Category: Antibiotics

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Antibiotic Use Impedes Athletes’ Performance

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Tired woman after exercise
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New research published in the journal Behavioural Processes demonstrates that by killing essential gut bacteria, antibiotics ravage athletes’ motivation and endurance. This study, which examined mice, suggests there is a big difference in the gut microbiome of athletes and couch potatoes.

Much research has been done on how exercise impacts the gut microbiome, but this study is one of few to examine the reverse – how gut bacteria also impact voluntary exercise behaviours. Engaging in voluntary exercise involves both motivation and athletic ability.

“We believed an animal’s collection of gut bacteria, its microbiome, would affect digestive processes and muscle function, as well as motivation for various behaviours, including exercise,” said Theodore Garland, UCR evolutionary physiologist in whose lab the research was conducted. “Our study reinforces this belief.”

Researchers confirmed through faecal samples that after 10 days of antibiotics, gut bacteria were reduced both in a group of ‘athletic’ mice bred for running on wheels and those that were not. Since no sickness behaviour was seen in the mice, exercise changes were ascribed solely to changes in antibiotic-induced changes in the gut bacteria.

Wheel running in the athletic mice was reduced by 21%, and the high runner mice did not recover their running behaviour even 12 days after the antibiotic treatment stopped.

Meanwhile, for the normal mice, antibiotics caused no difference in the running behaviour.

“A casual exerciser with a minor injury wouldn’t be affected much. But on a world-class athlete, a small setback can be much more magnified,” said Monica McNamara, UCR evolutionary biology doctoral student and the paper’s first author. “That’s why we wanted to compare the two types of mice.” Knocking out the normal gut microbiome might be compared with an injury.

One way the microbiome might affect exercise in mice or in humans is how carbohydrate metabolites are used by the muscles.

“Metabolic end products from bacteria in the gut can be reabsorbed and used as fuel,” Garland said. “Fewer good bacteria means less available fuel.”

The researchers would next like to identify the gut bacteria contributing to increased athletic performance. “If we can pinpoint the right microbes, there exists the possibility of using them as a therapeutic to help average people exercise more,” Garland said.

Lack of exercise is a risk factor for many diseases, and researchers would like to find ways of encouraging it more.

“Though we are studying mice, their physiology is very similar to humans. The more we learn from them, the better our chances of improving our own health,” Garland said.

Research into foods that can increase desirable gut bacteria is ongoing, and Garland recommends a balanced diet in addition to regular exercise to promote health.

Source: University of California, Riverside

Categories : Antibiotics Cardiovascular DiseaseTags :

Gut Bacteria can Reduce Effectiveness of Antihypertensive Drugs

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A new study published this month in the journal Hypertension has shown gut bacteria can reduce the effectiveness of certain antihypertensive drugs. The research provides the first clues into why some people not respond well to medication.

Among those with hypertension, an estimated 20% have resistant hypertension, where their blood pressure remains high despite aggressive treatment.

“The only thing doctors can really do in these patients is adding or switching medications and increasing the dose with the hope they can find something that works,” said Dr Tao Yang, an assistant professor at University of Toledo and the study’s first and lead author. “Until now, we haven’t had any clear indication what the mechanism is for resistant hypertension. Our research could provide a first step toward identifying new ways to effectively overcome treatment-resistant hypertension.”

Recent research has focused on the link between blood pressure and the gut microbiome. That work has helped to unravel potential causes of hypertension beyond diet and exercise. However, Dr Yang’s research is the first to examine the impact of gut bacteria on blood pressure medication itself.

In the study, UToledo scientists compared the effectiveness of the antihypertensive drug quinapril in rats with normal gut bacteria against those with gut microbiota depleted by high doses of antibiotics.

Researchers found a clear difference between the two, with animals that were given antibiotics first responding much better to quinapril.

Analysis of the gut bacteria composition in the animals identified the bacteria Coprococcus as the culprit. Laboratory experiments proved that Coprococcus comes, a dominant bacteria species in this genus, can break down quinapril and ramipril, resulting in the compromised blood pressure-lowering effects.

While the study was confined to animal models and lab experiments, researchers did find at least one intriguing case study that seems to support the notion that this could be applicable to humans.

That 2015 report, published in the International Journal of Cardiology, described a woman with a long history of treatment-resistant hypertension whose blood pressure was controlled without any antihypertensive medication for the two weeks she was taking antibiotics for a post-surgical infection. Her blood pressure was able to be controlled with only one medication for six months after stopping antibiotics, before again becoming treatment-resistant.

