Marine biofilms as reservoirs of antimicrobial bacteria

A new research paper of interest:

Marine biofouling communities constitute a rich reservoir of microbial diversity and represent a promising source of bioactive metabolites. In this study, we investigated culturable epibiotic bacteria associated with fouling invertebrates from the Marina in northern Tunisia, with a focus on their enzymatic activities, antimicrobial potential, and antibiotic resistance profiles. A total of 52 bacterial isolates were recovered from 23 fouling invertebrate hosts and characterized using DNA barcoding and molecular identification. 

The epibiotic culturable bacterial community was dominated by members of the genera Vibrio, Photobacterium, Halomonas, and Pseudomonas. Enzymatic screening revealed a high hydrolytic potential, with DNase (71.2%), lipase (65.4%), and gelatinase (59.6%) being the most prevalent activities. Antimicrobial assays showed that a substantial proportion of isolates exhibited inhibitory activity against at least one pathogenic indicator strain, whereas antibiotic susceptibility testing revealed frequent resistance, particularly to fosfomycin and cefoxitin. Together, these findings highlight the dual nature of epibiotic culturable bacteria in the Marina in northern Tunisia, acting both as a reservoir of biotechnologically valuable antimicrobial producers and as potential carriers of antibiotic resistance, underscoring their ecological relevance and public health significance in Mediterranean coastal ecosystems.

The paper is titled "Marine biofilms as reservoirs of antimicrobial bacteria: molecular identification and functional characterization of epibiotic culturable communities from biofouling invertebrates in northern Tunisia."

To access, see Frontiers 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

Latest twist with the antimicrobial properties of graphene

 

Image by: AlexanderAlUS CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=11294534  

Scientists have uncovered how graphene oxide pulls off a remarkable trick: it hunts down and destroys harmful bacteria while leaving human cells completely unharmed. By targeting a molecule found only in bacterial membranes, this ultra-thin carbon-based material acts with laser-like precision—offering a powerful new alternative to traditional antibiotics. Even more exciting, it works against drug-resistant “superbugs,” promotes faster wound healing, and keeps its antibacterial strength even after repeated washing.

Hygiene is essential for everyday items that come into close contact with the body, including clothing, masks, and toothbrushes. Scientists have now uncovered how graphene can selectively eliminate bacteria while leaving human cells unharmed. This discovery points to a new class of antibacterial materials that could be both safe for people and capable of reducing reliance on traditional antibiotics.

Recently, KAIST announced that a collaborative research team led by Professor Sang Ouk Kim from the Department of Materials Science and Engineering and Professor Hyun Jung Chung from the Department of Biological Sciences identified the mechanism behind the antibacterial properties of Graphene Oxide (GO). This material consists of a single atomic layer of carbon with oxygen groups attached, giving it the ability to disperse well in water and perform a range of functions.

Until now, scientists did not fully understand how graphene achieved its antibacterial effects. This study provides clear molecular-level evidence explaining how the material works.

Selective Antibacterial Action Explained

The researchers found that graphene oxide carries out what they describe as "selective antibacterial action." It attaches to and disrupts the membranes of bacteria while leaving human cells unaffected. The process is similar to how a magnet only sticks to certain metals.

This selectivity comes from oxygen-containing groups on the surface of graphene oxide. These groups bind specifically to a molecule called POPG, which is found in bacterial cell membranes but not in human cells. In simple terms, graphene oxide identifies a unique feature of bacteria, attaches to it, and breaks down the cell structure. Phospholipids make up the membrane surrounding cells, and POPG is a type mainly present in bacteria.

Effective Against Superbugs and Promotes Healing

When applied in nanofiber form, this material was able to stop the growth of a wide range of harmful bacteria, including antibiotic-resistant superbugs. Tests in animals also showed that it helped wounds heal more quickly without causing inflammation.

Another advantage is durability. Fibers made with graphene oxide retained their antibacterial properties even after repeated washing, suggesting strong potential for use in clothing, medical fabrics, and other practical applications.

