Tag: antibiotic resistance

Temperature may be a New Weapon in the Battle against Antibiotic Resistance

Scientists from the University of Groningen in the Netherlands, together with colleagues from other European universities, have tested how a fever could affect the development of antimicrobial resistance. In laboratory experiments, they found that a small increase in temperature from 37 to 40 degrees Celsius drastically changed the mutation frequency in E. coli bacteria, which facilitates the development of resistance. If these results can be replicated in human patients, fever control could be a new way to mitigate the emergence of antibiotic resistance.

There are two ways to fight the threat of antimicrobial resistance: by developing new drugs, or by preventing the development of resistance. ‘We know that temperature affects the mutation rate in bacteria’, explains Timo van Eldijk, co-first author of the paper published in JAC-Antimicrobial Resistance. ‘What we wanted to find out was how the increase in temperature associated with fever influences the mutation rate towards antibiotic resistance.’

‘Most studies on resistance mutations were done by lowering the ambient temperature, and none, as far as we know, used a moderate increase above normal body temperature,’ Van Eldijk reports. Together with Master’s student Eleanor Sheridan, he cultured E. coli bacteria at 37 or 40 degrees Celsius, and subsequently exposed them to three different antibiotics to assess the effect. ‘Again, some previous human trials have looked at temperature and antibiotics, but in these studies, the type of drug was not controlled.’ In their laboratory study, the team used three different antibiotics with different modes of action: ciprofloxacin, rifampicin, and ampicillin.

The results showed that for two of the drugs, ciprofloxacin and rifampicin, increased temperature led to an increase in the mutation rate towards resistance. However, the third drug, ampicillin, caused a decrease in the mutation rate toward resistance at fever temperatures. ‘To be certain of this result, we replicated the study with ampicillin in two different labs, at the University of Groningen and the University of Montpellier, and got the same result,’ says Van Eldijk.

The researchers hypothesized that a temperature dependence of the efficacy of ampicillin could explain this result, and confirmed this in an experiment. This explains why ampicillin resistance is less likely to arise at 40 degrees Celsius. ‘Our study shows that a very mild change in temperature can drastically change the mutation rate towards resistance to antimicrobials,’ concludes Van Eldijk. ‘This is interesting, as other parameters such as the growth rate do not seem to change.’

If the results are replicated in humans, this could open the way to tackling antimicrobial resistance by lowering the temperature with fever-suppressing drugs, or by giving patients with a fever antimicrobial drugs with higher efficacy at higher temperatures. The team concludes in the paper: ‘An optimized combination of antibiotics and fever suppression strategies may be a new weapon in the battle against antibiotic resistance.’

Source: University of Groningen

Milk Samples From the 1940s Reveal Antibiotic Resistance in the Pre-antibiotic Era

Photo by Robin Worrall on Unsplash

Using stored milk samples as a kind of time capsule, veterinary researchers at the University of Connecticut have uncovered insights about the presence of antibiotic resistance even in the pre-antibiotic era.

Sometime in the 1940s or so, someone in what is now the Department of Pathobiology and Veterinary Science got a lyophiliser, a piece of equipment that freeze-dries samples, says Director of the Connecticut Veterinary Medical Diagnostic Laboratory (CVMDL) Dr Guillermo Risatti. Risatti explains that at that time, the microbiology lab was very active in testing milk for the dairy farms in the region. With an exciting new piece of equipment, it seems they started lyophilising hundreds of samples.

The samples have been in storage ever since. Beyond the scant details that these are milk samples containing Streptococcus bacteria from the 1940s, Risatti explains that he and his colleagues – CVMDL Research Associate Dr. Zeinab Helal, Ji-Yeon Hyeon and Dong-Hun Lee – were interested in exploring their microbial history.

Risatti says that over the years, the data was lost, so researchers don’t have precise details of the provenance of the samples. But knowing a bit of history about the department, they can deduce some information.

“We believe that most of them came from Connecticut or perhaps from cases from the region, but we cannot say which parts,” Risatti says. “Most likely, this lab provided a testing service to locals, as this was mainly a pathology lab. Now it’s more like a diagnostic lab, and we receive samples from all over the region, including New York and New Jersey.”

Learning about what these historical samples hold could help with research in unexpected ways, but the first step is piecing together the lost details. To do this, Risatti explains that the team established a workflow using standard techniques to streamline processes to analyse the visual characteristics, called phenotype, and to analyse their genotype with genomic sequencing.

