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Published on Leave a comment on A Mix of Bacteria Protect Against Infections?

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.

A Clostridium difficile cell.                                                     Credit: Centers for Disease Control and Prevention

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Drawing of colon seen from front (the appendix is colored red). Credit: Wikipedia.

For more than 100 years, the standard treatment for appendicitis has been surgery. Now a large Finnish study provides the best evidence to date that most patients can be treated with antibiotics alone.

How did the usual treatment of doing an appendectomy (appendix removal) arise? In 1886 Dr. Reginald Fitz, while investigating pelvic infections (which resulted in many deaths in those days), decided that an inflamed appendix progresses from a mild inflammation, to gangrene, then perforation, which would result in pelvic abscess.

This reason for an appendectomy (that it would prevent serious infection) became established in medical thought and still guides appendicitis management today. But nowadays we have antibiotics! And the researchers noted that some cases resolved on their own without any treatment.

And instead of the prevailing view for many years that the appendix is a "vestigial organ with no purpose",  it turns out that the appendix has a great reason for existence. It seems to provide a safe haven for good bacteria when gastrointestinal illness flushes those bacteria from the rest of the intestines. This reservoir of gut microbes then repopulates the digestive system following the illness.

It makes me wonder why some people get appendicitis and others don't - do they have inflammation for some reason so that their bacterial communities are out of whack (dysbiosis)? Would dietary changes help prevent recurrences?

From the NY Times: Antibiotics Are Effective in Appendicitis, Study Says

For more than 100 years, the standard treatment for appendicitis has been surgery. Now a large Finnish study provides the best evidence to date that most patients can be treated with antibiotics alone. The study, published Tuesday in JAMA, involved 530 patients aged 18 to 60 who agreed to have their treatment — antibiotics or surgery — decided at random. Three out of four who took antibiotics recovered easily, the researchers found. And none who had surgery after taking antibiotics were worse off for having waited.

The new study comes amid growing questions about the routine use of surgery to treat appendicitis, which strikes about 300,000 Americans a year, afflicting one out of 10 adults at some point in their lives.

The results only apply to uncomplicated appendicitis, stressed Dr. Paulina Salminen, a surgeon at Turku University Hospital in Finland and lead author of the new study. She and her colleagues excluded from their trial the 20 percent of patients with complicated cases — people with perforated appendices or abdominal abscesses, and those with a little, rock like blockage of the appendix called an appendicolith.

In the 1950s, soon after antibiotics were discovered, some doctors reported success using them to treat patients with appendicitis. But, Dr. Livingston wrote in his editorial, “So powerful is the perceived benefit of appendectomy for appendicitis that surgical treatment for appendicitis remains unquestioned, with seemingly little interest in studying the problem.”

Dr. Livingston also found that most appendices that perforate have already done so by the time the patient shows up at an emergency room. Those that have not perforated when the patient seeks medical help almost never do so. People with so-called uncomplicated appendicitis, he concluded, seem to have a different disease — one that can be treated with antibiotics.

“The reason we take the appendix out and do it as an emergency is the belief, dating back to 1886, that the appendix will eventually become gangrenous and cause a pelvic abscess,” Dr. Livingston said.

Even with the results of the Finnish study, many questions remain. A person who has had one episode of appendicitis is at higher than usual risk for another....Accumulating data has led other experts to raise an even more controversial idea: Perhaps antibiotics aren’t always necessary, either. It is possible, some researchers say, that most people with appendicitis would get better on their own if doctors did nothing. The Finnish team is now planning a clinical trial to test that theory.

Published on Leave a comment on Some Childbirth Practices Mess With Needed Microbes

Currently, during birth there are many potential disruptions to the healthy development of the infant's microbial ecosystem. Some practices to be concerned about: the use of antibiotics during pregnancy and during delivery, c-sections, newborns routinely given antibiotics, and then bottle feeding instead of breastfeeding. Sometimes one or more of these practices are medically necessary, but currently they are being done much too frequently and casually. In these ways we are conducting an experiment on every baby's microbial ecosystem with unknown long-term consequences. The following excerpts from Dr.Martin Blaser's popular 2014 book Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues, even though written a year ago, are a nice summary of these issues. From Wired:

The Way You’re Born Can Mess With the Microbes You Need to Survive

THROUGHOUT THE ANIMAL kingdom, mothers transfer microbes to their young while giving birth....And for millennia, mammalian babies have acquired founding populations of microbes by passing through their mothers’ vagina. This microbial handoff is also a critical aspect of infant health in humans. Today it is in peril.