“This is just one report and more research is needed. However, this suggests that gut bacteria can play a very real and very important role in regulating the efficacy of blood pressure medication,” Dr Yang said.

The research group intends to further explore the interaction between additional blood pressure medications and other common types of gut bacteria.

Though long-term use of antibiotics isn’t a realistic strategy for addressing treatment-resistant hypertension, Dr Yang said it should be possible for someone to alter their microbiota through probiotics, prebiotics and changes in diet.

“The ultimate goal of my research is to identify ways we can specifically target the bacteria in an individual’s gut to improve drug efficacy,” he said. “This has the potential to benefit a lot of people.”

Source: University of Toledo

Categories : AntibioticsTags :

Fungal Infections Occur When Antibiotics Disrupt Gut Immune System

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Photo by Andrea Piacquadio on Unsplash

Patients prescribed antibiotics in hospital are more likely to get fungal infections because of disruption to the gut immune system, according to a new study published in Cell Host and Microbe.

The study authors suggested that using immune-boosting drugs alongside the antibiotics could reduce the health risks from these complex infections.

Invasive candidiasis is an invasive fungal infection that can endanger hospitalised patients receiving antibiotics to prevent sepsis and other bacterial infections (such as C. diff). Fungal infections can be more difficult to treat than bacterial infections, but the underlying factors causing these infections are not well understood.

The study’s researchers discovered that antibiotics disrupt the immune system in the intestines, meaning that fungal infections were poorly controlled in that area. Unexpectedly, the team also found that where fungal infections developed, gut bacteria were also able to escape, leading to the additional risk of bacterial infection.

Not only does the study demonstrate the potential for immune-boosting drugs, but also it also highlights how antibiotics can other effects on the immune system. This in turn underscores the importance of careful stewardship of available antibiotics.

Lead author Dr Rebecca Drummond said: “We knew that antibiotics make fungal infections worse, but the discovery that bacterial co-infections can also develop through these interactions in the gut was surprising. These factors can add up to a complicated clinical situation — and by understanding these underlying causes, doctors will be better able to treat these patients effectively.”

In the study, the team administered a broad-spectrum antibiotic cocktail to mice and then infected them with Candida albicans, the most common fungus that causes invasive candidiasis in humans. They found that although infected mice had increased mortality, this was caused by infection in the intestine, rather than in the kidneys or other organs.

In a further step, the team pinpointed what parts of the immune system were missing from the gut after antibiotic treatment, and then added these back into the mice using immune-boosting drugs similar to those used in humans. They found this approach helped reduce the severity of the fungal infection.

The researchers followed up the experiment by studying hospital records, where they were able to show that similar co-infections might occur in humans after they have been treated with antibiotics.

“These findings demonstrate the possible consequences of using antibiotics in patients who are at risk of developing fungal infections,” added Dr Drummond. “If we limit or change how we prescribe antibiotics we can help reduce the number of people who become very ill from these additional infections — as well as tackling the huge and growing problem of antibiotic resistance.”

Source: University of Birmingham

Categories : AntibioticsTags :

Fungal Microbiota May Explain Antibiotics’ Long Term Effects in Infants

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Gut microbiome. Credit: Darryl Leja, NIH

In infants treated with antibiotics, fungal gut microbiota are more abundant and diverse compared with the control group even six weeks following the start of the antibiotic course, according to a study published in the Journal of Fungi. The study’s authors suggest that reduced competition from gut bacteria being killed by antibiotics left more space for fungi to multiply.

“The results of our research strongly indicate that bacteria in the gut regulate the fungal microbiota and keep it under control. When bacteria are disrupted by antibiotics, fungi, Candida in particular, have the chance to reproduce,” explained PhD student Rebecka Ventin-Holmberg from the University of Helsinki.

A new key finding in the study was that the changes in the fungal gut microbiota, together with the bacterial microbiota, may be partly responsible for the long-term adverse effects of antibiotics on human health.

Antibiotics are the most commonly prescribed drugs for infants, causing changes in the gut microbiota at its most important developmental stage. These changes are more long-term compared to those in adults.

“Antibiotics can have adverse effects on both the bacterial and the fungal microbiota, which can result in, for example, antibiotic-associated diarrhoea,” Ventin-Holmberg said.

