SoylentNews

Sir Finkus writes:

The World Health Organization has warned that the rise of antibiotic-resistant bacterial infections poses a major threat to global health. The report [PDF 3.9MB] paints a bleak picture, noting that previously treatable infections such as urinary tract infections caused by E. coli are becoming increasingly difficult to treat in all regions.

It goes on to recommend:

1. Using antibiotics only when prescribed by a doctor
2. Completing the full prescription, even if they feel better
3. never sharing antibiotics with others or using leftover prescriptions.

GoonDu writes:

This article started off with an introduction to superbugs before proceeding to talk about the bacteria Staphylococcus aureus, specifically the microbe USA300, and how the epidemic is spreading to households as well.

While the presence of Staph on skin has always put people at risk for infection, two features make CA-MRSA (community associated methicillin-resistant Staphylococcus aureus) riskier. It can cause severe disease in previously healthy people. In about one in every ten cases, CA-MRSA infections lead to deadly pneumonia, severe sepsis, or the dreaded "flesh-eating disease" (aka necrotizing fasciitis). They also have the ability to spread rapidly, which has helped propel them to a global epidemic.

The bacteria spreads by contact, which makes it easy to spread amongst family, as sharing common household items, like a door knob, counts. To make matters worse, research shows that it is able to evolve into a more harmful version.

Tracing the bug by whole-genome sequencing, researchers managed to "determine that USA300 first arose around 1993. The molecular signatures allowed them to also home in on the geographic location where this happened, which they determined to be right in Columbia's neighborhood: northern Manhattan."

migz writes:

The Independent reports that a new study will be published in Nature today.

Scientists at East Anglia University have discovered a new avenue to combat antibiotic resistant bacteria. The paper discusses attacking the cell membranes of gram negative bacteria, using lipopolysaccharides to inhibit membrane growth. This membrane normally protects the bacteria from the immune system. The technique has not yet been tested invitro against infection causing bacteria, and so looks like a long way from practical application.

Hugh Pickens writes:

Drug resistant strains of many diseases are emerging faster than new antibiotics can be made to fight them with drug-resistant bacteria infecting at least two million people a year in the United States and killing 23,000. Now Denise Grady reports at the NYT that scientists have developed a new method, which extracts drugs from bacteria that live in dirt, that has yielded a powerful new antibiotic, teixobactin, that was tested in mice and easily cured severe infections, with no side effects. Better still, the drug works in a way that makes it very unlikely that bacteria will become resistant to it. And the method developed to produce the drug has the potential to unlock a trove of natural compounds to fight infections and cancer — molecules that were previously beyond scientists’ reach because the microbes that produce them could not be grown in the laboratory.

The new research is based on the premise that everything on earth — plants, soil, people, animals — is teeming with microbes that compete fiercely to survive. Trying to keep one another in check, the microbes secrete biological weapons: antibiotics. “The way bacteria multiply, if there weren’t natural mechanisms to limit their growth, they would have covered the planet and eaten us all eons ago,” says Dr. William Schaffner. The problem is that about 99 percent of the microbial species in the environment are bacteria that do not grow under usual laboratory conditions (PDF). But the researchers have found a way to grow them using a process that involves diluting a soil sample and placing it on specialized equipment. Then, the secret to success is putting the equipment into a box full of the same soil that the sample came from. “Essentially, we’re tricking the bacteria,” says Dr. Kim Lewis. Back in their native dirt, they divide and grow into colonies. Once the colonies form, the bacteria are “domesticated,” and researchers can scoop them up and start growing them in petri dishes in the laboratory.

Experts not involved with the research say the technique for isolating the drug had great potential. They also say teixobactin looked promising, but expressed caution because it has not yet been tested in humans. “What most excites me is the tantalizing prospect that this discovery is just the tip of the iceberg,” says Mark Woolhouse. “It may be that we will find more, perhaps many more, antibiotics using these latest techniques.”

"gewg_" writes:

The Center for American Progress reports

After being treated at UCLA's Ronald Reagan Medical Center, nearly 180 people may have been exposed to a potentially dangerous bacteria that's resistant to antibiotic treatment, the Los Angeles Times reported [February 19]. Two deaths have been linked to the outbreak so far. And federal officials are warning that the source of the "superbug" spread is probably a commonly used medical scope.

Seven patients at UCLA have been officially infected with CRE [Carbapenem resistant enterobacteriaceae], the deadly superbug that's been rapidly spreading throughout the United States' hospitals over the past several years. CRE bacteria are virtually untreatable with our current antibiotics. In the medical community, CRE are known as "nightmare bacteria" because they have a particularly high mortality rate compared to other bugs.

The medical scope in question is called a duodenoscope, a tool in the field of gastroenterology that offers a less invasive way(PDF) to examine a patient's digestive tract.

The flexible nature of the duodenoscope makes it hard to effectively sterilize, and medical investigators have linked the tools to an increased risk of CRE infections. In previous outbreaks in Chicago and Seattle, duodenoscopes have infected dozens of people with CRE. At the Virginia Mason Medical Center in Seattle, eleven people died.

jdccdevel writes:

The CBC has an article about a medieval recipe found in a 1,000-year-old book that can kill antibiotic-resistant superbugs.

The recipe's ingredients include: garlic, onion or leek, wine, and oxgall (bile from a cow's stomach). Oh, yeah, it's also supposed to be "brewed in a brass vessel, strained and then left to sit for nine days before use."

From the article:

A recipe for the potion, originally an eye salve, was found in Bald's Leechbok, a 10th-century book of Anglo-Saxon medical advice and recipes for medicines, salves and treatments found in the British Library.
...
When tested in mice on wounds infected with methicillin-resistant Staphylococcus aureus (MRSA), it performed at least as well as conventional antibiotics, reported scientists at the Annual Conference of the Society for General Microbiology this week in the United Kingdom.

"We were absolutely blown away by just how effective the combination of ingredients was," Freya Harrison, the University of Nottingham microbiologist who led the study, said in a statement.

Apparently, this recipe is even effective against biofilms which modern antibiotics really struggle to combat.

More details from The University of Nottingham and BBC News.

Runaway1956 writes:

A patient with extensively drug-resistant TB flew from Mumbai to Chicago, and the deadly disease could become an infamous export due to problems in India's public health system

[...] Now, difficult-to-kill TB is no longer just India's nightmare. In June U.S. health authorities confirmed that an Indian patient carried this extreme form of the infection, called XDR-TB, across the ocean to Chicago. The patient drove from there to visit relatives as far away as Tennessee and Missouri. Health officials in several states are tracking down everyone with whom the patient—who is now quarantined and being treated at the National Institutes of Health in Maryland—had prolonged contact. The disease can be cured in only 30 percent of patients and sometimes requires surgery to remove infected parts of lungs. Although TB's slow rate of infection makes explosive epidemics unlikely, the Chicago episode shows how easy it might be for the illness to become a worldwide export.

Yet until recently Indian public health officials remained reluctant to admit there's a problem, says Nerges Mistry, director of the Mumbai-based Foundation for Medical Research. "They were always trying to deny it [existed]," she says. (Neither the head of India's Revised National Tuberculosis Control Program (RNTCP) nor Mumbai's main tuberculosis control official—both of whom are new to their posts—responded to interview requests from Scientific American.)

