Tag Archives: bacteria


Researchers, at long last, develop effective tool to study soil-borne microbes

Novel research is allowing us to see what different microbes in the soil are up to.


Image via Pixabay.

Researchers from the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) report being the first to successfully isolate active microbes from a soil sample. These germs underpin life on Earth today, so the research has the potential to branch out into many other fields including ecosystem science, environmental rehabilitation, and agriculture.

Soil searching

Soils are probably the most diverse microbial communities on the planet,” said Estelle Couradeau, first author of the study. “In every gram of soil, there are billions of cells from tens of thousands of species that, all together, perform important Earth nutrient cycles. They are the backbone of terrestrial ecosystems, and healthy soil microbiomes are key to sustainable agriculture.”

“We now have the tools to see who these species are, but we don’t yet know how they do what they do. This proof-of-concept study shows that BONCAT is an effective tool that we could use to link active microbes to environmental processes.”

For the past two years, Couradeau and her co-authors have been collaborating with other researchers in a Berkeley Lab-led scientific focus area called ENIGMA (Ecosystems and Networks Integrated with Genes and Molecular Assemblies) to better understand soil microbiomes. ENIGMA’s projects are of great interest to researchers in the field of biology, energy, and Earth sciences.

Soil microbes are hard to study because they won’t grow in lab cultures, and because they come in an extremely wide palette in natural habitats. Many of these microbes as much as 95% at a time, according to the team can also lie inactive at any given time, further complicating efforts to tie their activity to observed effects. Because of this, researchers usually study such microbes by collecting samples and then sequencing bulk DNA to determine which strains are present therein. However, most of the commonly used techniques can’t differentiate active microbes from those that are dormant or from free-floating bits of DNA found in soil and sediment.

Sleeper cells

“There are many barriers to measuring microbial activities and interactions,” said Trent Northen, lead author and director of biotechnology for ENIGMA

Enter BONCAT (Bioorthogonal Non-Canonical Amino Acid Tagging), a microbial sorting tool that allows researchers to tell apart active vs inactive microbes in a sample. Northen’s team is the first one to successfully use this technique on a sample of soil, and they hope the research will help us understand how soil microbiomes affect large-scale environmental events. BONCAT was developed by Caltech geneticists in 2006 as a way to isolate newly made proteins in cells, and was later adapted into a tool that could identify active, symbiotic clusters of dozens to hundreds of microbes within ocean sediment. Further refinement of this method led to the development of BONCAT Fluorescent Activated Cell Sorting (BONCAT+FACS), which is able to detect individual active microbes.

With BONCAT+FACS, researchers sort through single-celled organisms using a fluorescent tagging molecule, which binds to a modified version of methionine (an amino acid). A fluid solution containing the modified methionine is introduced to a sample of microbes, and those that are active — i.e. that are synthesizing proteins — will incorporate the modified methionine into their structures. The process is much more streamlined and reliable than previous microbial identification methods, and only takes a few hours to perform (which means it can tag active cells even when they are not replicating).

The team spent three months tweaking and optimizing the technique, which resulted in a protocol that can smoothly and reliably identify active microbes in a sample — “most importantly”, according to a press release accompanying the study, the technique “gives very reproducible results”.

“BONCAT+FACS is a powerful tool that provides a more refined method to determine which microbes are active in a community at any particular time,” said  Rex Malmstrom, co-author of the study who previously worked on refining BONCAT for marine use.

“It also opens the door for us to experiment, to assess which cells are active under condition A and which cells become active or inactive when switched to condition B.”

“With BONCAT, we will be able to get immediate snapshots of how microbiomes react to both normal habitat fluctuations and extreme climate events—such as drought and flood—that are becoming more and more frequent,” said Northen.

BONCAT+FACS will be available through the user programs set up by the Department of Energy’s Joint Genome Institute (JGI), the authors write. They hope to promote research in other lines of study, among which they cite assessing antibiotic susceptibility in unculturable microbes and investigating the completely unknown roles of Candidatus Dormibacteraeota, a phylum of soil bacteria, found across the world, that appear to remain dormant most of the time. The technique will also help fill in the gaps of our understanding of environmental functions and point the way for new research into drought-resistance in crops, the sustainable production of fuel and other bioproducts, environmental rehabilitation, and many others.

The paper “Probing the active fraction of soil microbiomes using BONCAT-FACS” has been published in the journal Nature.

Kitchen Sponge.

Phages in kitchen sponges could help us wipe antibiotic resistant bacteria clean off

New student research from the New York Institute of Technology (NYIT) could help us stem the tide of antibiotic-resistant infections — using your kitchen sponge.

Kitchen Sponge.

The savior we didn’t want, but the one we need.
Image credits Hans Braxmeier.

Research at the NYIT has zoomed in on bacteriophages — viruses that infect bacteria — living in our kitchen sponges. These biological particles, often shorthanded as ‘phages’, may prove useful in fighting antibiotic-resistant bacteria, the team reports.

Spongy science

“Our study illustrates the value in searching any microbial environment that could harbor potentially useful phages,” said Brianna Weiss, a Life Sciences student at New York Institute of Technology.

Kitchen sponges aren’t exactly the cleanest items in your house. In fact, it’s exposed to all kinds of different microbes every day and is pretty much crawling with a microbiome of bacteria. And where there are bacteria, there are also bacteriophages, viruses that target, infect, and multiply on the back of bacteria.

Students in a research class at NYIT isolated bacteria from their own used kitchen sponges and then used them as bait to see which phages could attack them. Two of the students successfully baited phage strains that could infect these bacteria. The team then decided to ‘swap’ these two phage strains and check whether they could cross-infect the bacteria isolated by the other student — and it turned out they could. The phage strains successfully infected and then killed bacteria recovered from the other sponge.

“This led us to wonder if the bacteria strains were coincidentally the same, even though they came from two different sponges,” said Weiss.

To get to the bottom of things, the team isolated and compared the DNA of these bacterial strains. They report that both belong to the Enterobacteriaceae family, a vast grouping of rod-shaped bacteria that are commonly found in feces. Some members of the Enterobacteriaceae family have been recorded to cause infections in hospital settings. Although related, the researchers do add that lab analysis revealed chemical variations between the two strains.

“These differences are important in understanding the range of bacteria that a phage can infect, which is also key to determining its ability to treat specific antibiotic-resistant infections,” said Weiss.

“Continuing our work, we hope to isolate and characterize more phages that can infect bacteria from a variety of microbial ecosystems, where some of these phages might be used to treat antibiotic-resistant bacterial infections.”

The project fits into a larger drive to develop non-chemical avenues of fighting bacteria. Such measures are meant, on the one hand, to reduce the incidence and spread of antibiotic resistance in bacterial strains by limiting exposure to such drugs. On the other hand, they aim to give us a functioning defense against strains that have already acquired partial or (much worse) complete immunity to our antibiotics. Some of these ideas that we’ve looked at in the past include laying down antibacterialspike pits‘, shredding them with polymers and nanomaterials, using (Komodo) dragon blood, and straight-up causing some bacterial civil war.

Still, the World Health Organization is concerned that, despite drug-resistant bacteria being “one of the biggest challenges mankind has to face in the near, as well as distant future,” and despite these strains claiming hundreds of thousands of lives every year, the world is simply not prepared to deal with the threat. “Only 34 out of 133 questioned countries have even a basic plan to combat the misuse of antibiotics fuelling drug resistance,” Andrei reported at the time.

Hopefully, research such as the one we’re discussing today will mature before our antibiotics become powerless in the face of bacteria. We’re simply over-relying on antibiotics, a study published last May explained, and methods such as the use of phages could help us break the pattern before it is too late.

The findings have been presented at ASM Microbe, the annual meeting of the American Society for Microbiology.

Escherichia Coli.

Researchers film bacteria sharing antibiotic resistance in real time — and find a potential fix

New research into how antibiotic resistance spreads among bacterial populations points the way forward to fighting this growing threat.

Escherichia Coli.

Escherichia Coli.
Image credits Gerd Altmann.

Growing levels of antibiotic resistance, both in scope and sheer effectiveness, is a very real threat for us. It’s easy, in this day and age, to consider most bacteria and the diseases they cause as simple nuisances. But that safety is owed to the antibiotics and active compounds we’ve developed to protect us — should they turn ineffective, we’re as much at the mercy of these germs as any other organism on the planet.

