Tag Archives: bacteria

Metal-eating bacteria discovered in dirty lab glassware

Manganese oxide nodules generated by the bacteria discovered by the Caltech team. The nodules are generally about 0.1 to 0.5 millimeters in diameter. Credit: Hang Yu/Caltech

His dark material

One regular day, Jared Leadbetter left a jar soiled with manganese to soak with tap water in his Caltech office sink. Upon his return from fieldwork several months later, the environmental microbiology professor was surprised to find the jar was coated in some dark material.

“I thought, ‘What is that?'” he said. “I started to wonder if long-sought-after microbes might be responsible, so we systematically performed tests to figure that out.”

Turns out, Leadbetter had identified bacteria that consume the metal for energy, something that has been theorized for over a hundred years but which has only recently been confirmed.

The black coating that the scientist found inside the walls of his glassware was in fact oxidized manganese — a dark, clumpy substance that is very commonly found in nature, particularly in subsurface deposits and water-distribution systems.

“There is a whole set of environmental engineering literature on drinking-water-distribution systems getting clogged by manganese oxides,” says Leadbetter. “But how and for what reason such material is generated there has remained an enigma. Clearly, many scientists have considered that bacteria using manganese for energy might be responsible, but evidence supporting this idea was not available until now.”

Scientists have been aware for some time that some bacteria degrade pollutants like manganese oxide, through a process called bioremediation. The microorganisms reduce the manganese oxide, meaning they donate electrons, similarly to how humans use oxygen to breathe.

It’s striking when you realize that it is also bacteria that likely form most of the manganese oxide in the first place.

Lurking in the waters, eating metal

The two newly found microorganisms, a type of Nitrospirae and betaproteobacterium that lurk in groundwater and tap water, strip electrons off of manganese to convert carbon dioxide into biomass — a process that scientists call chemosynthesis.

“The bacteria we have discovered can produce it, thus they enjoy a lifestyle that also serves to supply the other microbes with what they need to perform reactions that we consider to be beneficial and desirable,” says Leadbetter.

In order to be sure that microorganisms were indeed oxidizing the manganese, the researchers coated more jars with the substance and then sterilized some of them with scorching steam. Even a year later, the sterilized flasks didn’t darken at all, while those that hadn’t been steamed were smudged.

Manganese is one of the most abundant metals on Earth. We actually regularly ingest this metal from foods such as nuts and tea, which our bodies use to process fats or form bone. It’s then not that surprising to learn that bacteria use the metal for energy. Another microorganism, a soil-living, rod-shaped bacterium called Cupriavidus metallidurans, is known for eating toxic metals and ‘pooping’ gold nuggets as a byproduct.

Manganese oxide also deposits on the seafloor under the form of nodules. These grapefruit-sized metallic balls have been identified since the days of the HMS Challenger in the 1870s. Today, mining companies are interested in harvesting these nodules since rare metals are often found inside them.

However, little is understood about how the metal balls form in the place. The new study suggests that perhaps other microorganisms that are adapted to seawater rather than freshwater may be responsible.

“This underscores the need to better understand marine manganese nodules before they are decimated by mining,” says postdoctoral scholar Hang Yu, co-author of the new study alongside Leadbetter.

“This discovery from Jared and Hang fills a major intellectual gap in our understanding of Earth’s elemental cycles, and adds to the diverse ways in which manganese, an abstruse but common transition metal, has shaped the evolution of life on our planet,” says Woodward Fischer, professor of geobiology at Caltech, who was not involved with the study.

The findings were reported in the journal Nature.

Even underground ecosystems are being influenced by humanity

Not even underground systems are free from the effects of pollution, according to a new study.

A cave in the Municipality of Quezon, Philippines (not Monte Conca).
Image via Wikipedia.

The research focused on the Monte Conca cave system, a sprawling gallery of springs and pools below a nature preserve in Sicily. According to the team, despite its isolation underground, even the Monte Conca system shows signs of changes in its microbe communities with species associated with human waste.

Nowhere to hide

Monte Conca is Sicily’s longest and deepest gypsum karst system and was dug out by sulfuric acid eating into the rock. It’s not a unique occurrence, and caves of this type have been found throughout the world.

Given how secluded it is, the system was believed to be pristine, but pollution seems to make an impact even here. The team reports that the cave system experiences seasonal changes in microbial communities between its wet and dry seasons. Their results suggest that such changes are driven by surface water percolating through soils beneath agricultural and urban areas that collect contaminants and deposit them in the cave.

These chemicals then alter the makeup of the cave’s microbial communities.

While the research focused on the Monte Conca spring pool, the team says it’s indicative of the impact surface runoff has on cave microbes throughout the world. Exactly what the long-term effect of these changes will be is not well known, says lead author Dr. Madison Davis of USF’s Department of Cell Biology, Microbiology and Molecular Biology.

During the dry season, biological activity in the cave is dominated by sulfur-oxidizing bacteria, which mix oxygen from the cave with hydrogen sulfide in the water for energy. They represent over 90% of the bacteria in this ecosystem.

After heavy rainfall, however, (which is especially likely during the wet season), this type of bacteria was overshadowed by surface-derived species which the team identified as being primarily human-associated strains, including Escherichia coli and other fecal bacteria.

One sampling (the team took four samplings between 2015 and 2016) appeared to show a transition between the wet and dry seasons when potential man-made contaminants (such as Escherichia and Lysinibacillus), sulfur-oxidizing bacteria, and nitrogen-fixing bacteria all were present within the spring pool after heavy rains. This helped show that what the team picked up on was indeed the effect of surface events and not a natural occurrence in the cave.

The paper “Surface runoff alters cave microbial community structure and function” has been published in the journal PLOS ONE.

Newly discovered bacteria feeds on toxic plastic

Credit: Pixabay.

Human activity has produced over eight billion tons of plastic since the material entered mass production in the 1950s — most of which have been discarded in huge landfills and the world’s oceans after products made from it fell out of use.

Plastic is extremely cheap and durable, which explains its popularity. These characteristics also make plastic a bane for the environment.  Not only do plastic fragments threaten wildlife when they ingest them, they also release toxic and carcinogenic chemicals when they break down.  

But we know that life finds a way to thrive even in the most unexpected and inhospitable places.

Newly discovered bacteria not only survive in landfills, they also seem to feed solely on the toxic chemicals formed by the breakdown of plastics. Specifically, the bacteria munch on polyurethane (PET), the authors wrote in their new study published in the journal Frontiers in Microbiology.

About 50 million tons of Polyethylene terephthalate (PET) are made each year to satisfy our growing needs for fabrics, electrics and beverage containers. Alas, half of all PETs end up either in landfills or the ocean.

According to researchers at theHelmholtz Centre for Environmental Research-UFZ in Leipzig, Germany, the new strain of Pseudomonas bacteria can use the components of polyurethane as their sole source of carbon, nitrogen, and energy.

Previously, scientists had discovered fungi that could break down polyurethane and even accidentally created a mutant enzyme in the lab that could break down plastic bottles. This month, biologists at Brandon University in the US described a plastic-munching wax moth caterpillar. However, bacteria are much more reliable to use at an industrial scale.

