Tag Archives: resistance

Your microbiota will be having non-stop sex this Valentine’s Day

Even if you’re alone this Valentine’s Day, there’s no need to worry: some parts of your body will be getting plenty of action. In fact, your body will host a veritable carnival of the sensual in your tummy, as your microbiota will engage in an orgy of sex and swinger’s parties — where they’ll be swapping genes instead of keys.

A medical illustration of drug-resistant, Neisseria gonorrhoeae bacteria. Original image sourced from US Government department: Public Health Image Library, Centers for Disease Control and Prevention. Image in the public domain.

The salacious gene

Imagine you have a severe disease with a very unusual cure: you can treat by making love with someone who then passes on the necessary genes to cure your ailment. It is, as they say, sexual healing. Using sex to protect or heal themselves is precisely what bacteria can do, and it’s a crucial defense mechanism.

In the past, the research community thought bacterial sex (or conjugation, as scientists call it) was a terrible threat for humans, as this ancient process can spread DNA capable of conveying antibiotic resistance to their neighbors. Antibiotic resistance is one of the most pressing health challenges the world is facing, being projected to cause 10 million deaths a year by 2050.

But there’s more to this bacterial sex than meets the eye. Recently, scientists from the University of Illinois at Urbana-Champaign and the University of California Riverside witnessed gut microbes sharing the ability to acquire a life-saving nutrient with one another through bacterial sex. UCR microbiologist and study lead Patrick Degnan says:

“We’re excited about this study because it shows that this process isn’t only for antibiotic resistance. The horizontal gene exchange among microbes is likely used for anything that increases their ability to survive, including sharing vitamin B12.”

For well over 200-years, researchers have known that bacteria reproduce using fission, where one cell halves to produce two genetically identical daughter cells. However, in 1946, Joshua Lederberg and Edward Tatum discovered bacteria could exchange genes through conjugation, an entirely separate act from reproduction.

Conjugation occurs when a donor and a recipient bacteria sidle up to each other, upon which the donor creates a tube, called a pilus that attaches to the recipient and pulls the two cells together. A small parcel of DNA is then passed from the donor to the recipient, providing new genetic information through horizontal transfer.

Ironically, it wasn’t until Lederberg met and fell in love with his wife, Esther Lederberg, that they made progress regarding bacterial sex.

Widely acknowledged as a pioneer of bacterial genetics, Esther still struggled for recognition despite identifying the horizontal transfer of antibiotic resistance and viruses, which kill bacteria known as bacteriophages. She discovered these phages after noticing small objects nibbling at the edges of her bacterial colonies. Going downstream to find out how they got there, she found these viral interlopers hiding dormant amongst bacterial chromosomes after being transferred by microbes during sex.

Later work found that environmental stresses such as illness activated these viruses to replicate within their hosts and kill them. Still, scientists assumed that bacterial sex was purely a defense mechanism.

Esther Ledeberg in her Stanford lab. Image credits: Esther Lederberg.

Promiscuity means longevity

The newly-published study builds on Esther’s work. The study authors felt this bacterial process extended beyond antibiotic resistance. So they started by investigating how vitamin B12 was getting into gut microbial cells, where the cells had previously been unable to extract this vitamin from their environment — which was puzzling as, without vitamin B12, most types of living cells cannot function. Therefore, many questions remained about how these organisms survived without the machinery to extract this resource from the intestine.

The new study in Cell Reports uses the Bacteroidetes species, which comprise up to 80% of the human microbiome in the intestines, where they break down complex carbohydrates for energy.

“The big, long molecules from sweet potatoes, beans, whole grains, and vegetables would pass through our bodies entirely without these bacteria. They break those down so we can get energy from them,” the team explained.

This bacteria was placed in lab dishes mixing those that could extract B12 from the stomach with some that couldn’t. The team then watched in awe while the bacteria formed their sex pilus to transfer genes enabling the extraction of B12. After the experiment, researchers examined the total genetic material of the recipient microbe and found it had incorporated an extra band of DNA from the donor.

Among living mice, something similar happens. When the group-administered two different subgroups of Bacteroidetes to a mouse – one that possessed the genes for transferring B12 and another that didn’t — they found the genes had ‘jumped’ to the receiving donee after five to nine days.

“In a given organism, we can see bands of DNA that are like fingerprints. The recipients of the B12 transporters had an extra band showing the new DNA they got from a donor,” Degnan said.

Remarkably, the team also noted that different species of phages were also transferred during conjugation, exhibiting bacterial subgroup specificity in some cases. These viruses also showed the capacity to alter the genomic sequence of its bacterial host, with the power to promote or demote the life of its microbic vessel when activated.