Microbes play a hidden role in the course of every pregnancy. During the first trimester, certain species of bacteria become overrepresented while others become less common. By the third trimester, just before the baby is born, even greater shifts occur. These changes, involving scores of species, are not random. The compositions change in the same direction across the dozens of women who have been studied.... Women of reproductive age carry bacteria, primarily lactobacilli, which make the vaginal canal more acidic. This environment provides a hardy defense against dangerous bacteria that are sensitive to acid. Lactobacilli also have evolved a potent arsenal of molecules that inhibit or kill other bacteria.

Whether the birth is fast or slow, the formerly germ-free baby soon comes into contact with the lactobacilli. The baby’s skin is a sponge, taking up the vaginal microbes rubbing against it. The first fluids the baby sucks in contain mom’s microbes, including some fecal matter.

Once born, the baby instinctively reaches his mouth, now full of lactobacilli, toward his mother’s nipple and begins to suck. The birth process introduces lactobacilli to the first milk that goes into the baby. This interaction could not be more perfect. Lactobacilli and other lactic acid–producing bacteria break down lactose, the major sugar in milk, to make energy. The baby’s first food is a form of milk called colostrum, which contains protective antibodies. The choreography of actions involving vagina, baby, mouth, nipple, and milk ensures that the founding bacteria in the baby’s intestinal tract include species that can digest milk for the baby.

Breast milk, when it comes in a few days later, contains carbohydrates, called oligosaccharides, that babies cannot digest. But specific bacteria such as Bifidobacterium infantis, another foundational species in healthy babies, can eat the oligosaccharides. The breast milk is constituted to give favored bacteria a head start against competing bacteria.

Cesarian delivery is a largely unrecognized threat to the microbial handoff from mother to child. Instead of traveling down the birth canal picking up lactobacilli, the baby is surgically extracted from the womb through an incision in the abdominal wall....For all of these reasons, U.S. C-section rates increased from fewer than one in five births in 1996 to one in three births in 2011—a 50 percent increase.

The founding populations of microbes found on C-section infants are not those selected by hundreds of thousands of years of human evolution. A few years ago in Puerto Ayacucho, Venezuela, my wife, Gloria, conducted the first study of its kind to test whether the microbes found on newborn babies delivered vaginally or by C-section varied in any way....The mouths, skin, and first bowel movements of babies born vaginally were populated by their mother’s vaginal microbes: Lactobacillus, Prevotella, or Sneathia species. Those born by C-section harbored bacterial communities found on skin, dominated by Staphylococcus, Corynebacterium, and Propionibacterium.

In other words, their founding microbes bore no relationship to their mother’s vagina or any vagina. At all the sites—mouth, skin, gut—their microbes resembled the pattern on human skin and organisms floating in the air in the surgery room. They were not colonized by their mother’s lactobacilli. The fancy names of these bacteria don’t matter as much as the notion that the founding populations of microbes found on C-section infants are not those selected by hundreds of thousands of years of human evolution or even longer.

Another threat to a baby’s newly acquired resident microbes involves antibiotics given to the mother. Most doctors consider it safe to prescribe penicillins for all sorts of mild infections in pregnancy—coughs, sore throats, urinary tract infections. Sometimes when doctors think that the mother has a viral infection they also give antibiotics just in case it is actually a bacterial infection.

Then comes the birth itself. Women in labor routinely get antibiotics to ward off infection after a C-section....Antibiotics are broad in their effects, not targeted....The problem, of course, is that we know antibiotics are broad in their effects, not targeted. While the antibiotic kills Group B strep, it also kills other often-friendly bacteria, thus selecting for resistant ones. This practice is altering the composition of the mother’s microbes in all compartments of her body just before the intergenerational transfer is slated to begin.

The baby also is affected in similar unintended ways. Any antibiotic that gets into the bloodstream of the fetus or into the mother’s milk will inevitably influence the composition of the baby’s resident microbes, but we are only beginning to understand what this means.