There is still much work to be done before enzymes extracted from the bacteria can be sprayed on landfills to almost magically make plastic disappear. It’s much more complicated than meets the eye and it might take ten years before we see wide-scale use of biotech to tackle plastic pollution.

Nevertheless, this is very good news within a backdrop of doom and gloom, dominated by news of increasing pollution, global warming, and now a life-threatening pandemic.

Many existential threats to mankind are of our own doing. It is thus our responsibility to make amends by recycling more and using plastic-free products, besides radical solutions such as biotech. We made plastic; now it’s up to us to clean it up.

New species of soil bacteria can break down soil pollutants

Researchers at Cornell University discovered a new species of bacteria that can break down organic contaminants in the soil.

Image via Pixabay.

The new species was named Paraburkholderia madseniana in honor of the late Gene Madsen, the microbiology professor who started the research. The species is particularly adept at breaking down aromatic compounds (ring-like molecules of carbon), a large class of organic compounds that includes several types of pollutants.

Cleaning the soiled

“Microbes have been here since life began, almost 4 billion years. They created the system that we live in, and they sustain it,” said Dan Buckley, professor of microbial ecology at Cornell’s School of Integrative Plant Science. “We may not see them, but they’re running the show.”

Professor Madsen discovered the bacteria in soil samples from the Turkey Hill road meadow, an experimental forest stewarded by the Cornell Botanic Gardens. However, he passed away in 2017 before he could prove the bacteria’s abilities, which this study reports on.

The species belongs to the genus Paraburkholderia, which are known for their ability to decompose aromatic compounds. Some species in this genus are also known to form symbiotic relationships with plants, creating nodules around their roots and supplying nitrogen.

Madsen, however, focused his work on biodegradation — the process by which bacteria break organic matter down to extract energy, — with a particular eye towards organic pollutants called polycyclic aromatic hydrocarbons (PAHs). His work helped further our understanding of how natural tools can be applied to clear waste areas in which soils can’t be easily de-contaminated or removed.

The first step of the research was to sequence the bacteria’s RNA, which showed it to be a new species. Subsequent observation showed that madseniana can break down aromatic hydrocarbons; this ability, the team explains, was likely evolved as it allows madseniana to break down lignin, a major structural component of wood and plant tissues. Luckily for us, this also allows it to attack a wide range of organic pollutants generated through the use of fossil fuels.

“We know remarkably little about how soil bacteria operate,” Buckley said. “Soils, every year, process about seven times more carbon than all of the human emissions from cars, power plants and heating units, all over the world, just in their natural work of decomposing plant material.”

“Because it’s such a large amount of carbon going through the soil, small changes in how we manage soil could make a big impact on climate change.”

In the future, the team plans to investigate the relationship between madseniana and forest trees. Their findings so far suggest that trees trade carbon with colonies of the bacteria around their roots, which break down organic matter and return vital nutrients such as phosphorous and nitrogen.

The paper “Paraburkholderia madseniana sp. nov., a phenolic acid-degrading bacterium isolated from acidic forest soil” has been published in the International Journal of Systematic and Evolutionary Microbiology.

New compounds fight drug-resistant bacteria by turning their membranes into prison cells

Two new antibiotic compounds join the fight against drug-resistant bacteria.

Staphylococcus aureus seen under the electron microscope.
Image credits Mogana Das Murtey, Patchamuthu Ramasamy.

The compounds have been named corbomycin and complestatin, and are part of the glycopeptide family of antibiotics produced by soil bacteria (the Actinomycetes family in particular). The unique way in which they attack bacteria makes them very promising candidates against drug-resistant infections, the study reports.

Don’t tear down this wall

The study reports that laboratory studies on mice showed that these two substances interact with bacteria in a completely different way from anything we’ve seen before.

“Bacteria have a wall around the outside of their cells that gives them shape and is a source of strength,” said study first author Beth Culp, a PhD candidate in biochemistry and biomedical sciences at McMaster.

“Antibiotics like penicillin kill bacteria by preventing building of the wall, but the antibiotics that we found actually work by doing the opposite — they prevent the wall from being broken down. This is critical for cell to divide.”

Both corbomycin and complestatin have proven themselves effective in combating Methicillin-resistant Staphylococcus aureus (MRSA), a family of bacteria that is highly resistant to antibiotics and is responsible for many serious, potentially life-threatening infections today.

Glycopeptides inhibit the growth of cell membranes by blocking the synthesis of peptidoglycan, which is a vital building block. It may not sound like much of a hassle but this effectively prevents bacteria from multiplying, as they need to generate extra membrane before dividing. These two compounds essentially ensures the bacteria are “trapped in a prison, and can’t expand or grow.”

For the study, the team started with a list of known glycopeptides — a chemical class that includes some of the most powerful and dangerous antibiotics humanity has ever wielded — and the microbial genes that encode their synthesis. They hoped that compounds encoded in different genes would also engage bacteria in different ways. This step set them on the trail of corbomycin and complestatin.

Looking at the family tree of known members of the glycopeptides, researchers studied the genes of those lacking known resistance mechanisms, with the idea they may be antibiotics demonstrating a different way to attack bacteria. Further testing in collaboration with Yves Brun and his team from the Université de Montréal carried out with cell imaging equipment, revealed how they acted on bacterial membranes.

“This approach can be applied to other antibiotics and help us discover new ones with different mechanisms of action,” Culp explains. “We found one completely new antibiotic in this study, but since then, we’ve found a few others in the same family that have this same new mechanism.”

One of the most exciting findings of the study is that the compounds show efficiency even against Enterococcus strains resistant to vancomycin and S. aureus strains that show an intermediate resistance to vancomycin. Vancomycin is used as a last-line-of-defense antibiotic against gram-positive infections that do not respond to any other treatment.

The paper “Evolution-guided discovery of antibiotics that inhibit peptidoglycan remodelling” has been published in the journal Nature.

Researchers develop new bandage that senses and treats drug-resistant bacteria

Resistance to antibiotics is one of the main threats to global health, with two million new infections in the US every year showing resistance to antibiotics. That’s why identifying and treating bacterial infections earlier is key, helping to improve patients’ recovery and reducing the spread of microbes.

Credit Wikipedia Commons

A team of researchers reporting in the American Chemical Society developed a set of bandages that change their color by sensing drug-resistant and drug-sensitive bacteria in wounds, also treating them accordingly.

Xiaogang Qu from the University of Science and Technology of China and a group of colleagues created a material that goes from green to yellow by contacting the acidic microenvironment caused by a bacterial infection. The material is incorporated into the bandage and releases an antibiotic that kills the drug-resistant bacteria.

“We constructed a portable paper-based band-aid (PBA) which implements a selective antibacterial strategy after sensing of drug resistance. The colors of PBA indicate bacterial infection (yellow) and drug resistance (red), just like a bacterial resistance colorimetric card,” the researchers wrote.

The bandages turn red in color if in the presence of a drug-resistant bacterium, all thanks to the action of an enzyme produced by said microbes. When that happens, the researchers shine light on the bandage, which causes the release of reactive oxygen species that kill or weaken the bacteria.