From Lab Discovery to Real-World Products

This technology is already being used in consumer products. A graphene antibacterial toothbrush developed through patents from the faculty-led startup 'Materials Creation Co., Ltd.,' has sold more than 10 million units, demonstrating strong commercial success. In addition, GrapheneTex, a textile material incorporating this technology, was used in uniforms worn by the Taekwondo demonstration team at the 2024 Paris Olympics.

For further details see:

Sujin Cha, Ju Yeon Chung, Seungju Yang et al.. Biocompatible but Antibacterial Mechanism of Graphene Oxide for Sustainable Antibiotics. Advanced Functional Materials, 2026; DOI: 10.1002/adfm.74695 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

Genomes reveal five E. coli 'armor' types behind most multidrug-resistant bloodstream infections

                                                            Image designed by Tim Sandle

The first large-scale genetic study of E. coli's protective armour has identified the five capsule types that are responsible for 70% of all multidrug-resistant bloodstream infections in Europe. Researchers, including those at the Wellcome Sanger Institute, the University of Oslo, and their collaborators, analysed over 18,000 bacterial genomes from samples across all continents to investigate E. coli's armour and find new ways to penetrate it. 

Provided by Wellcome Trust Sanger Institute 

The study, published in Nature Microbiology, uncovered 90 different types of protective capsules, of which only 34% had been previously documented. The team also identified the capsule types that enable the bacterium to have the highest invasive potential, meaning it can transition from a harmless gut resident to a dangerous bloodstream invader.

By providing a blueprint of the armor that each E. coli strain has, this research can help in designing targeted vaccines and new treatments that can combat the most dangerous strains of E. coli while minimizing harm to beneficial strains of E. coli gut bacteria.

Science and microbiology gifts via Babbling Bacteria 

Escherichia coli (E. coli) is the leading cause of bloodstream infections worldwide. Most strains of E. coli are harmless and commonly found in the gut, however, if the bacterium gets into the bloodstream or the urinary tract, it can cause infections that range from mild to severe, particularly in people with a weakened immune system.

As an added challenge for health care providers, antibiotic resistance has become a frequent feature of such infections. Rates of antibiotic resistance in E. coli vary globally and, in the UK, over 40% of E. coli bloodstream infections are resistant to a key antibiotic.

Some bacteria, such as E. coli, have protective capsules that help shield the bacteria from the immune system and certain treatments, influencing the bacteria's ability to cause infections. Each bacterial strain has a different capsule makeup, and the capsules have markers, called antigens.

These antigens are often used as targets for new vaccines and treatments. However, for effective therapies to be developed, researchers need to know which capsule commonly causes the infection.

Traditional methods of mapping E. coli capsules are labor-intensive and uncommon. To address this, the team at the Sanger Institute and their collaborators genetically analyzed 18,000 E. coli samples. This allowed them to create the first digital database mapping capsule type and E. coli strain. They were then able to determine how common each type is using samples from nearly 8,000 people, ranging from newborns to those over 80 years old.

They found that capsule types are much more diverse than previously thought, mapping 90 different types, including 69 that had not been previously documented. The team also noted that different capsules were common in high-resource settings, such as the UK, compared to less industrialized regions such as Malawi and Pakistan.

For example, the researchers found that five specific capsule types (K1, K5, K52, K2, and K14) account for over 50% of all E. coli bloodstream infections and urinary tract infections across the UK, Norway, and France. Furthermore, a slightly different set (K1, K5, K52, K2, and K100) is responsible for 70% of multidrug-resistant E. coli infections in Europe.

While two of these (K1 and K5) do cause infections globally, there is more diversity in the strains that cause serious infections in low and middle-income countries than in Europe.

Due to these differences, the researchers highlight the importance of global data in future research, especially around drug and vaccine development, as the bacterial capsule types being targeted would vary depending on where the individual lived.

The team also found that E. coli has the ability to swap the genes that encode the capsule, sharing the information to build different types of armor between them.

Dr. Rebecca Gladstone, first and corresponding author at the University of Oslo, said, "By creating a digital library from over 18,000 bacterial genomes, we can see the true complexity of how E. coli protects itself, and how this armor is encoded in the genes. This research has expanded our scientific map from just a handful of known bacterial shields to a comprehensive database of 90 unique types, including nearly two-thirds that were previously unknown.