Finally, the babies are directly exposed. Most parents are not aware that all American-born babies today are given an antibiotic immediately after birth. The reason is that many years ago, before antibiotics, women who unknowingly had gonorrhea would pass the infection to their babies, giving the newborns terrible eye infections that could cause blindness...The dose is low but is likely affecting the composition of the infant’s resident microbes just when the founding populations are developing. We should be able to develop a better way to screen, so we can target those babies at the highest risk, perhaps a few hundred among the millions of births a year.

Although babies are born into a world replete with diverse bacteria, the ones that colonize them are not accidental. These first microbes colonizing the newborn begin a dynamic process. We are born with innate immunity, a collection of proteins, cells, detergents, and junctions that guard our surfaces based on recognition of structures that are widely shared among classes of microbes. In contrast, we must develop adaptive immunity that will clearly distinguish self from non-self. Our early-life microbes are the first teachers in this process, instructing the developing immune system about what is dangerous and what is not.

A newborn infant, seconds after delivery. Amniotic fluid glistens on the child's skin.  Credit: Wikipedia, Ernest F

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Further reasons to be cautious of using antibiotics, and more support for finding beneficial bacteria and other microbes to outcompete the "bad" microbes. I especially liked the last paragraph that stressed for a healthy microbiota (microbial community):"Instead of trying to kill the "bad" bacteria causing an illness, a healthy and functioning microbiota may be able to outcompete the unwanted microbes and improve immune function." From Medical Xpress:

Unwanted impact of antibiotics broader, more complex than previously known

Researchers at Oregon State University have discovered that antibiotics have an impact on the microorganisms that live in an animal's gut that's more broad and complex than previously known. The findings help to better explain some of the damage these medications can do, and set the stage for new ways to study and offset those impacts.

Researchers have known for some time that antibiotics can have unwanted side effects, especially in disrupting the natural and beneficial microbiota of the gastrointestinal system. But the new study helps explain in much more detail why that is happening, and also suggests that powerful, long-term antibiotic use can have even more far-reaching effects. Scientists now suspect that antibiotic use, and especially overuse, can have unwanted effects on everything from the immune system to glucose metabolism, food absorption, obesity, stress and behavior.

The issues are rising in importance, since 40 percent of all adults and 70 percent of all children take one or more antibiotics every year, not to mention their use in billions of food animals. Although when used properly antibiotics can help treat life-threatening bacterial infections, more than 10 percent of people who receive the medications can suffer from adverse side effects.

This research used a "cocktail" of four antibiotics frequently given to laboratory animals, and studied the impacts."Prior to this most people thought antibiotics only depleted microbiota and diminished several important immune functions that take place in the gut," Morgun said. "Actually that's only about one-third of the picture. They also kill intestinal epithelium. Destruction of the intestinal epithelium is important because this is the site of nutrient absorption, part of our immune system and it has other biological functions that play a role in human health."

The research also found that antibiotics and antibiotic-resistant microbes caused significant changes in mitochondrial function, which in turn can lead to more epithelial cell death....Mitochondria plays a major role in cell signaling, growth and energy production, and for good health they need to function properly.

Morgun and Schulzhenko's research group also found that one of the genes affected by antibiotic treatment is critical to the communication between the host and microbe. "When the host microbe communication system gets out of balance it can lead to a chain of seemingly unrelated problems," Morgun said. Digestive dysfunction is near the top of the list, with antibiotic use linked to such issues as diarrhea and ulcerative colitis. But new research is also finding links to obesity, food absorption, depression, immune function, sepsis, allergies and asthma.

Healthy microbiota may also be another way to address growing problems with antibiotic resistance, Morgun said. Instead of trying to kill the "bad" bacteria causing an illness, a healthy and functioning microbiota may be able to outcompete the unwanted microbes and improve immune function.

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After my January 9, 2015 post I was asked more about the microbial differences in babies who had been born by cesarean vs vaginal deliveries. What could be done about this? Should this be of concern when C-section rates in some places are approaching 50% of all births?

Well, some researchers are concerned, including Dr. Dominguez-Bello, who is doing ground-breaking research in this area. She is doing a long-term study in which babies born by cesarean section are immediately swabbed with a gauze cloth laced with the mother's vaginal fluids and resident microbes. Several (but not all) articles that I looked at said that the gauze is a "saline-soaked gauze".