“Compared with traditional PDT-based antibacterial strategies, our design can alleviate off-target side effects, maximize therapeutic efficacy, and track the drug resistance in real-time with the naked eye. This work develops a new way for the rational use of antibiotics,” the researchers wrote.

Thanks to their work, the team proved that the bandage speeds up the healing of wounds in mice that had been infected with drug-sensitive or drug-resistant bacteria. Now, the challenge will be to expand its use to practical applications, which the teams believes possible due to the low cost and the easy operation of the device.

This is not the first time a smart band-aid is developed for diverse applications. Researchers in Zurich developed a type of bandage that simultaneously repels blood and promotes clotting, while researchers in the US are looking at synthesizing spider silk for a new time of bandage.

Bacteria-laden materials point the way to living, growing, healing buildings

New research at the University of Colorado Boulder (UCB) aims to pave the way to living, breathing buildings by mixing concrete with bacteria.

One of the shapes the team used to test their material.
Image credits UCB College of Engineering & Applied Science.

Walls that heal, scrub the air clean, or even glow on demand — that’s what the team envisions for the future. Led by engineer Wil Srubar from the UCB, they’re trying to make it happen by mixing living bacteria with sand and gelatin and then having them produce concrete on the spot, out of thin air. In addition, such an approach would help scrub CO2 out of the atmosphere.

Tiny building blocks

“We already use biological materials in our buildings, like wood, but those materials are no longer alive” said Srubar, an assistant professor in the Department of Civil, Environmental and Architectural Engineering at the UCB.

“We’re asking: Why can’t we keep them alive and have that biology do something beneficial, too?”

The bacteria-laden material isn’t commercially available just yet. However, the little bugs have survived in the hardened mixture for several weeks, suggesting that the approach is viable.

Mineralization comparison of the gelatin scaffold for the experimental (A, B) and bacteria-free control (C, D) bricks.
Image credits Chelsea M. Heveran et al., (2020), Matter.

Srubar and colleagues experimented with cyanobacteria belonging to the genus Synechococcus. Under the right conditions, these green microbes absorb carbon dioxide gas to help them grow and make calcium carbonate—the main ingredient in limestone and, it turns out, cement. The researchers bred colonies of these cyanobacteria and injected them into the sand and gelatin matrix, which serves to provide the shape and other materials required for the desired piece of concrete.

With the right tweaks, the calcium carbonate mineralizes with the gelatin that binds the grains of sand together, producing a brick.

“It’s a lot like making rice crispy treats where you toughen the marshmallow by adding little bits of hard particles,” Srubar said.

The material effectively acts as carbon storage, because it scrubs the gas from the air and chemically binds it into a stable compound. Because the bacteria don’t die off after crystallization, they could be used to repair any cracks or similar damage sustained by the brick (or a whole building), much like the living cells in our bones. The team managed to keep around 9-14% of the bacterial colonies in their material alive for 30 days, having spent three different generations in brick form.

“We know that bacteria grow at an exponential rate,” Srubar said. “That’s different than how we, say, 3-D-print a block or cast a brick. If we can grow our materials biologically, then we can manufacture at an exponential scale.”

But are they any good as far as bricks go? It seems so — the team found that the bacteria-laden bricks have similar strength to Portland cement-based mortars humidity conditions. In the future, they see their material as being delivered in bags on-site, where it would just be mixed with water and shaped, then allowed to develop.

 Cyanobacteria growing and mineralizing in the sand-hydrogel framework.
Image credits UCB College of Engineering & Applied Science.

The team also hopes to help slash emissions and energy use related to construction material manufacturing. Cement and concrete production for roads, bridges, skyscrapers and other structures generates nearly 6% of the world’s annual emissions of carbon dioxide, they explain.

However, there is still a lot of work to be done before such material becomes commercially available. One of the team’s goals right now is to grow cyanobacteria that is more resistant to dry conditions (the team’s bacteria currently need humid conditions to survive) so that they can be employed in hotter, drier areas.

The paper “Biomineralization and Successive Regeneration of Engineered Living Building Materials” has been published in the journal Matter.

Birds and bats have very weird gut bacteria, and it’s likely linked to flying

Bats and birds don’t seem to need gut bacteria the way other animals do, a new study finds.

Our microbiota or microflora — communities of bacteria making home in our digestive tract — play quite a central role in our health and wellbeing. These tiny helpers aid us in fighting bad bacteria and aid digestion. It’s not just us. Most vertebrates rely on similar bacterial communities for the same tasks.

A phylosymbiosis tree diagram showing a microbiome composition in bats and birds (marked with black bars) compared to other mammalian species.
Image credits Se Jin Song et al., (2020), mBio.

But not birds and bats, a new study found. By drawing on field samples and museum specimens, a team of US researchers has compared the makeup of mammal, bird, reptile, and amphibian microbiota, finding that species which evolved for flight tend not to rely on symbiotic bacteria almost at all.

You can’t fly with us

“If you’re carrying a lot of bacteria in your gut, it can be pretty heavy and may take resources away from you,” says Holly Lutz, a research associate at Chicago’s Field Museum and postdoctoral researcher at the University of California San Diego and co-author of the study.

“So if you’re an animal that has really high energetic demands, say because you’re flying, you may not be able to afford to carry all those bacteria around, and you may not be able to afford to feed them or deal with them.”

The study is the first of its kind and the first to showcase how different the microbiota of flight-capable species are compared to those of other vertebrates. The team believes that the necessities of flight are exactly what caused this difference in gut bacteria.

To the best of our knowledge, animals that are closely related to each other have similar gut microbiomes, because they evolved together — a pattern referred to by scientists as phylosymbiosis. Thus, Se Jin Song, the paper’s co-first author from UC San Diego, says that before the study the team assumed they would “see similar associations between animals and their gut microbes when the animals shared a similar diet.”

“Our pie-in-the-sky idea was that flight could impose a similar type of selection on which microbes animals host,” he explains. “What was shocking was that we didn’t find that birds and bats share a similar microbiome per se, but rather that both lack a specific relationship with microbes.”

For the study, the team analyzed fecal samples from roughly 900 species of vertebrates on a global scale. Researchers, museum collections, and zoo directors from around the world participated in the efforts, which ranged from zoo work to venturing deep into remote Ugandan and Kenyan caves with a flashlight to collect samples from African bats.

An African fruit bat.
Image via Pixabay.

After collecting the needed material, the team used high throughput genetic sequencing to process them. In essence, they extracted all DNA from all the samples, and then used individual genes to sift through the bacterial communities within each sample. For the final step, they pooled all of the data together to form the comparisons between species.

The microbiomes of bats and birds didn’t fit in with the rest of the vertebrates, the team found. While their gut bacteria makeup was quite similar, they had very little in common with other vertebrates. The team believes that it’s their shared lifestyle, not their ancestry (bats and birds are only very distantly related), that shapes their gut flora. In other words, their ability to fly.

