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Tag: Antibiotic

  • Minocycline fails to slow vision loss in people with dry age-related macular degeneration

    Minocycline fails to slow vision loss in people with dry age-related macular degeneration

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    The drug minocycline, an antibiotic that also decreases inflammation, failed to slow vision loss or expansion of geographic atrophy in people with dry age-related macular degeneration (AMD), according to a phase II clinical study at the National Eye Institute (NEI), part of the National Institutes of Health.

    Dry AMD affects the macula, the part of the eye’s retina that allows for clear central vision. In people with dry AMD, patches of light-sensing photoreceptors and their nearby support cells begin to die off, leaving regions known as geographic atrophy. Over time, these regions expand, causing people to lose more and more of their central vision. Microglia, immune cells that help maintain tissue and clear up debris, are present at higher levels around damaged retinal regions in people with dry AMD than in people without AMD. Scientists have suggested that inflammation – and particularly microglia – may be driving the expansion of geographic atrophy regions.

    This study, led by Tiarnan Keenan, M.D., Ph.D., a Stadtman Tenure-Track Investigator at the NEI’s Division of Epidemiology and Clinical Applications, tested whether inhibiting microglia with minocycline might help slow geographic atrophy expansion and its corresponding vision loss. The trial enrolled 37 participants at the NIH Clinical Center in Bethesda, Maryland, and at the Bristol Eye Hospital, United Kingdom. After a nine-month period where the researchers tracked each participant’s rate of geographic atrophy expansion, the participants took twice-daily doses of minocycline for two years. The researchers compared each participant’s rate of geographic atrophy expansion while taking minocycline to their baseline rate, and found there was no difference in geographic atrophy expansion rate or vision loss with minocycline. 

    Previous studies have shown that minocycline can help reduce inflammation and microglial activity in the eye, including the retina. The drug has shown beneficial effects for conditions such as diabetic retinopathy, but has not previously been tested for dry AMD.

    The clinical study was funded by the NEI Intramural Program, and took place in part at the NIH Clinical Center. Clinical trial number NCT02564978.

    Source:

    NIH/National Eye Institute

    Journal reference:

    Keenan, T. D. L., et al. (2024). Phase 2 Trial Evaluating Minocycline for Geographic Atrophy in Age-Related Macular Degeneration: A Nonrandomized Controlled Trial. JAMA Ophthalmology. doi.org/10.1001/jamaophthalmol.2024.0118.

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  • Antibiotics can effectively target gut bacteria that harbor COVID-19 virus, study shows

    Antibiotics can effectively target gut bacteria that harbor COVID-19 virus, study shows

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    New research indicates that antibiotics can effectively target bacteria in the gut that harbor the virus that causes COVID-19 and produce toxin-like peptides that contribute to COVID-19-related symptoms. In the study, which involved 211 participants and was published in the Journal of Medical Virology, individuals who received early antibiotic treatment after having COVID-19 recovered more quickly than those who did not receive antibiotics.

    The authors had already evaluated the efficacy of certain antibiotics in SARS-CoV-2-infected bacterial cultures in vitro, and this new study demonstrates promising results with the use of the combination of 2 antibiotics (amoxicillin and rifaximin) within the first 3 days.

    Furthermore, a significant number of patients who received antibiotics within the first 3 days and for a duration of 7 days during the acute phase of COVID-19 did not develop long COVID.

    Our findings suggest that antibiotics should be considered in acute infection and Long COVID. The study also lays the foundation for additional vaccine strategies.”

    Marina Piscopo, PhD, co-corresponding author of the University of Naples Federico, Italy

    Source:

    Journal reference:

    Brogna, C., et al. (2024) A retrospective cohort study on early antibiotic use in vaccinated and unvaccinated COVID-19 patients. Journal of Medical Virology. doi.org/10.1002/jmv.29507.

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  • Antimicrobial resistance prevalence tied to patient age and sex

    Antimicrobial resistance prevalence tied to patient age and sex

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    A person’s age and sex are correlated with the chance that they have a bloodstream infection caused by a bacterium that is resistant to antibiotics, according to a new study published in PLOS Medicine.