Sexual activity in our intestines keeps us healthy

Interestingly, the authors note they could not observe conjugation in all subgroups of the Bacteroidetes species, suggesting this could be due to growth factors in the intestine or a possible subgroup barrier within this large species group slowing the process down.

Despite this, Degnan states, “We’re excited about this study because it shows that this process isn’t only for antibiotic resistance.” And that “The horizontal gene exchange among microbes is likely used for anything that increases their ability to survive, including sharing [genes for the transport of] vitamin B12.”

Meaning that bacterial sex doesn’t just occur when microbes are under attack; it happens all the time. And it’s probably part of what keeps the microbiome and, by extension, ourselves fit and healthy.

Bangladesh’s waters are heavily contaminated with medicine, pesticides, and other chemicals

Researchers from the University at Buffalo (UB) and icddr,b, a leading global health research institute in Bangladesh, report that the waters in the city of Dhaka, the country’s capital, are awash with chemicals.

The city of Dhaka.
Image via Pixabay.

The research effort began in 2019 and it involved testing a lake, a canal, and a river in Dhaka, which is also the country’s largest city. The team also sampled water from ditches, ponds, and drinking wells in a rural area known as Matlab. All in all, the analysis revealed the existence of a mix of both pharmaceutical and non-pharmaceutical compounds including antibiotics, antifungals, anticonvulsants, anesthetics, antihypertensive drugs, pesticides, and flame retardants — among others.


“When we analyzed all these samples of water from Bangladesh, we found fungicides and a lot of antibiotics we weren’t looking for,” says Diana Aga, PhD, Henry M. Woodburn Professor of Environmental Chemistry in the UB College of Arts and Sciences and corresponding author of the study. “This kind of pollution is a problem because it can contribute to the development of bacteria and fungi that are resistant to the medicines we have for treating human infection.”

To conduct the study, members of the team traveled to Bangladesh to sample water and train scientists there on sample collection and preparation techniques. The samples were analyzed in the Buffalo laboratory using state-of-the-art analytical methods.

Dhaka’s canal and river contained several families of chemicals, with the team noting multiple antibiotics and antifungals at these two sites. Rural test sites generally showed lower levels of antimicrobials, but antifungal agents were commonly seen, as were some antibiotics.

While not all chemicals were identified at all test sites and sometimes present only in low amounts, the team says the ubiquity of contamination seen in Dhaka is very concerning. Carbendazim, an antifungal agent, alongside insect repellent DEET, and flame retardants, were found in each and every sample the team retrieved.

“The fact that we found so many different types of chemicals is really concerning,” Aga says. “I recently saw a paper, a lab study, that showed exposure to antidepressants put pressure on bacteria in a way that caused them to become resistant to multiple antibiotics. So it’s possible that even chemicals that are not antibiotics could increase antibacterial resistance.”

Finding antimicrobial compounds in the water around urban areas isn’t surprising, as such chemicals are often released through urine and eventually wind up in rivers. At rural sites, the presence of antibiotics and antifungals in water is most likely tied to local agriculture.

Furthermore, such contamination is not unique to Bangladesh, but “is expected in many countries throughout the world where antimicrobial use is poorly regulated in both human medicine and agriculture,” says study co-author Shamim Islam, MD, clinical associate professor of pediatrics in the Jacobs School of Medicine and Biomedical Sciences at UB.

“As undertaken in this study, we feel analyzing and characterizing such environmental antimicrobial contamination is a critically important component of global antimicrobial resistance surveillance and mitigation efforts,” Islam concludes.

The paper “Retrospective suspect screening reveals previously ignored antibiotics, antifungal compounds, and metabolites in Bangladesh surface waters” has been published in the journal Science of The Total Environment.

New shape-shifting metal particles shred drug-resistant bacteria to bits

New research at RMIT University is looking into liquid metals as a solution to drug-resistant bacteria.

Image credits Aaron Elbourne et al., (2020), ACS Nano.

The approach the team is working on involves using magnetic particles of liquid metals to physically destroy bacteria, side-stepping the use of antibiotics entirely. The study describes how this technique can be used to destroy both bacteria and bacterial biofilms — protective, layered structures that house bacteria — without harming human cells.

A shred of hope

“We’re heading to a post-antibiotic future, where common bacterial infections, minor injuries and routine surgeries could once again become deadly,” says Dr Aaron Elbourne, a Postdoctoral Fellow in the Nanobiotechnology Laboratory at RMIT, and the paper’s lead author.

“It’s not enough to reduce antibiotic use, we need to completely rethink how we fight bacterial infections.”

The rising levels of antibiotic resistance recorded throughout the world is a very scary development, one that we’ll have to tackle sooner rather than later. Modern antibiotics fundamentally changed the rules of life for us when they were first developed 90 years ago. Before that, any infection was basically the luck of the draw: even a routine medical intervention or the most unassuming of wounds could become infected, and even the humblest infection could kill.