Both groups evolved this ability independently, but no matter which way you cut it, flying is very energy-intensive and requires a light body. Bats and birds both have much shorter digestive tracts than comparable land mammals, and they both carry fewer bacteria, which likely helps reduce weight. The authors write that it’s also possible that diet plays a role here; due to the huge energy requirements of active flight, there may simply not be enough food to spare to maintain a symbiotic relationship with the bacteria.

Another important finding is that the few bacteria that do live in the digestive tract of both birds and bats tend to be very varied. Various types of individual bacteria live in the guts of different species of bats or birds, most other groups of amphibians, reptiles, and mammals apart from bats follow specific patterns.

“It’s almost like they’re just picking up whatever’s around them and they don’t really need their microbes to help them in ways that we do,” says Lutz.

“If we ever are putting ourselves in some kind of extreme situation where we’re disrupting our microbiome, there is something that we can learn from animals that don’t need their microbiomes as much.”

Lutz notes that this study wouldn’t have been possible without museum collections from around the world. Specimens of bird and bat kept in cryogenic chambers in the Field Museum’s Collections Resource Center were pulled out to help provide the broad samples needed for a study of this size.

“The scope of this paper —in terms of species that we sampled— is really remarkable. The diversity of collaborators that came together to make this study happen shows how much we can achieve when we reach out and have these big and inter-institutional collaborations,” says Lutz.

The paper “Comparative Analyses of Vertebrate Gut Microbiomes Reveal Convergence between Birds and Bats” has been published in the journal mBio.

Scientists make plastic self-cleaning surface that repels even the worst superbugs

Credit: McMaster University

Researchers at McMaster University in Canada made a self-cleaning plastic surface that repels most substances, like blood, water, and other liquids, but also some of the most dangerous antibiotic-resistant bacteria. The transparent plastic wrap is ideal for packaging food or insulating surfaces that are vulnerable to contamination, such as those found in hospitals or kitchens.

The material is basically a conventional transparent wrap that went through chemical treatment and some nanoscale alterations to its surface.

In fact, the self-cleaning material was heavily inspired by the lotus leaf, whose surface naturally repels liquids — a process known as superhydrophobicity. Just like the lotus leaf, the new material has a roughened surface — a wrinkled texture that creates miniature air pockets, minimizing the contact area between the surface and a liquid, almost like standing on a bed of needles.

“We’re structurally tuning that plastic,” said Leyla Soleymani , an engineering physicist at McMaster. “This material gives us something that can be applied to all kinds of things.”

Researchers further enhanced the plastic wrap’s repelling properties through a chemical treatment.

The resulting material acts as a firm barrier against even the meanest superbugs. For instance, it could be wrapped around door handles, railings, and any surface that typically attracts bacteria like MRSA, E. coli, Salmonella, and C. difficile.

“We can see this technology being used in all kinds of institutional and domestic settings,” Didar says. “As the world confronts the crisis of anti-microbial resistance, we hope it will become an important part of the anti-bacterial toolbox.”

The researchers verified the effectiveness of the material by spraying two of the most challenging strains of antibiotic-resistant bacteria onto it. An analysis performed with an electron microscope showed no trance of bacterial transfer on the surface of the material.

In the future, the researchers hope to bring their product to market by partnering with select industry partners.

The findings appeared in the journal ACS Nano.

That make-up you’re using? It’s probably riddled with superbugs

Make-up is used by millions of people every day, but they might want to reconsider that after reading a new study.

Researchers from Aston University in Birmingham, UK, have found dangerous microbes such as E.coli and Staphylococci in more than nine out of ten in-use beauty products.

Make-up products are almost never cleaned, and they are often used far beyond their expiration date. In fact, for many of the products, it would be realistically impossible to use them within the expiration date.

A total of 467 make-up products were analyzed. The products were donated by consumers from the UK, following a social media campaign (donors also answered a few questions about make-up habits). This comprised of lipstick (96), eyeliner (92), mascara (93), lip-gloss (107) and beauty blenders (79).

When the team scanned these for pathogens, the results were pretty concerning. The bacteria found in these beauty products range from pathogens that can cause skin infections to some that can cause blood infections, particularly if they are used on sensitive tissue such as eyes or mouth. Given that make-up is sometimes applied over areas with cuts or grazes, the risk of infection with opportunistic bacteria is even higher, particularly in immunocompromised people.

The vast majority of the products were never cleaned — only 6.4% of all collected samples had ever been cleaned. Potentially unsanitary practices were also common: 27.3% of products (largely eyeliner), had been applied in a bathroom, and 28.7% of products had been dropped on the floor.

Beauty blenders, sponges used to apply skin foundation products, were among the biggest culprits. They’ve recently become a sensation in the make-up world, but 35.6% of beauty blenders were used or stored in a bathroom, and 64.4% had been dropped on the floor at least once. As you’d expect from a sponge, the beauty blenders tend to absorb water, dirt, and bacteria, which makes them excellent hosts for all sorts of unwanted bugs.

“Beauty blenders have only been recently introduced as an application product and limited information is available on how best to use or clean them. Our results have shown that these products carried the highest bacterial load during use and more than a quarter were contaminated with Enterobacteriaceae,” the study reads. Several Enterobacteriaceae strains have been shown to be antibiotic-resistant.

Sharing makeup products and makeup testers found on beauty counters may also provide a route for contamination and infection researchers say. Testers are not commonly cleaned regularly, and are often left exposed to the environment and to passing customers.

Although previous research has suggested that make-up products can have disease risk, this is one of the very few studies that analyzes products coming from the real world — and is probably the first one to look at beauty blenders. It’s estimated that 6.5 million such sponges are sold every year, and the figure continues to grow as they are endorsed by celebrities. Since these products are an ideal breeding ground for bacteria, they should be looked at more closely, researchers warn.

Brushes and sponges are great environments for bacteria to reproduce and spread, researchers warn.

The study also highlights that consumers are putting themselves at risk — and they are probably doing so unwittingly (how many consumers out there are aware that beauty blenders are an ideal breeding ground for bacteria?). Producers and regulators should take more action to protect consumers. Cosmetic regulations clearly state that products should not contain pathogenic. organisms, yet 70-90% of all used products were contaminated with bacteria.

Commenting on the new findings, co-author Dr. Amreen Bashir said:

“Consumers’ poor hygiene practices when it comes to using make-up, especially beauty blenders, is very worrying when you consider that we found bacteria such as E.coli – which is linked with faecal contamination – breeding on the products we tested.

“More needs to be done to help educate consumers and the make-up industry as a whole about the need to wash beauty blenders regularly and dry them thoroughly, as well as the risks of using make-up beyond its expiry date.”

There are even more reasons to worry when you consider that make-up products in the European Union are subject to much more scrutiny than those in other parts of the world. EU guidance holds make-up brands to strict hygiene standards of manufacture. People in the US, for instance, are at a much greater risk because the cleanliness of make-up products is less regulated, and there are no requirements to put expiry dates on make-up packaging.