[...] If there are indeed many people with resistant germs, it heightens the chances of those pathogens leaving the country for the rest of the world. Nearly a million Indians traveled to the U.S. in 2014, compared with less than three million from all of central Asia. More and more middle-class Indians are being diagnosed with TB, and although the patient who carried XDR-TB to the U.S. was immediately placed in isolation, India has no provisions for quarantines or travel restrictions.

http://www.scientificamerican.com/article/supercharged-tuberculosis-made-in-india1/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+ScientificAmerican-News+%28Content%3A+News%29

http://www.cdc.gov/tb/publications/factsheets/drtb/xdrtb.htm
http://www.medicinenet.com/extensively_drug-resistant_tuberculosis_xdr_tb/article.htm
http://www.who.int/tb/challenges/xdr/faqs/en/

Yes, their headline is sensationalist - but there really IS a problem here, as evidenced by the CDC, WHO, and other organizations. Perhaps the problem wasn't created by India's restructured medical school system, but it has almost certainly been increased by it.

As reported by The Times of India last year:

The SN Medical College's trauma centre which became 'functional' in 2011 is yet to conduct a surgery. This came to UP chief minister Akhilesh Yadav's attention when he conducted a surprise inspection of the centre on Friday.

[...] "Not a single serious patient has ever been treated at the centre. Whenever a minister or a dignitary plans to pay a visit to the centre, a few are admitted in the intensive care unit (ICU) to 'show' them," said a doctor, who did not wish to be named. He added that a ward boy has been put on duty in the ICU just to keep an eye that no one steals anything from there.

Arthur T Knackerbracket suggests the following story from Phys.org:

To fight a pathogen that's highly resistant to antibiotics, first understand how it gets that way.

Klebsiella pneumoniae strains that carry a particular enzyme are known for "their ability to survive any antibiotics you throw at them," said Corey Hudson of Sandia National Laboratories in California.

Using Sandia's genome sequencing capabilities, Hudson and colleagues Robert Meagher and Kelly Williams, along with former postdoctoral employee Zach Bent, identified several mechanisms that bacteria use to share genes and expand their antibiotic resistance. They found that in some cases, bacteria can receive a new set of genes all at once and in the process become pathogenic.

To better understand how the process works, they focused on the large mobile DNAs, such as plasmids, which exist as free DNA circles apart from the bacterial chromosome, and genomic islands, which can splice themselves into the chromosome. These mobile DNAs are major mechanisms for evolution in organisms that lack a true nucleus. Genomic islands and plasmids carry genes that contribute to everything from metabolism to pathogenicity, and move whole clusters of genes all at once between species.

Identifying how genomic islands move and their effect on bacterial physiology could lead to new approaches to bypass bacterial defenses, Hudson said.

Eventually, the effort might lead to a way to predict new pathogens before they emerge as public health threats.

Original Submission

Bobs writes:

New study details from http://www.reuters.com/article/us-olympics-rio-superbacteria-exclusive-idUSKCN0YW2E8 "Exclusive: Studies find 'super bacteria' in Rio's Olympic venues, top beaches":

The Zika thing seems bad, but this sounds imminently deadly to athletes and provides the potential for the Olympics to rapidly spread these infectious super-bugs around the world.

I don't like being 'alarmist', but this appears to be a likely, credible threat to world health. How logical is it to be concerned about this? Are Soylents aware of any good, practical way for participants and attendees to the Olympics in Brazil to reduce the risk of exposure and infection and then spreading this? Are you planning on attending?

Other Soylent discussion on Zika / Olympics:

• Why Concerns for Global Spread of Zika Means Rio de Janeiro's 2016 Olympics Must Not Proceed"
• Maybe "It's Not the Zika Virus".

Original Submission

Arthur T Knackerbracket has found the following story:

They may be slimy, but they are a perfect environment for microorganisms: biofilms. Protected against external influences, here bacteria can grow undisturbed, and trigger diseases. Scientists at Kiel University, in cooperation with colleagues at the Hamburg University of Technology (TUHH) in Hamburg-Harburg, are researching how it can be possible to prevent the formation of biofilms from the beginning. On this basis, alternatives to antibiotics could be developed, as many pathogens are already resistant to most commercially used antibiotics. The biologists have published their findings in the scientific journal Frontiers in Microbiology. Their study shows that strategies from nature are particularly effective at inhibiting biofilms.

A thin layer floating on water, dental plaque, or slimy black coatings in the washing machine detergent drawer: biofilms originate when cells attach to surfaces, and organise themselves into coordinated three-dimensional consortia, embedded in an extracellular matrix. It becomes problematic when biofilms form on medical devices or implants. Pathogenic bacteria, which trigger deseases, pose a particularly serious threat, as they cannot be treated with normal antibiotics when growing within a biofilm. Therefore: "One way to prevent illnesses is to stop biofilms forming in the first place," according to Professor Ruth Schmitz-Streit from the Institute of General Microbiology at Kiel University.

In order to coordinate themselves and establish consortia on surfaces, the bacteria must communicate with each other via signal molecules (so-called "autoinducers"). If this communication is disrupted, no biofilm can be formed. This cell-to-cell communication, known as "quorum sensing" (QS), can be influenced by disruptive biomolecules ("quorum quenching" or QQ proteins). "Proteins can break down these signal molecules, or modify them in such a way that they are no longer functional," explained Schmitz-Streit. Therefore, the goal of the study, financed by the Federal Ministry of Education and Research (BMBF), was to find QQ proteins which disrupt this communication between bacteria as effectively as possible.

[...] The research group discovered even more: the communication-disrupting protein QQ-2 proved itself to be particularly effective during the investigations. "This protein is very robust and can prevent many different types of biofilms," explained Weiland-Bräuer. Previous studies focused more on disrupting a particular language of bacteria. "In contrast, the QQ-2 protein is orientated towards a 'universal language', and can disrupt the communication of different bacteria. This makes it a 'general troublemaker'."

Original Submission

takyon writes:

Three young scientists thing they have a way to defeat antibiotic resistance:

Three college-age scientists think they know how to solve a huge problem facing medicine. They think they've found a way to overcome antibiotic resistance. Many of the most powerful antibiotics have lost their efficacy against dangerous bacteria, so finding new antibiotics is a priority. It's too soon to say for sure if the young researchers are right, but if gumption and enthusiasm count for anything, they stand a fighting chance.

[...] Last October, Stanford launched a competition for students interested in developing solutions for big problems in health care. Not just theoretical solutions, but practical, patentable solutions that could lead to real products. The three young scientists thought they had figured out a way to make a set of proteins that would kill antibiotic resistant bacteria. They convinced a jury of Stanford faculty, biotech types and investors that they were onto something, and got $10,000 to develop their idea.

[...] "The way that our proteins operate, that if the bacteria evolve resistance to them, actually the bacteria can no longer live anymore," says Rosenthal. "We target something that's essential to bacterial survival." Bacteria have managed to evolve a way around even the most sophisticated attempts to kill them, so I was curious to know more about how the proteins these young inventors say they've found worked. "We're not able to disclose, unfortunately," says Filsinger Interrante. It's their intellectual property, she explains, that they hope will attract investors. "We think that our protein has the potential to target very dangerous, multidrug-resistant bacteria."

Peer review, meet news review.