They still can, but modern antibiotics offer us a level of protection that people in the past could only pray for. Still, overuse and misuse of these compounds are forcing pathogens to adapt and survive, and they’re doing so much faster than we can develop new, more powerful drugs. It’s estimated that antibiotic-resistant bacteria cause in excess of 700,000 deaths per year, a figure which could reach 10 million a year by 2050 (which would make it deadlier than cancer). Bacteria’s ability to form biofilms further complicates the matter, as such structures render them virtually immune to all existing antibiotics.

Antibiotics are chemical compounds that prevent bacteria from functioning properly. They can do this through a range of methods: by blocking their ability to form proteins, by breaking down their membrane, or by interfering with their ability to reproduce. Human cells and bacterial cells are similar but different enough that antibiotics can be made to target the latter and leave the former unaffected.

The team wanted to develop a whole new method to attack pathogens, one that does away completely with chemical means (which bacteria can adapt to).

“Bacteria are incredibly adaptable and over time they develop defences to the chemicals used in antibiotics, but they have no way of dealing with a physical attack,” Dr. Elbourne explains.

“Our method uses precision-engineered liquid metals to physically rip bacteria to shreds and smash through the biofilm where bacteria live and multiply.”

The team’s approach involves the use of nano-sized droplets of liquid metal. When exposed to a low-intensity magnetic field, these droplets change shape and grow sharp edges.

To check how effective they would be at the task, the team placed droplets in contact with a bacterial biofilm then made them change shape. The sharp edges broke down the biofilm and physically ruptured the bacterial cells inside, the team found. They proved effective against both Gram-positive and Gram-negative bacterial biofilms. After 90 minutes of exposure to the particles, both biofilms were destroyed and 99% of the bacteria inside were killed, the team explains, suggesting that they would be effective as a wide-range treatment option. Human cells were left unaffected by the nanoparticles.

The team says that their method is versatile enough to be used in multiple settings and approaches. For example, a coating of the nanoparticles could be sprayed on implants to help prevent infections for hip or knee replacements. They also plan to explore its effectiveness against fungal infections, cancerous tumors, and build-ups such as cholesterol plaques.

“There’s also potential to develop this into an injectable treatment that could be used at the site of infection,” said Dr Vi Khanh, a Postdoctoral Research Fellow at the North Carolina State University and co-author of the paper.

The nanoparticles are currently undergoing preclinical trials in animals. If all goes well, human trials could start in a few years.

The paper “Antibacterial Liquid Metals: Biofilm Treatment via Magnetic Activation” has been published in the journal ACS Nano.

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.

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.

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.

Medicinal plants used in the Civil War can stomp our modern antibiotic-resistant germs

New research into old germ-fighting methods suggests they could prove effective in combating antibiotic-resistant bacteria today.


Bronze statue of Abraham Lincoln in Virginia, USA.
Image credits Dennis Larsen

At the height of the Civil War, the paper reports, the Confederate Surgeon General released a guide of traditional plant remedies from the South that battlefield physicians could draw upon when faced with shortages of conventional medicine. Three of the plants in this guide — white oak (Quercus alba), tulip poplar (Liriodendron tulipifera), and devil’s walking stick (Aralia spinosa) — have antiseptic properties that could be useful today, the authors explain.

The seeds of salvation

“Our findings suggest that the use of these topical therapies may have saved some limbs, and maybe even lives, during the Civil War,” says Cassandra Quave, senior author of the paper and assistant professor at Emory’s Center for the Study of Human Health and the School of Medicine’s Department of Dermatology.

The team found that extracts from these three plants have significant antimicrobial properties in the face of three dangerous species of multi-drug-resistant bacteria: Acinetobacter baumannii, Staphylococcus aureus, and Klebsiella pneumoniae. These bacteria are often seen in wound-associated infections.

Quave’s research focuses on understanding the role of plants in traditional healing and other practices, a field known as ethnobotany.

“Ethnobotany is essentially the science of survival—how people get by when limited to what’s available in their immediate environment,” she says. “The Civil War guide to plant remedies is a great example of that.”

“Our research might one day benefit modern wound care, if we can identify which compounds are responsible for the antimicrobial activity,” adds Micah Dettweiler, the first author of the paper.

If the active ingredients in these plants are identified, explains co-author Daniel Zurawski from the Wound Infections Department at the Walter Reed Army Institute of Research, they can be tested through modern “models of bacterial infection.” In a way, he says, this is mixing the “wisdom of our ancestors” with modern techniques to create new solutions for the problems we’re facing today.

