says it may be necessary to seek out ancestral microbial communities—the ones all humans hosted before the advent of the antibiotic era—within people in Africa or the Amazon. “It’s just a disappearing resource,” he says.

By the beginning of April 2014, nearly 30 fecal transplant clinical trials were underway around the world. Roughly half were aimed at C. diff., including two testing the therapy in combination with vancomycin, and another multi-center trial evaluating the effectiveness of fresh versus frozen donor poo.

As the therapy becomes more widely established, via something akin to a “poop pill” or “crapsule,” perhaps the infectious pool of C. diff. patients may start to dwindle. More clinicians, then, might feel emboldened to explore how our bowel flora may affect not only the gastrointestinal system but also the immune and neurological systems. At least a dozen trials are now investigating whether fecal transplants can help treat some form of inflammatory bowel disease, be it Crohn’s disease or ulcerative colitis. Another is looking into Type 2 diabetes, and one is even using lean donors to test fecal transplants on patients with metabolic syndrome. Researchers say it won’t be along before they’re joined by studies investigating whether the therapy might aid diseases like multiple sclerosis and autism.

For those who want to know more, another article form The Pacific Standard:

6 Ways to Transplant Fecal Matter, at Home or at the Hospital

And the following two groups:  The Fecal Transplant Foundation

The Power of Poop

There is a new procedure in which microbiota (the microbes) from a healthy individual are introduced into the gastrointestinal system of a diseased individual via a fecal transplant.  The purpose of the fecal transplant is to replace good bacteria which has been suppressed or killed (usually by antibiotics) , and which has caused bad bacteria, such as Clostridium difficile, to overpopulate the gut. This is having amazing success rates.  It has been used the most for Clostridium difficile (C. difficile) infections, which sickens about half a million Americans annually. This infection can be so debilitating and so resistant to all antibiotics that about 14,000 Americans die each year from it. Even though not that many have been done, fecal transplants are gaining in popularity (some even being done by do-it-yourselfers using fecal enemas at home) because fecal transplants can have a 95 to 98% success rate.                      

New research is starting to see if the fecal transplant can be made even easier (via a "poop pill"), and also if fecal transplants will work for Inflammatory Bowel Diseases (IBD). This would mean the future treatment possibility of transplanting microbiota from healthy individuals to individuals sick with IBD. From the October 4, 2013 Science Daily:  

 Fecal Transplant Pill Knocks out Recurrent C. Diff Infection

C. diff infection can occur after people take antibiotics, wiping out the good bacteria in the gastrointestinal (GI) system, allowing C. diff to flourish and leading to severe diarrhea. In some patients, infection continues to recur despite standard treatment with antibiotics. For patients trapped in that cycle, doctors have transplanted feces from healthy donors into their GI system to rebalance the bacteria and stop infections from recurring.

University of Calgary researchers reported a 100 percent success rate -- none of the 27 patients who took the tablet-sized pills had a recurrence of C. diff, even though all of them previously had had at least four bouts of the infection. Patients ingested between 24 and 34 capsules containing fecal bacteria, often donated by family members.

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There is even the site The Power of Poop  which calls itself a "patient information resource dedicated to promoting safe accessible Fecal Microbiota Transplant (FMT) and to raising awareness of the role of the human microbiome in digestive illness."    http://thepowerofpoop.com