Original Submission

Phoenix666 writes:

Tiny, star-shaped molecules are effective at killing bacteria that can no longer be killed by current antibiotics, new research shows.

The study, published today in Nature Microbiology, holds promise for a new treatment method against antibiotic-resistant bacteria (commonly known as superbugs).

The star-shaped structures, are short chains of proteins called 'peptide polymers', and were created by a team from the Melbourne School of Engineering.
...
tests undertaken on red blood cells showed that the star-shaped polymer dosage rate would need to be increased by a factor of greater than 100 to become toxic. The star-shaped peptide polymer is also effective in killing superbugs when tested in animal models.

Furthermore, superbugs showed no signs of resistance against these peptide polymers. The team discovered that their star-shaped peptide polymers can kill bacteria with multiple pathways, unlike most antibiotics which kill with a single pathway.

Let's hope any such molecules are thoroughly vetted with long-term studies before being introduced to medical therapies.

Original Submission

takyon writes:

A lethal and drug-resistant fungal infection is beginning to creep into the United States. Healthcare facilities are at risk:

Thirteen individuals have become ill from a serious and sometimes fatal fungal infection previously unseen in the United States, the Centers for Disease Control and Prevention said Friday. The fungus, Candida auris, is known to occur in health care settings such as hospitals and nursing homes. Seven cases occurred between May 2013 and August 2016 in four states: Illinois, Maryland, New Jersey and New York. As of August 31, four of these seven patients, all with bloodstream infections, died, though it is unclear whether their deaths were due to C. auris. The remaining six cases were identified after August and are still under investigation. "It appears that C. auris arrived in the United States only in the past few years," Dr. Tom Chiller, chief of the CDC's Mycotic Diseases Branch, said in statement. He added that scientists are working to better understand the fungus so they can develop recommendations to protect those at risk.

C. auris bloodstream infections have a 50% fatality rate in some countries, according to one study. Some strains of this yeast are multidrug-resistant and cannot be treated by the three major classes of antifungal medications. First reported in 2009 in Japan, cases have been recorded in South Korea, India, South Africa, Kuwait, Colombia, Venezuela, Pakistan and the United Kingdom. "Experience outside the United States suggests that C. auris has high potential to cause outbreaks in healthcare facilities," the CDC notes on its website. Importantly, this deadly organism is difficult to identify using traditional laboratory biochemical methods.

CDC's Candida auris page; CDC's report on these first seven cases.

Original Submission

charon writes:

Researchers at Imperial College London and the University of Nottingham have found a novel way of killing harmful bacteria that cause infection — setting predator bacteria loose to eat the harmful ones.

Experiments showed a dose of Bdellovibrio bacteriovorus acted like a "living antibiotic" to help clear an otherwise lethal infection.

The animal studies, published in Current Biology , suggested there would be no side effects.

[...] Dr Michael Chew, from the Wellcome Trust medical research body, said: "It may be unusual to use a bacterium to get rid of another, but in the light of the looming threat from drug-resistant infections the potential of beneficial bacteria-animal interactions should not be overlooked.

"We are increasingly relying on last-line antibiotics, and this innovative study demonstrates how predatory bacteria could be an important additional tool to drugs in the fight against resistance."

Original Submission

hubie writes:

A big challenge in modern wastewater treatment is the removal of micropollutants and multiresistant bacteria (MRB). Micropollutants, which includes such things as pesticides, pharmaceuticals, personal care products, food additives, and hormones, are dangerous for the environment and human health as we have previously reported. MRBs, and their antibiotic resistant genes (ARG), have been rated as a global health threat by the World Health Organization. Modern wastewater treatment plants are fairly effective at reducing the total number of MRBs, but it turns out they may also help select particular highly resistant strains that make it through the processing and they are only moderately successful at removing micropollutants. To address these new threats, many treatment facilities are discussing adding an additional treatment step. One of the more promising treatments being implemented is the use of ozone because it is economically feasible, and it significantly abates micropollutants.

What is largely unknown is the effect of ozonation on MRBs. Ozone is a strong oxidant and disinfectant and it is very effective on organic materials. A group of Swiss researchers investigated the extent that ozone kills MRBs and destroys ARGs when applied at the levels implemented by wastewater treatment plants. They performed laboratory experiments, and also took samples from a wastewater treatment plant. Their results are presented in a paper [Paywalled] in the journal Environmental Science & Technology. In the lab they found ozonation to be very effective at disrupting ARGs, but unfortunately it was not effective when applied to the secondary effluent at a treatment facility. What this means is that the new ozonation systems being implemented to deal with micropollutants, although they have much potential, will not be effective against antibiotic resistant bacteria.

Inactivation of Antibiotic Resistant Bacteria and Resistance Genes by Ozone: From Laboratory Experiments to Full-Scale Wastewater Treatment [DOI: 10.1021/acs.est.6b02640][DX]

Original Submission

Phoenix666 writes:

Scientists have found a superbug— hidden 1,000 feet underground in a cave — which is resistant to 70 percent of antibiotics and can totally inactivate many of them.

But here's the kicker. This bacterium has been isolated from people, society — and drugs — for 4 million years, scientists report Thursday in the journal Nature Communications.

That means it hasn't been exposed to human drugs in a clinic or on a farm that uses them. But it has the machinery to knock out these drugs. And that machinery has been around for millions of years.

...

Because, Barton says, the bacterium is helping scientists understand where antibiotic resistance comes from and, hopefully, new ways to stop it. And the bacterium — called Paenibacillus (pronounced "penny-bacillus") — isn't pathogenic. It won't hurt you. It's just capable of evading many, many antibiotics.

Original Submission

AnonTechie writes:

If it sometimes seems like the idea of antibiotic resistance, though unsettling, is more theoretical than real, please read on.

Public health officials from Nevada are reporting on a case of a woman who died in Reno in September from an incurable infection. Testing showed the superbug that had spread throughout her system could fend off 26 different antibiotics.

"It was tested against everything that's available in the United States ... and was not effective," said Dr. Alexander Kallen, a medical officer in the Centers for Disease Control and Prevention's division of health care quality promotion. Although this isn't the first time someone in the US has been infected with pan-resistant bacteria, at this point, it is not common. It is, however, alarming.

[Source]: https://www.scientificamerican.com/article/woman-killed-by-a-superbug-resistant-to-every-available-antibiotic/

[Journal Ref.]: https://www.cdc.gov/mmwr/volumes/66/wr/mm6601a7.htm

Original Submission

takyon writes:

Researchers have found that an extract from an invasive weed in Florida can disrupt Methicillin-resistant Staphylococcus aureus bacteria:

The researchers showed that a refined, flavone-rich composition extracted from the berries inhibits formation of skin lesions in mice infected with methicillin-resistant Staphylococcus auereus (MRSA). The compound works not by killing the MRSA bacteria, but by repressing a gene that allows the bacteria cells to communicate with one another. Blocking that communication prevents the cells from taking collective action, a mechanism known as quorum quenching.

"It essentially disarms the MRSA bacteria, preventing it from excreting the toxins it uses as weapons to damage tissues," Quave says. "The body's normal immune system then stands a better chance of healing a wound."