However, new research shows it isn’t unstoppable. Robust, yes; backed-up with redundancy systems, yes — but not unstoppable.

The tiny pump that could

The research was carried out by a team of researchers from the Université Lyon and CNRS, the French National Center for Scientific Research. They successfully filmed the process of antibiotic resistance acquisition in real time, thus finding a new and central player that takes part in this process.

Antibiotic resistance primarily spreads among bacteria through a process known as (bacterial) conjugation, which is basically the sharing of genetic material. Systematic genetic sequencing of both pathogenic and environmental strains of bacteria suggests that a very wide range of genetic elements can be shared via conjugation which encodes resistance to most or all of the antibiotic classes currently in use.

So we know how it goes down, but we’re still in the dark in regards to how long it takes for conjugation to work its magic and how antibiotics interfere with the process. That’s what the present research aimed to find out.

The team worked with a strain of Escherichia Coli (E.coli) bacteria resistant to tetracycline, a commonly used antibiotic. Tetracycline works by attaching itself to the bacteria’s molecular mechanisms, rendering them unable to produce proteins. The team exposed the bacteria to tetracycline in the presence of another strain that was not resistant to the substance. Previous research told the team that, in such conditions, the spread of antibiotic resistance hinges on the first strain clearing the drug out using “efflux pumps” on their membrane before it can wreak havoc internally, thus conferring them some degree of resistance to the drug.

The team reports seeing DNA transmission being carried out between individuals of the two strains with one specific efflux pump, the TetA pump. Using fluorescent marking and live-cell microscopy, the researchers tracked the spread the DNA encoding this pump from resistant bacteria and how the recipient ones expressed the genes.

It only took 1 to 2 hours for the single-stranded DNA fragments put out by the efflux pumps to be turned into a double-stranded DNA molecule and, subsequently, into a functional protein, they report. In effect, that is the timeframe required for resistance to spread between different strains of bacteria. You can see the process in the video below; green bacteria are the donors (i.e. resistant E.coli strain) and the red ones are the recipients. In effect, everything you see turning green is learning tetracycline resistance from its peers.


Given the way tetracycline works — by blocking the production of proteins — you’d reasonably expect it to block the ‘red’ bacteria from synthesizing TetA efflux pumps (they’re made of proteins). However, the team is surprised to report that this isn’t the case. Paradoxically, the bacteria were able to survive and develop a resistance to tetracycline even in the presence of this drug — which suggested there’s another, unknown factor at work here.

It seems to be another efflux pump, they explain. Called AcrAB-TolC (scientists are good with naming stuff), this pump is present in virtually all bacteria, but serves a general role. As such, it’s less efficient than TetA at ejecting tetracycline, but it is still able to remove a small quantity from the cell, allowing the bacteria to carry out a minimal level of protein synthesis. This process allows bacteria to become durably resistant to antibiotics should they be provided with the right genes from the environment.

However, the findings also point the way to a potential fix for acquired antibiotic resistance.

“We could even consider a therapy combining an antibiotic and a molecule able to inhibit this generalist pump,” says Christian Lesterlin, a researcher at Lyon’s Molecular Microbiology and Structural Biochemistry laboratory and the paper’s corresponding author.

“While it is still too soon to envisage the therapeutic application of such an inhibitor, numerous studies are currently being performed in this area given the possibility of reducing antibiotic resistance and preventing its spread to the various bacterial species.”

The paper “Role of AcrAB-TolC multidrug efflux pump in drug-resistance acquisition by plasmid transfer” has been published in the journal Science.


Study proposes five new rules to prevent antibiotic resistance “disaster”

Efforts to fight antibiotic resistance aren’t “nearly radical enough” today, according to a new study.


Image credits Emilian Danaila.

Relying too much on reducing antibiotic use and implementing new drugs could lead to “disaster”, says Dr. Ben Raymond, of the University of Exeter. In a new study, Dr. Raymond proposes five rules for the “sustainable use” of antibiotics which would help us maintain the efficiency of this class of drugs and prevent antibiotic resistance from becoming a deadly problem.

Resistance fighters

“People think the best way to tackle antibiotic resistance is to give out fewer antibiotics and find new drugs. Those are important steps, but this approach alone is not nearly radical enough,” says Dr. Raymond, of the Centre for Ecology and Conversation on the University of Exeter’s Penryn Campus in Cornwall.

“Even if we can keep finding new drugs, disaster will follow if we use them in the same way as we use current ones. No drug yet discovered is evolution proof, and the typical practice of using single drugs at once, in unprotected ‘monotherapies’ is unsustainable.”

What he proposes instead is a multi-pronged approach intended to prevent what the World Health Organisation calls “a post-antibiotic era in which common infections and minor injuries can once again kill.” The measures include taking steps to protect new drugs before resistance becomes a problem, diversifying the range of antimicrobials currently in use to avoid relying too much on a handful of drugs (which also speeds up the evolution of resistance for those drugs), and using data to design management plans for particular superbugs.

“This ‘business as usual’ approach can be disastrous, as exemplified by the history of resistance in gonorrhoea and the emergence of untreatable infections,” Dr. Raymond explains. “Resistance to new antibiotics can become widespread in two or three years, so new drugs must be partnered with more sustainable patterns of use.”

The five ‘rules’ outlined in the study are:

  1. Prevention. Echoing the old adage, Dr. Raymond wisely notes that “resistance is easier to deal with before it becomes severe.” Avoiding heavy use of single drugs for extended periods of time creates less evolutionary pressure for its active compound (i.e. bugs have less need and opportunities opportunity to develop resistance to a particular compound, as they don’t see it that frequently).
  2. Don’t rely on “fitness costs.” Some approaches call for break periods in the use of a particular drug, in the hope that bacteria resistant to it will die off to their competition because they carry resistance genes that are no longer useful (i.e. genetic dead weight.) While the idea behind the approach can work, resistance to a drug does not necessarily vanish because of an interruption in the use of a drug.
  3. Limit bacteria’s ability to mutate drug-resistance genes. One approach is to use antibiotic cocktails, as microbes rarely develop resistance to multiple antibiotics at once. Slowly building a massive reservoir of antibiotic-resistance genes in the wild is “madness” according to Dr. Raymond. Traces of antibiotics in wastewater, or the use of antibiotics in livestock farming, are doing exactly that. “As an individual you are very unlikely to have acquired an antibiotic resistant microbe from an animal, but it’s highly likely that environmental contamination has helped some of the microbes in your body acquire resistance,” he says.
  4. Low doses don’t work, but short courses might. A greater pool of mutations can give microbes the chance to resist low doses of antibiotics, so lowering the dose doesn’t prevent resistance from evolving. However a shorter, more intense course of treatment might benefit patients without giving the bugs a chance to evolve, he says.
  5. Know your enemy. “If you don’t know what kind of resistance is around among patients or in your hospital, you could give people the wrong drug at the wrong time,” he says. “The more data you have, the better you can design your resistance management programmes. Resistance management programmes should target specific microbes or groups of microbes, rather than resistance in general.”

“Some humility in the face of natural selection can ensure that human creativity keeps pace with evolutionary innovation,” he adds, noting that other disciplines have a broader knowledge of resistance management, but that their input is “not widely appreciated” among microbiologists.

The paper “Five rules for resistance management in the antibiotic apocalypse, a road map for integrated microbial management” has been published in the journal Evolutionary Applications.

Bacteria steal genetic material from predator viruses using Spam gene

Just like we have bacteria, dangerous microscopic organisms that can cause serious problems, bacteria have bacteriophages (or phages) — viruses that prey on them. Phages are so devastating to bacteria that they’re estimated to kill about half of the bacteria in the world’s oceans every two days. Now, researchers have uncovered a surprising mechanism through which some bacteria defend themselves from phages: by stealing genetic material.

“This study shows bacteria’s ability to transform an implement of war into a tool to create life,” said the study’s lead author, Amelia Randich. “It’s like watching evolution beat a sword into plowshare.”

Watch a video of bacteria-killing phages in action.

Like human viruses, bacteriophages can’t reproduce by themselves, so they inject their own genetic material into cells, hijacking their victims to copy their own genes, thereby producing new virus particles that break open and kill the cells. This process is called lysis, and the toxic enzymes that produce cell death are called lysins. However, a family of bacteria called Caulobacterales seem to have developed an antidote.