    Antimicrobial resistance (AMR), which encompasses infections that cannot be treated with antibiotics, is a major global public health threat. Little has been known about how the prevalence of resistance varies with patient’s age and sex, despite both factors being linked to variation in antibiotic usage, changes in immune function and exposure to high-risk settings.

    In the new study, led by researchers from the London School of Hygiene & Tropical Medicine (LSHTM), data collected as part of routine surveillance between 2015 and 2019 on bloodstream infections in 944,520 individuals across 29 European countries were analyzed. 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 the prevalence of resistance 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.

    Our findings highlight important gaps in our knowledge of the spread and selection of antimicrobial resistance (AMR) and may help us understand why the epidemiology has been difficult to explain through known patterns of antibiotic exposure and healthcare contact.


    They also suggest 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.


    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 antimicrobial resistance being seen.”


    Dr Gwen Knight, Associate Professor and Co-Director of the AMR Centre at LSHTM

    Source:

    London School of Hygiene & Tropical Medicine (LSHTM)

    Journal reference:

    Waterlow, N. R., et al. (2024). Antimicrobial resistance prevalence in bloodstream infection in 29 European countries by age and sex: An observational study. PLOS Medicine. doi.org/10.1371/journal.pmed.1004301.

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  • Innovative plasma-activated hydrogel dressings revolutionize chronic wound care

    Innovative plasma-activated hydrogel dressings revolutionize chronic wound care

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    An effective treatment for chronic wounds that does not involve antibiotics, but an ionized gas to activate a wound dressing, has been developed by a team of international scientists.

    The treatment involves the plasma activation of hydrogel dressings (that are commonly used in wound dressings) with a unique mix of different chemical oxidants that are effective in decontaminating and aid healing in chronic wounds.

    Researchers from the University of Sheffield and University of South Australia, who led the study, believe the new method is a significant advance in tackling antibiotic resistance pathogens and has the potential to change the treatment of diabetic foot ulcers and internal wounds. 

    Professor Rob Short, Professor of Chemistry at the University of Sheffield who co-authored the study, said: “More than 540 million people are living with diabetes worldwide, of which 30 per cent will develop a foot ulcer during their lifetime. This is a neglected global pandemic which is set to increase further in the coming years due to a rise in obesity and lack of exercise.

    “In England alone between 60,000 and 75,000 people are being treated for diabetic foot ulcers per week. Infection is one of the major risks. Increasingly, many infections do not respond to normal antibiotic treatment due to resistant bacteria which results in 7,000 amputations per year.

    “There is an urgent need for innovation in wound management and treatment and it is a real privilege to be part of the international team who have been working on this alternative treatment for over 10 years.” 

    The cost of managing chronic wounds such as diabetic foot ulcers already exceeds $17 billion US dollars annually.

    The benefits of cold plasma ionized gas have already been proven in clinical trials, showing it controls not only infection but also stimulates healing. This is due to the potent chemical cocktail of oxidants, namely reactive oxygen and nitrogen species (RONS) it produces when it mixes and activates the oxygen and nitrogen molecules in the ambient air.

    Dr Endre Szili, from the University of South Australia who led the study, published this week in the journal Advanced Functional Materials, said: “Antibiotics and silver dressings are commonly used to treat chronic wounds, but both have drawbacks.

    “Growing resistance to antibiotics is a global challenge and there are also major concerns over silver-induced toxicity. In Europe, silver dressings are being phased out for this reason.”

    The international team of scientists have shown that plasma-activating hydrogel dressings with RONS makes the gel far more powerful, killing common bacteria.

    Although diabetic foot ulcers were the focus of this study, the technology could be applied to all chronic wounds and internal infections.

    Despite recent encouraging results in the use of plasma-activated hydrogel therapy (PAHT), we faced the challenge of loading hydrogels with sufficient concentrations of RONS required for clinical use. We have overcome this hurdle by employing a new electrochemical method that enhances the hydrogel activation.” 

    Dr. Endre Szili, University of South Australia

    As well as killing common bacteria (E. coli and P. aeruginosa) that cause wounds to become infected, the researchers say that the plasma-activated hydrogels might also help trigger the body’s immune system, which can help fight infections.