Different species of Streptococcus use different strategies to inflict disease in the organisms they infect. These virulence factors are used to differentiate one species of Streptococcus from another and are one way to distinguish samples through phenotypic analysis. Another phenotypic analysis includes testing bacteria for their susceptibility to antibiotics.

The researchers started with 50 samples collected from 1941 to 1947, and they found that the samples contained seven different Streptococcus species, including two subspecies of S. dysgalactiae. Interestingly, the researchers found some of the samples were resistant to the antibiotic tetracycline and did not carry antibiotic resistance genes typically seen in today’s antibiotic-resistant bacterial strains. Since these samples were collected prior to the antibiotic era, the results add to a growing body of literature showing that antibiotic resistance occurred naturally before humans discovered and began to use antibiotics.

“Antibiotic resistance is a very big area of research, and it has been for many years,” says Risatti. “We did not go any further with our analysis because we don’t have the tools here, but we hope to bring this information to the public. I think it could be the jumpstart for somebody to study further.”

Risatti explains the hope is to partner with large agencies like the CDC and the Department of Public Health to help bolster antibiotic resistance research.

First-line Antibiotic for C. Diff may be Weakening

Clostridioides difficile. Credit: CDC

The antibiotic vancomycin, recommended as first-line treatment for infection caused by the deadly superbug Clostridioides difficile, may not be living up to its promise, according to new US-based research.

C. diff infection is the leading cause of death due to gastroenteritis in the US. It causes gastrointestinal symptoms ranging from diarrhoea and abdominal pain to toxic megacolon, sepsis and death.

Based on 2018 clinical practice guidelines, the use of oral vancomycin has increased by 54% in the past six years, but the clinical cure rates have decreased from nearly 100% in the early 2000’s to around 70% in contemporary clinical trials.

“Despite the increasing prevalence of data showing reduced effectiveness of vancomycin, there is a significant lack of understanding regarding whether antimicrobial resistance to these strains may affect the clinical response to vancomycin therapy,” reports Anne J. Gonzales-Luna, research assistant professor in the Department of Pharmacy Practice and Translational Research, UH College of Pharmacy, in the journal Clinical Infectious Diseases. “In fact, the prevailing view has been that antibiotic resistance to these strains are unlikely to impact clinical outcomes, given the high concentrations of vancomycin in stools.”

But the University of Houston College of Pharmacy team arrived at a different conclusion after sifting through research included in a multicentre study, which included adults treated with oral vancomycin between 2016-2021 for C. diff infection.

“We found reduced vancomycin susceptibility in C. difficile was associated with lower 30-day sustained clinical response and lower 14-day initial cure rates in the studied patient cohort,” said Gonzales-Luna.

The finding is cause for concern.

“It’s an alarming development in the field of C. diff as there are only two recommended antibiotics,” said Kevin Garey, professor of pharmacy practice and translational research. “If antimicrobial resistance increases in both antibiotics, it will complicate the management of C. diff infection leading us back to a pre-antibiotic era.”

Source: University of Houston

Large Study Finds Antibiotics are Ineffective for Most Lower Respiratory Tract Infections

Photo by Robina Weermeijer on Unsplash

Use of antibiotics provided no measurable impact on the severity or duration of coughs, even if a bacterial infection was present, finds a large prospective study of people seeking care for lower-respiratory tract infections. The study by researchers at Georgetown University Medical Center and colleagues appeared in the Journal of General Internal Medicine.

“Upper-respiratory tract infections usually include the common cold, sore throat, sinus infections and ear infections and have well established ways to determine if antibiotics should be given,” says the study’s lead author, Dan Merenstein, MD, professor of family medicine. “Lower-respiratory tract infections tend to have the potential to be more dangerous, since about 3% to 5% of these patients have pneumonia. But not everyone has easy access at an initial visit to an X-ray, which may be the reason clinicians still give antibiotics without any other evidence of a bacterial infection. Plus, patients have come to expect antibiotics for a cough, even if it doesn’t help. Basic symptom-relieving medications plus time brings a resolution to most people’s infections.”

The antibiotics prescribed in this study for lower-tract infections were all appropriate, commonly used antibiotics to treat bacterial infections. But the researchers’ analysis showed that of the 29% of people given an antibiotic during their initial medical visit, there was no effect on the duration or overall severity of cough compared to those who didn’t receive an antibiotic.