The key to the antidote is a gene called SpmX, commonly known as “Spam X.” Caulobacterales are a bacterial order whose members grow long appendages called stalks. Spam X appears where cell stalks grow, assigning proteins to support the development of the stalk. However, the gene appears to have originated in bacteriophages and was originally used to destroy bacterial cell walls.

The red section shows the process by which viruses kill bacterial cells to produce new virus particles with help from an enzyme, represented as a ‘Pac-Man’ with razor-sharp teeth. In Caulobacterales, the ‘teeth’ are now blunt, no longer able to kill bacteria, instead helping grow new stalks through the process shown in blue. Credit: Amelia Randich, Indiana University.

Using X-ray crystallography to create 3-D models of SpmX and related protein structures, researchers found remarkable similarities between SpmX and the gene producing the viral lysins. But instead of cracking open cells in Caulobacter, they seem to help guide SpmX to the future position of the stalk.

“Even though it was very, very similar to phage genes, we found a specific mutation in Caulobacter—in the area of the protein used to cut through the bacterial cell wall—that reduced its efficiency,” Brun said.

“Because the sequence was so closely related to the genes in phage, you would expect it to have the same function: to cut the cell wall,” he added. “But instead its activity was reduced to the point where it no longer killed the bacteria. It’s quite remarkable.”

The similarities are too large to be a coincidence, and genetic analysis suggests that bacteria developed and tweaked this gene around 1 billion years in the past. More importantly for us, it could be a way to keep viral infections at bay, or even to use bacteria for innovative uses, such as delivering compounds such as insulin or antibiotics.

The study has been published in Current Biology.


There are arsenic-breathing microbes in the tropical Pacific, a new study finds

Arsenic is generally viewed as a life-ending element, but new research shows how some organisms rely on it to breathe.


Image credits fdecomite / Flickr.

Certain microorganisms in the Pacific Ocean respire arsenic, according to a new study from the University of Washington. The findings are quite surprising as, although arsenic-based respiration has been documented in ancient and current organisms, it is extremely rare on the planet. Moreover, ocean water just doesn’t have that much arsenic, to begin with.

Doing without

“We’ve known for a long time that there are very low levels of arsenic in the ocean,” said co-author Gabrielle Rocap, a UW professor of oceanography. “But the idea that organisms could be using arsenic to make a living—it’s a whole new metabolism for the open ocean.”

The team analyzed Pacific seawater samples taken from water layers at depth intervals where oxygen is almost absent. Given the lack of oxygen here, organisms had to adapt and seek other sources of energy, the team writes. The results are interesting and may become very important in our understanding of marine ecosystems, as these areas — known as oxygen-deficient zones, ODZs or oxygen minimum zones, OMZs — will likely expand under climate change, according to other recent research.

The most common alternatives to oxygen that biology draws upon today are nitrogen and sulfur. However, previous research carried out by Jaclyn Saunders, this paper’s first author, suggested that arsenic might also do the trick. She was curious to see whether this was the case, which spurred the present paper.

The samples used in this study were collected during a 2012 research cruise to the tropical Pacific, off the coast of Mexico. Analysis of eDNA material recovered from the samples showed two genetic pathways that process arsenic-based molecules to extract energy. Two different forms of arsenic seem to be targeted by these pathways, leading the authors to believe that we’re looking at two organisms that cycle arsenic back and forth between the different forms. Which, as far as ecosystems are concerned, is quite a nifty trick.

“Thinking of arsenic as not just a bad guy, but also as beneficial, has reshaped the way that I view the element,” said Saunders, who did the research for her doctoral thesis at the UW and is now a postdoctoral fellow at the Woods Hole Oceanographic Institution and the Massachusetts Institute of Technology.

While arsenic might be beneficial, it’s certainly not very popular. Only about 1% of the microbe population in the samples seems to breathe arsenic, judging by the ratios of genetic material. Most likely, these strains are loosely-related to arsenic-breathing microbes found in hot springs or contaminated sites on land. Saunders recently collected samples from the same region and is now trying to grow the arsenic-breathing marine microbes in a lab in order to study them more closely.

“Right now we’ve got bits and pieces of their genomes, just enough to say that yes, they’re doing this arsenic transformation,” Rocap said. “The next step would be to put together a whole genome and find out what else they can do, and how that organism fits into the environment.”

“What I think is the coolest thing about these arsenic-respiring microbes existing today in the ocean is that they are expressing the genes for it in an environment that is fairly low in arsenic,” Saunders said. “It opens up the boundaries for where we could look for organisms that are respiring arsenic, in other arsenic-poor environments.”

Arsenic respiration is most likely a ‘retro’ type of respiration, passed down over the eons. When life first sprung up on Earth, oxygen was very scarce both in the air and in the ocean (as oxygen is very reactive and forms chemical bonds readily). Until photosynthesizing plants became widespread, there simply wasn’t enough output of this gas to maintain any meaningful levels available for organisms to use up. As such, early life had to use something else for energy — and arsenic was likely common in the oceans at that time.

Climate change may, sadly, breathe new life into arsenic-breathing life. Low-oxygen regions are projected to expand as thermal imbalances shift water currents, and dissolved oxygen is also predicted to drop across the board in marine environments.

The paper “Complete arsenic-based respiratory cycle in the marine microbial communities of pelagic oxygen-deficient zones” has been published in the journal Proceedings of the National Academy of Sciences.


Our immune systems may actually help create cavities, a new study finds

Researchers in the University of Toronto’s Faculty of Dentistry have found evidence that our own bodies could be the major driver of tooth decay and filling failure.


Image via Pixabay.

The study shows how the decay of dentin (the hard substance beneath our teeth’s enamel) and fillings isn’t the work of bacteria alone. Rather, they report, it’s the product of an unintentional ‘collaboration’ between bacteria and immune cells known as neutrophils. As these two do battle, our teeth suffer the collateral damage.

Carpet bombing

“No one would believe that our immune system would play a part in creating cavities,” says Associate Professor Yoav Finer, the lead author of the study and the George Zarb/Nobel Biocare chair in prosthodontics at the Faculty of Dentistry. “Now we have evidence.”

Neutrophils are a type of short-lived immune system cells that play an important role in combating inflammation throughout the body. These cells make their way into the oral cavity via the gums around our teeth, where they fight off any bacterial invaders. But as they track and engage these bacteria, neutrophils also inflict damage on the surrounding environment.

“It’s like when you take a sledgehammer to hit a fly on the wall,” Finer says. “That’s what happens when neutrophils fight invaders.”

Byproducts of these engagements are the problem, the team explains. On their own, neutrophils can’t cause meaningful damage to teeth; these cells can’t produce any acid to attack the mineral-rich compounds. However, as they engage in an attack, oral bacteria do employ acids in a bid to defend themselves — and these demineralize teeth.

It’s here that the problem starts. The now-weakened teeth become susceptible to enzymes released both by bacteria and neutrophils, and these enzymes start boring through the demineralized area of teeth and tooth-colored fillings. Dentin and tooth-colored fillings sustain damage “within hours” of a bacteria-neutrophil showdown, the team reports. The research helps better explain why so many patients who had cavities filled with tooth-colored fillings face high rates of recurrence of the cavities. Most tooth-coloured fillings fail within five to seven years, costing Canadians an estimated $3 billion a year, the paper explains.

“It’s a collaboration of destruction – with different motives,” says study author Michael Glogauer, professor of the Faculty of Dentistry and acting chief dentist at the Princess Margaret Cancer Centre.

“Ours is the first basic study to show that neutrophils can break down resin composites (tooth-coloured fillings) and demineralize tooth dentin,” says master’s student and first author of the paper, Russel Gitalis. “This suggests that neutrophils could contribute to tooth decay and recurrent caries.”

While the findings may seem bleak, they actually point the way towards new potential treatment strategies. The findings may also help us develop new filling materials and test their resilience in the lab, potentially leading to much more durable fillings.

The paper “Human neutrophils degrade methacrylate resin composites and tooth dentin” has been published in the journal Acta Biomaterialia.

Tracy Caldwell Dyson in ISS Cupola.

The International Space Station is teeming with bacteria and fungi

Where humanity goes, microorganisms boldly follow.

Tracy Caldwell Dyson in ISS Cupola.