Summary of the method:1) Incubate gauze in mother's vagina for 1 hour 2) Extract gauze before C-section  3) Expose newborn to the vaginal gauze (Mouth first, then face, then rest of body). If for some medical reason they don’t (and there is a C-section), then this is a restoring intervention.

Note that Dr. Dominguez-Bello always first checks to make sure the mother is HIV-negative and strep-B negative, and showing no signs of a STD. The basic premise is that babies should have crossed the mother's birth canal to be "seeded" with the mother's microbes, but if for some medical reason they don’t (and there is a C-section), then this is a (somewhat) restoring intervention.

From Feb. 2014 New York Academy of Sciences: Hats Off to Bacteria!

Why are bacteria in the body? What do we, and the bacteria, gain from this arrangement? And who's in charge? "There is a dialogue," Dominguez-Bello said, "sometimes a fight, sometimes a good dialogue. We have evolved with them. The first form of life on Earth was bacteria. Whatever came after had to deal with bacteria, cope with bacteria, associate with bacteria ...  ...continue reading "Can Missing Birth Canal Bacteria Be Restored to Cesarean Birth Babies?"

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Considering all the antibiotics that the typical sinusitis sufferer takes over the years, reading this article was depressing. One wonders, can the gut microbiome (community of microbes) recover from many rounds of antibiotics and how long does it take? Please note: CD is Crohn's disease, UC is ulcerative colitis, and IBD is inflammatory bowel disease. Dysbiosis means that the community of microbes (microbiome) is out-of-whack. From Medscape:

Antibiotics Associated With Increased Risk of New-onset Crohn's Disease but not Ulcerative Colitis

The objective of this study was to perform a meta-analysis investigating antibiotic exposure as a risk factor for developing inflammatory bowel disease (IBD).A literature search using Medline, Embase, and Cochrane databases was performed to identify studies providing data on the association between antibiotic use and newly diagnosed IBD. 

Conclusions: Exposure to antibiotics appears to increase the odds of being newly diagnosed with CD but not UC. This risk is most marked in children diagnosed with CD.

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Environmental factors have a key role in the pathogenesis of inflammatory bowel disease (IBD)...Furthermore, the incidence of IBD has been increasing worldwide over time. Developing countries have seen an increase in IBD incidence as they have Westernized.

Emerging evidence suggests that certain medications are associated with an increased risk of new-onset IBD. In particular, antibiotics have been linked to the development of both Crohn's disease (CD) and ulcerative colitis (UC).Growing research suggests that the microbiome and its interaction with the mucosal immune system are important in the pathogenesis of IBD.Antibiotics can cause alterations to the microbiome that may potentially contribute to the dysbiosis and dysregulated immune response seen in IBD.

Previous studies have investigated the association of antibiotic exposure with newly diagnosed IBD in both adult and pediatric populations. CD has been more consistently associated with antibiotic use, with some studies demonstrating an increased risk of CD but not UC. It also appears that patients who receive more frequent courses of antibiotics have a higher likelihood of developing IBD.

The results of this meta-analysis suggest that exposure to antibiotics increases the risk of new-onset IBD. When stratifying by type of IBD, antibiotic exposure was associated with an increased risk of developing CD but not UC. We found that the magnitude of risk of new CD is greater for children than for adults. All classes of antibiotics studied, with the exception of penicillins, were associated with new diagnoses of IBD. Interestingly, the types of antibiotics showing the strongest association were fluoroquinolones and metronidazole.

Although it is impossible to draw causal links on the basis of these data, there are some possible implications and explanations for our findings. First, our findings may support the importance of disruptions in the microbiome in the pathogenesis of IBD. The link between antibiotic exposure and new IBD seems biologically plausible. It is known that the microbiome likely has an important role in the pathogenesis of IBD. Studies have shown a decrease in the diversity and stability of both mucosa-associated bacteria and fecal bacteria in patients with CD and UC.For example, the largest cohort microbiome study to date recently found that newly diagnosed CD patients have increased Enterobacteriaceae,Pasteurellaceae, Veillonellaceae, and Fusobacteriaceae, and decreased Erysipelotrichales, Bacteroidales, and Clostridiales.