“Physicians know, but probably overestimate, the percentage of lower-tract infections that are bacterial; they also likely overestimate their ability to distinguish viral from bacterial infections,” says Mark H. Ebell, MD, MS, a study author and professor in the College of Public Health at the University of Georgia. “In our analysis, 29% of people were prescribed an antibiotic, while only 7% were given an antiviral. But most patients do not need antivirals, as there exist only two respiratory viruses where we have medications to treat them: influenza and SARS-CoV-2. There are none for all of the other viruses.”

To determine if there was an actual bacterial or viral infection present, beyond the self-reported symptoms of a cough, the investigators confirmed the presence of pathogens with advanced lab tests to look for microbiologic results classified as only bacteria, only viruses, both virus and bacteria, or no organism detected. Very importantly, for those with a confirmed bacterial infection, the length of time until illness resolution was the same for those receiving an antibiotic versus those not receiving one –about 17 days.

Overuse of antibiotics can result in dizziness, nausea, diarrhoea and rash, along with about a 4% chance of serious adverse effects including anaphylaxis, which is a severe, life-threatening allergic reaction; Stevens-Johnson syndrome, a rare, serious disorder of the skin and mucous membranes; and Clostridioides difficile-associated diarrhoea. The World Health Organization considers antibiotic resistance to be a major an emerging threat.

“We know that cough can be an indicator of a serious problem. It is the most common illness-related reason for an ambulatory care visit, accounting for nearly 3 million outpatient visits and more than 4 million emergency department visits annually,” says Merenstein. “Serious cough symptoms and how to treat them properly needs to be studied more, perhaps in a randomized clinical trial, as this study was observational and there haven’t been any randomized trials looking at this issue since about 2012.”

Source: Georgetown University School of Medicine

New Enzymatic Cocktail can Kill Tuberculosis-causing Mycobacteria

Mycobacterium tuberculosis drug susceptibility test. Photo by CDC on Unsplash

With resistance to chemical antibiotics on the rise, the world needs entirely new forms of antibiotics. A new study published in Microbiology Spectrum, a journal of the American Society for Microbiology, shows that an enzymatic cocktail can kill a variety of mycobacterial species of bacteria, including those that cause tuberculosis. The research was carried out by scientists at Colorado State University and Endolytix Technologies.

“We have a mycobacterial drug that works for Nontuberculous Mycobacteria and M. tuberculosis that is biological, not phage therapy, and not small molecule antibiotics,” said Jason Holder, Ph.D., a study coauthor and Founder and Chief Science Officer at Endolytix Technology.

“Mycobacterial infections are particularly hard to treat due to poor efficacy with standard of care drugs that are used in multidrug regimens resulting in significant toxicities and treatments lasting 6 months to years. This is often followed up by reemergence of the bacterial infection after a year of testing negative.”

In the new proof of principle study, the researchers took a biological approach instead of a chemical one to develop a cocktail of enzymes that attack the cell envelope of mycobacteria.

The cocktail of enzymes contains highly specific biochemical catalysts that target and degrade the mycobacteria cell envelope that is essential for mycobacterial viability.

To increase efficacy, the researchers delivered the enzymatic drug inside of host macrophages where mycobacteria grow. In laboratory experiments, the drug was effective against M. tuberculosis and Nontuberculous Mycobacteria (NTMs), both lethal pulmonary lung diseases (PD). TB kills roughly 1.5 million people per year.

“We characterised the mechanism of bactericide as through shredding of the bacterial cells into fragments,” Holder said.

“We’ve shown we can design and develop biological antibiotics and deliver them to the sites of infection through liposomal encapsulation. By combining drug delivery science with enzymes that lyse bacteria, we hope to open up treatment options in diseases such as NTM pulmonary disease, tuberculosis pulmonary disease and others.”

According to study coauthor Richard Slayden, PhD, a professor in the Department of Microbiology, Immunology and Pathology at Colorado State University, the new therapy complements current standard-of-care drugs and does not have many of the drug-drug interactions that are problematic with many anti-mycobacterial drugs in use. “Endolytix enzymes work powerfully with standard-of-care antibiotics to kill bacteria with lower drug concentrations,” Holder said. “This has the potential to reduce the significant toxicities associated with multi-drug regimens that are the standard for mycobacterial infections and hopefully lead to more rapid cures.”

Source: American Society for Microbiology

Steroid Drugs Used for HRT could be Repurposed to Combat E. coli and MRSA

Methicillin resistant Staphylococcus aureus (MRSA) – Credit: CDC

Researchers from the University of Kent’s School of Biosciences have combined computational and microbiology laboratory approaches to identify existing drugs that can be repurposed to combat antibiotic-resistant bacterial infections, instead of developing new ones.