Self-portrait of Tracy Caldwell Dyson in the Cupola module of the International Space Station observing the Earth below during Expedition 24.
Image credits NASA / Tracy Caldwell Dyson via Wikimedia.

New research is pinpointing exactly who makes up the microflora on the International Space Station. The study — the first comprehensive catalogue of the bacteria and fungi on the inside surfaces of the ISS — can be used to develop safety measures for NASA for long-term space travel or living in space.

Space bugs

“Whether these opportunistic bacteria could cause disease in astronauts on the ISS is unknown,” says Dr Checinska Sielaff, first author of the study. “This would depend on a number of factors, including the health status of each individual and how these organisms function while in the space environment. Regardless, the detection of possible disease-causing organisms highlights the importance of further studies to examine how these ISS microbes function in space.”

Microflora can have a range of impacts on human health, so it pays to know exactly what you’re up against — especially in space. Astronauts show an altered immune response during missions, which is compounded by the difficulty of giving them proper medical care. The team hopes that their catalog can give future space mission planners a better idea of which bugs accumulate in the unique environments associated with spaceflight, how long each strain survives, and their possible impact on the crew and the ship itself.

Despite the exotic setting, the team used pretty run-of-the-mill culture techniques to sample the microflora of eight different locations inside the ISS. These included the viewing window, toilet, exercise platform, dining table, and sleeping quarters. The samples were taken during three flights across 14 months’ time, so the team could get an idea of how the tiny organisms fared over time. Genetic sequencing methods were used to identify the strains in these samples.

All in all, the team reports finding mostly human-associated microbes on the ISS. The most prominent included Staphylococcus (26% of total isolates), Pantoea (23%), and Bacillus (11%). The analysis also revealed the presence of bugs considered to be opportunistic pathogens here on Earth — such as Staphylococcus aureus (10% of total isolates identified), which is commonly found on the skin and in the nasal passages, and Enterobacter, which is associated with the human gastrointestinal tract. Opportunistic pathogens are regulars in gyms, offices, and hospitals, the team explains, suggesting that the ISS’s microbiome is also shaped by human occupation, as is similar in microbiome to other built environments.

But it’s not all about the crew.

“Some of the microorganisms we identified on the ISS have also been implicated in microbial induced corrosion on Earth. However, the role they play in corrosion aboard the ISS remains to be determined,” says Dr Urbaniak, joint first author of the study.

“In addition to understanding the possible impact of microbial and fungal organisms on astronaut health, understanding their potential impact on spacecraft will be important to maintain structural stability of the crew vehicle during long term space missions when routine indoor maintenance cannot be as easily performed.”

Fungal communities were quite stable over the study’s period, but microbial communities changed over time (but not across locations). Samples taken during the second flight mission had higher microbial diversity than samples collected during the first and third missions. The authors suggest that these temporal differences may come down to which astronauts are aboard the ISS at any given time. Dr Venkateswaran hopes this data can help NASA improve on-board safety measures, and that they will pave the way to safe, deep space human habitation.

“The results can also have significant impact on our understanding of other confined built environments on the Earth such as clean rooms used in the pharmaceutical and medical industries,” he adds.

The paper “Characterization of the total and viable bacterial and fungal communities associated with the International Space Station surfaces” has been published in the journal Microbiome.

The Caulobacter ethensis-2.0 genome in a micro tube. Credit: ETH Zurich.

Scientists present first computer-generated artificial genome

The Caulobacter ethensis-2.0 genome in a micro tube. Credit: ETH Zurich.

The Caulobacter ethensis-2.0 genome in a micro tube. Credit: ETH Zurich.

Researchers at ETH Zurich have demonstrated a new method for producing genomes that is cheaper and faster than ever before. The authors produced the first fully computer-generated genome — the Caulobacter ethensis-2.0 for which a corresponding organism does not yet exist. However, the genome was physically produced and inserted into an existing organism with similar genetic material.

Computers and synthetic life

In 2010, researchers at the J. Craig Venter Institute reported a landmark advancement in synthetic biology: the first bacterial DNA engineered from scratch. This was the culmination of more than a decade of hard work and a $40 million investment. But while the bacterial genome made by Craig Venter was an exact copy of a natural genome, researchers at ETH Zurich radically altered the genome of a model organism called Caulobacter crescentus. What’s more, their research spanned a time frame of a year and cost les than half a million dollars, which shows that synthetic biology is on the brink of a revolution.

Caulobacter crescentus is a harmless freshwater bacterium whose genome has been extensively studied. Previous research showed that out of the bacterium’s 4,000 genes only about 680 were crucial to the survival of the organism in laboratory conditions. Beat Christen, Professor of Experimental Systems Biology at ETH Zurich, and his brother, Matthias Christen, a chemist at ETH Zurich, used this minimum set of crucial genes as a starting point.

The researchers designed a computer algorithm that scanned this minimally viable natural genome and computed the ideal DNA sequence for the synthesis and construction of the genome. The algorithm replaced a sixth of all the 800,000 DNA letters found in the minimal genome.

“Through our algorithm, we have completely rewritten our genome into a new sequence of DNA letters that no longer resembles the original sequence. However, the biological function at the protein level remains the same,” says Beat Christen.

The hard part was only just beginning. Next, the researchers had to produce a DNA molecule which contained the artificial bacterial genome, and this had to be done step by step. The researchers synthesized 236 separate genome segments, which they then had to delicately piece together.

“The synthesis of these segments is not always easy,” explains Matthias Christen. “DNA molecules not only possess the ability to stick to other DNA molecules, but depending on the sequence, they can also twist themselves into loops and knots, which can hamper the production process or render manufacturing impossible,” explains Matthias Christen.

An electron microscope image of Caulobacter crescentus, a harmless bacterium living in fresh water. Credit: ETH Zurich.

An electron microscope image of Caulobacter crescentus, a harmless bacterium living in fresh water. Credit: ETH Zurich.

As an experiment, the researchers produced strains of bacteria in the lab that contained the naturally occurring Caulobacter genome as well as segments of the new artificial genome. By switching off certain natural genes in the bacteria, the researchers were able to test the functions of the artificial genes introduced earlier. The rewritten genome was designed by an algorithm which could only parse information that was understood at the time of the DNA sequence. Naturally, there are also DNA sequences that have yet to be understood by scientists, and this can be lost in the process of creating the new code.

“Our method is a litmus test to see whether we biologists have correctly understood genetics, and it allows us to highlight possible gaps in our knowledge,” explains Beat Christen.

These experiments showed that only 580 of the 680 artificial genes were functional, showing that the algorithm needs tweaking before researchers can hope to achieve a truly functional genome in version 3.0.

Even though this version isn’t perfect, the new study demonstrates how modern technology can streamline artificial DNA synthesis. And who knows: in the future scientists might finally create synthetic organisms that would serve a wide array of biotech applications. For instance, custom-made bacteria could be used to produce active molecule for drugs or DNA vaccines.

“We believe that it will also soon be possible to produce functional bacterial cells with such a genome,” says Beat Christen.

“As promising as the research results and possible applications may be, they demand a profound discussion in society about the purposes for which this technology can be used and, at the same time, about how abuses can be prevented,” he added. It is still not clear when the first bacterium with an artificial genome will be produced – but it is now clear that it can and will be developed. “We must use the time we have for intensive discussions among scientists, and also in society as a whole. We stand ready to contribute to that discussion, with all of the know-how we possess.”

The findings were reported in the Proceedings of the National Academy of Sciences

Butterfly in a jar.

Researchers develop way to trap and study bacteria so we can fight disease and antibiotic resistance

New research from the University of York (UoY) will allow us to capture and study individual bacteria — hundreds of them at a time.

Butterfly in a jar.

The secret is to trap them!
Image credits Isabel Perelló.

When scientists want to see how a certain strain of bacteria will react to a given drug, they’ll flood a culture with different levels of the compound and see what happens. For the most part, this is a pretty effective technique and tells us what we need to know — does drug A kill bacterium Q, for example?

However, this approach has its own limitations. A novel method detailed in a new study wants to address these limitations by allowing researchers to look at individual bacteria rather than whole populations.

I’m not like the other bacteria

“Individual bacteria behave differently from one another and so looking at them as one large group can mean that inaccurate assumptions are made. This can lead to delayed or prolonged treatment regimes,” says Giampaolo Pitruzzello, a PhD student from the UoY’s Department of Physics and lead author of the study.