“In addition, antibiotics increase the risk of developing chronic inflammatory diseases, such as inflammatory bowel disease (IBD), and they have been found also to have a link to overweight,” she added.

These long-term effects are thought to be caused, at least in part, by an imbalance in the gut microbiota.

This study involved infants with a respiratory syncytial virus (RSV) infection who had never previously received antibiotics. While some of the children were given antibiotics due to complications, others received no antibiotic therapy throughout the study.

“Investigating the effects of antibiotics is important for the development of techniques that can be used to avoid chronic inflammatory diseases and other disruptions to the gut microbiota in the future,” Ventin-Holmberg emphasised.

While there have been many studies on the effect of antibiotics on bacterial microbiota, there has been a lack of studies on fungal microbiota. This study’s findings indicate that fungal microbiota may also have a role in the long-term effects of imbalance in the gut microbiota.

“Consequently, future research should focus on all micro-organisms in the gut together to better understand their interconnections and to obtain a better overview of the microbiome as a whole,” Ventin-Holmberg noted.

Source: University of Helsinki

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Nanoparticle Could Boost Polymyxin B for Gram-negative Sepsis

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Patient's hand with IV drip
Photo by Anna Shvets on Pexels

To treat Gram-negative sepsis, Purdue University researchers are developing an injectable nanoparticle that can safely deliver Polymyxin B at high enough levels to inactivate endotoxins. Their research is published in Science Advances.

With an estimated annual mortality of between 30 and 50 deaths per 100 000 population,this condition ranks in the top 10 causes of death. One in three patients who die in a hospital has sepsis. Sepsis is a systemic illness caused by microbial invasion of normally sterile parts of the body, occurring when the body’s immune response to an infection or injury goes unchecked. The condition makes blood vessels leaky, leading to inflammation and blood clots, leading to impaired blood flow and possible death.

Professor Yoon Yeo leads a Purdue University team developing biocompatible nanoparticles that treat sepsis systemically through intravenous injection.

Prof Yeo said Polymyxin B, a traditional antibiotic, can inactivate endotoxins that cause a specific type of sepsis, but it may be too toxic for systemic application. For sepsis therapy, it mostly has been tested in extracorporeal blood cleaning, which is cumbersome and time consuming.

“Our nanoparticle formulations reduce dose-limiting toxicity of Polymyxin B without losing its ability to inactivate endotoxins,” Prof Yeo said.

In mouse models of sepsis, 100% treated with the Purdue nanoparticle were protected from excessive inflammation and survived.

“This technology holds promise as a safe, convenient option for patients and physicians,” Prof Yeo said.

Source: Purdue University

Categories : Antibiotics Medical Research & TechnologyTags :

Gut Bacteria Alter Gene Expression to Evade Phage Therapy

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A bacteriophage, Credit: CC0

Phage therapy is a long-standing technique which makes use of bacteriophage viruses to kill bacteria, but poses the challenge of some strains working in vitro but failing in vivo. Scientists have now found that gut bacteria alter their gene expression to avoid attack by bacteriophages. This research, published in Cell Host & Microbe, helps explains the difference in bacteriophage efficacy.

Phage therapy is a medical approach that involves treating bacterial infectious diseases using the natural ability of certain viruses, known as bacteriophages, to kill bacteria that they specifically recognise. Following the development of antibiotics, the West saw a significant decline in the use of this century-old therapeutic strategy. In the face of the growing threat of antibiotic resistance, scientists are returning to bacteriophages and to understand their mechanism of action.

Bacteria and bacteriophages are the most abundant entities in the human gut microbiota. Although bacteriophages kill bacteria, the two antagonist populations coexist in a balance in the gut.

To date, there has been little data on how phage therapy works in vivo. Interactions between bacteria and bacteriophages have, in contrast, been extensively studied in vitro. In these conditions, bacteriophages quickly infect bacteria, replicate, and destroy bacteria, while releasing new viruses capable of infecting other bacteria. However, the dynamics observed between these two microorganisms are very different in mammalian guts. Some bacteriophages that are effective in culture medium are totally ineffective in the gut environment.

In order to understand this difference, scientists decided to compare the gene expression profile, or transcriptome, of the bacterium Escherichia coli in both contexts: culture media and the gut. Using this method, they revealed genetic regulations that characterise the bacterium’s adaptation to the gut environment.