The discovery may hold potential for new ways to treat and prevent antibiotic-resistant infections, a growing international problem. Antibiotic-resistant infections annually cause at least two million illnesses and 23,000 deaths in the United States, according to the Centers for Disease Control and Prevention. The United Nations last year called antibiotic-resistant infections a "fundamental threat" to global health and safety, citing estimates that they cause at least 700,000 deaths each year worldwide, with the potential to grow to 10 million deaths annually by 2050.

Schinus terebinthifolius .

Virulence Inhibitors from Brazilian Peppertree Block Quorum Sensing and Abate Dermonecrosis in Skin Infection Models (open, DOI: 10.1038/srep42275) (DX)

Original Submission

An Anonymous Coward writes:

On February 27, World Health Organization published its first ever list of the top 12 "priority pathogens."

The list was drawn up in a bid to guide and promote research and development (R&D) of new antibiotics, as part of WHO's efforts to address growing global resistance to antimicrobial medicines.

The list highlights in particular the threat of gram-negative bacteria that are resistant to multiple antibiotics. These bacteria have built-in abilities to find new ways to resist treatment and can pass along genetic material that allows other bacteria to become drug-resistant as well.

[...] "Antibiotic resistance is growing, and we are fast running out of treatment options. If we leave it to market forces alone, the new antibiotics we most urgently need are not going to be developed in time."

[...] The most critical group of all includes multidrug resistant bacteria that pose a particular threat in hospitals, nursing homes, and among patients whose care requires devices such as ventilators and blood catheters. They include Acinetobacter, Pseudomonas and various Enterobacteriaceae (including Klebsiella, E. coli, Serratia, and Proteus). They can cause severe and often deadly infections such as bloodstream infections and pneumonia.

These bacteria have become resistant to a large number of antibiotics, including carbapenems and third generation cephalosporins – the best available antibiotics for treating multi-drug resistant bacteria.

More analysis at NPR: WHO's First-Ever List Of The Dirty Dozen Superbugs

Original Submission

Phoenix666 writes:

Antibiotic resistance is one of medicine's most pressing problems. Now, a team from Korea is tackling this in a unique way: using bacteria to fight bacteria.

Before the discovery of penicillin in 1928, millions of lives were lost to relatively simple microbial infections. Since then, antibiotics have transformed modern medicine. The World Health Organization estimates that, on average, antibiotics add 20 years to each person's life. However, the overuse of antibiotics has put pressure on bacteria to evolve resistance against these drugs, leading to the emergence of untreatable superbugs.

Now, researchers at South Korea's Ulsan National Institute of Science and Technology (UNIST) aim to fight fire with fire by launching predatory bacteria capable of attacking other bacteria without harming human cells. "Bacteria eating bacteria. How cool is that?" asks Professor Robert Mitchell, the team leader. He and his colleagues are also developing a natural compound called violacein to tackle Staphylococcus, a group of around 30 different bacteria known to cause skin infections, pneumonia and blood poisoning. Some Staphylococcus bacteria such as MRSA (methicillin-resistant Staphylococcus aureus) are resistant to antibiotics, making infections harder to treat.

Violacein is a so-called 'bisindole': a metabolite produced by bacteria from the condensation of two molecules of tryptophan (an essential amino acid used in many organisms to ensure normal functioning and avoid illness and death). This compound is vibrant purple in colour and of interest to researchers for its anticancer, antifungal and antiviral properties. Researchers have discovered that it can stop bacteria from reproducing, and even kill the multidrug resistant bacterium Staphylococcus aureus, when used in the right doses. It also works well in conjunction with other existing antibiotics.

Previously on SoylentNews: Predatory Bacteria could be a New Weapon Against Superbugs

Original Submission

Phoenix666 writes:

Inspired by viruses that attack and kill bacteria, researchers at The Rockefeller University have created an entirely new weapon against disease-causing bacteria that shows great promise for treating drug-resistant infections.

In work described in the Proceedings for the National Academy of Sciences on April 17, the team engineered molecules that accomplish something viruses do much better than the human immune system; namely, targeting specific carbohydrate molecules that appear on the surfaces of bacterial cells.

"Bacteria-infecting viruses have molecules that recognize and tightly bind to these common components of the bacterial cell's surface that the human immune system largely misses. We have co-opted these molecules, and we've put them to work helping the human immune system fight off microbial pathogens," says Vincent A. Fischetti, head of the Laboratory of Bacterial Pathogenesis and Immunology.

In experiments with mice, Fischetti's team used this approach to successfully treat life-threatening infections by MRSA, a bacterium that is resistant to conventional antibiotics—results that suggest they may have found a new way to fight superbugs like MRSA.

Original Submission

An Anonymous Coward writes:

Dr. Lowe, from In the Pipeline, writes about new discoveries in the field of antibiotics:

Anyone who's done antibiotic research can tell you about what a slog it is. Just looking at the rate of approval of new ones will tell you that, too – it really is like breaking rocks, except breaking rocks is a lot more straightforward and rewarding most of the time. As I've said before, when I look back at all the mammalian cells that I've killed with my molecules over the years, and compare that to the experience I had working against gram-negative bacteria, it's pretty sobering. Killing gram-negative pathogens is hard. And killing them with a compound that (A) hasn't already been discovered, in one form or another and (B) doesn't kill everything else it touches is a challenge indeed.

There are two new papers, though, that give a person some hope. And we need some, because resistant bacteria, as everyone has been saying for years now, could really give our industrial civilization fits. Here's some work by the Hergenrother group at Illinois, though, that sheds light on one of the biggest problems in antibiotic drug discovery: what kinds of structures should we be looking at?

That's a real puzzle, because antibiotic compounds in general tend to have pretty wooly structures, especially the ones derived from natural products. They tend to be outliers in most any rule-of-thumb property screen, and often break several of them simultaneously. Yet they work, and that's impressive, since to "work" in this context means to penetrate a lipopolysaccharide outer membrane, survive on the other side of it without being pumped right back out of the bacterial cell entirely, and penetrate that a second inner membrane in quantities sufficient to serve as a drug.

This paper looks through a set of compounds, carefully measuring the degree to which each accumulate in E. coli, and tried to draw some general structural lessons.

After identifying properties that allow compounds to penetrate Gram-negative bacteria, the research group demonstrates that they can convert an antibiotic that was limited to Gram-positive bacteria to have activity in Gram-negative bacteria.

The second discovery involves greatly improving the potency of a specific antibiotic:

MrPlow writes:

Submitted via IRC for Bytram

Scientists from Rutgers University-New Brunswick, the biotechnology company NAICONS Srl., and elsewhere have discovered a new antibiotic effective against drug-resistant bacteria: pseudouridimycin. The new antibiotic is produced by a microbe found in a soil sample collected in Italy and was discovered by screening microbes from soil samples. The new antibiotic kills a broad spectrum of drug-sensitive and drug-resistant bacteria in a test tube and cures bacterial infections in mice.

In a paper published in Cell today, the researchers report the discovery and the new antibiotic's mechanism of action.

Pseudouridimycin inhibits bacterial RNA polymerase, the enzyme responsible for bacterial RNA synthesis, through a binding site and mechanism that differ from those of rifampin, a currently used antibacterial drug that inhibits the enzyme. Because pseudouridimycin inhibits through a different binding site and mechanism than rifampin, pseudouridimycin exhibits no cross-resistance with rifampin, functions additively when co-administered by rifampin and, most important, has a spontaneous resistance rate that is just one-tenth the spontaneous resistance rate of rifampin.