“We wanted a method that allowed clinical decisions to be made faster and more accurately. This meant finding a way of trapping individual bacteria and testing multiple features at once, rather than growing large cultures in a dish.”

Knowing how individual bacteria react to certain drugs could help doctors pick the right antibiotic for the right infection more quickly, reducing treatment times. This would also reduce the risk of complications developing before or during treatment (as the bacteria can be dealt with sooner, before they have a chance to run amok) and nip the rise of antibiotic resistance in the bud (as we can ensure that most if not all of these bugs die off).

Compared to current methods — which rely on growing whole cultures, billions of organisms strong — which take about 24-48 hours to run a full test, the team’s method can analyze bacterial susceptibility to certain drugs within a single hour. Even better, the team showed that their method can be used to look at hundreds of individual bacteria at the same time. As a proof of concept, they analyzed the shape and swimming ability of multiple bacteria and how different drugs interfere with their function.

The most effective drugs, they report, are those that messed up an organism’s shape and ability to move at the same time. The team explains that, while they chose to look at these two traits in particular, the method can be used to analyze virtually any property of bacteria.

“This method would allow clinicians to prescribe effective, targeted antibiotics early on in an infection which would lead to improved clinical outcomes whilst reducing overall levels of antibiotic use,” says Professor Thomas Krauss, from the UoY’s Department of Physics, who led the research efforts. “The aim is to get the right drug, to the right patient, at the right time.”

So how do they do it? Well, the team basically created a bacteria trap. They used very narrow channels filled with fluids and made bacteria swim along their length. The channels fed into microscopic traps where bacteria would come to a halt. Once there, the team injected different drugs into each trap and placed the bacteria under the microscope to see how they fared.

The approach yielded very encouraging results in a lab setting, and the team now hopes to expand their testing to include clinical samples (those taken directly from patients). Ultimately, they hope to refine the technique so it can be used in medical settings, such as clinics and hospitals, where it can save actual lives.

“This new technique offers a quick result so we can target more precisely which antibiotic to use to get patients better quicker,” explains Dr Adrian Evans, co-author and specialist in Urogynaecology at York Hospital. “This may well help reduce the burden of sepsis in our communities, which is an ever-increasing problem.”

The paper “Multiparameter antibiotic resistance detection based on hydrodynamic trapping of individual E. coli” has been published in the journal Lab on a Chip.


Treated wastewater could release antibiotic-resistance genes into the wild



Image credits Iva Balk.

These compounds end up in the water supply, potentially driving the spread of antibiotic resistance.

A team from the University of Southern California Viterbi School of Engineering say that even low concentrations of a single type of antibiotic can lead to the spread of resistance to multiple classes of these drugs in the wild. The team reports that antibiotics present in wastewater plants are a key driver of such resistance in the wild.

Drug dumping

“We’re quickly getting to a scary place that’s called a “post-antibiotic world,” where we can no longer fight infections with antibiotics anymore because microbes have adapted to be resilient against those antibiotics,” said Adam Smith, assistant professor of civil and environmental engineering at USC and lead investigator of the study. “Unfortunately, engineered water treatment systems end up being sort of a hot-bed for antibiotic resistance.”

While most of the antibiotics we ingest get metabolized (broken down) inside our bodies, small amounts find their way into urine and end up in wastewater treatment plants. So far, so good.

The problem starts inside these plants, the team explains. One of the most common ways in which wastewater is treated is through a membrane bioreactor, a process that relies on filtration systems and bacteria to remove and break down waste products. While doing their job, some of these bacteria encounter those trace-levels of antibiotics. They either die upon exposure or adapt to become (more) resistant to the compounds.

Those that do adapt pass their genes off to later generations — or to their neighbors via horizontal gene transfer.

One of the more dire possible scenarios, the team writes, is for these antibiotic-resistant bacteria (or free-floating bits of their DNA) to make it through the filtration membrane, into waterways, eventually reaching the ocean. Treated wastewater is also sometimes recycled for use in irrigation, car washes, firefighting, or to replenish groundwater supplies — so these bacteria could reach human populations directly.

The team believes that the amount of antibiotic-resistant organisms in treatment plants could be reduced through alterations in the treatment processes. For example, the use of anaerobic (oxygen free) processes rather than aerobic processes, or more aggressive filtration, could help limit their development. The team tested a small-scale anaerobic membrane bioreactor and compared the resulting antibiotic-resistant populations to those in treatment plants and their effluents for different types of antibiotics.

They report that these profiles are different in the treatment plants and effluents, and therefore one cannot be used to predict the other. However, they also found that there wasn’t a clear-cut correlation between the antibiotics they introduced into the system and the resulting resistance — they found bacteria with genes allowing for resistance to multiple classes of antibiotics, although only one such compound was tested at a time.

“The multi-drug resistance does seem to be the most alarming impact of this,” Smith said. “Regardless of the influent antibiotics, whether it’s just one or really low concentrations, there’s likely a lot of multi-drug resistance that’s spreading.”

This is probably generated by gene elements called plasmids, which can carry resistance genes for several types of antibiotics at a time. Because of their extremely small size — 1,000 times smaller than bacteria — plasmids can easily make it through filtration systems in the treatment process and reach the environment. Needless to say, that would not be good.

The paper “Evaluating Antibiotic Resistance Gene Correlations with Antibiotic Exposure Conditions in Anaerobic Membrane Bioreactors” has been published in the journal Environmental Science & Technology.

N. aromaticivorans bacteria.

Slightly-tweaked microbe could create plastics from a common plant waste material

A few genetic modifications can induce a strain of soil bacteria to convert a renewable material, lignin, into plastics. The best part? Lignin is so cheap and plentiful we don’t even bother trying to use it right now.

N. aromaticivorans bacteria.

N. aromaticivorans bacteria.
Image credits Great Lakes Bioenergy Research Center / UoW.

Woody plants show great promise as a potential replacement for petroleum in various uses — such as fuel, plastics, and chemical production. They contain a lot of sugars, which can be used for those applications, but they’re kept out of reach behind the cellulose in their cellular walls.

Those walls are so durable and hard (read: ‘expensive’) to break down industrially, that we generally don’t really bother extracting the materials.

Mister bacteria, break down this wall

A team of researchers at the Great Lakes Bioenergy Research Center (based at the University of Wisconsin-Madison-based and funded by the Department of Energy) hopes that a bacteria species can point the way to woody-plants-based replacements for petroleum. Their plan is to take this microscopic critter, tweak its genome around a bit, and unleash it on the plants’ cells — where it will transform all the lignin, a polymer that ties cellulose to the sugars, into something we can actually use.

Lignin is actually super abundant. It’s the second-most abundant type of aromatic compound (those ‘rings’ you see in organic chemistry) on the planet after petroleum, the team explains. However, isn’t very valuable right now. That’s actually an understatement. Lignin today is so cheap that paper mills — which have been in the business of stripping lignin from wood for centuries — can’t even bother trying to sell the stuff; they just dispose of it in huge boilers.

“They say you can make anything from lignin except money,” says Miguel Perez, a UW-Madison graduate student in civil and environmental engineering and the paper’s first author.

The bacteria in question is Novosphingobium aromaticivorans. It was first isolated in soils that were previously contaminated by petroleum products. And, in this environment where most other organisms find it hard to eek out a living, N. aromaticivorans was thriving. Its name aromaticivorans means ‘aromatic-eater’ as a nod to its unique adaptations.

Lignin is a large molecule that’s very difficult to break down into smaller pieces. But N. aromaticivorans already had a natural appetite for lignin-like products when discovered — in fact, it’s the only known organism so far that can digest many parts of the lignin molecule and excrete smaller aromatic compounds.

“Other microbes tried before may be able to digest a few types of aromatics found in lignin,” Perez says. “When we met this microbe, it was already good at degrading a wide range of compounds. That makes this microbe very promising.”

During this process, N. aromaticivorans produces 2-pyrone-4,6-dicarboxylic acid or PDC. The team engineered the bacteria by removing three genes in its genome, further stabilizing the digestion process and coaxing it reducing all its meal into PDC. In the end, what they obtained was an organism which could be fed any part of the lignin molecule and produce PDC.