The study has been published in the Journal of Applied Microbiology

New, free app modifies antibiotics to work against drug-resistant infections

A new web tool could help us find novel antibiotics that work against Gram-negative bacteria (which tend to gain antibiotic resistance). The app works by offering instructions on converting drugs that kill other bacteria into compounds that work against Gram-negative strains.

Image credits Sheep purple / Flickr.

Gram-negative bacteria have an extra, outer membrane, that renders most antibiotics useless. It helps the bacteria to survive out in nature where many organisms (like fungi) naturally produce antibiotics. This would be fine except for the fact that some Gram-negative bacteria like to cause nasty infections in humans — which don’t respond to treatment and put patients at risk. In order to prove that their tool works, the team used it to modify a drug and successfully tested it against three different Gram-negative bacterial strains.

Computer, design a drug

“It’s really hard to find new antibiotics for Gram-negative pathogens, because these bacteria have an extra membrane, an outer membrane, that’s very good at keeping antibiotics out,” said University of Illinois chemistry professor Paul Hergenrother, who led the research.

Hergenrother explains that no new antibiotics against Gram-negative bacteria have been approved by the Food and Drug Administration in 50 years, leaving us virtually exposed to the pathogens. His team has been hard at work finding a solution for several years now. His team “discovered the molecular features that allowed an antibiotic compound to surpass this barrier” a few years ago, he said, adding that this tool is the implementation of those findings.

The team’s app/web tool is called eNTRyway, and evaluates the potential of known drug compounds to pierce the outer membrane of Gram-negative bacteria. It also estimates whether the drug can perform this at high enough levels to accumulate inside the bacterial cells in functional doses. Even better, this app can also point out how to modify existing drugs for the task of tackling Gram-negative pathogens.

The team used eNTRyway to identify a drug that’s currently in use against Gram-positive infections that, with a little bit of tweaking, could potentially hurt Gram-negative strains. The team then synthesized the drug (by adding an amine group to the original one) and tested it on Gram-negative infections in mice. It proved effective against several different strains, the team reports, successfully accumulating behind the outer membrane of these pathogens.

The whole process took only a few weeks, Hergenrother said. The team hopes that their app will greatly speed up the development of such drugs in the future.

“We can use this tool to rapidly identify compounds that accumulate in Gram-negative bacteria,” he said.

“Keep in mind that before this, over 100 derivatives of this same compound had been made. We found them in patents and papers,” he said. “And none of these other derivatives had notable Gram-negative activity.”

The team went on to identify over 60 antibiotics that could be converted to fight Gram-negative bacteria using a variety of chemical pathways. For example, one of their newly-developed drugs (christened Debio-1452-NH3) disturbs fatty acid synthesis in bacterial cells, but not in mammalian ones.

The paper “Implementation of permeation rules leads to a FabI inhibitor with activity against Gram-negative pathogens” has been published in the journal Nature Microbiology.

Copper-lined hospital beds harbor up to 95% less bacteria, can help save patient lives

Lining hospital beds with copper could be a cheap and easy way to reduce healthcare-associated infections (HAIs), especially among the most vulnerable patients.

Image via Pixabay.

A new study led by Michael G. Schmidt, PhD, Professor of Microbiology and Immunology at the Medical University of South Carolina, Charleston, reports that copper hospital beds in the Intensive Care Unit (ICU) carry an average of 95% fewer bacteria than conventional beds. Better yet, this reduced bacterial population remained constant throughout the patients’ stay in hospital.

Copper solutions

“Hospital-acquired infections sicken approximately 2 million Americans annually, and kill nearly 100,000, numbers roughly equivalent to the number of deaths if a wide-bodied jet crashed every day,” said coauthor Michael G. Schmidt, PhD, Professor of Microbiology and Immunology, Medical University of South Carolina, Charleston. They are the eighth leading cause of death in the US.

Hospital beds are among the most contaminated surfaces in medical settings, the team explains. Although healthcare workers do clean and sanitize them, these efforts fall short — the beds are cleaned either not often enough, or not well enough to remove all pathogens, the team explains. And, while the antimicrobial properties of copper have been known for a long time now, patient beds that incorporate copper-lined surfaces aren’t commercially available.

In an effort to quantify the effectiveness of such beds — and potentially bring them to hospital settings around the world — the team performed an on-site experiment using five ICU beds, which see some of the heaviest patient use. The team compared the relative contamination levels of beds lined with copper rails, footboards, and bed controls to traditional hospital beds (which have plastic surfaces). All in all, they report that 90% of bacterial samples taken from plastic surfaces had bacteria concentrations that exceeded safe levels. Meanwhile, copper-lined surfaces “harbored significantly fewer bacteria throughout the patient stay than control beds,” they explain, “at levels below those considered to increase the likelihood of HAIs”. Furthermore, if daily and terminal cleaning regimes are respected, these beds don’t tarnish and don’t require additional cleaning or maintenance.

Copper-lined surfaces for hospital beds can help keep them hygienic for longer (provided they are cleaned regularly) and reduce the risk of HAIs spreading between patients. The use of copper-lined equipment can help improve patient outcomes, save lives, and reduce healthcare expenditures, the team concludes.

“Based on the positive results of previous trials, we worked to get a fully encapsulated copper bed produced,” said Dr. Schmidt. “We needed to convince manufacturers that the risk to undertake this effort was worthwhile.”

The paper “Self-Disinfecting Copper Beds Sustain Terminal Cleaning and Disinfection (TC&D) Effects Throughout Patient Care” has been published in the journal Applied and Environmental Microbiology.

Sanitizing homes gets rids of bacteria but makes room for fungi

Researchers have found that using cleaning products is effective at eradicating bacteria. However, the downside is cleansing the home of bacteria makes room for other microbes, such as fungi.

The findings were reported by researchers at the University of Oklahoma, who compared the microbial diversity in rural and urban homes from Peru and Brazil. They took samples from four locations in increasingly urban settings: from huts in the rainforest to city apartments in Manaus, the capital and largest city of the Brazilian state of Amazonas.

Samples were taken off the walls, floors, and countertops of the homes, as well as skin swabs from pets and people.

As the researchers converged towards more urban homes, bacterial diversity decreased, including so-called ‘good’ bacteria, some of which live in our gut. Meanwhile, fungal diversity actually increased in urban homes. Among them are fungi from the Malassezia genus, which contains strains that are known to cause infections.

This is probably due to the cleaning solutions that specifically target bacteria. Fungi, which have thick cell walls, are much harder to kill than your run-off-the-mill bacteria. And since urban homes are such good insulators, trapping CO2 and blocking sunlight, they’re also hospitable environments for the fungi. These differences in bacteria and fungi were also found on the skin of humans, not just in their homes.

“Maybe they’re scrubbing away all the bacteria and now you have this big open surface for fungi to grow on; maybe [the fungi] are also becoming more resistant to the cleaning agents that we use,” Laura-Isobel McCall, a biochemist at the University of Oklahoma, told NPR.

Besides bacteria, fungi, and some parasites, the researchers also tested the chemicals found inside the apartments. They found many more synthetic chemicals inside urban homes than in rural ones, sourced from items such as building materials, medications, and personal care products. In other words, urban environments are extremely artificial compared to rural ones — and these findings likely aren’t limited to Peru and Brazil.