Source: https://www.sciencedaily.com/releases/2017/06/170615142842.htm

Journal reference: Sonia I. Maffioli, et. al. Antibacterial Nucleoside-Analog Inhibitor of Bacterial RNA Polymerase. Cell, 2017; 169 (7): 1240 DOI: 10.1016/j.cell.2017.05.042

Original Submission

MrPlow writes:

Submitted via IRC for Bytram

The number of drug-resistant tuberculosis (TB) cases is rising globally. But a newly discovered natural antibiotic — produced by bacteria from the lung infection in a cystic fibrosis patient — could help fight these infections. Lab testing reported in the Journal of the American Chemical Society shows that the compound is active against multi-drug resistant strains.

Starting with the famous first discovery of penicillin from mold, scientists have continued to search for natural sources of antibiotics. And as pathogens develop resistance to once-reliable medicines, the search has taken on a new urgency. By 2040, more than a third of all TB cases in Russia, for example, could show resistance to first-line drugs currently used to fight the disease, a recent report published in Lancet estimates. Among potential new drug sources are species of the bacterial genus Burkholderia that thrive in a wide range of habitats, from soil to the human lung. One way these microbes have adapted to these diverse environments is by making potent antibiotics to take out their competition. In light of the growing threat of drug-resistant bacteria, particularly among TB strains, Gregory L. Challis, Eshwar Mahenthiralingam and colleagues wanted to see if Burkholderia might produce a promising anti-TB compound.

Source: https://www.acs.org/content/acs/en/pressroom/presspacs/2017/acs-presspac-june-14-2017/bacteria-from-cystic-fibrosis-patient-could-help-thwart-antibiotic-resistant-tb.html

Original Submission

An Anonymous Coward writes:

Dr. Lowe, from In the Pipeline, writes about the origins of MRSA (methicillin-resistant Staphylococcus aureus), a type of multi-drug resistant bacteria that is responsible for approximately 11,000 deaths each year in the US:

OK, everyone recognizes the problem that we face with drug-resistant bacteria. MRSA (methicillin-resistant Staphylococcus aureus) is the most well-known variety, and it's bad news. Penicillin was introduced in the 1940s, and methicillin was brought to market in 1959, largely because so many infections were becoming resistant to penicillin by then. The first methicillin-resistant strains were noted in the early 1960s, which would seem to make the story pretty clear.

But it isn't. [...] MRSA bacteria actually predate the introduction of methicillin. So does that mean that they aren't a product of antibiotic use? Not at all – it's just that the antibiotic that brought them on was penicillin, not methicillin.

From the primary research:

It therefore appears that the first MRSA clone emerged, and developed resistance to two of the earliest antibiotics—streptomycin and penicillin—almost immediately after the S. aureus population would have been first exposed to them.

At the time of its discovery, the incidence of MRSA in the general population is likely to have been very low. This is demonstrated by the fact that screening of over 5000 samples at Public Health England yielded only three methicillin-resistant isolates. Therefore, it is likely that when methicillin was introduced to circumvent penicillin resistance in S. aureus, it did not select for emergence of MRSA at that time, but instead provided the selective pressure, which drove the nosocomial spread of a pre-existing variant, at a time when infection control measures in UK hospitals were limited.

Nosocomial spread: hospital-acquired infection or spread of infections within a hospital.

Blog Post: http://blogs.sciencemag.org/pipeline/archives/2017/08/07/where-mrsa-came-from
Scientific Paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5517843/
MRSA: https://en.wikipedia.org/wiki/Methicillin-resistant_Staphylococcus_aureus

Original Submission

martyb writes:

Researchers have found a way to modify vancomycin — a last-ditch antibacterial — and "supercharge" it to create vancapticins which are far more effective against antibiotic-resistant bacterial infections:

Antibiotic-resistant bacteria – superbugs – cause 700,000 deaths worldwide each year, and a UK government review has predicted this could rise to 10 million by 2050.

[University of Queensland's] Dr Blaskovich said the old drug, vancomycin, was still widely used to treat extremely dangerous bacterial infections, but bacteria were becoming increasingly resistant to it.

“The rise of vancomycin-resistant bacteria, and the number of patients dying from resistant infections that cannot be successfully treated, stimulated our team to look at ways to revitalise old antibiotics,” Dr Blaskovich said.

“We did this by modifying vancomycin’s membrane-binding properties to selectively bind to bacterial membranes rather than those of human cells, creating a series of supercharged vancomycin derivatives called vancapticins.”

The rebooted vancomycin has the potential to treat methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococci (VRE).

[...] “Drug development is normally focused on improving binding to a biological target, and rarely focuses on assessing membrane-binding properties.

“This approach worked with the vancapticins, and the question now is whether it can be used to revitalise other antibiotics that have lost effectiveness against resistant bacteria.

“Given the alarming rise of multi-drug resistant bacteria and the length of time it takes to develop a new antibiotic, we need to look at any solution that could fix the antibiotic drug discovery pipeline now,” Professor Cooper said.

Having been treated for an infection with vancomycin, I can attest it's a scary feeling when, after three days' treatment, the infection commences to spread! Fortunately, an increased dose turned the tide, but it was touch-and-go for a while. Sadly, is this just another step in the cat-and-mouse battle of increasing bacterial resistance?

Journal Reference:

1. Mark A. T. Blaskovich, et. al. Protein-inspired antibiotics active against vancomycin- and daptomycin-resistant bacteria. Nature Communications, 2018; 9 (1) DOI: 10.1038/s41467-017-02123-w

Original Submission

Fnord666 writes:

Colistin is a last resort antibiotic used against multi-drug resistant pathogens. Now scientists have found a strain of bacterium that can evade it.

For the first time, researchers have discovered strains of a deadly, multidrug-resistant bacterium that uses a cryptic method to also evade colistin, an antibiotic used as a last-resort treatment. That's according to a study of US patients published this week by Emory University researchers in the open-access microbiology journal mBio.

The wily and dangerous bacteria involved are carbapenem-resistant Klebsiella pneumoniae or CRKP, which are already known to resist almost all antibiotics available, including other last-line antibiotics called carbapenems. The germs tend to lurk in clinical settings and can invade the urinary tract, bloodstream, and soft tissues. They're members of a notorious family of multidrug-resistant pathogens, called carbapenem-resistant Enterobacteriaceae (CRE), which collectively have mortality rates as high as 50 percent and have spread rapidly around the globe in recent years. A 2013 report by the Centers for Disease Control and Prevention estimated that there were more than 9,300 CRE infections in the US each year, leading to 600 deaths. Both the CDC and the World Health Organization have listed CRE as one of the critical drug-resistant threats to public health, in need of "urgent and aggressive action."

That's what we knew about CRKP before this week.

In the new study, the Emory researchers discovered two strains of CRKP—isolated from the urine of patients in Atlanta, Georgia—that can also resist colistin. But they do so in a poorly understood, surreptitious way. At first, they appear vulnerable to the potent antibiotic in standard clinical tests, but with more advanced testing and exposure to the drug, they reveal that they can indeed survive it. In mice, the strains caused infections that couldn't be cured by colistin and the mice died of the infections. Mice infected with typical CRKP were all saved with colistin.