    “Chronic wound infections are a silent pandemic threatening to become a global healthcare crisis,” added Dr Szili.

    “It is imperative that we find alternative treatments to antibiotics and silver dressings because when these treatments don’t work, amputations often occur.”

    “A major advantage of our PAHT technology is that it can be used for treating all wounds. It is an environmentally safe treatment that uses the natural components in air and water to make its active ingredients, which degrade to non-toxic and biocompatible components.”

    “The active ingredients could be delivered over a lengthy period, improving treatment, with a better chance of penetrating a tumor.

    “Plasma has massive potential in the medical world, and this is just the tip of the iceberg,” Dr Szili says.

    The next step will involve clinical trials to optimize the electrochemical technology for treatment in human patients.

    Source:

    Journal references:

    Sumyea Sabrin, et al. (2024). Electrochemically Enhanced Antimicrobial Action of Plasma‐Activated Poly(Vinyl Alcohol) Hydrogel Dressings. Advanced Functional Materials. doi.org/10.1002/adfm.202314345.

     

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  • New study highlights the urgent need for typhoid vaccination in sub-Saharan Africa

    New study highlights the urgent need for typhoid vaccination in sub-Saharan Africa

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    There is a high burden of typhoid fever in sub-Saharan African countries, according to a new study published today in The Lancet Global Health. This high burden combined with the threat of typhoid strains resistant to antibiotic treatment calls for stronger prevention strategies, including the use and implementation of typhoid conjugate vaccines (TCVs) in endemic settings along with improvements in access to safe water, sanitation, and hygiene.

    The findings from this 4-year study, the Severe Typhoid in Africa (SETA) program, offers new typhoid fever burden estimates from six countries: Burkina Faso, Democratic Republic of the Congo (DRC), Ethiopia, Ghana, Madagascar, and Nigeria, with four countries recording more than 100 cases for every 100,000 person-years of observation, which is considered a high burden. The highest incidence of typhoid was found in DRC with 315 cases per 100,000 people while children between 2-14 years of age were shown to be at highest risk across all 25 study sites.

    There are an estimated 12.5 to 16.3 million cases of typhoid every year with 140,000 deaths. However, with generic symptoms such as fever, fatigue, and abdominal pain, and the need for blood culture sampling to make a definitive diagnosis, it is difficult for governments to capture the true burden of typhoid in their countries.

    “Our goal through SETA was to address these gaps in typhoid disease burden data,” said lead author Dr. Florian Marks, Deputy Director General of the International Vaccine Institute (IVI). “Our estimates indicate that introduction of TCV in endemic settings would go to lengths in protecting communities, especially school-aged children, against this potentially deadly-;but preventable-;disease.”

    In addition to disease incidence, this study also showed that the emergence of antimicrobial resistance (AMR) in Salmonella Typhi, the bacteria that causes typhoid fever, has led to more reliance beyond the traditional first line of antibiotic treatment. If left untreated, severe cases of the disease can lead to intestinal perforation and even death. This suggests that prevention through vaccination may play a critical role in not only protecting against typhoid fever but reducing the spread of drug-resistant strains of the bacteria.

    There are two TCVs prequalified by the World Health Organization (WHO) and available through Gavi, the Vaccine Alliance. In February 2024, IVI and SK bioscience announced that a third TCV, SKYTyphoid™, also achieved WHO PQ, paving the way for public procurement and increasing the global supply.

    Alongside the SETA disease burden study, IVI has been working with colleagues in three African countries to show the real-world impact of TCV vaccination. These studies include a cluster-randomized trial in Agogo, Ghana and two effectiveness studies following mass vaccination in Kisantu, DRC and Imerintsiatosika, Madagascar.

    Through these vaccine effectiveness studies, we aim to show the full public health value of TCV in settings that are directly impacted by a high burden of typhoid fever.” He adds, “Our final objective of course is to eliminate typhoid or to at least reduce the burden to low incidence levels, and that’s what we are attempting in Fiji with an island-wide vaccination campaign.”


    Dr. Birkneh Tilahun Tadesse, Associate Director General at IVI and Head of the Real-World Evidence Department

    As more countries in typhoid endemic countries, namely in sub-Saharan Africa and South Asia, consider TCV in national immunization programs, these data will help inform evidence-based policy decisions around typhoid prevention and control.