If anything, this study shows that our efforts to sanitize our homes may never be satisfying. When you throw out one kind of germs, you’re just making room for other germs to break in.

The findings appeared in the journal Nature Microbiology.

Bacteria’s social lives influence how they develop drug resistance

How bacteria live influences how they develop antibiotic resistance, a new study reports.

Independent and communal bacteria react differently to antibiotics and develop resistance to medicine in different ways, according to researchers at the University of Pittsburgh School of Medicine. The findings could help shape more efficient methods of infection control and antimicrobial therapies.

Together we stand

“What we’re simulating in the lab is happening in the wild, in the clinic, during the development of drug resistance,” said senior author Vaughn Cooper, Ph.D., director of the Center for Evolutionary Biology and Medicine at Pitt. “Our results show that biofilm growth shapes the way drug resistance evolves.”

According to study lead author Alfonso Santos-Lopez, Ph.D., the results could be used to find a chink in the armor of drug-resistant bacteria.

For the study, the team repeatedly exposed bacterial cultures to ciprofloxacin (a broad-spectrum antibiotic) to force them to develop resistance — and they did. However, the team was surprised to see that the ‘lifestyle’ of individual species led to them developing specific mechanisms for drug resistance.

The paper showcases the role “collateral sensitivity” can play in our fight against drug-resistant pathogens. In simple terms, when bacteria evolve to be more resistant to one drug or class of drugs, this can make them vulnerable to other antibiotics. If you know which drug that is, then you have an effective tool against the bugs.

In the team’s experiment, communal bacterias — which bunch together into biofilms — that developed resistance to ciprofloxacin also lost virtually all resistance to the cephalosporin class of antibiotics. In contrast, free-floating (individual) bacteria didn’t become susceptible to cephalosporins and developed, on average, 128 times the resistance to ciprofloxacin of the biofilm-grown bacteria.

“Biofilms are a more clinically relevant lifestyle,” said study coauthor Michelle Scribner, a doctoral student in Cooper’s lab. “They’re thought to be the primary mode of growth for bacteria living in the body. Most infections are caused by biofilms on surfaces.”

The paper “Evolutionary pathways to antibiotic resistance are dependent upon environmental structure and bacterial lifestyle” has been published in the journal eLife.

Dolphins are seeing a rise of antibiotic-resistant bacteria and it’s our fault

Antibiotic resistance is reaching dramatic levels in some wild ecosystems, reports a study on bottlenose dolphins living in Florida’s Indian River Lagoon.

Image credits Claudia Beer.

One of the scariest public health issues we’re contending with today is the rise of antibiotic resistance. Many common bacterial strains are evolving to resist the drugs we rely on to treat them, making even mundane infections potentially deadly — and antibiotic development isn’t keeping up.

Once primarily confined to health care settings, these resistant strains of bacteria are now commonly found in other places, especially marine environments, a new study reports.

No cure for the porpoise

“In 2009, we reported a high prevalence of antibiotic resistance in wild dolphins, which was unexpected,” said Adam M. Schaefer, MPH, lead author and an epidemiologist at Florida Atlantic University’s (FAU) Harbor Branch. “Since then, we have been tracking changes over time and have found a significant increase in antibiotic resistance in isolates from these animals.”

“This trend mirrors reports from human health care settings.”

The team from Florida Atlantic University’s Harbor Branch Oceanographic Institute, in collaboration with the Georgia Aquarium and the Medical University of South Carolina and Colorado State University, conducted a long-term study from 2003 to 2015 of antibiotic resistance among bacteria retrieved from dolphins (Tursiops truncatus) in Florida’s Indian River Lagoon. The site was picked because this lagoon has a large coastal human population with a pronounced environmental impact.

Using the Multiple Antibiotic Resistance (MAR) index, the researchers obtained a total of 733 pathogen isolates from 171 individual bottlenose dolphins. Several of these strains are important human pathogens, the team explains.

“Based on our findings, it is likely that these isolates from dolphins originated from a source where antibiotics are regularly used, potentially entering the marine environment through human activities or discharges from terrestrial sources,” Schaefer explains.

The overall prevalence of resistance to at least one antibiotic for the 733 isolates was 88.2%. The highest prevalence of resistance found by the team were to erythromycin (91.6% of isolates), ampicillin (77.3%) and cephalothin (61.7%), and resistance to cefotaxime, ceftazidime, and gentamicin increased significantly between sampling periods for all the isolates.

Resistance to ciprofloxacin among E. coli isolates more than doubled between sampling periods, the team reports, reflecting recent trends in human clinical infections. The MAR index increased significantly from 2003-2007 and 2010-2015 for Pseudomonas aeruginosa and Vibrio alginolyticus. P. aeruginosa causes respiratory system and urinary tract infections among others, while the latter is a common pathogenic strain of Vibrio found to cause serious seafood-poisoning.

“The nationwide human health impact of the pathogen Acinetobacter baumannii is of substantial concern as it is a significant nosocomial pathogen with increasing infection rates over the past 10 years,” said Peter McCarthy, Ph.D., co-author, a research professor and an associate director for education at FAU’s Harbor Branch.

“The high MAR index for this bacteria isolated from dolphins in the Indian River Lagoon represents a significant public health concern.”

The paper “Temporal Changes in Antibiotic Resistance Among Bacteria Isolated from Common Bottlenose Dolphins (Tursiops truncatus) in the Indian River Lagoon, Florida, 2003-2015” has been published in the journal Aquatic Mammals.

Cigarette smoke breeds drug-resistant bacteria

In what could be a new reason against smoking, new research from the University of Bath in the UK showed that cigarette smoke can make bacterial strains more resistant to antibiotics.

Credit: Flickr


Some strains of Staphylococcus aureus, a microbe present in a large part of the global population and responsible for many diseases, can become more invasive and persistent due to exposure to the smoke from cigarettes, according to the researchers, whose work was published in Scientific Reports.

“We expected some effects, but we didn’t anticipate smoke would affect drug-resistance to this degree. It seems reasonable to hypothesize that stressful conditions imposed by smoking induce responses in microbial cells,” said Dr. Maisem Laabei, the lead author.

Working with colleagues from Spanish research institutes, the experts at Bath carried out a set of lab-based experiments. They exposed six reference strains of the most important ‘superbug’ Methicillin-resistant S. aureus (MRSA) clones to cigarette smoke.

The strains were chosen for their clinical relevance and genetic diversity, known to cause several infections. While not all responded the same way, the strains showed increased resistance to the antibiotic rifampicin and increased invasiveness and persistence after being exposed to cigarette smoke.

The changes seen on the trains were linked by researchers to the emergence of so-called Small Colony Variants (SCVs), a slow-growing subpopulation of bacteria with distinctive phenotypic and pathogenic traits. SCVs have been linked to chronic infections in smokers in previous research.

“These Small Colony Variants are highly adhesive, invasive and persistent. They can sit around for a long time, are difficult to kick out, and are linked to chronic infections. We hope that our work provides another reason for people not to smoke and for current smokers to quit,” said Laabei.