Original Submission

takyon writes:

A new class of antibiotics to combat drug resistance

Called odilorhabdins, or ODLs, the antibiotics are produced by symbiotic bacteria found in soil-dwelling nematode worms that colonize insects for food. The bacteria help to kill the insect and, importantly, secrete the antibiotic to keep competing bacteria away. Until now, these nematode-associated bacteria and the antibiotics they make have been largely understudied.

[...] UIC's Alexander Mankin and Yury Polikanov are corresponding authors on the study and led the research on the antibiotic's mechanism of action. They found that ODLs act on the ribosome — the molecular machine of individual cells that makes the proteins it needs to function — of bacterial cells. "Like many clinically useful antibiotics, ODLs work by targeting the ribosome," said Polikanov, assistant professor of biological sciences in the UIC College of Liberal Arts and Sciences, "but ODLs are unique because they bind to a place on the ribosome that has never been used by other known antibiotics."

Odilorhabdins, Antibacterial Agents that Cause Miscoding by Binding at a New Ribosomal Site (DOI: 10.1016/j.molcel.2018.03.001) (DX)

Meanwhile, an IBM research team has designed a polymer that can target at least five types of drug-resistant bacteria:

Earlier versions of synthetic polymers created problems because they essentially exploded the bacteria, releasing dangerous toxins into the bloodstream. While other scientists are researching different approaches to avoid resistance, most involve finding new molecules or proteins. IBM's synthetic molecule employs a completely different strategy.

It carries a negative electrical charge, so is drawn — like a magnet — to the positively charged surfaces of infectious cells. Then it binds to the cell, pierces the membrane, enters it and turns the inner liquid contents into solids. The new ninja polymer kills bacteria so quickly, they don't have time to mutate.

The eventual goal, said Hedrick, is to create an entirely new class of therapeutics that could treat a spectrum of infectious diseases with a single mechanism — without the onset of resistance.

Also at IBM.

A macromolecular approach to eradicate multidrug resistant bacterial infections while mitigating drug resistance onset (open, DOI: 10.1038/s41467-018-03325-6) (DX)

Original Submission

Arthur T Knackerbracket has found the following story:

Antimicrobial resistance is on the rise worldwide. This is becoming a problem for infectious diseases like tuberculosis as there are only a few active substances available to combat such diseases. Pharmacists at Martin Luther University Halle-Wittenberg (MLU) have now found a way to increase the efficacy of a common tuberculosis agent while, at the same time, reducing resistance to it. The research group presents its latest developments in the international journal Molecules.

Tuberculosis (TB) is a disease transmitted by the bacterium Mycobacterium tuberculosis and it often affects the respiratory tract. TB is usually treated with antibiotics. "Increasingly, however, bacteria are developing a resistance to common antibiotics," says Professor Andreas Hilgeroth from the Institute of Pharmacy at MLU. If a patient does not respond to the standard treatment, stronger substances are required, which are sometimes accompanied by stronger side-effects. But bacteria can also become resistant to these stronger antibiotics. If a bacterial strain is resistant to several antibiotics, it is termed multi-resistant tuberculosis. In 2016, the World Health Organisation (WHO) recorded 490,000 cases of multi-resistant TB.

To remedy this problem, the researchers from Halle pursued an alternative approach: Instead of developing a new active substance, they sought a way to improve the efficacy of the existing drugs. The tuberculosis bacteria defend themselves against the antibiotics by pumping the substances out of their cell interior before they can take effect. "If this pumping mechanism is blocked, or at least hindered, inside the bacteria, this could improve the efficacy of current drugs," Hilgeroth adds. The pharmacists developed a new chemical compound, combined it with conventional tuberculosis antibiotics and tested the effectiveness. They were able to demonstrate that the compound achieves very good results with the antibiotic isoniazid, and blocks the pumping mechanism in the bacteria. "This improves the effects of the isoniazid," concludes Hilgeroth.

Journal reference: Fabian Lentz, Norbert Reiling, Ana Martins, Joseph Molnár, Andreas Hilgeroth. Discovery of Novel Enhancers of Isoniazid Toxicity in Mycobacterium tuberculosis. Molecules, 2018; 23 (4): 825 DOI: 10.3390/molecules23040825

Original Submission

MrPlow writes:

Submitted via IRC for takyon

There’s a little-known sexually transmitted disease (STD) that’s on the rise – and could soon become a very big problem.

Sexual health experts warn that Mycoplasma genitalium (MG) has the potential to become a drug-resistant superbug within a matter of years.

Research by the British Association for Sexual Health and HIV (BASHH) found that over 70 percent of sexual health experts said that if current practices do not change, MG will become resistant to first and second line antibiotics within a decade. Left unchecked, they say this could result in thousands of women each year at increased risk of infertility from pelvic inflammatory disease caused by MG.

As a result of these daunting statistics, BASHH have just released draft guidelines to help the public and health services deal with this impending crisis.

“MG is rapidly becoming the new superbug: it’s increasingly resistant to most of the antibiotics we use to treat chlamydia and changes its pattern of resistance during treatment so it's like trying to hit a moving target,” Dr Peter Greenhouse, sexual health consultant from the UK, said in a statement.

Source: http://www.iflscience.com/health-and-medicine/this-littleknown-std-could-become-the-next-superbug-within-a-decade/

Original Submission

takyon writes:

Bacteria are becoming resistant to alcohol-based disinfectants:

Because of the growing numbers of so-called superbugs, hospitals have introduced more stringent cleaning routines. Part of the regimen involves alcohol-based disinfectants, such as hand rubs, positioned in and around hospital wards. Since their introduction, there has been a significant reduction in the number of hospital-based infections. Containing 70 percent isopropyl or ethyl alcohol, alcohol-based hand rubs kill bacteria quickly and effectively.

Over recent years, researchers have noted a steady rise in the number of serious infections caused by one particular drug-resistant bacterium — Enterococcus faecium. Despite the wide use of alcohol-based disinfectants, E. faecium is now a leading cause of hospital-acquired infections. Dr. Sacha Pidot and his colleagues at the University of Melbourne in Australia set out to understand whether this increased infection rate might be because the bacterium is growing resistant to alcohol. Their findings were published this week in the journal Science Translational Medicine [DOI: 10.1126/scitranslmed.aar6115] [DX].

Also at Live Science.

Increasing tolerance of hospital Enterococcus faecium to handwash alcohols:

Arthur T Knackerbracket writes:

Story:

Scientists have traditionally believed that combining more than two drugs to fight harmful bacteria would yield diminishing returns. The prevailing theory is that that the incremental benefits of combining three or more drugs would be too small to matter, or that the interactions among the drugs would cause their benefits to cancel one another out.

Now, a team of UCLA biologists has discovered thousands of four- and five-drug combinations of antibiotics that are more effective at killing harmful bacteria than the prevailing views suggested. Their findings, reported today in the journal npj Systems Biology and Applications, could be a major step toward protecting public health at a time when pathogens and common infections are increasingly becoming resistant to antibiotics.

[...] Working with eight antibiotics, the researchers analyzed how every possible four- and five-drug combination, including many with varying dosages a total of 18,278 combinations in all worked against E. coli. They expected that some of the combinations would be very effective at killing the bacteria, but they were startled by how many potent combinations they discovered.