“There’s no industrial process for doing that, because PDC is so difficult to make by existing routes,” says Daniel Noguera, the study’s corresponding author. “But if we’re making biofuels from cellulose and producing lignin — something we used to just burn — and we can efficiently turn the lignin into PDC, that potentially changes the market for industrial use of this compound.”

“The compound performs the same or better than the most common petroleum-based additive to PET polymers — like plastic bottles and synthetic fibers — which are the most common polymers being produced in the world,” Perez adds.

PDC is also biodegradable and doesn’t leach any by-products while it degrades.

For now, the engineered variation on N. aromaticivorans can turn at least 59% of lignin’s potentially useful compounds into PDC. The team suggests that a greater efficiency is possible through further genetic manipulation of the microbe. They’re currently at work implementing such changes and “might create a new industry,” Noguera says.

The paper “Funneling aromatic products of chemically depolymerized lignin into 2-pyrone-4-6-dicarboxylic acid with Novosphingobium aromaticivorans” has been published in the journal Green Chemistry.

Burkholderia ambifaria. Credit: Genome Portal.

Bacteria might become a natural, toxin-free alternative to pesticides

Burkholderia ambifaria. Credit: Genome Portal.

Burkholderia ambifaria. Credit: Genome Portal.

Man-made pesticides are essential to our modern way of life. They not only protect crops and improve farmers’ yields, but also ward off pests around homes or prevent vegetation from clogging powerlines and highways. Synthetic pesticides also have their downsides, such as their toxicity which can threaten some ecosystems. For instance, the worldwide collapse of bee populations has been at least partly pinned on certain classes of pesticides. This is why some scientists are experimenting with a different kind of pesticides. Instead of toxic chemicals, researchers at Cardiff University are investigating the possibility of using living pesticides — bacteria that protect crops against diseases.

Biopesticides that use bacteria or bacteria-derived substances aren’t exactly new. In the 1990s, the industry experimented with Burkholderia ambifaria bacteria which produce one or more antibiotics that are active against a broad range of plant pathogenic fungi. These antibiotics appear, in many cases, to be important for disease suppression and their use in biocontrol can be an effective substitute for chemical pesticides which may pose risks to human health and the environment. However, their use has been linked with lung infections in people with cystic fibrosis (CF), leading to their withdrawal from the biopesticide market.

Cardiff University researchers, led by Eshwar Mahenthiralingam, want to exploit Burkholderia‘s biopesticide qualities while controlling the adverse effects it might pose the health of some people. For many years, they have been studying Burkholderia-plant interactions in order to find out how they protect plants against diseases.

Researchers sequenced the genome of the bacteria, identifying Burkholderia’s antibiotic-making gene called Cepacin. Subsequent tests showed that the gene protected plants against damping off — a soil-borne fungal disease that affects seeds and new seedlings.

According to Mahenthiralingam, the biopesticide bacteria splits its genomic DNA into 3 fragments, called replicons. By removing the smallest of these 3 replicons, the researchers created a mutant strain which demonstrated effective biopesticidal properties. Experiments with mice show that the mutant strain did not persist in animals with lung infections, suggesting that in the future similar strains could protect our crops without causing health issues.

“Beneficial bacteria such as Burkholderia that have co-evolved naturally with plants, have a key role to play in a sustainable future. We have to understand the risks, mitigate against them and seek a balance that works for all,” said Professor Mahenthiralingam.

“Through our work, we hope to make Burkholderia viable as an effective biopesticide, with the ultimate aim of making agriculture and food production safer, more sustainable, and toxin-free.”

The findings appeared in the journal Nature Microbiology.


Over 100 new species of bacteria discovered in your gut

An international research team has created the most comprehensive record of human intestinal flora to date. Over 100 of the species they list are completely new to science.


Image via Pixabay.

Our intestinal microbiome is essential in keeping us healthy, well-fed, and in good spirits. Each one of us carries around 2% of our overall body weight in bacteria. However, we don’t have a very clear idea of what strains call our innards ‘home’. A new study, published by researchers from the Wellcome Sanger Institute, Hudson Institute of Medical Research, Australia, and EMBL’s European Bioinformatics Institute comes to flesh out our understanding of these bugs with the most comprehensive look at human intestinal flora to date.

The resource will allow scientists to better understand our bacterial compadres and make it easier to analyze the particular microbiome of each individual. All in all, the team hopes their work will point the way towards new treatments for diseases such as gastrointestinal disorders, infections, and immune conditions.


“This study has led to the creation of the largest and most comprehensive public database of human health-associated intestinal bacteria,” says first author Dr Samuel Forster from the Wellcome Sanger Institute.

“The gut microbiome plays a major in health and disease. This important resource will fundamentally change the way researchers study the microbiome.”

The team worked with fecal samples collected from 20 people in the UK and Canada. They isolated, grew, and DNA-sequenced 737 individual strains of bacteria from this material. Further analysis showed these strains make up 273 separate bacterial species — strains are roughly equivalent to a sub-species — including 173 that have never before been sequenced. Of these latter ones, 105 have never been isolated before.

So why is that important? Well, when researchers need to study the effect of microbiomes on human health, they usually sequence the DNA of the whole sample (which is to say, the genomes of all species in a sample), and then try to tease apart its different component species. It works really well if you know what each individual species’ genome looks like — however, we didn’t have reference material for all the inhabitants of our bellies. That’s where the present study comes into the picture.

The data collected by the team will make it cheaper, faster, and easier for researchers to determine which bacteria are present in a certain community, and to research their role in diseases. If researchers need to check a particular hypothesis — that certain bacteria increase in the case of a disease, for example — they can get an isolate from the collection and run it through tests in the lab. Up to now, researchers would have to obtain stool samples from which to isolate particular strains or species — which took a lot of time and incurred costs.

“For researchers trying to find out which species of bacteria are present in a person’s microbiome, the database of reference genomes from pure isolates of gut bacteria is crucial,” says coauthor Dr Rob Finn from EMBL’s European Bioinformatics Institute.

“This culture collection of individual bacteria will be a game-changer for basic and translational microbiome research,” adds senior author Dr Trevor Lawley (also from the Wellcome Sanger Institute). “Ultimately, this will lead us towards developing new diagnostics and treatments for diseases such as gastrointestinal disorders, infections and immune conditions.”

The paper “Human Gastrointestinal Bacteria Genome and Culture Collection” has been published in the journal Nature Biotechnology.

New bacteria strain.

Irish dirt might cure the world of (most) multi-drug-resistant bacteria

Irish soil might win us the fight against drug-resistant superbugs. Literally!

New bacteria strain.

Growth of the newly discovered Streptomyces sp. myrophorea. Although superficially resembling fungi, Streptomyces are true bacteria and are the source of two-thirds of the various frontline antibiotics used in medicine.
Image credits G Quinn / Swansea University

An international team of researchers based at the Swansea University Medical School, UK, reports finding a new strain of bacteria that can murder pathogens that our antibiotics increasingly cannot. The bacteria has been found in soil samples recovered from an area of Fermanagh, Northern Ireland.

Bad bugs get grounded

“This new strain of bacteria is effective against 4 of the top 6 pathogens that are resistant to antibiotics, including MRSA. Our discovery is an important step forward in the fight against antibiotic resistance,” says Professor Paul Dyson of Swansea University Medical School, paper co-author.

The finding is far from inconsequential. The World Health Organisation (WHO) describes rising antibiotic resistance as “one of the biggest threats to global health, food security, and development today”. Further research also estimated that antibiotic-resistant ‘superbugs’ could lead up to 1.3 million deaths in Europe alone by 2050.

The team named their discovery Streptomyces sp. myrophorea. It was discovered in the Boho Highlands, County Fermanagh, Northern Ireland, hiding in the soil. The researchers investigated the soils there as Dr. Gerry Quinn, a previous resident of the area, became curious to investigate local healing traditions.

Those traditions called for a small amount of soil to be wrapped up in cotton cloth and applied to cure ailments varying from toothaches to throat or neck infections. The team notes that the area has been inhabited for at least 4,000 years — first by Neolithic tribes and later druidic tribes — who may have started this tradition.

