What microbes are living in public bathrooms?

Do you ever wonder how clean our bathrooms are, or question what kinds of bacterial communities are lurking in the public bathrooms you use? Well lucky for you and I, a team of scientists wondered the same exact thing. Published in Applied and Environmental Microbiology, the scientists sampled the microbial communities of four public restrooms at San Diego State University to better understand how they shifted over time.

At the beginning of the study, the restrooms were sterilized using a bleach solution.  Just one-hour post sterilization, the bathrooms were already filled with microbes again and as you can imagine, a significant portion of the microbes were of fecal origin.  They found that despite varying frequency of use and sampling bathrooms of both sexes, the four bathrooms all eventually had microbial communities that were very similar to one another.

The scientists found one specific bacterium, Staphylococcus, was prevalent in all the restrooms. One kind of staph can be very pathogenic, specifically when it is resistant to antibiotics (MRSA), however Staphylococcus does often live harmless in our bodies.  They did not find any Staphylococcus that was resistant to antibiotics in any of the restrooms. The restrooms were cleaned regularly using soap and water over the course of this study, yet the microbial communities remained largely stable.

You may read this and be grossed out about bacteria being prevalent in public restrooms even after regular cleaning, but they are most likely harmless, or even beneficial. Perhaps bleaching a bathroom may be like taking antibiotics - it leaves open the possibility for harmful bacteria to colonize, like what Clostridium difficile does in the gut.

A recreational drug may cause memory loss due to the microbiome

There is a common method to induce schizophrenia-like symptoms in mice that is often used in research.  The method involves dosing the mice with a molecule called phenylcyclidine (PCP), better known as the drug angel dust.  There are neurological reasons why this drug should cause schizophrenia-like symptoms in mice, and one consequence of its administration is memory loss.  Researchers from Denmark recently tested if this memory loss was connected to the microbiome and published their results in Physiology and Behavior.

The researchers devised an experiment where groups of mice were either given PCP or a control.  All the mice had their microbiomes tested and underwent a memory test.  The scientists discovered that the PCP did heavily change the microbiome, with many genera increasing in abundance, like Roseburia, Dorea, and Odoribacter.  In addition, the memory performance also seemed to correlate with the microbiome.  As the microbiome rebounded after a 3 week time frame, so did the memory of the mice, even though some other symptoms of the PCP persisted.  Finally, the researchers gave some of the mice that were given PCP antibiotics so as to decrease the population of the microbiome.  The antibiotics were effective in restoring the memory of the mice even within 3 weeks, suggesting a microbiome connection.

The researchers hypothesize that stress caused from taking PCP may be the root cause of the microbiome shifts and memory loss.  Interestingly, some of the bacteria that they identified in the PCP microbiomes had been associated with stress in previous studies.  Here at the AMI we don’t like to preach to our readers, but if any of you use PCP and have a big exam coming up, you may want to consider stopping, or at least taking a probiotic.

Our microbiome has a taste for beer

Many humans enjoy the taste of bread, beer, soy sauce, and other yeasty treats because they taste so darn good.  As it turns out though, we may not be only ones who like these flavors.  A report published last week in Nature describes the discovery of bacteria in our guts that survive by off the yeast in our diets.

The researchers noted that many gut bacteria from the phylum bacteroidetes have genomes that contain genes for enzymes that are capable of degrading complex carbohydrates, including one called α-mannan.  Curiously, the primary source of α-mannan in the gut is on cell walls of ingested yeasts such as Saccharomyces cerevisiae.  The researchers performed a variety of experiments that confirmed that at least one of the bacteroidetes, Bacteroides thetaiotaomicron, could metabolize the yeast cell wall molecule.  The scientists also hypothesize that B. thetaiotaomicron evolved this ability as an adaptation to the changing human diet which includes yeasts from of leavened bread and fermented alcohols. The ability to break down and utilize yeast cell wall components as energy gives B. thetaiotaomicron a competitive edge in living in the gut over other bacteria with less metabolic options.

The B. thetaiotaomicron can thrive in the human intestine because of their evolved symbiotic relationship with the human host: the bacteria breaks down the yeast for the human, while at the same time gaining a source of energy.  This type of relationship is probably quite common in the gut and likely extends to other popular foods.  Who knows, but knowing what we do about the gut-brain axis, maybe these bacteria are actually causing our cravings for bread and beer.

How our body's normal bacteria avoid destruction by the immune system

The human gut is exposed to toxins, pathogens, dietary changes, antibiotics, and other disturbances that can cause alterations to our microbiome. So how is it that the gut of healthy individuals remains largely stable despite these perturbations? When we get sick, why is it that our body’s “good” bacteria remain in the gut while the bacteria causing the infection are killed off by our immune system?  A study out of Yale, published last week in Science, identified a single gene in bacteria that allows for these bacteria to resist inflammation-associated antimicrobial peptides that are released by the body to kill off harmful bacteria.

The scientists found that this gene, lpxF, encodes for an enzyme in the cell membrane of bacteria to be slightly altered from bacteria lacking this specific gene.  To figure this out, they exposed 17 commensal (or normal) bacteria to antimicrobial peptides (AMPs) and found that they were more resistant than pathogens that were also exposed to the same AMPs. They then mutated the genes of five species of Bacteroidetes at various points and checked to see which ones became less resistant to AMPs.  They found one gene that was common across all five species, lpxF.