By closely examining the genes involved in this adaptation, they revealed four genes that modulate the bacterium’s susceptibility to bacteriophages. “We observed that certain genes required for infection by bacteriophages are expressed less in the gut than in vitro, thus protecting bacteria from bacteriophages,” commented Laurent Debarbieux, last author of the study.

The scientists verified their theory by eliminating the expression of one particular gene. They observed that bacterial susceptibility to a bacteriophage was significantly reduced. As a result, bacteria in the gut are able to resist predation by bacteriophages by modulating the expression of certain genes rather than mutating their genome.

This study therefore demonstrates that environment plays a predominant role in interactions between bacteria and bacteriophages. These findings pave the way for improved use of bacteriophages for therapeutic purposes.

Source: Pasteur Institute

Categories : Antibiotics CancerTags :

Unlikely Allies: Bacteria can Promote Cancer Metastasis

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Scanning Electron Micrograph of a breast cancer cell. Credit: NIH

Researchers have found that bacteria lurking inside tumours promote cancer metastasis. They do so by enhancing the strength of host cells against mechanical stress in the bloodstream, promoting cell survival during tumour progression, researchers report in the journal Cell.

“Our study reveals that the cancer cell’s behaviour is also controlled by the microbes hiding inside tumours, the majority of which were originally thought to be sterile,” said senior author Shang Cai of the Westlake Laboratory of Life Sciences and Biomedicine. “This microbial involvement is distinct from the genetic, epigenetic, and metabolic components that most cancer drugs target.”

“However, our study does not mean that using antibiotics during cancer treatment will benefit patients,” he cautioned. “Therefore, it is still an important scientific question of how to manage the intratumor bacteria to improve cancer treatment in the future.”

It is known that microbes play a critical role in affecting cancer susceptibility and tumour progression, particularly in colorectal cancers. New evidence suggests however that, in a broad range of cancer types, they also form integral components of the tumour tissue itself, such as pancreatic cancer, lung cancer, and breast cancer. Microbial features are linked to cancer risk, prognosis, and treatment responses, yet the biological functions of tumour-resident microbes in tumour progression remain unclear.

Whether these microbes are actually drivers of tumour progression has been an intriguing question. “Tumour cells hijacked by microbes could be more common than previously thought, which underscores the broad clinical value of understanding the exact role of the tumour-resident microbial community in cancer progression,” Cai explained.

To find answers, Cai’s team utilised a mouse model of breast cancer with significant amounts of bacteria inside cells, similar to human breast cancer. The bacteria were found to be capable of travelling through the circulatory system with the cancer cells, playing critical roles in tumour metastasis. These passenger bacteria have the capacity to modulate the cellular actin network, promoting cell survival against mechanical stress in circulation.

“We were surprised initially at the fact that such a low abundance of bacteria could exert such a crucial role in cancer metastasis. What is even more astonishing is that only one shot of bacteria injection into the breast tumour can cause a tumour that originally rarely metastasises to start to metastasise,” Cai said. “Intracellular microbiota could be a potential target for preventing metastasis in broad cancer types at an early stage, which is much better than to have to treat it later on.”

While intratumour bacteria was found to have a clear role in promoting cancer cell metastatic colonisation, the authors did not exclude the possibility that the gut microbiome and immune system may act together with intratumour bacteria to determine cancer progression. Future in-depth analyses of how bacteria invade tumour cells, how intracellular bacteria are integrated into the host cell system, and how bacteria-containing tumor cells interact with the immune system will help inform how to properly deploy antibiotics in cancer treatment.

Source: ScienceDaily

Categories : Antibiotics UncategorizedTags :

It’s in the Mix: Certain Combinations of Pathogens Resist Antibiotics

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Pseudomonas
Scanning Electron Micrograph of Pseudomonas aeruginosa. Credit: CDC/Janice Carr

A study has found that much higher doses of antibiotics are needed to eliminate a bacterial infection of the airways when certain other microbes are present. This helps explain why treatment often fails to treat respiratory infections in people with diseases such as cystic fibrosis.

The study’s researchers, whose findings are published in The ISME Journal, say that even a low level of one type of microbe in the airways can have a significant impact on the response of other microbes to antibiotics.

The results highlight the need to consider the interaction between different species of microbe when treating infections with antibiotics – and to adjust dosage accordingly.