"Ultimately, this database provides the missing blueprint to identify strains most likely to cause serious infections, and design targeted vaccines and treatments to stop these."

Professor Jukka Corander, senior author at the Wellcome Sanger Institute and the University of Oslo, said, "This new research enables us to identify the strains of E. coli that are the biggest threats to human health. With this database, we can now see the bacterial capsule types that are prevalent in different countries, whether they cause serious infections, or if they are resistant to treatments.

"What our research also shows is the stark differences between capsule groups found in different regions, highlighting the need for systematic and standardized global data collection. Especially as we have found that E. coli can trade the genes for their protective shields between different genetic lineages.

"Understanding how these bacteria, especially the most drug-resistant ones, swap their coats, and having the global data to track this, is crucial for staying one step ahead of them in the fight against serious bloodstream infections."

Dr. Trevor Lawley, co-author at the Wellcome Sanger Institute, said, "Our microbiomes are made up of thousands of bacteria, and while the majority of these are beneficial, some strains can cause infections if they get into the bloodstream, such as E. coli.

"Large-scale population studies, such as the Baby Biome study, that provide a high-resolution view into the microbiome are essential for understanding the risk associated with certain bacterial strains, the genetic tools they use to cause infections, and how often they are found in the population.

"Understanding and tracking the E. coli strains that are most able to use their protective shield to move into the bloodstream and cause infection allows for the development of future targeted treatments while minimizing the harmful effects on the microbiome."

Publication details

Identification of transporter-dependent capsular K loci associated with invasive potential of Escherichia coli, Nature Microbiology (2026). DOI: 10.1038/s41564-026-02283-w

Journal information: Nature Microbiology 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

List of new antibiotics approved since 2000

List of antibiotics,  since 2000:

 2000: Linezolid (Zyvox) — The first oxazolidinone, a new class effective against vancomycin-resistant enterococci (VRE) and MRSA.

2003: Daptomycin (Cubicin) — The first lipopeptide approved for skin and skin structure infections.

2005: Tigecycline (Tygacil) — First glycylcycline, a derivative of minocycline designed to overcome resistance. 

2010: Ceftaroline fosamil (Teflaro) — First cephalosporin with activity against MRSA.

2011: Fidaxomicin (Dificid) — A macrocyclic antibiotic for Clostridioides difficile.

2012: Bedaquiline (Sirturo) — First diarylquinoline for multi-drug resistant tuberculosis (MDR-TB).

2014: Dalbavancin (Dalvance) & Oritavancin (Orbactiv) — Lipoglycopeptides for acute bacterial skin and skin structure infections (ABSSSI).

2014: Tedizolid (Sivextro) — A second-generation oxazolidinone.

2014: Ceftolozane/tazobactam (Zerbaxa) — Cephalosporin/β-lactamase inhibitor combination.

2015: Ceftazidime/avibactam (Avycaz) — Novel β-lactamase inhibitor combination for serious Gram-negative infections.

2017: Meropenem/vaborbactam (Vabomere) — Combination targeting carbapenem-resistant Enterobacteriaceae (CRE).

2017: Delafloxacin (Baxdela) — An anionic fluoroquinolone with activity against MRSA.

2017: Ozenoxacin (Ozanex) — Topical quinolone.

2018: Plazomicin (Zemdri) — Next-generation aminoglycoside.

2018: Eravacycline (Xerava) — Novel synthetic fluorocycline.

2018: Omadacycline (Nuzyra) — Aminomethylcycline for pneumonia and skin infections.

2018: Sarecycline (Seysara) — Tetracycline for acne.

2019: Cefiderocol (Fetroja) — Siderophore cephalosporin for MDR Gram-negative infections.

2019: Lefamulin (Xenleta) — First systemic pleuromutilin for community-acquired pneumonia (CABP).

2019: Pretomanid — Nitroimidazole for extensively drug-resistant TB (XDR-TB)

 

The Threat: Microbes change over time, rendering drugs ineffective and leading to "superbugs".