Antibiotics have been shown to alter the composition of the human gut microbiota by decreasing taxonomic richness and diversity....Although the microbiome may recover to its initial state within days to weeks after antibiotic treatment, some studies have shown a longer-term impact of antibiotics on specific microbial populations that can persist for months to years.

It is unclear as to why antibiotic exposure was associated with new-onset CD and not UC. Studies have suggested a difference in the microbiota between CD and UC patients....Our finding that pediatric populations appear to have an increased association of antibiotic use with new-onset CD compared with adults may reflect the less stable nature of the microbiome earlier in life. During the first 3 years of life, the microbiome appears to undergo marked changes and significant maturation toward an adult-like composition with greater interpersonal variation. It is possible that antibiotics may therefore have a greater impact during childhood when the gut microbiota composition is still developing.

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Another research result from the American Gut Project, an amazing crowdsourced project. While differences were found in the fecal microbiome (microbial community) of adults born by cesarean section vs vaginal delivery, it is unknown whether this has any possible effects on diseases or risks of diseases during adulthood. This study is online as of 8 November 2014, but still In Press. From EBioMedicine:

Diversity and Composition of the Adult Fecal Microbiome Associated with History of Cesarean Birth or Appendectomy: Analysis of the American Gut Project

Adults born by cesarean section appear to have a distinctly different composition of their fecal microbial population. Whether this distinction was acquired during birth, and whether it affects risk of disease during adulthood, are unknown.

Prenatal and early postnatal exposures and events can affect the entire life course. As one example, cesarean birth has been associated with an increased likelihood of asthma and cardiovascular disease in children (Renz-Polster et al., 2005, Thavagnanam et al., 2008 and Friedemann et al., 2012), hypertension in young adults (Horta et al., 2013), and obesity in both children and adults (Pei et al., 2014, Darmasseelane et al., 2014,Blustein et al., 2013 and Mueller et al., 2014). ... As well summarized by Arrieta and colleagues, several studies have noted differences in the neonatal fecal microbiota by route of delivery (Arrieta et al., 2014). ... More recently, with comprehensive analysis based on next generation sequencing of 16S rRNA genes, Dominguez-Bello and colleagues reported that route of delivery was associated with differences in the composition of the microbial populations that initially colonized the offspring. Notably, neonates who were born vaginally were colonized by vagina-associated bacteria, whereas those born by cesarean section were initially colonized by skin-associated bacteria ( Dominguez-Bello et al., 2010).

Early life alteration of the gut microbiota may have a lasting effect. Trasande et al. observed that exposure to antibiotics up to age 6 months was associated with elevated body mass index (BMI) up to age 7 years (Trasande et al., 2013).

The 16S rRNA V4 region was sequenced by the American Gut Project....Of the 1097 participants, cesarean birth was reported as “yes” by 92, “no” by 948, and missing or uncertain by 57. Likewise, appendectomy was reported as “yes” by 155, “no” by 961, and missing or uncertain by 21.

This analysis was primarily motivated by the observation that the composition of the microbiome of neonates differed significantly between those born vaginally and those born by cesarean section (Arrieta et al., 2014 and Dominguez-Bello et al., 2010). With vaginal delivery, the neonatal microbiome resembled the vaginal microbiome, with high relative abundance of Prevotella and especially Lactobacillus taxa. In contrast, cesarean-delivered neonates had a diverse array of taxa resembling the skin microbial community, including Staphylococcus, Streptococcus, Propionibacterineae, Haemophilus, and Acinetobacter ( Dominguez-Bello et al., 2010). Cesarean-delivered neonates and infants typically have a paucity of Bifidobacterium and Bacteroides species ( Arrieta et al., 2014).

In the current analysis, we observed that the fecal microbiome composition differed in adults who reported that they had been delivered by cesarean section. This suggests that a difference by route of delivery may persist into adulthood. Of the taxa noted to be increased in cesarean-delivered neonates and infants ( Arrieta et al., 2014, Penders et al., 2006 and Dominguez-Bello et al., 2010), only Haemophilus and certain Clostridia genera had elevated abundance in the fecal microbiome of cesarean-delivered adults ( Table 3).