Around 1 in 13 soldiers that lived through the Civil War went back home with missing limbs, the authors report. “Far more Civil War soldiers died from disease than in battle,” Zurawski explains, adding that he was surprised to see how “common amputation was as a medical treatment for an infected wound.” At the time, germ theory was still crude, and very much a work-in-progress. The training medical personnel at the time received was also shoddy at best.

An antiseptic was simply defined as a tonic used to prevent “mortification of the flesh.” Iodine and bromine were sometimes used to treat infections, according to the National Museum of Civil War Medicine, although the reason for their effectiveness was unknown. Other conventional medicines available at the time included quinine for treating malaria, and morphine and chloroform to block pain.

Union blockade

The Confederacy, however, didn’t have reliable access to these compounds. In the 1863 copy of “Resources of the Southern Fields and Forests,” Francis Peyre Porcher (who was commissioned by the Confederacy for this task) set about detailing alternatives to the essential but lacking medicine. Porcher was a botanist and surgeon from South Carolina, and his book represents a compilation of medicinal plants of the Southern states, including plant remedies used by Native Americans and enslaved Africans. Among others, the book contains a description of 37 species for treating gangrene and other infections. His work formed the foundation upon which Samuel Moore, the Confederate Surgeon General, produced the “Standard supply table of the indigenous remedies for field service and the sick in general hospitals.”

The team collected samples of the three plants from around their university’s campus, abiding to the specifications Porcher set out in his book. Extracts were produced from white oak bark and galls; tulip poplar leaves, root inner bark and branch bark; and the devil’s walking stick leaves, and were then tested on multi-drug-resistant bacteria commonly found in wound infections.

White oak and tulip poplar extracts inhibited the growth of S. aureus, while the white oak extracts also inhibited the growth of A. baumannii and K. pneumoniae, the team writes. Extracts from both of these plants also inhibited S. aureus from forming biofilms, which can insulate it against antibiotics.

Staphylococcus aureus is considered the most dangerous of the staph bacteria, and can spread from skin infections or medical devices to infect internal organs. Klebsiella pneumoniae is a leading cause of hospital infection and can result in life-threatening cases of pneumonia and septic shock. Aceinetobacter baumannii is particularly worrisome as it exhibits extensive resistance to most first-line antibiotics, and is closely associated with combat wounds. Extracts from the devil’s walking stick inhibited both biofilm formation and quorum sensing — a signaling system that staph bacteria use to manufacture toxins — in S. aureus.

“There are many more ways to help cure infections, and we need to focus on them in the era of drug-resistant bacteria,” says Quave.

“Plants have a great wealth of chemical diversity, which is one more reason to protect natural environments,” Dettweiler adds.

The paper “American Civil War plant medicines inhibit growth, biofilm formation, and quorum sensing by multidrug-resistant bacteria” has been published in the journal Nature Scientific Reports.


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.

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.

Staphylococcus epidermidis biofilm.

One bacteria lives on everybody’s skin — and it’s becoming resistant to antibiotics

Researchers at the University of Bath, UK, report that an extremely common bacterium is developing antibiotic resistance.

Staphylococcus epidermidis biofilm.

A Staphylococcus epidermidis biofilm formed on a titanium substrate.

MRSA, E. coli, they’re all very scary. But new research says there’s a newcomer to the Scary Table: Staphylococcus epidermidis, a widespread species that lives on our skins. A close relative of MRSA, this bacteria is a leading cause of infections (some of them life-threatening) following surgery.

It’s abundant, widespread, generally overlooked — and rapidly becoming resistant to antibiotics, warn researchers at the Milner Centre for Evolution at the University of Bath.

Staphil-oh no no no.

The team says we should take the threat posed by S. epidermidis much more seriously than we do today. They recommend taking extra precautions especially in the case of patients with heightened risk of infection that are due to undergo surgery.

The researchers started by retrieving samples of the bacteria from patients who developed infections following following hip replacement, knee joint replacement, and fracture fixation operations. Then, they compared the genetic material of these strains with those in swab samples harvested from the skin of healthy volunteers.

They report identifying a set of 61 genes that allow some strains of S. epidermidis to cause life-threatening infection. These genes help the bacterium grow in the bloodstream, avoid the host’s immune response, make the cell surface sticky so that the organisms can form biofilms, and make the bug resistant to antibiotics, they write. This finding, the team hopes, will further our understanding of why some strains can become infectious — in the future, this should help us keep the risk of post-surgery infection with S. epidermidis at bay.

The team also found that a small number of (healthy) individuals carry a much more deadly strain of the bacteria on their skin. Determining which strain (relatively harmless, dangerous, or one of these very dangerous ones) a potential patient carries on their skin before surgery would help doctors prepare extra hygiene precautions as needed.