[...] Yeh added that although the results are very promising, the drug combinations have been tested in only a laboratory setting and likely are at least years away from being evaluated as possible treatments for people.

"With the specter of antibiotic resistance threatening to turn back health care to the pre-antibiotic era, the ability to more judiciously use combinations of existing antibiotics that singly are losing potency is welcome," said Michael Kurilla, director of the Division of Clinical Innovation at the National Institutes of Health/National Center for Advancing Translational Science. "This work will accelerate the testing in humans of promising antibiotic combinations for bacterial infections that we are ill-equipped to deal with today."

Original Submission

Arthur T Knackerbracket has found the following story:

Gram-negative bacteria like the Klebsiella pneumoniae... have an outer membrane that makes them impervious to many drugs, but a new compound from Genentech can breach the border and cripple them.

[...] A team led by evolutionary biologist Peter Smith at Genentech, the biotech pioneer in South San Francisco, California, began with a class of natural compounds called arylomycins. Various arylomycins can penetrate the outer membrane of gram-negatives, but they have trouble binding to their target, an enzyme embedded in the inner membrane that juts into the space between the inner and outer walls. So Smith and colleagues chemically modified an arylomycin to "systematically optimize" it such that the drug could more easily reach that space—and bind to the enzyme.

The molecule they created, dubbed G0775, was at least 500 times more potent than a naturally found arylomycin against some of the biggest gram-negative bacterial threats to humans, including Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Acinetobacter baumannii. What's more, it remained potent against all 49 isolates of multidrug-resistant forms of these bacteria that the researchers obtained from patients. In a coup de grâce, when tested against a notoriously drug-resistant strain of K. pneumoniae that has defied 13 different classes of antibiotics, G0775 walloped the bacterium in lab dish experiments, they report today in Nature. "We're really excited," Smith says. "We've made the necessary changes to the molecules so that they can hit the real deal."

G0775 also showed in mice it could stymie infections from six strains of four different gram-negative bacteria. It also hasn't exhibited any potential toxicities in mammalian cells. But the road to antibiotic approval is littered with compounds that later proved toxic in larger animals or during early human trials—or that simply failed to retain their potency.

doi:10.1126/science.aav4019

Original Submission

upstart writes:

Submitted via IRC for Bytram

A new drug may boost dwindling treatment options for gonorrhea

Gonorrhea is a wily foe. But doctors may soon have another drug to fight the sexually transmitted infection that's become resistant to nearly every antibiotic thrown its way. In clinical trials, a new antibiotic was effective at stopping the bacteria that causes the disease.

A single oral dose of the drug, called zoliflodacin, cured 96 percent of people who had gonorrhea infections in the urinary and genital organs, researchers report in the Nov. 8 New England Journal of Medicine. In comparison, 100 percent of patients given ceftriaxone — the remaining antibiotic that's effective against the disease in the United States — were successfully treated.

Caused by Neisseria gonorrhoeae, gonorrhea can be passed from an infected person to a sexual partner or from an infected mother to her baby at birth. The consequences of the infection are especially severe for women, who can develop pelvic inflammatory disease and become infertile (SN: 6/10/00, p. 376), and for babies, who can lose their sight. The United States had more than half a million new gonorrhea cases reported in 2017, up about 75 percent from the historical low point in 2009. Worldwide, an estimated 78 million new gonorrhea infections occur each year.

[...] A larger, international clinical trial of the drug is underway.

Original Submission

Arthur T Knackerbracket has found the following story:

Researchers analysing soil from Ireland long thought to have medicinal properties have discovered that it contains a previously unknown strain of bacteria which is effective against four of the top six superbugs that are resistant to antibiotics, including MRSA.

[...] They have named the new strain Streptomyces sp. myrophorea.

The soil they analysed originated from an area of Fermanagh, Northern Ireland, which is known as the Boho Highlands. It is an area of alkaline grassland and the soil is reputed to have healing properties.

The search for replacement antibiotics to combat multi-resistance has prompted researchers to explore new sources, including folk medicines: a field of study known as ethnopharmacology. They are also focusing on environments where well-known antibiotic producers like Streptomyces can be found.

One of the research team, Dr Gerry Quinn, a previous resident of Boho, County Fermanagh, had been aware of the healing traditions of the area for many years.

Traditionally a small amount of soil was wrapped up in cotton cloth and used to heal many ailments including toothache, throat and neck infections. Interestingly, this area was previously occupied by the Druids, around 1500 years ago, and Neolithic people 4000 years ago.

[...] The main findings of the research were that the newly-identified strain of Streptomyces:

RandomFactor writes:

According to the CDC a suberbug acquired during bariatric surgery in Tijuana just got worse.

The superbug that infected nearly a dozen Americans who recently underwent weight-loss surgery at a Tijuana hospital had a particularly nasty genetic mutation that set off alarm bells after patients began showing up in hospitals and doctors officers[sic] with painful wounds.

Pseudomonas is a common bacteria found normally in the environment the world over and generally poses little threat unless you have a weakened immune system or are sick.

Dr. David “Cal” Ham, a CDC medical officer, said Friday that the particular strain of pseudomonus bacteria involved in 11 confirmed cases had metallo-beta lactamase genes. Often called “VIM” by the epidemiological community, Ham explained that these genes cause the microbes that carry them to excrete enzymes that destroy carbapenems, a workhorse class of antibiotics with some of the broadest efficacy in medicine.

One patient has died, some have recovered, and others

are still in hospitals suffering as doctors work down a dwindling list of available options.

Dr. Ham added

“Several of the isolates involved are susceptible only to a couple of, I would say, less-than-optimal antibiotics that have significant side effect profiles.”

The pseudomonus strains in question were already drug resistant, adding the ability to ward off carbapenems makes the already serious threat even more deadly.

The inexorable decline of antibiotics continues.

Original Submission

upstart writes:

Submitted via IRC for Bytram

'Superbug gene' found in one of the most remote places on Earth

Soil samples taken in the Kongsfjorden region of Svalbard have now confirmed the spread of blaNDM-1 into the High Arctic -- an ARG [antibiotic-resistant genes] originally found in Indian clinical settings, which conditionally provides multidrug resistance (MDR) in microorganisms.

Worldwide spread of blaNDM-1 and other MDR genes is a growing concern because they often target "last resort" classes of antibiotics, including Carbapenems.

Carried in the gut of animals and people, the research team, led by Newcastle University's Professor David Graham, say that blaNDM-1 and other medically-important ARGs were found in Arctic soils that were likely spread in the faecal matter of birds, other wildlife and human visitors to the area.

"Polar regions are among the last presumed pristine ecosystems on Earth, providing a platform for characterizing pre-antibiotic era background resistance against which we could understand rates of progression of AR 'pollution'," says Professor Graham, an environmental engineer at Newcastle University who has spent 15 years studying the environmental transmission of antibiotic resistance around the world.

"But less than three years after the first detection of the blaNDM-1 gene in the surface waters of urban India we are finding them thousands of miles away in an area where there has been minimal human impact. "Encroachment into areas like the Arctic reinforces how rapid and far-reaching the spread of antibiotic resistance has become, confirming solutions to AR must be viewed in global rather than just local terms."