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Sad, but not surprising results. It highlights the damage repeated courses of antibiotics, and even illness, do to gut microbial communities. The researchers write that during a prolonged stay in ICU they found the emergence of "ultra-low-density communities" (only 1 to 4 bacteria species) in patients. From Science Daily:

Critically ill ICU patients lose almost all of their gut microbes and the ones left aren't good

Researchers at the University of Chicago have shown that after a long stay in the Intensive Care Unit (ICU) only a handful of pathogenic microbe species remain behind in patients' intestines. The team tested these remaining pathogens and discovered that some can become deadly when provoked by conditions that mimic the body's stress response to illness.

"Our hypothesis has always been that the gut microflora in these patients are very abnormal, and these could be the culprits that lead to sepsis," he says. The current study supports this idea. Alverdy and Olga Zaborina, a microbiologist, wanted to know what happens to the gut microbes of ICU patients, who receive repeated courses of multiple antibiotics to ward off infections.

They found that patients with stays longer than a month had only one to four types of microbes in their gut, as measured from fecal samples -- compared to about 40 different types found in healthy volunteers.

Four of these patients had gut microbe communities with just two members-- an infectious Candida yeast strain and a pathogenic bacterial strain, such as Enterococcus faecium or Staphylococcus aureus and other bugs associated with hospital-associated infections. Not surprisingly, almost all of the pathogenic bacteria in these patients were antibiotic resistant.

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Published on 4 Comments on Which Probiotic Treatment is Best For Sinusitis?

[PLEASE NOTE THAT AN UPDATED VERSION OF THIS POST WITH NEW INFORMATION, INCLUDING NEW PRODUCTS, WAS PUBLISHED IN MAY 2018: The One Probiotic That Treats Sinusitis. Comments can be posted there.]

We now know that antibiotics, especially repeated courses of antibiotics, kills off bacteria and alters the microbial community in the sinuses (sinus biome). Research by Abreu et al (in 2012) showed that it is Lactobacillus sakei that is missing in chronic sinusitis sufferers, and that Lactobacillus sakei successfully treats sinusitis. From this research it is clear that Lactobacillus sakei is a  beneficial bacteria that can be used as a probiotic to cure sinustis.

It turns out that many brands of live fermented kimchi contain Lactobacillus sakei, and this is what my family used to treat and cure ourselves of chronic sinusitis (and acute sinusitis). So yes, kimchi can be probiotics for sinusitis. It is now over 85 weeks since I've been off all antibiotics and feeling great!

Until now I avoided naming the kimchi brand we used on this site because I believe that many brands of fermented kimchi (with cabbage) contain Lactobacillus sakei, and should be effective in curing sinusitis (this is by dabbing or smearing it in the nostrils - see Sinusitis Treatment Summary link for the METHOD and details).

WHAT BRANDS OR PRODUCTS WITH Lactobacillus sakei WORK?

The brand I use is Sunja's Kimchi (from Vermont). We originally were successful with the Medium Spicy Cabbage Kimchi and when that stopped being fully effective last winter (from overuse? recipe change?), we switched to Sunja's Medium Spicy Cucumber Kimchi (fermented at least 14 days and the jar opened less than 1 week).

Recently I heard from a woman in Nevada who wrote me stating that smearing/dabbing Sinto Gourmet Mild White Napa Cabbage Kimchi into her nostrils was successfully treating her chronic sinusitis (using the method described in the Sinusitis Treatment page)

One person wrote that he successfully cured chronic and acute sinusitis with a fermented sausage starter from Chr. Hansen containing L. sakei and another bacteria. He used it after mixing very small amounts in his  Neti pot - initially used it 1 x per day until cured, and then sparingly only as needed (after a cold) or as a maintenance booster once every 3 or 4 months (see his comment in the Contact page for more details). (UPDATE: one name for this product is Bactoferm F-RM-52, which contains Lactobacillus sakei and Staphylococcus carnosus  . See 1/12/15 post for more, including my experience with it.)

Eating kimchi does not seem to treat sinusitis, even though it may be good for the gut. Only smearing or dabbing it in the nostrils works.

Several people have reported that using sauerkraut has not helped their sinusitis, and scientific studies report that sauerkraut contains minimal L.sakei, if at all.

Others have also mentioned thinking about using lactic acid starter cultures containing L. sakei , whether using it alone or making kimchi with it, but I don't know how it went.