Causes: Overuse of antibiotics for viral infections (like colds/flu), not finishing prescribed courses, and environmental contamination.

Prevention: Proper antimicrobial stewardship, including only using them when prescribed and practicing good hygiene to prevent infections.

 

 Thanks to Microbiology Matters for the list. 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

New insights into antimicrobial tolerance

Antimicrobial tolerance is

the ability of a normally susceptible, often dormant, bacterial population to survive, rather than die, during extended exposure to bactericidal drugs without changing their minimum inhibitory concentration (MIC). Unlike resistance, which allows growth despite drugs, tolerant bacteria temporarily endure treatment, leading to chronic, relapsing infections and potential evolution into resistant strains. This represents an important area of inquiry for pharmaceutical microbiologists. 

 

The following video provides some insights, looking at recent research: 

 

 

 

Key Aspects of Antimicrobial Tolerance:

• Mechanism: Often involves low metabolic states (dormancy) or specialized stress responses (e.g., SOS DNA damage repair, cell envelope stress systems).
• Persistence vs. Tolerance: Tolerance typically describes the survival of the entire population, whereas persistence describes a small subpopulation ("persister cells") that survives high drug concentrations.
• Clinical Impact: Contributes to treatment failure in infections like tuberculosis, as bacteria "reawaken" once the antibiotic is removed.
• Distinction from Resistance: Tolerant cells do not grow in the presence of the drug, unlike resistant cells.
• Evolutionary Role: Tolerance can serve as a stepping stone for the development of full resistance.

Common Tolerance Mechanisms:

• Metabolic Slowdown: Reduced metabolic rate makes cells less susceptible to metabolic-dependent antibiotics.
• Biofilm Formation: Bacteria in biofilms often exhibit higher tolerance due to nutrient limitation and stress responses.
• Stress Responses: Activation of pathways (e.g., SOS response) that repair damage caused by antibiotics.

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

5,000 year old ice cave bacterium resists modern antibiotics

 Cave. Image by Tim Sandle

Bacteria are remarkably adaptable, thriving in some of the harshest places on Earth, from boiling hot springs to deep freezes far below zero. Ice caves are one such extreme habitat, home to diverse microorganisms that scientists are only beginning to understand. These frozen environments may contain vast stores of genetic material that have gone largely unexplored. 

Deep inside a Romanian ice cave, locked away in a 5,000-year-old layer of ice, scientists have uncovered a bacterium with a startling secret: it’s resistant to many modern antibiotics. Despite predating the antibiotic era, this cold-loving microbe carries more than 100 resistance-related genes and can survive drugs used today to treat serious infections like tuberculosis and UTIs.

Psychrobacter 

The Psychrobacter SC65A.3 bacterial strain isolated from Scarisoara Ice Cave, despite its ancient origin, shows resistance to multiple modern antibiotics and carries over 100 resistance-related genes.

The bacterium can also inhibit the growth of several major antibiotic-resistant 'superbugs' and shows important enzymatic activities with important biotechnological potential.

Psychrobacter SC65A.3 belongs to a group of cold-adapted bacteria known as Psychrobacter. While some members of this genus can cause infections in people or animals, they are also considered promising for biotechnology applications. Until now, however, little was known about how these bacteria respond to antibiotics. 

Studying microbes such as Psychrobacter SC65A.3 retrieved from millennia-old cave ice deposits reveals how antibiotic resistance evolved naturally in the environment, long before modern antibiotics were ever used.

How the organism was isolated 

To retrieve the organism, the team drilled a 25-meter ice core from a section of the cave called the Great Hall, capturing a frozen record spanning 13,000 years. To prevent contamination, ice samples were sealed in sterile bags and transported in frozen conditions back to the laboratory. There, scientists isolated bacterial strains and sequenced their genomes to identify genes responsible for surviving extreme cold, as well as genes linked to antimicrobial resistance and activity.