Lab tests later revealed the presence of the strain in local soils, and clued the team in on their impressive antibacterial properties. This bacteria inhibited the growth of four of the top six multi-resistant pathogens (those listed by the WHO as being responsible for healthcare-associated infections): Vancomycin-resistant Enterococcus faecium (VRE), methicillin-resistant Staphylococcus aureus (MRSA), Klebsiella pneumonia, and Carbenepenem-resistant Acinetobacter baumanii. It was also successful in inhibiting both gram positive and gram negative bacteria, which differ in the structure of their cell wall. Gram-negative bacteria are, generally speaking, more resistant to antibiotics.

It is not yet clear exactly how the bacteria do this, but the team is hard at work finding out.

New bacteria strain.

Zone of inhibition (light brown) produced by Streptomyces sp myrophorea (brown spot) on a lawn of MRSA.
Image credits G Quinn / Swansea University.

The active compounds secreted by Streptomyces sp.myrophorea could help create a new class of treatment against multi-drug resistant bacteria, the study reports. These pathogens are one of the most pressing threats to public health currently, as doctors are often left powerless to treat them. They’re especially dangerous in hospitals, where the large density of patients (often with weakened or compromised immune systems) means easy pickings for such pathogens.

“Our results show that folklore and traditional medicines are worth investigating in the search for new antibiotics,” Professor Dyson says. “Scientists, historians, and archaeologists can all have something to contribute to this task. It seems that part of the answer to this very modern problem might lie in the wisdom of the past.”

“We will now concentrate on the purification and identification of these antibiotics. We have also discovered additional antibacterial organisms from the same soil cure which may cover a broader spectrum of multi-resistant pathogens.”

The paper “A Novel Alkaliphilic Streptomyces Inhibits ESKAPE Pathogens” has been published in the journal Frontiers in Microbiology.

There’s a massive ecosystem of ‘deep life’ right beneath our feet

A study that has been a decade in the making has finally documented one of the largest and least understood ecosystems on the planet — the deep biosphere, which can extend over several kilometers into the crust. According to the analysis, Earth’s subsurface is teeming with life, totaling 245 to 385 times more carbon mass than all humans on the surface.

This is a species of Methanobacterium, which produces methane. Found in samples from a buried coal bed 2 km below the Pacific Ocean floor off the coast of Japan. Credit: Hiroyuki Imachi (Japan Agency for Marine-Earth Science and Technology (JAMSTEC).

Scientists have always presumed that there is a lot of biodiversity beneath the planet’s continents and ocean floors. But reality seems to have beaten even the wildest speculations.

Researchers at the Deep Carbon Observatory project collected samples from hundreds of sites around the world, from mines and boreholes 5 km (3.1 mi) deep and up to 2.5 km (1.6 mi) under the seafloor. This data was extrapolated to cobble together a broader picture of much and what kinds of life exist in the deep subsurface — under the greatest extremes of pressure, temperature, and low nutrient availability. The researchers estimated that the volume of the deep biosphere is about 2 to 2.3 billion cubic km, almost twice the volume of all oceans. They also estimated the total biomass of deep-Earth life: 15 to 23 billion tonnes, a figure that sums 2 to 6 × 10^29 cells — that’s 6 followed by 29 zeroes.

“Ten years ago, we knew far less about the physiologies of the bacteria and microbes that dominate the subsurface biosphere,” says Karen Lloyd, University of Tennessee at Knoxville, USA. “Today, we know that, in many places, they invest most of their energy to simply maintaining their existence and little into growth, which is a fascinating way to live.

“Today too, we know that subsurface life is common. Ten years ago, we had sampled only a few sites – the kinds of places we’d expect to find life. Now, thanks to ultra-deep sampling, we know we can find them pretty much everywhere, albeit the sampling has obviously reached only an infinitesimally tiny part of the deep biosphere.”

Candidatus Desulforudis audaxviator (the orange carbon spheres are carbon that the bacteria eats) collected from under Mponeng gold mine in South Africa. Credit: University of Queensland.

Candidatus Desulforudis audaxviator (the orange carbon spheres are carbon that the bacteria eats) collected from under Mponeng gold mine in South Africa. Credit: University of Queensland.

All three domains of life are represented in the deep biosphere: bacteria, archaea (single-celled organisms that lack a well-defined nucleus), and eukarya (multicellular organisms). However, as one might expect, bacteria and archaea dominate subsurface life — a whopping 70% of all bacteria and archaea live in the subsurface. What’s also striking is that the genetic diversity of such organisms is comparable and in some instances greater than their surface counterparts.

Perhaps the most important takeaway is that life is extremely resilient, never ceasing to amaze us. Even kilometers beneath the surface, where the only available energy comes from rocky surroundings, some organisms have found a way to survive. Some of the strangest organisms are so-called “zombie” bacteria that have life cycles of millions, even tens of millions of years — a necessary adaptation to their low-nutrient environment. The fact that some organisms exist at such incredible depths — let alone for millennia — is mind-boggling!

Altiarchaeales (Archaea) found in sulfidic springs in Germany. Credit: Medical University of Graz, Austria.

Altiarchaeales (Archaea) found in sulfidic springs in Germany. Credit: Medical University of Graz, Austria.

Even now, we still don’t know what the absolute limits for life on Earth in terms of temperature, pressure, and energy availability are. The record depth at which life has been found in the continental subsurface is 5 km. For marine waters, the record is 10.5 km from the ocean’s surface. As scientists drill even deeper for life, such records will likely be broken time and time again.

“Our studies of deep biosphere microbes have produced much new knowledge, but also a realization and far greater appreciation of how much we have yet to learn about subsurface life,” says Rick Colwell from Oregon State University. “For example, scientists do not yet know all the ways in which deep subsurface life affects surface life and vice versa. And, for now, we can only marvel at the nature of the metabolisms that allow life to survive under the extremely impoverished and forbidding conditions for life in deep Earth.”

Deep Carbon Observatory’s findings were released on the eve of the American Geophysical Union’s annual meeting. Some of the studies were published in the journals Geobiology and Nature Geoscience.

Credit: Wikimedia Commons.

Purple bacteria turns sewage waste into clean energy

Wastewater is not something you usually want to be around — but that doesn’t mean it can’t be valuable. Your typical household sewage is rich in bioplastics, organic compounds that can be turned into energy, or even proteins for animal feed. The challenge lies in separating contaminants from the valuable organic compounds — the gold from the trash, so to speak. Now, researchers say they’ve found a new cost-effective and environmentally-friendly method that does just that using purple bacteria.

Credit: Wikimedia Commons.

Credit: Wikimedia Commons.

In most people’s minds, photosynthesis is associated with the color green. However, photosynthetic pigments come in all sorts of colors (think of yellow, orange, and red leaves in the autumn), but also in a variety of different organisms. For instance, a group phototrophic bacteria use energy from the sun via a variety of different pigments, such as orange, red, brown, but also purple — they’re even called purple bacteria.

However, it’s not their color that interests scientists but rather their unique metabolism. In the presence of light, these microbes use organic molecules and nitrogen gas to make carbon and nitrogen, all while releasing electrons. A byproduct of this metabolic reaction is hydrogen gas, which can be used to generate electricity in a fuel cell.

Dr. Daniel Puyol and colleagues at King Juan Carlos University, Spain designed a biorefinery process that harvests green energy from wastewater using a mixture of purple bacteria species. In a new study published in the Frontiers in Energy Researchthe research team analyzed the optimal conditions for maximizing hydrogen product and found a nutrient blend that not only outputs the highest rate of hydrogen, but also minimizes the production of CO2.

One of the biggest environmental problems associated with wastewater treatment is its significant carbon emissions which warm up the planet’s atmosphere. So, having a technical solution that not only removes this excess carbon from the atmosphere but also produces a useful, clean fuel is a great combo.

“Our group manipulates these conditions to tune the metabolism of purple bacteria to different applications, depending on the organic waste source and market requirements,” says co-author Professor Abraham Esteve-Núñez of University of Alcalá, Spain.

“But what is unique about our approach is the use of an external electric current to optimize the productive output of purple bacteria.”

The most interesting result, however, was obtained when the Spanish researchers found that purple bacteria are capable of using electrons from the cathode (negative electrode) to capture CO2 via photosynthesis. The bioelectrochemical system is the first demonstration of any phototroph shifting metabolism due to interaction with a cathode.

“Recordings from our bioelectrochemical system showed a clear interaction between the purple bacteria and the electrodes: negative polarization of the electrode caused a detectable consumption of electrons, associated with a reduction in carbon dioxide production,” Esteve-Núñez said in a statement.