This research, which has been published in the Journal of Infectious Diseases, revealed that a class of steroid drugs currently used in hormone replacement therapy (HRT) can also stop the growth of antibiotic-resistant E. coli and effectively kill MRSA.

These drugs are particularly good at binding to a protein complex, cytochrome bd, which is important for the growth and survival of a range of disease-causing bacterial species. The researchers made an in silico screening for drugs that could inhibit bd activity, and identified quinestrol, ethinyl estradiol and mestranol, then evaluated their effectiveness in vitro.

The steroid drugs ethinyl estradiol and quinestrol inhibited E. coli bd-I activity. The IC50 of quinestrol for inhibiting oxygen consumption in E. coli bd-I-only membranes as 0.2µg/mL, although residual activity remained at around 20% at higher concentrations Quinestrol exhibited potent bactericidal effects against S. aureus but not E. coli.

It is expected that steroids may provide an alternative to conventional antibiotics that are becoming increasingly ineffective.

Dr Mark Shepherd, Reader in Microbial Biochemistry at Kent and the corresponding author on the paper, said: “These exciting developments will help to advance research into new antimicrobials, and we are enthusiastic to use our powerful experimental approach to discover drugs that can target other bacterial proteins and combat a wide range of antibiotic-resistant infections.”

Source: University of Kent

Age and Sex Associated with Patient’s Likelihood of Antimicrobial Resistance

Photo by CDC on Unsplash

A person’s age, sex and location are correlated with the chance that they have a bloodstream infection that is resistant to antibiotics, according to a new study published March 14th in PLOS Medicine by Gwenan Knight of the London School of Hygiene and Tropical Medicine, UK, and colleagues.

Antimicrobial resistance (AMR), in which infections cannot be treated with antibiotics, is a major global public health threat.

Little has been known about how the prevalence of resistance varies with age and sex even though antibiotic usage, changes in immune function, and exposure to high-risk settings are all linked to age and sex.

In the new study, researchers analyzed data collected as part of routine surveillance between 2015 and 2019 on bloodstream infections in 944,520 individuals across 29 European countries.

The team looked at which bacterial species were isolated and sent to the surveillance service, and which antibiotics were used to treat the infections.

Distinct patterns in resistance prevalence by age were observed throughout Europe but varied across bacterial species.

For most but not all bacteria, peaks in resistance were seen at the youngest and oldest ages.

The occurrence of methicillin-resistant Staphylococcus aureus (MRSA) increased with age and the occurrence of aminopenicillin resistance in Escherichia coli decreased with age.

Some antimicrobial resistance profiles peaked in middle-age; Pseudomonas aeruginosa was most likely to be resistant to several antibiotics around 30 years of age and, for women, the incidence of bloodstream infections due to E. coli peaked between ages 15 and 40. There were other important differences between sexes; in general, men had a higher risk of antimicrobial resistance than women.

“These findings highlight important gaps in our knowledge of the epidemiology of antimicrobial resistance that are difficult to explain through known patterns of antibiotic exposure and healthcare contact,” the authors say.

“Our findings suggest that there may be value in considering interventions to reduce antimicrobial resistance burden that take into account important variations in antimicrobial resistance prevalence with age and sex.”

The authors add, “Our findings, that the prevalence of resistance in bloodstream infections across Europe varies substantially by age and sex, highlights important gaps in our knowledge of the spread and selection of AMR. In order for us to address this growing threat to public health, we now need data from a wider range of sources to determine the contribution that cultural versus natural history differences have in driving these patterns globally and the role that they play in the increasing rates of AMR being seen.”

Breaching Stubborn Bacterial Biofilms with a ‘Trojan Horse’

Methicillin resistant Staphylococcus aureus (MRSA) – Credit: CDC

A new study has tricked bacteria into sending death signals to stop the growth of biofilms that lead to deadly infections. The discovery by Washington State University researchers could someday be harnessed as an alternative to antibiotics for treating difficult infections.

Reporting in the journal, Biofilm, the researchers used the messengers, which they named death extracellular vesicles (D-EVs), to reduce growth of the bacterial communities by up to 99.99% in laboratory experiments.

“Adding the death extracellular vesicles to the bacterial environment, we are kind of cheating the bacteria cells,” said Mawra Gamal Saad, first author on the paper and a graduate student in WSU’s Gene and Linda Voiland School of Chemical Engineering and Bioengineering.