Finally, I would like feedback from you: 1) What brands of kimchi have worked for you in treating or curing sinusitis?     2) What other products containing Lactobacillus sakei have worked successfully for you? And how did you use it?   3) What other bacteria have worked for you in curing sinusitis?

Please let me know by commenting in the comments section or writing me an email. This way I can update this list.  The goal is to find ways to improve the beneficial bacteria in the sinuses and so treat, cure, and eventually prevent sinusitis.   Thanks!

[PLEASE NOTE THAT AN UPDATED VERSION OF THIS POST WITH NEW INFORMATION WAS PUBLISHED IN MAY 2018: The One Probiotic That Treats Sinusitis. Comments can be posted there.]

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If taking Clostridia as a probiotic for food allergies works, it would be amazing for food allergy sufferers. Very exciting research. From Time:

The Bacteria That May One Day Cure Food Allergies

Every round of antibiotics a person takes will wipe out strains of bacteria inside the body, some of which are eliminated forever. Considering how early and how often antibiotics are administered to kids—coupled with our increasingly antimicrobial lifestyles—we’ve become more prone to allergies and other ailments, the hygiene hypothesis goes. There’s no cure for food allergies, just lifestyle adjustments and abstention. But Nagler and her team may have the germ of an idea for treatment using gut bacteria, according to a new mice study published in the Proceedings of the National Academy of Sciences.

The team dosed two groups of mice with peanut allergens. One group of mice had been bred to be entirely without gut germs; the other group had sparsely populated gut bacteria due to treatment with antibiotics. Both groups of mice had higher levels of the allergen in their bloodstream compared to mice with healthy gut-bacteria populations.

After giving those same mice a mix that contained the bacteria strain Clostridia, their allergen levels plummeted. Infusing the mice with another group of intestinal bacteria, Bacteroides, didn’t help—so the researchers think the effect is special to Clostridia. “These bacteria are very abundant and they reside very close to the epithelial lining, so they’re in intimate contact with the immune system,” Nagler says.

Next, they’ll transfer gut bacteria from food-allergic infants and healthy infants into germ-free mice, Nagler says. “If we give back Clostridia to a mouse that has the bacteria of an allergic child, can we now reverse susceptibility in that mouse?”

This is a more in-depth article of the research. From Science Daily:

Gut bacteria that protect against food allergies identified

The presence of Clostridia, a common class of gut bacteria, protects against food allergies, a new study in mice finds. The discovery points toward probiotic therapies for this so-far untreatable condition. Food allergies affect 15 million Americans, including one in 13 children, who live with this potentially life-threatening disease that currently has no cure, researchers note.

Although the causes of food allergy -- a sometimes deadly immune response to certain foods -- are unknown, studies have hinted that modern hygienic or dietary practices may play a role by disturbing the body's natural bacterial composition. In recent years, food allergy rates among children have risen sharply -- increasing approximately 50 percent between 1997 and 2011 -- and studies have shown a correlation to antibiotic and antimicrobial use.

"Environmental stimuli such as antibiotic overuse, high fat diets, caesarean birth, removal of common pathogens and even formula feeding have affected the microbiota with which we've co-evolved," said study senior author Cathryn Nagler, PhD, Bunning Food Allergy Professor at the University of Chicago. "Our results suggest this could contribute to the increasing susceptibility to food allergies."

To test how gut bacteria affect food allergies, Nagler and her team investigated the response to food allergens in mice. ...This sensitization to food allergens could be reversed, however, by reintroducing a mix of Clostridia bacteria back into the mice. Reintroduction of another major group of intestinal bacteria, Bacteroides, failed to alleviate sensitization, indicating that Clostridia have a unique, protective role against food allergens.

To identify this protective mechanism, Nagler and her team studied cellular and molecular immune responses to bacteria in the gut. Genetic analysis revealed that Clostridia caused innate immune cells to produce high levels of interleukin-22 (IL-22), a signaling molecule known to decrease the permeability of the intestinal lining.

While complex and largely undetermined factors such as genetics greatly affect whether individuals develop food allergies and how they manifest, the identification of a bacteria-induced barrier-protective response represents a new paradigm for preventing sensitization to food. Clostridia bacteria are common in humans and represent a clear target for potential therapeutics that prevent or treat food allergies.