“[S. epidermidis has] always been ignored clinically because it’s frequently been assumed that it was a contaminant in lab samples or it was simply accepted as a known risk of surgery,” says  Professor Sam Sheppard, Director of Bioinformatics at the Milner Centre for Evolution at the University of Bath and the study’s lead author. “Post-surgical infections can be incredibly serious and can be fatal. Infection accounts for almost a third of deaths in the UK so I believe we should be doing more to reduce the risk if we possibly can.

“Because the bug is so abundant, they can evolve very fast by swapping genes with each other,” he explains. “If we do nothing to control this, there’s a risk that these disease-causing genes could spread more widely, meaning post-operative infections that are resistant to antibiotics could become even more common.”

The paper “Disease-associated genotypes of the commensal skin bacterium Staphylococcus epidermidis” has been published in the journal Nature Communications.

International Space Station.

Antibiotic-resistant bacteria found on the ISS — they’ve been up there for at least two years

That the ISS is laden with germs isn’t, honestly, much of a surprise. But some of them are highly resistant to antibiotics, and that’s worrying.

International Space Station.

The International Space Station as seen on May 2010.
Image credits NASA / Crew of STS-132.

The International Space Station might sound spacey-clean but it is, in fact, crawling with microbes. JPL-NASA scientists report identifying several strains of Enterobacter in samples collected from the space station’s toilet and exercise area. Enterobacter is best known for infecting patients with weakened immune systems in hospitals, and being extremely resistant to antibiotics.


Luckily, the strains identified on the ISS aren’t pathogenic to (they don’t infect) humans. And, while it’s virtually impossible to have humans without bacteria — we trail our own microbiomes around anywhere we go — just finding any strain of Enterobacter on the station is enough cause for concern.

The genus is infamous for its preying on immunocompromised patients here on Earth; it’s also renowned for its ridiculous resistance to antibiotics. Space is (pardon the quip) an environment out of this world. There’s more radiation, there’s virtually no gravity, there are humans everywhere, crammed up in a tube with a lot of their carbon dioxide. All of these constraints could alter how the microbes live and multiply — these changes, could, in turn, cause them to become pathogenic to humans.

NASA employs quite a handful of microbiologists at its Jet Propulsion Laboratory, who regularly analyze microbe samples sent down from the ISS to see whether space life alters their populations or habits. The microbiologists also keep an eye on any potential biological hazards to either equipment or the astronauts’ health. This is the first time they’ve identified antibiotic-resistant Enterobacter strains in the station.

“To show which species of the bacteria were present on the ISS, we used various methods to characterise their genomes in detail. We revealed that genomes of the five ISS Enterobacter strains were genetically most similar to three strains newly found on Earth,” explained microbiologist Kasthuri Venkateswaran.

“These three strains belonged to one species of the bacteria, called Enterobacter bugandensis, which had been found to cause disease in neonates and a compromised patient, who were admitted to three different hospitals (in east Africa, Washington state and Colorado).”

The samples were collected in 2015. Since no astronauts have been struck down since then, the bugs seem not to be an immediate threat. However, the team says this state of affairs can quickly change — and it would be bad. The space-borne Enterobacter were found to be resistant to a wide range of antibiotics, and virtually completely immune to cefazolin, cefoxitin, oxacillin, penicillin, and rifampin.

Enterobacter cloacae.

Enterobacter cloacae.
Image credits CDC Public Health Image Library (PHIL #6552).

The strains also share 112 genes with clinical strains, associated with virulence, disease, and defense. The team reports that computer models show a 79% probability that the space strains will develop a human pathogen and cause disease.

Right now, however, the astronauts are safe. The possibilities, however worrying, have yet to be tested in living organisms. So the team is working to better understand the situation and develop a response procedure (that they hope never to use) against these bacteria.

“Whether or not an opportunistic pathogen like E. bugandensis causes disease and how much of a threat it is, depends on a variety of factors, including environmental ones,” Venkateswaran said. “Further in vivo studies are needed to discern the impact that conditions on the ISS, such as microgravity, other space, and spacecraft-related factors, may have on pathogenicity and virulence.”

The paper “Multi-drug resistant Enterobacter bugandensis species isolated from the International Space Station and comparative genomic analyses with human pathogenic strains” has been published in the journal BMC Microbiology.

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.

Antibiotic resistance infograph.

The CDC thwarted 220 cases of pathogens with ‘unusual’ antibiotic resistance last year alone

Over 220 instances of germs with ‘unusual’ antibiotic resistance genes were reported to the CDC across the U.S., the CDC’s Vital Signs report states.


Image via Pixabay.

The increasing prevalence of drug-resistant bacteria is, for good reason, one of the most worrying trends in modern medicine. Simply put, we’re developing new treatment options much more slowly than bacteria and their ilk can adapt (read: become immune) to the ones currently at our disposal.