The researchers then tested SC65A.3 against 28 antibiotics across 10 different classes. These drugs are commonly prescribed or reserved for serious bacterial infections. Some had already been associated with known resistance genes or mutations, allowing the team to compare predicted resistance mechanisms with actual laboratory results. "The 10 antibiotics we found resistance to are widely used in oral and injectable therapies used to treat a range of serious bacterial infections in clinical practice," Purcarea noted. Among them were rifampicin, vancomycin, and ciprofloxacin, medications used to treat conditions such as tuberculosis, colitis, and UTIs.

SC65A.3 is the first Psychrobacter strain found to resist certain antibiotics, including trimethoprim, clindamycin, and metronidazole. These drugs are typically used to treat UTIs and infections affecting the lungs, skin, bloodstream, and reproductive system. The strain's resistance profile suggests that bacteria adapted to cold environments could serve as reservoirs of resistance genes, which are segments of DNA that enable survival when exposed to antibiotics.

Significance of the discovery 

Genetic analysis of Psychrobacter SC65A.3 revealed nearly 600 genes with unknown functions, pointing to a largely untapped resource for uncovering new biological processes. The team also identified 11 genes that may have the ability to kill or inhibit bacteria, fungi, and even viruses.

As antibiotic resistance continues to rise worldwide, insights from ancient microbes are becoming increasingly valuable. Studying genomes preserved in ice helps scientists trace how resistance emerged and spread long before modern medicine existed.

Research paper

Victoria Ioana Paun, Corina Itcus, Paris Lavin, Mariana Carmen Chifiriuc, Cristina Purcarea. First genome sequence and functional profiling of Psychrobacter SC65A.3 preserved in 5,000-year-old cave ice: insights into ancient resistome, antimicrobial potential, and enzymatic activities. Frontiers in Microbiology, 2026; 16 DOI: 10.3389/fmicb.2025.1713017 

 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

Fully synthetic bacteriophage engineering system propels long-obstructed bacteriophage research

 

As antibiotic-resistant infections increasingly threaten public health, interest in bacteriophages as therapeutics has seen a resurgence. However, laborious strain engineering techniques have limited the pace of discovery and the creation of tailored therapeutic strains. 

In a PNAS study scheduled for publication on January 23rd, researchers from New England Biolabs and Yale University describe the first fully synthetic bacteriophage engineering system for Pseudomonas aeruginosa, an antibiotic-resistant bacterium of global concern. 

By leveraging golden gate assembly, the method:

• Uses digital sequence data rather than bacteriophage isolates

• Removes the need to propagate physical phage isolates or specialized host bacteria

• Allows for many simultaneous edits instead of iterative editing

• Works with therapeutically relevant bacteriophages that have previously required extremely specialized expertise to study
  
  

A related study, which described engineering high-GC content Mycobacterium (tuberculosis) phages, was published in November, and a December study applied the method to engineer biosensing bacteriophages for detecting E. coli in drinking water.

 

Some antibiotics stop bacteria from growing without actually killing them, allowing infections to return later. Scientists at the University of Basel created a new test that tracks individual bacteria to see which drugs truly eliminate them. When tested on tuberculosis and other serious lung infections, the method revealed big differences in how bacteria tolerate treatment. The findings could lead to more precise therapies and better predictions of treatment success.

Dormant Bacteria and Lingering Infections

Even bacteria that are not resistant can sometimes survive antibiotic treatment. This often happens when bacteria enter a dormant state. In this condition, they stop multiplying, but antibiotics may fail to kill them. Once treatment ends, these dormant bacteria can become active again and restart the infection.

This challenge is especially severe in diseases such as tuberculosis and other complex infections that require many months of therapy. In such cases, choosing drugs that fully eliminate bacteria and completely clear the infection is essential.

A New Way to Predict Treatment Success

Traditional laboratory tests mainly show whether a drug prevents bacteria from growing, rather than confirming whether the bacteria are dead. To overcome this limitation, researchers led by Dr. Lucas Boeck from the Department of Biomedicine at the University of Basel and University Hospital Basel developed a new testing method designed to better predict real world treatment outcomes. Their findings were published in the scientific journal Nature Microbiology.