“The cells don’t know which type of EVs they are, but they take them up because they are used to taking them from their environment, and with that, the physiological signals inside the cells change from growth to death.”

Bacterial resistance is a growing problem around the world. In the US, at least 2 million infections and 23 000 deaths are attributable to antibiotic-resistant bacteria each year, according to the U.S. Centers for Disease Control.

When antibiotics are used to treat a bacterial infection, some of the bacteria can hide within their tough-to-penetrate biofilm. These subpopulations of resistor cells can survive treatment and are able to grow and multiply, resulting in chronic infections.

“They are resistant because they have a very advanced and well-organised adaptive system,” said Saad.

“Once there is a change in the environment, they can adapt their intracellular pathways very quickly and change it to resist the antibiotics.”

In their new study, the researchers discovered that the extracellular vesicles are key to managing the growth of the protective biofilm.

The vesicles, tiny bubbles from 30 to 50nm or about 2000 times smaller than a strand of hair, shuttle molecules from cells, entering and then re-programming neighbouring cells and acting as a cell-to-cell communications system.

As part of this study, the researchers extracted the vesicles from one type of bacteria that causes pneumonia and other serious infections.

They determined that the bacteria initially secrete vesicles, called growth EVs, with instructions to grow its biofilm, and then later, depending on available nutrients, oxygen availability and other factors, send EVs with new instructions to stop growing the biofilm.

The researchers were able to harness the vesicles with the instructions to stop growth and use them to fool the bacteria to kill off the biofilm at all stages of its growth.

Even when the biofilms were healthy and rapidly growing, they followed the new instructions from the death EVs and died. The death EVs can easily penetrate the biofilm because they are natural products secreted by the bacteria, and they have the same cell wall structure, so the cells don’t recognise them as a foreign enemy.

“By cheating the bacteria with these death EVs, we can control their behaviour without giving them the chance to develop resistance,” said Saad.

“The behavior of the biofilm just changed from growth to death.”

WSU Professor and corresponding author Wen-Ji Dong, who has been studying the vesicles for several years initially thought that all of the bacterial-secreted vesicles would promote cell growth.

The researchers were surprised when they found that older biofilms provided instructions on shutting themselves down.

“So now we’re paying attention to the extracellular vesicles secreted by older biofilms because they have therapeutic potential,” he said.

Source: Washington State University

Treating Tuberculosis when Antibiotics Become Ineffective

Tuberculosis bacteria. Credit: CDC

An international research team has found a number of substances with a dual effect against tuberculosis (TB): They make the bacteria causing the disease less pathogenic for human immune cells whilst boosting the activity of conventional antibiotics. They published their findings in the journal Cell Chemical Biology.

Infectious disease specialist Dr Jan Rybniker and colleagues have identified new, antibiotic molecules that target Mycobacterium tuberculosis and make it less pathogenic for humans.

Diagram by the United States-based National Institute of Allergy and Infectious Diseases showing the medicine options for drug-resistant tuberculosis. (Via Flickr, CC BY 2.0 Deed)

In addition, some of the discovered substances may allow for a renewed treatment of tuberculosis with available medications – including strains of the bacterium that have already developed drug resistance.

Although treatable with antibiotics, it still ranks among the infectious diseases that claim the most lives worldwide: According to the World Health Organization (WHO), only COVID was deadlier than TB in 2022. The disease also caused almost twice as many deaths as HIV/AIDS. More than 10 million people continue to contract TB every year, mainly due to insufficient access to medical treatment in many countries.

Limited targets

Multidrug-resistant tuberculosis is emerging especially in eastern Europe and Asia. That is of particular concern to researchers because like all bacteria that infect humans, Mycobacterium tuberculosis possesses only a limited number of targets for conventional antibiotics.

That makes it increasingly difficult to discover new antibiotic substances in research laboratories.

Working together with colleagues from the Institute Pasteur in Lille, France, and the German Center for Infection Research (DZIF), the researchers at University Hospital Cologne have now identified an alternative treatment strategy for the bacterium.

The team utilized host-cell-based high-throughput methods to test the ability of molecules to stem the multiplication of bacteria in human immune cells: From a total of 10,000 molecules, this procedure allowed them to isolate a handful whose properties they scrutinized more closely in the course of the study.

Two-pronged attack

Ultimately, the researchers identified virulence blockers that utilise target structures that are fundamentally distinct from those targeted by classical antibiotics.