The next step for the researchers will be to study how air pollution, from diesel exhaust fumes and other sources, might affect the microbes in nasal passages as many of the pollution compounds are the same as in cigarette smoke.

“Smoking is the leading cause of preventable death worldwide, and cigarette smoke has over 4,800 compounds within it,” said Laabei. “We wanted to study S. aureus because it’s so common in humans and it can cause a range of diseases, so we wanted to see what happened when we exposed it to smoke.

Hospital room.

Hospitals in Europe are contributing to the spread of extremely drug-resistant bacteria

New research from the Wellcome Sanger Institute is mapping the spread of extremely drug-resistant (XDR) strains of Klebsiella pneumoniae through hospitals in Europe.

Hospital room.

Image via Pixabay.

As far as antibiotics go, our last line of defense are carbapenem antibiotics; when all other antibiotics fail in dealing with a certain infection, these are sent in to finish the job. However, a Europe-wide survey of the Enterobacteriaceae family of bacteria found that antibiotic-resistant strains of Klebsiella pneumoniae, an opportunistic pathogen that can cause respiratory and bloodstream infections in humans, are spreading through hospitals in Europe. The findings are based on samples taken from patients in 244 hospitals in 32 countries.


“In the case of carbapenem-resistant Klebsiella pneumoniae, our findings imply hospitals are the key facilitator of transmission — over half of the samples carrying a carbapenemase gene were closely related to others collected from the same hospital, suggesting that the bacteria are spreading from person-to-person primarily within hospitals,” says Dr. Sophia David, first author of the study.

It is estimated that carbapenem-resistant K. pneumoniae caused 341 deaths in Europe in 2007, a figure that grew to 2,094 by 2015 (a six-fold increase), the authors explain. This high number of deaths is owed to the fact that once carbapenems lose the ability to fight a population of antibiotic-resistant bacteria, doctors have very few options left. Infants, the elderly, and immuno-compromised individuals, whose bodies can’t take the strain of said options, are thus particularly at risk.

The survey, its authors write, is the largest of its kind and the first concrete step towards consistent surveillance of carbapenem-resistant bacteria in Europe. It was built from over 2,000 samples of K. pneumoniae collected from patients across 244 hospitals and sent to the Wellcome Sanger Institute, where the genomes of 1,700 of them were sequenced. The team identified a small cluster of genes that, when expressed, cause a strain to produce enzymes called carbapenemases that neutralizes the antibiotics.

The emergence of certain strains that carry one or more carbapenemase genes is of particular concern to public health, the authors explain, as these strains have spread relatively rapidly. Today’s heavy use of antibiotics in hospitals likely stacks the playing field in favor of these bacteria, the team adds, as they outcompete other strains that are more easily treatable with antibiotics. Samples used in the study were also more likely to be closely related to other samples in the same country rather than across countries, which suggests that national healthcare systems as a whole contribute to spread the strains around.

Not all is lost, however. The team explains that despite the deadliness of this carbapenem-resistant strains, infection control procedures in hospitals — ranging from consideration of how patients move between hospitals to hygiene interventions — still have an important impact.

“We are optimistic that with good hospital hygiene, which includes early identification and isolation of patients carrying these bacteria, we can not only delay the spread of these pathogens, but also successfully control them,” says Professor Hajo Grundmann, co-lead author and Head of the Institute for Infection Prevention and Hospital Hygiene at the Medical Centre, University of Freiburg.

“This research emphasises the importance of infection control and ongoing genomic surveillance of antibiotic-resistant bacteria to ensure we detect new resistant strains early and act to combat the spread of antibiotic resistance.”

The results were made available through MicroReact, a publicly-available web-based tool developed by the Centre for Genomic Pathogen Surveillance to help researchers and healthcare systems chart the spread of antibiotic resistance in pathogens like K. pneumoniae. A second survey is currently being planned.

“Genomic surveillance will be key to tackling the new breeds of antibiotic-resistant pathogen strains that this study has identified,” says Professor David Aanensen, co-lead author and Director of the Centre for Genomic Pathogen Surveillance.

“Currently, new strains are evolving almost as fast as we can sequence them. The goal to establish a robust network of genome sequencing hubs will allow healthcare systems to much more quickly track the spread of these bacteria and how they’re evolving.”

The paper “Epidemic of carbapenem-resistant Klebsiella pneumoniae in Europe is driven by nosocomial spread” has been published in the journal Nature Microbiology.

Tower Bridge.

London’s waterways found to contain antibiotic-resistant bacterial genes

London’s waterways are rife with antibiotic resistant genes.

Tower Bridge.

Image via Pixabay.

The Regent’s Canal, Regent’s Park Pond, and the Serpentine contained high level of antibiotic resistance genes, a new study reports, but none were worse than the Thames. These genes encode resistance to common antibiotics such as penicillin, erythromycin, and tetracycline. They found their way into the water from bacteria in human and animal waste.

Laced waters

“This [study] shows that more research is needed into the efficiency of different water treatment methods for antibiotic removal, as none of the treatments currently used were designed to incorporate this,” says lead author Dr. Lena Ciric from UCL Civil, Environmental and Geomatic Engineering.

“This is particularly important in the case of water bodies into which we discharge our treated wastewater, which currently still contains antibiotics. It is also important to look into the levels of antibiotics and resistant bacteria in our drinking water sources.”

When humans or animals take antibiotics, part of the active substance gets excreted (while still active) into sewer systems and, from there, into freshwater sources. Once there, they’re exposed to bacteria and create an environment that favors resistant microbes. These will multiply faster than their non-resistant counterparts, making the resistance genes more prevalent in the total population. Resistant microbes can also share their resistance with their peers via lateral gene transfer.

The team developed a DNA-analysis method that can be used to measure the quantity of fourteen types of antibiotic resistance genes per liter of water. They then applied it in different water systems throughout London and compared the results. The Thames River had the highest level of antibiotic resistance genes, followed by The Regent’s Canal, Regent’s Park Pond, and the Serpentine. Antibiotics entering the sewer system are diluted through flushing, but even low levels can encourage resistance genes to multiply and spread to more microbes. The Thames is likely to have higher levels of antibiotics and resistant genes because a large number of wastewater treatment works discharge into it both upstream and in London.

The authors note that there is currently no legislation in place which specifies that antibiotics or the genes that encode their resistance need to be scrubbed from water sources. This could mean that antibiotics and said genes could be present in small amounts in drinking water, although this would require testing.

The team is now working on finding a way to remove antibiotics, resistant bacteria, and antibiotic-resistance genes from London’s natural water system using slow sand filtration, which is a form of drinking water treatment. This technique is already in use around the world including at Thames’ Coppermills Water Treatment Works, they explain, which provides drinking water for most of north east London. Their plan is to beef-up this filtration technique by tweaking the properties of the sand and activated carbon used in the filters, and by varying water flow rates.

The paper ” Use of synthesized double-stranded gene fragments as qPCR standards for the quantification of antibiotic resistance genes” has been published in the journal Journal of Microbiological Methods.