The new approach, known as "antimicrobial single-cell testing," uses advanced microscopy to observe millions of individual bacteria across thousands of different test conditions. "We use it to film each individual bacterium over several days and observe whether and how quickly a drug actually kills it," explains Lucas Boeck.

This technique allows researchers to determine exactly how many bacteria are eliminated by a treatment and how efficiently that elimination occurs across an entire bacterial population.

To demonstrate the method, the team tested 65 different drug combinations against Mycobacterium tuberculosis, the bacterium responsible for tuberculosis. They also applied the approach to bacterial samples from 400 patients with another severe lung infection caused by Mycobacterium abscessus, a close relative of the tuberculosis pathogen.

Why Some Bacteria Outlast Antibiotics

The researchers observed clear differences between drug combinations, as well as differences between bacterial strains from different patients. Specialists refer to this second factor as antibiotic tolerance. Further analysis showed that specific genetic traits influence how well bacteria can endure treatment and effectively wait it out.

"The better bacteria tolerate an antibiotic, the lower the chances of therapeutic success are for the patients," says Lucas Boeck. When compared with results from clinical studies and animal models, the new testing method closely matched how well various treatments actually cleared infections.

Benefits for Patients and Drug Development

So far, antimicrobial single-cell testing has mainly been used in research settings, but it could eventually be applied in hospitals and the pharmaceutical industry. According to Boeck, the method could help doctors select antibiotic therapies that are better matched to the specific bacterial strain infecting each patient.

"Our test method allows us to tailor antibiotic therapies specifically to the bacterial strains in individual patients." He adds that a deeper understanding of the genetic factors behind antibiotic tolerance could lead to faster and simpler testing methods and improve predictions about how effective new antibiotics will be during development.

"Last but not least, the data can help researchers to better understand the survival strategies of pathogens and thus lay the foundation for new, more effective therapeutic approaches," says Boeck.

---

Journal Reference:

1. Alexander Jovanovic, Frederick K. Bright, Ahmad Sadeghi et al. Large-scale testing of antimicrobial lethality at single-cell resolution predicts mycobacterial infection outcomes. Nature Microbiology, 2026; DOI: 10.1038/s41564-025-02217-y

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

New images reveal how antibiotics shatter bacterial defenses

Composite image of E. coli exposed to the polymyxin antibiotic – the images show the changes to the outer layer of armor over time. From left to right: bacterium untreated by the antibiotic; bacterium after 15 minutes; after 30 minutes; after 60 minutes; after 90 minutes. The white scale bar is 250 nanometers across. Credit: Carolina Borrelli, Edward Douglas et al. / Nature Microbiology 

Researchers from University College London have revealed how polymyxins, crucial last-resort antibiotics, break down bacterial armor by forcing cells to overproduce and shed it. Astonishingly, the drugs only kill bacteria when they’re active, leaving dormant cells untouched. This discovery could explain recurring infections and inspire strategies to wake bacteria up before treatment. 

Polymyxins were discovered more than 80 years ago and are used as a last-resort treatment for infections caused by "Gram negative" bacteria. These bacteria have an outer surface layer that acts like armor and prevents certain antibiotics from penetrating the cell. Polymyxins are known to target this outer layer, but how they disrupt it and then kill bacteria is still not understood.

In the new study, the research team revealed in high-resolution images and biochemical experiments how the antibiotic Polymyxin B rapidly caused bumps and bulges to break out on the surface of an E. coli bacterial cell.

These protrusions, which appeared within minutes, were followed by the bacterium rapidly shedding its outer armor.

The antibiotic, the researchers concluded, had triggered the cell to produce and shed its armor. The more the cell tried to make new armor, the more it lost the armor it was making, at such a rate that it left gaps in its defenses, allowing the antibiotic to enter the cell and kill it.

However, the team found that this process - protrusions, fast production and shedding of armor, and cell death - only occurred when the cell was active. In dormant (sleeping) bacteria, armor production is switched off, making the antibiotic ineffective.