“People with chronic infections often have co-infection with several pathogens, but the problem is we don’t take that into account in deciding how much of a particular antibiotic to treat them with. Our results might help explain why, in these people, the antibiotics just don’t work as well as they should,” said Thomas O’Brien, PhD candidate and co-first author.

Chronic bacterial infections such as those in the human airways are very difficult to cure using antibiotics. Although these types of infection are often associated with a single pathogenic species, the infection site is frequently co-colonised by a number of other microbes, most of which are not usually pathogenic in their own right.

Treatment options usually revolve around targeting the pathogen, and take little account of the co-habiting species. However, these treatments often fail to resolve the infection. Until now scientists have had little insight into why this is.

To get their results the team developed a simplified model of the human airways, containing artificial sputum designed to chemically resemble the real thing, packed with bacteria.

The model allowed them to grow a mixture of different microbes, including pathogens, in a stable way for weeks at a time. This is a novel approach, as usually one pathogen will rapidly outgrow the others and spoil the experiment. It enabled the researchers to replicate and study poly-microbial infections in the laboratory.

The three microbes used in the experiment were the bacteria Pseudomonas aeruginosa and Staphylococcus aureus, and the fungus Candida albicans – a combination often found in the airways of cystic fibrosis patients.

The researchers treated this microbial mix with colistin, which kills P. aeruginosa effectively. But when the other pathogens were present alongside P. aeruginosa, the antibiotic didn’t work.

“We were surprised to find that an antibiotic that we know should clear an infection of Pseudomonas effectively just didn’t work in our lab model when other bugs were present,” said Wendy Figueroa-Chavez at the University of Cambridge, joint first author of the paper.

The same effect happened when the microbial mix was treated with fusidic acid – an antibiotic that specifically targets Staphylococcus aureus, and with fluconazole, which specifically targets C. albicans.

The researchers found that significantly higher doses of each antibiotic were needed to kill bacteria when it was part of poly-microbial infection, compared to when no other pathogens were present.

“All three species-specific antibiotics were less effective against their target when three pathogens were present together,” said Professor Martin Welch at the University of Cambridge, senior author of the paper.

Currently, antibiotics are usually only lab tested against the targeted pathogen, to determine the lowest effective dose. But when the same dose is used to treat infection in a person it is often ineffective, and this study helps to explain why. The new model system will enable the effectiveness of potential new antibiotics to be tested against a mixture of microbe species together.

Poly-microbial infections are common in the airways of people with cystic fibrosis. Despite treatment with strong doses of antibiotics, these infections often persist long-term. Chronic infections of the airways in people with asthma and chronic obstructive pulmonary disorder (COPD) are also often poly-microbial.

Genetically analysing the Pseudomonas in their lab-grown mix, the researchers were able to pinpoint specific mutations that give rise to this antibiotic resistance. The mutations were found to arise more frequently when other pathogens were also present.

Comparison with the genetic code of 800 samples of Pseudomonas from around the world revealed that these mutations have also occurred in human patients who had been infected with Pseudomonas and treated with colistin.

“The problem is that as soon as you use an antibiotic to treat a microbial infection, the microbe will start to evolve resistance to that antibiotic. That’s what has happened since colistin started to be used in the early 1990’s. This is another reminder of the vital need to find new antibiotics to treat human infections,” said Prof Welch.

Source: University of Cambridge

Categories : AntibioticsTags :

New Insights on Antibiotic-caused Diarrhoea

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Streptococcus pneumoniae. Credit: CDC

A study may have found that a effects on a key gut bacteria are the reason why some patients experience diarrhoea after receiving the widely prescribed antibiotic amoxicillin-clavulanate. 

Researchers, reporting in the journal iScience, found that the level of gut Ruminococcaceae, which plays a role in maintaining an individual’s gut health, strongly impacts diarrhoeal outcomes following antibiotic treatment.

One in three patients prescribed amoxicillin-clavulanate will develop diarrhoea. In some cases, it may be so severe that doctors have to prematurely halt the antibiotic, inadequately treating the infection or else forcing a change in antibiotics. The diarrhoea could also prolong patients’ hospital stays and further exposing them to hospital-acquired infections.

“The problem is very real for patients who are unable to take amoxicillin-clavulanate because it gives them diarrhoea, even though it is an effective and affordable antibiotic for their infection. Knowing why may help us identify those at risk of antibiotic-associated diarrhoea, and devise treatment strategies in the future to minimise or avoid such adverse effects,” said lead researcher Dr Shirin Kalimuddin.