They also did experiments in which they genetically manipulated bacteria to knock out the lpxF gene and put these bacteria into germ free mice along with the same bacteria with the functional lpxF gene. In the absence of a pathogen, the bacteria lacking the lpxF gene performed just as well as the bacteria with the gene.  When a pathogen was introduced into the mouse, inducing an immune response, the bacteria lacking the lpxF gene was greatly reduced in comparison to the other bacteria with functional lpxF.  This showed that the gene was protecting the bacteria from the AMPs. 

Lastly, they took fecal samples from twelve individuals and exposed bacteria from them to AMPs. They found that in comparison to pathogens that did not survive very well after exposure, the commensal bacteria performed very well.  This is a very important study as it opens up a new understanding of how bacteria in the body are saved from an immune response after exposure of a pathogen in the body.  There are most likely many more genes that play similar roles to lpxF and this work opens up new avenues to better understand how commensal microbes interact with the human body as well as pathogens in the body.   

Gut helminths harm individuals’ ability to combat some bacterial infections

Gut helminths are the worms that live in the gut.  While it should be no surprise that they infect many animals, they actually infect approximately 1 billion humans as well, mostly from traditional societies.  Their role and criticality to the microbiome has been an ongoing topic of research, and as we have written about before, there is research to show helminths can be both beneficial and harmful to humans.  A study published last week in Science shines a new light on this subject, showing helminths may be bad for individuals, but good for communities.

The study focused on wild Africa buffalo from Kruger National Park in South Africa.  Helminths naturally affect almost all of the wild buffalo, so the scientists gave some of them anti-helminth medication.  The scientists then measured how these buffalo survived bovine tuberculosis, a bacterial infection.  As it turns out, all buffalo, treated and untreated, were at equal risk for becoming infected with the tuberculosis.  However, the treated buffalo with no helminths had a 9 times higher survival rate from the disease.  The scientists believe that the immune system of these buffalo can exert all its resources to combat the bacteria, rather than having to deal with both the helminths and the tuberculosis at the same time.  Interestingly though, because all buffalo were at equal risk for infection, those buffalo that survived due to lack of helminths became efficient carriers of the disease.  Therefore the tuberculosis could spread to many more buffalo in the community, and a lack of helminths could usher in a buffalo tuberculosis outbreak.

I think the most important aspect of the paper as it relates to humans is that individual survival rates were much better in buffalo treated with anti-helminth drugs, so humans considering helminth therapy should keep this in mind.  The immune system has limited resources, and in buffalo it seems that helminth – bacterial co-infections increase morbidity.  Once again, though, research shows helminths to be a sort of double edged sword.  While individual buffalo may be better off without the worms, the overall population prospers with the worms.  

New antibiotic discovered that may not lead to resistance

iChip - the device used to identify the new antibiotic (image by Slava Epstein/Northeastern University)

Antibiotic resistance is a topic that we’ve written about extensively in the blog and a major public health concern in today’s society. In the US alone, over 20,000 deaths are caused by antibiotic resistant bacteria every year and several million illnesses can also be attributed annually to antibiotic resistant bacteria. Research led by Dr. Kim Lewis at Northeastern University resulted in the identification of a new antibiotic called teixobactin that looks as if it may not cause antibiotic resistanace. This discovery is being hailed as groundbreaking and a promising avenue to treat previously untreatable chronic infections.

The research published on Wednesday in Nature identified this new antibiotic by culturing bacteria that were previously difficult to grow in the laboratory.  Only about 1% of microbes can be grown in the laboratory making the identification of new antibiotics very difficult (antibiotics are generally developed using microbes).  Using a device called the iChip, they were able to successfully grow up to 50% of bacteria that were previously unable to be grown in the lab. 

Cells from different bacterium were placed individually into a chamber on the iChip that holds several hundred chambers. The device is then placed under the soil where the bacteria are able to grow in their natural environment. After they form colonies, the device was brought to the laboratory and the bacterial colonies were placed on a petri dish.  A target bacteria is then covered over the bacteria that were growing in the soil. If they see that there is no growth over a specific area, they know that the bacteria in that chamber is releasing a potential antibiotic. Through this method, the scientists identified 25 promising novel antibiotics in which teixobactin was the most promising. 

Two diseases we’ve discussed on the blog previously are MRSA (methicillin resistant Staphylococcus aureus) and Clostridium difficile infection. C. diff is a disease usually caused when the healthy bacteria in the gut are killed by an antibiotic and C. diff colonizes the gut. This can be very difficult to treat and a last resort is often a fecal microbiota transplant (FMT). An exciting development from this research is that this new antibiotic was particularly effective against both C. diff and S. aureus as well as the bacteria that causes tuberculosis. 

This is an incredibly exciting development but as an organization focused on the microbiome, we need to think about what the implications are on the microbiome.  The development of new antibiotics is incredibly important and we have seen the field move very slowly in recent times, but we still need to be careful with the overuse of antibiotics. Even if bacteria do not become resistant to this antibiotic, the same issues we’ve discussed pertaining to the overuse of antibiotics still exist.  This antibiotic seems to be quite powerful and ridding our guts of bacteria on a regular basis can cause increased levels of obesity in children among countless other public health problems. It is important that just because an antibiotic does not cause resistance, we do not overuse it. 

We look forward to the further developments with teixobactin and hope to see this move to clinical trials in the near future. This new antibiotic has only been tested so far in mice and will need to be tested further in animals and later humans.  The authors estimate that if all goes well, this new antibiotic could be on the market in about 4 or 5 years (they hope to be in clinical trials in two years with clinical trials taking an additional two to three years).