In light of this fact, I’m sure you’ll be comforted to hear that health departments working with CDC’s Antibiotic Resistance (AR) Lab Network throughout the U.S. found more than 220 instances of germs with ‘unusual’ antibiotic resistance genes last year, according to the Vital Signs report. This category includes germs that are impervious to most or all antibiotics we currently possess, are uncommon in one particular geographic area or the U.S. as a whole, or have genetic mechanisms that allow them to spread their resistance to other germs.

To kill a mockinggerm

Antibiotic resistance infograph.

Image credits CDC.

Needless to say, because of the danger they pose to public health, the CDC considers the early detection of these pathogens a top priority. After a threat is identified, the next step in the Centers’ strategy is containment: facilities working with the CDC’s AR Lab try to isolate infected patients as quickly as humanly possible, then initiate special procedures intended to root out any unknown infectees, as well as reduce or stop the pathogen’s spread to new patients.

Luckily, this strategy proved effective in all the reported cases.

“CDC’s study found several dangerous pathogens, hiding in plain sight, that can cause infections that are difficult or impossible to treat,” said CDC Principal Deputy Director Anne Schuchat, M.D. “It’s reassuring to see that state and local experts, using our containment strategy, identified and stopped these resistant bacteria before they had the opportunity to spread.”

The Vital Signs report explains that the CDC’s approach, when faced with such pathogens, calls for rapid identification of resistance, infection control assessments, testing patients who may carry and spread the germ (even those that don’t exhibit symptoms), coupled with continued infection control assessments until spread is stopped. Initial screening is performed within 48 hours of the initial report, and maintain follow-up procedures over several weeks to ensure the threat is neutralized.

CDC prevention strategy.

Image credits CDC.

The CDC estimates that such efforts prevented over one and a half thousand new cases of difficult-to-treat or potentially untreatable infections, including high-priority threats such as Candida auris and carbapenem-resistant Enterobacteriaceae (CRE). The AR Lab Network is crucial for this effort, as it allows for a coordinated response from several healthcare facilities, labs, health departments, and members of the CDC itself.

Other highlights published in the report include:

  • One in four germ samples sent to the AR Lab Network for testing had genetic mechanisms that allow them to spread resistance to other populations.
  • Investigations in facilities that work with unusual resistance pathogens show that about 10% of screening tests on patients without symptoms identified a hard-to-treat strain that spreads easily. This would suggest that germs can spread relatively undetected in such facilities.
  • For CRE alone, estimates show that the containment strategies would prevent as many as 1,600 new infections in three years’ time, in a single state — representing a 76% slash in the total number of cases.


So what can you do to help the CDC contain such dangerous pathogens in the future? Well, it’s not that much — as you can imagine, tackling populations of drug-resistant bacteria isn’t something you do for fun on a Wednesday evening if you want to be effective. But you can help by being the Center’s scout; its eyes on the ground, if you will. If you want to pitch in, the CDC recommends you:

  • Inform your health care provider if you recently received health care in another country or facility. This lets them tie the dots together and trace down a pathogen’s potential movements in case a threat is determined.
  • Talk to your healthcare provider about preventing infections, taking good care of chronic conditions and getting recommended vaccines. An ounce of prevention beats a pound of cure, as the old saying goes — especially if that pound of cure can’t even kill off the infection.
  • Lastly, practice good hygiene — such as keeping hands clean with handwashing or alcohol-based hand rubs — and make sure you keep cuts and other open wounds clean until healed.

The entire Vital Signs report, as well as more information on the CDC’s containment strategy,  can be accessed on the CDC’s website, here.

Petri dish.

New method developed to stop bacteria from sharing antibiotic resistance genes

The molecular mechanisms underpinning the spread of drug resistance in bacteria populations have been identified — and a new class of molecules has been designed to fight it.

Petri dish.

Image credits via Pixnio.

The rise of multi-drug resistant bacteria is often — and to my mind, as well as the WHO’s — rightly held to be one of the biggest current threats to global health. A large part of what constitutes this threat is that bacteria can share resistance among themselves — like IT guys swapping USB sticks with new firewall software, bacteria can share genes encoding antibiotic resistance.

In a bid to nip this growing threat in the bud, researchers at the European Molecular Biology Laboratory (EMBL) have uncovered and then unraveled one of the major resistance-transfer mechanisms. They’ve also developed proof-of-concept molecules to carry out this bacterial sabotage.

Resisting the resistance

Over time, bacteria have developed a certain resistance level to most drugs we use today. The worst are arguably those that have developed resistance to multiple classes of antibiotics; examples range from MRSA (methicillin-resistant Staphylococcus aureus), VRE (vancomycin-resistant enterococcus), and ESBL (extended spectrum beta-lactamase) producing Enterobacteriaceae.