“This indicates that the purple bacteria were using electrons from the cathode to capture more carbon from organic compounds via photosynthesis, so less is released as CO2.”

Capturing CO2 is useful not only to reduce carbon emissions but also for refining biogas for use as a fuel. What’s more, the researchers say that there may be even more surprises in store.

“One of the original aims of the study was to increase biohydrogen production by donating electrons from the cathode to purple bacteria metabolism. However, it seems that the PPB bacteria prefer to use these electrons for fixing CO2 instead of creating H2,” Puyol said in a statement.

“We recently obtained funding to pursue this aim with further research, and will work on this for the following years. Stay tuned for more metabolic tuning.”

Credit: Pixabay.

Sunlight kills indoor germs almost as well as UV rays

We know that sunlight is important to our health, regulating sleep and mood. A new study, however, suggests sunlight also keeps us healthy by destroying bacteria that lurk indoors. The sanitizing effects are impressively close to those of ultraviolet light.

Credit: Pixabay.

Credit: Pixabay.

For their experiment, researchers at the University of Oregon collected dust from homes in Portland and placed it in dollhouse-sized rooms. The dust inside the tiny rooms — and the microscopic creatures that lived within — stayed there for 90 days under three conditions: exposed to daylight through regular glass; UV light alone; and total darkness.

When the team counted and inspected the bacterial samples, they were surprised by what they found. Lit rooms seem to harbor only half as many viable bacteria when compared to dark rooms, and nearly as few as those in the UV room. Researchers found 12% of bacteria in dark rooms were viable, compared to 6.8% in daylit rooms and 6.1% in rooms with UV light only, according to the findings published in the journal Microbiome. 

Ultraviolet (UV) light is a form of light that is invisible to the human eye, occupying the portion of the electromagnetic spectrum between X-rays and visible light. One of the biological characteristics of UV light is that it is germicidal – meaning it is capable of inactivating microorganisms, such as bacteria, viruses, and protozoa.

Today, UV light-based devices are used for drinking and wastewater treatment, air disinfection, the treatment of fruit and vegetable juices, as well as a myriad of home devices for disinfecting everything from toothbrushes to tablet computers. But soon enough, smart blinds that allow some of the solar energy to pass through and kill germs for us may become commonplace in our homes.

The study’s results were quite unexpected, however, because glass is known to block out most UV rays. The findings suggest that having a well-lit room can help protect residents from all sorts of infections. For instance, some of the bacterial species that didn’t survive the daylight rooms are known to cause respiratory disease.

“Our experimental and simulation-based results indicate that dust contains living bacterial taxa that can be inactivated following changes in local abiotic conditions and suggest that the bactericidal potential of ordinary window-filtered sunlight may be similar to ultraviolet wavelengths across dosages that are relevant to real buildings,” the authors concluded.

Next, the team plans to gain a more nuanced look at the relationship between daylight exposure and bacterial inactivation. This way, architects can then design the perfect windows that are just big enough to let enough light in to kill dangerous germs. But, perhaps the most important takeaway is that you should pull the blinds and let some of that light shine your room for longer during the day.

E.coli rendering.

Some bacteria can ‘hibernate’ through antibiotic treatments, new paper finds

When antibiotics come knocking, bacteria may simply sleep the threat away.

E.coli rendering.

Digital rendering of E.coli bacteria.
Image via Fotolia.

Researchers from the University of Copenhagen report that pathogenic bacteria have a surprising defensive tactic against antibiotics: hibernation. The research might help us fight antibiotic-resistant infections.

Nap it out

Almost all types of pathogenic bacteria eventually develop strains that are tolerant of or resistant to antibiotic treatments. This is particularly problematic as the fraction of bacteria which survive treatment — although tiny — can later multiply, maintaining infection in the face of our antibiotic efforts.

However, a small number of bacterial species do away with this mechanism completely, yet still retain the ability to resist the drugs meant to kill them. In an effort to understand why, the Copenhagen team turned to E. coli.

“We studied E. coli bacteria from urinary tract infections that had been treated with antibiotics and were supposedly under control,” says Professor Kenn Gerdes of the University of Copenhagen’s Department of Biology, paper co-author.

“In time, the bacteria re-awoke and began to spread once again,” he explains

The team found that a few individuals in the overall bacterial population ‘hid’ from the antibiotics in a dormant, hibernation-like state. The bugs slept through the treatment, and only resumed their regular activity once the dangerous compounds were removed.

Antibiotics generally work by attacking a bacteria cell’s ability to grow — so these hibernating individuals are virtually immune to their effects.

“A bacterium in hibernation is not resistant. It is temporarily tolerant because it stops growing, which allows it to survive the effects of an antibiotic,” says Professor Gerdes.

Hibernating bacteria seem to share the same genetic characteristics as all other individuals in a given population, the team reports. So, as of right now, they can’t say exactly why some members enter a dormant state while their peers do not. The team did, however, identify an enzyme in dormant individuals that governs the ‘hibernation’ process. A compound that could interfere with this enzyme’s functioning, or its synthesis, could help to keep these bacteria from becoming invulnerable to antibiotics.

“The discovery of this enzyme is a good foundation for the future development of a substance capable of combating dormant bacteria cells,” says Professor Gerdes.

“The enzyme triggers a ‘survival program’ that almost all disease-causing bacteria deploy to survive in the wild and resist antibiotics in the body. Developing an antibiotic that targets this general programme would be a major advance,” he adds.

Although the findings are encouraging, it will still be several years before they can be turned into a safe and useable treatment, the team writes.

The paper “The kinases HipA and HipA7 phosphorylate different substrate pools in Escherichia coli to promote multidrug tolerance” has been published in the journal Science Signaling.

Scanning electron micrograph of Mycobacterium tuberculosis bacteria, which cause TB. Credit: NIAID, Flickr.

New non-antibiotic treatment hijacks tuberculosis bacterium

Scanning electron micrograph of Mycobacterium tuberculosis bacteria, which cause TB. Credit: NIAID, Flickr.

Scanning electron micrograph of Mycobacterium tuberculosis bacteria, which cause TB. Credit: NIAID, Flickr.

Although the vaccine for tuberculosis (TB) was developed more than a century ago, infections are on the rise with 7.3 million diagnosed cases recorded worldwide in 2018 — this is up from 6.3 million two years prior. Once the first symptoms of the infectious disease set in, the patient needs to undergo a lengthy treatment with a powerful cocktail of antibiotics, which isn’t foolproof.

This is where a promising new treatment pathway identified by researchers at the University of Manchester may come in. The team found a way to treat TB in animals with a non-antibiotic drug.

The treatment works by targeting Mycobacterium tuberculosis’ defenses rather trying to destroy the bacteria itself.

Mycobacterium tuberculosis secretes molecules called Virulence Factors, which block the immune system’s response to the infection, making it extremely difficult to combat it. This is why people need strong antibiotics, often over 6 to 8 months. But even after the treatment is over, there’s a 20% risk that the infection will resurface.

Professor Lydia Tabernero, the project’s lead researcher, and colleagues targetted a specific Virulence Factor called MptpB, which, when blocked, allows white blood cells to destroy the bacteria more efficiently. In trials, monotherapy with an orally bioavailable MptpB inhibitor reduced infection burden in acute and chronic guinea pig models.

“The fact that the animal studies showed our compound, which doesn’t kill the bacteria directly, resulted in a significant reduction in the bacterial burden is remarkable,” Tabernero said in a statement.

Because MptpB isn’t found in humans, nor anything similar to it, the compounds used to block it are non-toxic to our cells.

What’s more, because the bacteria aren’t threatened directly, they are less likely to develop resistance against the treatment. Currently, the world is facing an antibiotic-resistance crisis that is threatening to undermine decades-worth of medical progress.

Scientists think that one in three people around the world is infected with TB, which kills 1.7 million annually. The disease is the most prevalent in Africa, India, China, but is on the rise in some western countries, particularly in the UK’s capital, London.

“TB is an amazingly difficult disease to treat so we feel this is a significant breakthrough,” said Tabernero.

”The next stage of our research is to optimise further the chemical compound, but we hope Clinical trials are up to four years away.”

The findings appeared in the Journal of Medicinal Chemistry.