“These molecules probably lead to significantly less selective pressure on the bacterium, and thus to less resistance,” said Jan Rybniker, who heads the Translational Research Unit for Infectious Diseases at the Center for Molecular Medicine Cologne (CMMC) and initiated the study.

In deciphering the exact mechanism of action, the researchers also discovered that some of the newly identified chemical substances are dual-active molecules.

Thus, they not only attack the pathogen’s virulence factors, but also enhance the activity of monooxygenases — enzymes required for the activation of the conventional antibiotic ethionamide.

Ethionamide is a drug that has been used for many decades to treat TB. It is a so-called prodrug, a substance that needs to be enzymatically activated in the bacterium to kill it. Therefore, the discovered molecules act as prodrug boosters, providing another alternative approach to the development of conventional antibiotics.

In cooperation with the research team led by Professor Alain Baulard at Lille, the precise molecular mechanism of this booster effect was deciphered.

Thus, in combination with these new active substances, drugs that are already in use against tuberculosis might continue to be employed effectively in the future.

The discovery offers several attractive starting points for the development of novel and urgently needed agents against tuberculosis.

“Moreover, our work is an interesting example of the diversity of pharmacologically active substances. The activity spectrum of these molecules can be modified by the smallest chemical modifications,” Rybniker added.

However, according to the scientists it is still a long way to the application of the findings in humans, requiring numerous adjustments of the substances in the laboratory.

Source: University of Cologne

Skin Bacteria may Hold New Weapons against Antibiotic-resistant Bacteria

Methicillin resistant Staphylococcus aureus (MRSA) – Credit: CDC

Antibiotic-resistant bacteria are a growing global problem, but of the solution may lie in copying the bacteria’s own weapons. Researchers in the Norwegian city of Tromsø has found a new bacteriocin, in a very common skin bacterium, which they describe in Microbiology Spectrum. Bacteriocin inhibits the growth of antibiotic-resistant bacteria that are often the cause of disease and can be difficult to treat.

One million deaths each year

The fact that we have medicines against bacterial infections is something many people take for granted. But increasing resistance among bacteria means that more and more antibiotics do not work. When the bacteria become resistant to the antibiotics we have available, we are left without a treatment option for very common diseases. Over one million people die each year as a result of antibiotic resistance.

The first step in developing new antibiotics is to look for substances that inhibit bacterial growth.

Sami name for an exciting discovery

The research group for child and youth health at UiT The Arctic University of Norway has studied substances that the bacteria themselves produce to inhibit the growth of competitors. These substances are called bacteriocins. Through the work, they have discovered a new bacteriocin, in a very common skin bacterium. Bacteriocin inhibits the growth of antibiotic-resistant bacteria that can be difficult to treat with common antibiotics.

The researchers have called the new bacteriocin Romsacin, after the Sami name for Tromsø, Romsa. The hope is that Romsacin can be developed into a new medicine for infections for which there is currently no effective treatment.

Long way to go

At the same time, researcher Runa Wolden at the Department of Clinical Medicine at UiT emphasizes that there is a long way to go before it is known whether Romsacin will be developed and taken into use as a new medicine. Because that’s how it is with basic research; you cannot say in advance when someone will make use of the results you produce.

“This discovery is the result of something we have been researching for several years. Developing Romsacin – or other promising substances – into new antibiotics is very expensive and can take 10-20 years,” says Wolden, who is part of the research group for child and youth health.

Effective against bacterial types

Before new antibiotics can be used as medicines, one needs to make sure that they are safe to use. Currently, researchers do not know how the bacteriocin works in humans. A further process will involve comprehensive testing, bureaucracy and marketing.

“This naturally means that there is a long way to go before we can say anything for sure. What we already know, however, is that this is a new bacteriocin, and that it works against some types of bacteria that are resistant to antibiotics. It’s exciting,” says Wolden.

The new bacteriocin is produced by a bacterium called Staphylococcus haemolyticus. The bacteriocin is not produced by all S. haemolyticus, but by one of the 174 isolates that the researchers have available in the freezer.

“We couldn’t know that before we started the project, and that’s one of the things that makes research fun,” says Wolden.

She says that ten years ago the researchers collected bacterial samples from healthy people when they wanted to compare S. haemolyticus in healthy people with those found in patients in hospital.

“Subsequently, we have done many experiments with these bacteria, and this is the result from one of our projects,” says Wolden.

Source: UiT The Arctic University of Norway