One of the major drivers of resistance spread throughout bacterial populations are transposons. Also called ‘jumping DNA’, they are bits of genetic code that can autonomously move throughout the genome. When this movement occurs between bacteria, it spreads antibiotic resistance genes among individuals. Very bad for us.

Under the leadership of Orsolya Barabas, one research team at the EMBL became the first to determine the structure of a crystal-like, protein-DNA structure which inserts these transposons in recipient bacteria. Dubbed the transposase protein, this molecule could hold the key to throwing the whole process into disarray.

Protein structure.

The unusual shape of the transposase protein (blue) forces the transposon DNA (grey) to unwind and open up.
Image credits Cell.

The protein has an unusual shape, which allows it to bind to DNA in an inactive state, keeping the transposon safe from potential chemical or physical damage until it’s delivered to its new host. Its shape also forces the transposon DNA to unwind, the team notes, allowing the protein to insert these genes into a wide array of locations within the genomes of many different bacteria.

“If you think of ropes or wires, they are usually bundled and wound-up to make them stronger. If you want to tear or cut one, it’s much easier if you unwind and loosen it first,” says EMBL group leader Orsolya Barabas, who led the work.

“It’s the same for DNA, and the transposon transfer mechanism takes advantage of this.”

Because the transposase protein first unwinds and separates the transposon’s strands, they can more readily be cut and pasted to a new site in the recipient genome. Again, very bad for us.

Luckily, Barabas’ team used the protein’s crystal structure to develop molecules that should block the transposons’ movement through two mechanisms. The first prevents the transposase protein from activating by blocking its architecture with a newly designed peptide, a short chain of amino acids — in other words, it wedges itself in the transposase so that it can’t unfurl and deliver the DNA cargo.

The second method ‘corrupts’ the genetic data. This molecule, a DNA-mimic, binds to the transposon and blocks the DNA strand replacement in the host; no replacement, no resistance transfer.

“As we believe these features are broadly present in these jumping DNA elements, but not in related cellular systems, they may be quite specific to transposons. This way, we can target only the bacteria we want, and not the many good bacteria in our bodies and the environment,” Barabas explains.

The molecules are still far from trials with living hosts. For now, Barabas and her colleagues will focus on better understanding the transfer mechanisms, as well as on developing and testing new strategies to block it.

The paper “Transposase-DNA Complex Structures Reveal Mechanisms for Conjugative Transposition of Antibiotic Resistance” has been published in the journal Cell.


Small populations of bacteria can elude antibiotics — here’s how we’re fixing that

Small populations of bacteria respond differently to antibiotics than larger ones, a new study reports — offering clues as to why it’s so hard to kill these bugs off.


Image via Pixabay.

A population of bacteria that sports 100 or fewer cells doesn’t play by the rules; at least, not as far as antibiotics are concerned. Larger populations tend to respond homogeneously throughout their members, but with small populations, even antibiotics are more of a hail mary, new research shows — sometimes they work, sometimes they don’t, and it seems to be completely down to chance.

Strength in (small) numbers

Which, understandably, is not an ideal state of affairs for us hairless bipeds. Especially because for decades, the prevailing wisdom held that reducing the number of bacteria down to a few hundred individuals would be enough for the immune system to come in and carry the day.

“More recently, it became clear that small populations of bacteria really matter in the course of an infection,” says lead author Minsu Kim.

“The infectious dose — the number of bacterial cells needed to initiate an infection — turned out to be a few or tens of cells for some species of bacteria and, for others, as low as one cell.”

The researchers wanted to understand why antibiotic treatments sometimes work, and sometimes fail. They’ve started with the usual culprits: variations in immune responses between people, or possible mutations of bacteria that make them more virulent in some cases. Kim, however, wasn’t impressed. She suspected that something else was at work here, and her suspicions only became stronger when researchers working with model organism C. elegans recorded unexpected treatment failures even for antibiotic-susceptible infections.

Focusing their research only on small populations of bacteria, the team discovered that their interaction with antibiotics is based on a different dynamic than that of large populations. The researchers observed that antibiotics induce fluctuations in the density of bacterial populations as they kill off individuals, which they expected; however, they also noted that when the population’s rate of growth overcame the rate at which the antibiotics killed individuals, clearance failed.

Armed with this knowledge, they created a low-dose cocktail of drugs to preempt this quirky dynamic. This mix contained a bactericide (a compound that kills bacteria) and bacteriostat (a substance that slows the growth of bacteria). Taken together, these were intended to limit the random fluctuation seen by the team, and thus make it more probable to keep the population’s overall death rate higher than the growth rate. They then took this cocktail to the lab to see how it works. First, they showed that it was effective on a small population of drug-susceptible E. coli. Then they applied it to a clinically-isolated strand of antibiotic resistant E. coli — again, the cocktail worked.