The Wonderful World of Bacteriophages

We all know that the primary types of infection are viral and bacterial, but what about a virus that infects bacteria? Enter the bacteriophage, a virus that infects bacteria.

Read on to learn all about bacteriophages, how they infect their bacterial hosts, and how they might be used to solve the problem of antibiotic resistance in the near future.

A head-tail bacteriophage. Credit: Adenosine on WIkimedia Commons

What Does a Bacteriophage Look Like?

All bacteriophages infect bacteria, but the way they’re structured can be quite different. First of all, their genomes (their genetic material) can be made up of either DNA or RNA. Their genome can also vary in size. The smallest known bacteriophage genome actually contains only twenty genes, but they can contain hundreds. That means that they can function quite simply or their functioning can be incredibly complex.

The most well-studied bacteriophages look like the image above, called the head-tail phage. But some lack a tail, while others are shaped like a long strand (called filamentous phages). Bacteriophages have adapted over time to take on the shape best suited to infect their host bacteria of choice.

In fact, bacteriophages are so diverse that there’s an entire field to exploring their diversity. Metagenomics is the study of genetic material obtained from environmental samples, letting scientists examine bacteriophages that have some environmental significance.

How Does a Bacteriophage Infect Its Host?

Just like viruses, bacteriophages must infect a host so they can carry on their lineage. Now, bacteriophages have two possible ways to infect their host. They can either undergo what is called the lytic cycle, which ultimately kills the host bacteria, or the lysogenic cycle, which does not kill the host bacteria. Some bacteriophages, like lambda bacteriophages, can even switch between the two.

A visual depiction of the first two steps of host infection by a bacteriophage. Credit: Graham Colm on Wikimedia Commons

The first two steps are the same: the bacteriophage’s tail attaches to the surface of the bacterium, and the phage then injects its genome inside. In the lytic cycle, the genome copies itself once inside the bacterium. The DNA contains instructions for the bacteria to create proteins required to form more bacteriophages, called capsids. By hijacking the bacteria’s internal machinery, it creates many new bacteriophages.

Once enough have been made, these new bacteriophages poke holes in the membrane. Water rushes in until the bacterium expands and bursts, allowing these new bacteriophages to be free. Now they can go out and repeat the process. It’s called the lytic cycle because the cell bursting open is a process known as lysis.

It’s easy to see the pros and cons of this process. One bacteriophage can use a host bacterium to create tons of copies. But this process also kills its host, meaning that if a new suitable bacterium is not located, the new bacteriophages will soon die.

To overcome this, some bacteriophages have adapted by using the lysogenic cycle. Once the bacteriophage’s genome is inside the bacteria, it integrates into the host bacterium’s genome in a process called integration, creating what is called a prophage. This contains the information required to undergo the replication cycle of the bacteriophage. And this change is permanent: once the bacterium divides, the offspring will also have the prophage integrated into their genome.

This process keeps the bacteriophage’s genome safe until it’s time for replication. When the conditions are right, the prophage will exit the bacterium’s genome. Once the prophage exits, the lytic cycle begins in order to release a new set of bacteriophages.

A visual depiction of the two cycles of bacteriophage infection. Credit: Suly12 on Wikimedia Commons

Bacteriophages in Medicine

It may surprise you to learn that bacteriophages might be the answer to antibiotic resistance. In fact, long before we learned how to make and produce antibiotics, we used bacteriophages to treat bacterial infections. And this makes a lot of sense: bacteriophages target and kill bacteria via the lytic cycle, and they don’t target human cells.

So, why did we stop using them? Well, this treatment was started in the Soviet Union, so the Cold War almost certainly played some role in our reluctance to adopt them. Additionally, a lot of the research published on the subject was in Russian, so the international community wasn’t very familiar with these publications. Finally, antibiotics were simply easier to make, store, and administer.

Russia and several Eastern European countries still use these methods today. And while some may scoff at the idea of using medical techniques derived almost 100 years ago, these just might be the answer to our antibiotic woes. And a recent study presented at ASM Microbe shows that this idea is starting to catch on in America, too.

While bacteria can adapt to resist certain bacteriophages as well, researchers believe that resistance to a bacteriophage is actually a temporary trait. This means that any resistance formed will not force genetic divergence and therefore will not be relevant after a resting period of time, nor will it generalize to all types of phages.

Bacteriophages are all around us. In fact, there are estimated to be ten million trillion trillion. That’s more than every other organism on earth (including bacteria) put together. It just goes to show that when looking for the next big thing in medicine, maybe all we need to do is look at the diverse world around us.

Credit: Pixabay.

Elite athletes may owe some of their peak performance to unique gut microbes

Credit: Pixabay.

Credit: Pixabay.

The world’s foremost athletes owe their peak performance to both good genes and tremendous hard work — but that’s not all. According to a new study, microbes that are only found in the guts of athletes may enhance endurance, helping them perform better than regular people who live a sedentary lifestyle.

The findings were reported by researchers at Harvard University who initially analyzed stool samples from 15 competitors in the 2015 Boston Marathon. At the time, the researchers found high levels of a microbe called Veillonella, which spiked after an intense workout and skyrocketed after the marathon. This bacteria is known for breaking down lactate — a byproduct constantly produced in the body during normal metabolism and exercise. It’s what causes aching legs in runners during the last portion of a long race.

A side effect of high lactate levels is an increase in the acidity of the muscle cells, along with disruptions of other metabolites. The same metabolic pathways that permit the breakdown of glucose to energy perform poorly in this acidic environment. It might seem odd that working muscles would produce a substance that would slow their capacity for more work. However, there’s a good reason: lactate accumulation prevents permanent damage during extreme exertion by slowing down biological systems that are required for muscle contraction.

Veillonella absorbs lactate, converting the metabolite into a fuel called propionate. This short-chained fatty acid also has anti-inflammatory properties.

The Harvard researchers later confirmed these findings in another study involving 87 other athletes. Then, in an experiment involving only mice, the researchers colonized a strain of Veillonella collected from one of the athletes. The rodents which had the bacteria in their guts could run 13% longer on treadmills — a huge performance boost in the ultra-competitive world of elite sports where races can be won or lost due to a split-second difference.

The findings support the idea that lactate metabolism is an important component of extreme athlete performance. Previously, other studies had also shown that the microbiomes of athletes differ from those of sedentary individuals.

“Taken together, these studies reveal that V. atypica improves run time via its metabolic conversion of exercise-induced lactate into propionate, thereby identifying a natural, microbiome-encoded enzymatic process that enhances athletic performance,” the authors concluded.

In the future, the researchers would like to find out if they can augment endurance performance in humans as they did in mice. They would also like to see whether the endurance boost is due to the propionate’s anti-inflammatory properties. Perhaps one day you’ll be able to buy lab-made probiotics that contain Veillonella and other endurance-enhancing bacteria — that’s already the goal at an American startup called Fitbiomics. There’s also the possibility that the microbiomes of super-athletes might contain bacteria that help prevent diseases like irritable bowel syndrome, which is another compelling avenue of research.

The findings were reported in the journal Nature Medicine.