[...] Published today in the academic journal Environmental International, this latest research was carried out by an international team of experts from the Universities of Newcastle, York and Kansas and the Chinese Academy of Science in Xiamen, and was funded by the UK Natural Environmental Research Council and other agencies.

Analysing the extracted DNA from forty soil cores at eight locations along Kongsfjorden, a total of 131 ARGs were detected.

"The resistance genes detected were associated with nine major antibiotic classes, including aminoglycosides, macrolides and β-lactams, which are used to treat many infections. As an example, a gene that confers MDR in Tuberculosis was found in all cores, whereas blaNDM-1 was detected in more than 60% of the soil cores in the study.

"This finding has huge implications for global AR spread," warns Graham. "A clinically important ARG originating from South Asia is clearly not 'local' to the Arctic."

Journal Reference:
Clare McCann, Beate Christgen, Jennifer Roberts, Jian-Qiang Su, Kathryn Arnold, Neil Gray, Yong-Guan Zhu and David Graham. Understanding drivers of antibiotic resistance genes in High Arctic soil ecosystems. Environment International, 2019

Original Submission

upstart writes:

Submitted via IRC for AzumaHazuki

Deadly germs, Lost cures: A Mysterious Infection, Spanning the Globe in a Climate of Secrecy [Editor's Comment: Link has disappeared.]

https://www.nytimes.com/2019/04/06/health/drug-resistant-candida-auris.html [Alternative Link]

Last May, an elderly man was admitted to the Brooklyn branch of Mount Sinai Hospital for abdominal surgery. A blood test revealed that he was infected with a newly discovered germ as deadly as it was mysterious.

Doctors swiftly isolated him in the intensive care unit. The germ, a fungus called Candida auris, preys on people with weakened immune systems, and it is quietly spreading across the globe.

Over the last five years, it has hit a neonatal unit in Venezuela, swept through a hospital in Spain, forced a prestigious British medical center to shut down its intensive care unit, and taken root in India, Pakistan and South Africa .

Recently C. auris reached New York, New Jersey and Illinois, leading the federal Centers for Disease Control and Prevention to add it to a list of germs deemed "urgent threats."

The man at Mount Sinai died after 90 days in the hospital, but C. auris did not. Tests showed it was everywhere in his room, so invasive that the hospital needed special cleaning equipment and had to rip out some of the ceiling and floor tiles to eradicate it.

"Everything was positive — the walls, the bed, the doors, the curtains, the phones, the sink, the whiteboard, the poles, the pump," said Dr. Scott Lorin, the hospital's president. "The mattress, the bed rails, the canister holes, the window shades, the ceiling, everything in the room was positive."

upstart writes:

Submitted via IRC for Bytram

Fecal transplants may be best answer to antibiotic-resistant bacteria: Non-pharmaceutical treatment combats recurring Clostridium Difficile infections

Transplanting human donor fecal microbiota into the colon of a patient infected with Clostridiodes difficile (C. diff) may be the best treatment for those not helped by C. diff targeted antibiotics, according to an article in the Journal of the American Osteopathic Association.

C. diff is the most common healthcare-acquired infection in the United States. It affects nearly half a million patients each year and becomes a recurring infection for nearly a third of them. If untreated, C. diff can lead to sepsis and death.

"Twenty five years ago C. diff infections were easier to manage and often resolved with discontinuation of the initiating antibiotic," says Robert Orenstein, DO, an infectious disease specialist at Mayo Clinic and lead author on this article. "However, these infections have become increasingly common and pernicious."

RandomFactor writes:

Genetically engineered phage therapy has rescued a teenager on the brink of death

Isabelle Holdaway received a lung transplant and in the process picked up an antibiotic-resistant infection.
She was sent home from the hospital underweight, with liver failure, and with skin lesions from the infection. Her survival odds were "less than 1%."

Her consultant at Great Ormond Street Hospital in London worked with a team at the University of Pittsburgh to develop an untested phage therapy. This treatment used a cocktail of three phages: viruses that solely attack and kill bacteria. Two of the three phages, selected from a library of more more than 10,000 kept at the University of Pittsburgh, had been genetically engineered to be better at attacking the bacteria. The therapy was injected into her blood stream twice daily and applied to the lesions on her skin, according to Nature Medicine.

With this therapy, which is still ongoing, "virtually all her lesions have cleared." Her treatment team is planning to add a fourth phage to the treatment in hopes of clearing the infection completely.

The article notes this is a deeply personalized therapy approach and to be careful extrapolating from a single case study. Still, with the rise in antiobiotic resistance in bacteria in recent years, using viruses to kill superbugs has been getting attention.

Original Submission

RandomFactor writes:

A study led by scientists at Emory Univeristy has shown that extracts from plants used in the South during the civil war have antimicrobial properties effective against several modern multi-drug resistant bacteria.

During the height of the Civil War, the Confederate Surgeon General commissioned a guide to traditional plant remedies of the South, as battlefield physicians faced high rates of infections among the wounded and shortages of conventional medicines. A new study of three of the plants from this guide -- the white oak, the tulip poplar and the devil's walking stick -- finds that they have antiseptic properties.

The antebellum antimicrobials, harvested right on campus, were found to be effective in testing against modern Acinetobacter baumannii, Staphylococcus aureus and Klebsiella pneumoniae

"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 guide was named the "Standard supply table of the indigenous remedies for field service and the sick in general hospitals." and lists botanical names, dosages, and medical properties of various native southern plants.

Even so, amputation was a common treatment for infected wounds and one in 13 surviving Civil War soldiers went home missing one or more limbs.

Journal Reference: Micah Dettweiler, James T. Lyles, Kate Nelson, Brandon Dale, Ryan M. Reddinger, Daniel V. Zurawski, Cassandra L. Quave. American Civil War plant medicines inhibit growth, biofilm formation, and quorum sensing by multidrug-resistant bacteria. Scientific Reports, 2019; 9 (1) DOI: 10.1038/s41598-019-44242-y

Original Submission

takyon writes:

Artificial life form given 'synthetic DNA'

UK scientists have created an artificial version of the stomach bug E. coli that is based on an entirely synthetic form of DNA. At the same time, Syn61 as they are calling it, has had its genetic code significantly redesigned. It's been done in a manner that will pave the way for designer bacteria that could manufacture new catalysts, drugs, proteins and materials.

[...] Syn61's 4 million genetic letters make this the largest entire genome to be synthesised from scratch. They were ordered in short segments from a laboratory supplies company, before being assembled into half-million-letter lengths in yeast cells by natural cellular machinery.

At this point, the genome engineers' job became a bit like a railway engineer's maintenance programme - replacing the E. coli genome piecewise - section by section - rather than all at once. "The bacterial chromosome is so big," team leader Jason Chin told the BBC, "we needed an approach that would let us see what had gone wrong if there had been any mistakes along the way." So it was only after each half-million-letter segment had been tested in partially synthetic bacteria that the eight segments were brought together in Syn61.

The approach is more cautious than that used by bio-entrepreneur, Craig Venter, whose microbial replicant based on the tiny organism Mycoplasma genitalium was presented to the world in 2010.

Also at PLOS, NYT, and Smithsonian.

Total synthesis of Escherichia coli with a recoded genome (DOI: 10.1038/s41586-019-1192-5) (DX)

Original Submission