“We’ve shown that there may be nothing special about bacterial cells that aren’t killed by drug therapy — they survive by random chance,” said Kim. “This randomness is a double-edged sword. On the surface, it makes it more difficult to predict a treatment outcome. But we found a way to manipulate this inherent randomness in a way that clears a small population of bacteria with 100 percent probability.”

“By tuning the growth and death rate of bacteria cells, you can clear small populations of even antibiotic-resistant bacteria using low antibiotic concentrations.”

The team hopes that their model cocktail can help guide development of more refined antibiotic treatment courses. Their end goal is to help researchers develop treatments that use lower doses to kill an infection entirely, for as many different infections as possible.

“It’s important because if you treat a bacterial infection and fail to kill it entirely, that can contribute to antibiotic resistance,” says Kim.

Not all antibiotics available today fit the model they’ve developed, however. More research is needed get this approach ready for use in a clinical setting.

Antibiotic resistance is a huge and growing problem. Essentially, it means that at some point in the future our drugs won’t be able to reliably protect against bacteria — or they could become useless against them altogether. Antibiotic resistance could lead to 10 million people dying each year by 2050, a total health care burden of $100 trillion, and a reduction of 2% to 3.5% in world Gross Domestic Product (GDP) by the same year.

The paper “Antibiotic-induced population fluctuations and stochastic clearance of bacteria” has been published in the journal eLife.

Researchers at Max Planck developed a new fitness technology called Jymmin makes us less sensitive to pain. Credit: Max Planck Institute For Human Cognitive and Brain Sciences.

Jymmin combines working out with music, makes people feel less pain

Good news for all of us! Whether or not you’re enjoying exercising, scientists have developed new technology that makes working out more enjoyable than ever. The new study also found that it makes us more resistant to pain.

Researchers at Max Planck developed a new fitness technology called Jymmin makes us less sensitive to pain. Credit: Max Planck Institute For Human Cognitive and Brain Sciences.

Researchers at Max Planck developed a new fitness technology called Jymmin that makes us less sensitive to pain. Credit: Max Planck Institute For Human Cognitive and Brain Sciences.

Researchers at Max Planck Institute for Human Cognitive and Brain Sciences (MPI CBS) developed a new way of working out: they altered fitness machines to produce musical sounds during use. Scientists discovered that this novel approach, which they call Jymmin, increases pain threshold and makes people less sensitive to discomfort.

“We found that Jymmin increases the pain threshold. On average, participants were able to tolerate ten percent more pain from just ten minutes of exercise on our Jymmin machines, some of them even up to fifty percent”, said Thomas Fritz, head of research group Music Evoked Brain Plasticity at MPI CBS, in a press statement.

How do these machines work?

Scientists paired music composition software with sensors attached to the fitness machines. While exercising, the sensors captured and then transmitted signals to the software, which played back an accompaniment from each fitness machine. Basically, the researchers modified steppers and abdominal trainers to become our own musical instruments, so you can get really creative while working out.

Researchers discovered that, after Jymmin, participants were able to immerse their arms in ice water of 1°C (33.8°F) for five seconds longer compared to a conventional exercise session.

Scientists believe that the pain resistance experienced by the participants is due to the increased release of endorphins. Apparently, if music composition and physical activity are combined, endorphins are flushed into our systems in a more efficient way.

Researchers divided all 22 participants according to how they rated pain and discovered that participants with the highest pain threshold benefitted the most from this training method. Maybe this happens because these participants already release endorphins more effectively in comparison to those who are more pain sensitive.

“There are several possible applications for Jymmin that can be derived from these findings. Patients simply reach their pain threshold later,” Fritz added.

Jymmin could do wonders in treating chronic or acute pain. It could also be used as support in rehabilitation clinics by enabling more efficient training.

Scientists tested top swimmers in South Korea and the results were remarkable: athletes who warmed up using Jymmin machines were faster than those using conventional methods. In a pilot test, five of six athletes swam faster than in previous runs.

Previous studies showed that Jymmin has many positive effects on our well-being. They revealed that personal mood and motivation improved, and even the music produced while Jymmin was perceived as pleasant.

Scientific reference: Thomas H. Fritz, Daniel L. Bowling, Oliver Contier, Joshua Grant, Lydia Schneider, Annette Lederer, Felicia Höer, Eric Busch, Arno Villringer. Musical Agency during Physical Exercise Decreases PainFrontiers in Psychology, 2018; 8 DOI: 10.3389/fpsyg.2017.02312.