The study recruited 30 healthy volunteers, each receiving a three-day oral course of amoxicillin-clavulanate. Their stool samples were collected over four weeks and analysed using gene sequencing to look for changes in the gut microbiome.

Ruminococcaceae levels in the stools of study volunteers who developed diarrhoea were significantly lower when compared to those who did not, both before and during treatment with amoxicillin-clavulanate. This suggests that individuals may, depending on their gut composition, be predisposed to antibiotic-associated diarrhea. The team further devised a simple polymerase chain reaction (PCR) test based on levels of Faecalibacterium prausnitzii, a species within the Ruminococcaceae family, that could potentially be used in clinical settings to quickly determine an individual’s risk of developing diarrhea with amoxicillin-clavulanate treatment.

“People respond differently to medication. Understanding this response and the ability to predict those at risk will help guide the development of point-of-care diagnostics,” said lead researcher Professor Eric J. Alm.

“While a lot of attention has been paid to how DNA influences a person’s response to medication, the impact of the gut microbiome on the human drug response has not been widely researched. Our findings provide evidence that an individual’s gut microbial composition can influence the risk of developing antibiotics-associated diarrhoea. Tested against amoxicillin-clavulanate, the study provides a framework to identify other potential causes of antibiotic-associated diarrhoea in relation to other classes of antibiotics,” added Prof Alm.

The next step would be a clinical trial to determine whether certain Ruminococcaceae could be used as a probiotic to prevent diarrhoea in patients prescribed antibiotics.

Source: EurekAlert!

Categories : AntibioticsTags :

Nanoparticle and Antibiotic Polytherapy Defeats AMR Bacteria

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Polytherapy with PMB and cubosomes result in interactions with the bacterial OM in two consecutive ways: PMB initially interacts with the outer leaflet of OM via electrostatic interactions, leading to destabilised areas. Cubosomes then contact with the bilayer, causing further membrane perturbations via a lipid-exchange process. Credit: Monash University/Lai et al.

Researchers from Monash University have discovered a potential new method to circumvent antibiotic resistance, by means of a nanoparticle and antibiotic polytherapy. This approach could also reduce antibiotic intake.

The World Health Organisation (WHO) has declared antimicrobial resistance (AMR) to be among the top 10 global public health threats. A recent report found that in 2019, 1.27 million deaths were directly attributable to AMR infections – more than deaths from either HIV or TB.

AMR occurs when pathogens evolve to no longer respond to medicines, consequently infections become increasingly difficult or impossible to treat.

The study, which appears in Nature Communications, has found that the use of nanoparticles in combination with other antibiotics, is an effective strategy to improve bacterial killing.

For Gram-negative bacteria, polymyxins have been used as drugs of last resort as they disrupt the bacterial outer membrane (OM), causing it to become more permeable, causing cell contents to leak out and kill the bacteria.

The strategy involves administering polymyxin B (PMB) alongside cube-shaped nanoparticles called cubosomes. The PMB disrupted the OM first, but not enough to kill the cell. When the accompanying cubosome bound to the OM, disrupting it further, successfully killing the cell. Interestingly, loading PMB into the cubosomes as a carrier had little effect; in fact, the cubosome strengthened the OM.

“This is a stunning finding in how we deliver medicine and how the medicine we take impacts us in the future,” said lead researcher Dr Hsin-Hui Shen. 

This approach also means that lower dosages of antibiotics could be used. “Instead of looking for new antibiotics to counteract superbugs, we can use the nanotechnology approach to reduce the dose of antibiotic intake, effectively killing multidrug-resistant organisms.”

It has been 30 years since the discovery of the last new antibiotic, and in coming years, the growing crisis of antibiotics resistance will result in increased mortality from basic infections because they have developed antimicrobial resistance.

Without effective antimicrobials, the WHO warns that the success of modern medicine in treating infections, including during major surgery and cancer chemotherapy, would be at increased risk.

While nanoparticles had been used for a long time before as antimicrobial carriers,  “but the use of nanoparticles in polytherapy treatments with antibiotics in order to overcome antimicrobial resistance has been overlooked,” explained Dr Shen. “The use of nanoparticles-antibiotics combination therapy could reduce the dose intake in the human body and overcome the multidrug resistance.”

Research will now progress to the testing phase.

Source: Monash University