Co-senior author Dr Andrew Edwards, from Imperial, said: "For decades we've assumed that antibiotics that target bacterial armor were able to kill the microbes in any state, whether they're actively replicating or they were dormant. But this isn't the case. Through capturing these incredible images of single cells, we've been able to show that this class of antibiotics only work with help from the bacterium, and if the cells go into a hibernation-like state, the drugs no longer work -- which is very surprising."

Becoming dormant allows bacteria to survive unfavorable conditions such as a lack of food. They can stay dormant for many years and "wake up" when conditions become more favorable. This can allow bacteria to survive against antibiotics, for instance, and reawaken to cause recurrent infections in the body.

The E. coli cells were imaged at the London Centre for Nanotechnology at UCL. A tiny needle, only a few nanometers wide, was run over the bacterial cell, "feeling" the shape to create an image (a technique called atomic force microscopy) at much higher resolution than would be possible using light.

The team compared how active (growing) and inactive E. coli cells responded to polymyxin B in the lab, finding that the antibiotic efficiently eliminated active cells but did not kill dormant cells.

They also tested the E. coli cells' response with and without access to sugar (a food source that wakes up dormant cells). When sugar was present, the antibiotic killed previously dormant cells, but only after a delay of 15 minutes - the time needed for the bacteria to consume the sugar and resume production of its outer armor.

In conditions where the antibiotic was effective, the researchers detected more armor being released from the bacteria. They also observed the bulges occurring across the surface of the cell.

In conditions where it was ineffective, the antibiotic bound itself to the outer membrane but caused little damage.

The research paper can be found here: 

1. Carolina Borrelli, Edward J. A. Douglas, Sophia M. A. Riley, Aikaterini Ellas Lemonidi, Gerald Larrouy-Maumus, Wen-Jung Lu, Boyan B. Bonev, Andrew M. Edwards, Bart W. Hoogenboom. Polymyxin B lethality requires energy-dependent outer membrane disruption. Nature Microbiology, 2025; DOI: 10.1038/s41564-025-02133-1

 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)

Synthetic compound shows promise against multidrug resistance

Image: Antimicrobials, by Tim Sandle

Antimicrobial resistance directly causes more than 1 million deaths every year and contributes to more than 35 million more, according to the World Health Organization. Staphylococcus aureus and Enterococcus sp., 2 gram-positive pathogens highly likely to develop resistance to known treatments, can cause dangerous hospital-acquired and community-acquired infections.

Researchers have described a newly synthesised compound called Infuzide that shows activity against antimicrobial-resistant strains of S. aureus and Enterococcus in laboratory and mouse tests.

In addition, the findings suggest that Infuzide kills bacteria in ways that differ from other antimicrobials, which may help keep resistance at bay.

Infuzide (C17H14N4O4)

Infuzide emerged from more than a decade of work by interdisciplinary researchers looking for ways to create compounds that could act against pathogens in ways similar to known pharmaceutical compounds. Those include hydrazones, inorganic synthesised compounds that previous studies have shown to demonstrate antibacterial activity, including against resistant strains. The researchers synthesised 17 new compounds that contained hydrazones, and among those Infuzide showed activity against gram-positive S. aureus and Enterococcus.

The researchers found that Infuzide specifically attacks bacterial cells. In lab tests, they compared the antimicrobial effects of Infuzide against vancomycin, a powerful antibiotic that represents the standard of care in treating resistant infections. They found that Infuzide more quickly and effectively reduced the size of bacterial colonies than the standard drug. In tests of resistant S. aureus infections on the skin of mice, the compound effectively reduced the bacterial population. The reduction was even higher, the researchers reported, when infuzide was combined with linezolid, a synthetic antibiotic.

Infuzide did not show significant activity against Gram-negative pathogens, though Baltas said the group is looking for small changes to Infuzide that might expand its antimicrobial activity.

The researchers synthesised the compounds without the need of solvents, which can be expensive and environmentally hazardous. The simplicity of the chemical reactions, Baltas said, would make it easy to make large quantities to be used in new treatments.

Reference:

Rahul Maitra, Deepanshi Saxena, Abdul Akhir, Anna Kapusterynska, Michel Baltas, Sidharth Chopra. Comprehensive biological evaluation of infuzide as a potent antimicrobial, alone and in combination with gentamicin, linezolid, and minocycline targeting MDR Staphylococcus aureus and Enterococcus sp.. Microbiology Spectrum, 2025; DOI: 10.1128/spectrum.00279-25 

  

Innovation with transparent antimicrobial coatings

Image: Microorganisms. Designed by Tim Sandle

Hydrogen boride (HB) nanosheets can inactivate viruses, bacteria, and fungi within minutes in the dark conditions. By coating surfaces with HB nanosheets, it rapidly inactivates SARS-CoV-2, influenza virus, and other pathogens. The nanosheets work by denaturing microbial proteins, offering a safe, effective, and versatile antimicrobial coating for everyday items.

The global fight against infectious diseases faces two major challenges: the threat of new pandemic outbreaks and the alarming rise of antimicrobial resistance driven by the excessive use of antibiotics. As pathogens continue to evolve and spread, researchers are urgently seeking innovative technologies that can effectively combat viruses, bacteria, and fungi conveniently in everyday settings.

Microbiology books - at discount 

Two-dimensional nanomaterials have emerged as promising candidates in this search. Hydrogen boride (HB) nanosheets, initially invented by Professor Takahiro Kondo at the University of Tsukuba and his team, represent an exciting new frontier. Initially explored for potential applications in electronics, energy storage, and catalysis, the interactions between HB nanosheets and biomolecules have remained largely unexplored -- until now.

In a recent study, a research team involving Professor Masahiro Miyauchi and Associate Professor Akira Yamaguchi from the Department of Materials Science and Engineering at Institute of Science Tokyo, Japan discovered that HB nanosheets exhibit excellent antibacterial, antiviral, and antifungal properties. 

The researchers first fabricated transparent films by coating glass substrates with a dispersed solution of HB nanosheets. They then tested these films against a wide variety of microorganisms. Remarkably, the coated surfaces exhibited exceptional antimicrobial performance, inactivating the SARS-CoV-2, influenza, and feline caliciviruses down to detection limits within just 10 minutes at room temperature -- without the need for light activation. Similar effects were observed against various bacteriophages, and multiple types of bacteria, such as Escherichia coli and Staphylococcus aureus, and fungi, such as Aspergillus niger and Penicillium pinophilum.

The ability of HB nanosheets to inactivate these bacteria and fungi to the detection limit confirms the effectiveness of this material in combating a variety of microbial agents. The team then investigated the underlying mechanisms behind this broad-spectrum antimicrobial activity, revealing that it originates from the nanosheets' ability to denature microbial proteins through strong physicochemical interactions.

What makes these findings particularly exciting is the versatility of HB nanosheets as transparent coating materials. Unlike metal-based antimicrobials, which may leach or lack transparency, and photocatalyst-based coatings that require ultraviolet light activation, HB nanosheets function effectively in darkness and maintain optical clarity.

Laboratory tests further demonstrated their effectiveness under dry conditions, mimicking real-world scenarios where pathogens might be transferred by coughing or sneezing onto everyday surfaces. Amid concerns of another pandemic like the COVID-19 outbreak, HB nanosheets can be applied as transparent coatings for items and textiles to reduce infection risks. Additionally, due to their antifungal properties, they could also be used on various materials to help maintain cleanliness in everyday surroundings.

Overall, HB nanosheets offer a promising technology for creating safer environments and reducing pathogen transmission in daily life.

See:

 

Takeshi Nagai, Andi Mauliana, Keiichi Kobayashi, Akira Yamaguchi, Keisuke Miyazaki, Yue Yang, Jumpei Takeshita, Takeshi Fujita, Kayano Sunada, Hitoshi Ishiguro, Takahiro Kondo, Masahiro Miyauchi. Broad-spectrum antimicrobial effects of hydrogen boride nanosheets. Journal of Materials Chemistry B, 2025; 13 (19): 5723 DOI: 10.1039/D4TB02854F 

 

Posted by Dr. Tim Sandle, Pharmaceutical Microbiology Resources (http://www.pharmamicroresources.com/)