    Source:

    International Vaccine Institute

    Journal reference:

    Marks, F., et al. (2024) Incidence of typhoid fever in Burkina Faso, Democratic Republic of the Congo, Ethiopia, Ghana, Madagascar, and Nigeria (the Severe Typhoid in Africa programme): a population-based study. The Lancet Global Health. doi.org/10.1016/S2214-109X(24)00007-X.

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  • Novel genetic mechanisms of tetracycline resistance in gut bacteria discovered

    Novel genetic mechanisms of tetracycline resistance in gut bacteria discovered

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    Antibiotic resistance is a significant and growing medical problem worldwide. Researchers at the Marine Biological Laboratory (MBL) and collaborators have found a novel genetic arrangement that may help a common bacterium in the human gut, Bacteroides fragilis, protect itself from tetracycline, a widely used antibiotic.

    While these findings will not lead directly to new ways of combating tetracycline-resistant bacteria, the researchers have discovered previously unseen genetic arrangements that confer antibiotic resistance. Such understanding might help in developing new ways to limit the spread of antibiotic resistance genes, through genetic manipulation or other means.

    The findings were reported in the journal mBio by MBL scientists Joseph Vineis, Mitchell Sogin and Blair Paul, along with colleagues from MBL, Argonne National Laboratory, and the University of Chicago.

    The bacteria they studied, Bacteroides fragilis, was recovered from a patient with ulcerative colitis, where it was found to be abundant during periods of inflammation. The team had a large set of samples to analyze from patients with inflammatory bowel disease that had been surgically treated to alleviate the inflammation.

    These samples were studied at MBL using shotgun metagenomics, which produces sequences for all the genetic material in an entire community of microbial cells. It also facilitates cultivation of bacterial strains from the community, providing the data required to observe the activity of the tetracycline-resistance genes while growing in the presence of tetracycline. (At the time they started this work, Vineis says, “to be able to reconstruct genomes from metagenomic data was just getting started in the field. It was a novel approach, but now it’s common.”)

    “When we looked at the data,” Vineis says, “there was a very strong signal” showing high numbers of copies of particular regions of the bacterial genomes. One of these regions, encompassing many genes, “was very abundant” in the sample, and later they were able to determine “that this particular high-copy region contained tetracycline resistance… So we kept digging.”

    These high-copy sections of the genome contained DNA fragments that can move around in the genome or even jump into a different genome. Called transposons, these mobile genetic elements are “important ways for bacteria to develop adaptations to the environment without having to reinvent them themselves completely,” Vineis says. And in the human intestines, where vast numbers of species of gut bacteria are constantly in close proximity, “the potential for exchange is really high,” he says, and the rate increases when there is inflammation.

    Such exchange of genetic material between different species is called horizontal transfer. Blair Paul, an assistant scientist at MBL, says that “we think these transposons are actually a key vehicle for horizontal gene transfer.”

    In this case, the bacteria apparently sense when there is tetracycline in the environment and begin “a whole cascade” of production of a transposon containing the resistance gene, Vineis says.

    The part of the transposon containing the resistance gene, they found, occurred in two different forms within the same genome: Sometimes it is in its normal linear form, and sometimes rolled into a circle. Both forms occur at once in the Bacteroides fragilis genome, but the linear form contains a unique genomic insert in the region of DNA that encodes the machinery for mobilization into other cells.

    This hasn’t been seen before, to our knowledge, this particular type of transposon having a subregion amplified. And it’s occurring in bacteria that coincide with inflammation.”


    Blair Paul, MBL Scientist

    The increased expression of this group of genes is potentially associated with the success of Bacteroides fragilis during inflammation, although the connection is not yet proven and requires further research. But Paul says the findings “raise new questions about the role of gene transfer in human health, but also in terms of just how these transposons are controlled and how they may be changing evolutionarily over time.”

    “This finding is not going to change our understanding about the world of antibiotic resistance, but it’s a novel kind of mechanism that at least we can start looking for,” Vineis says. “There’s a lot of offense and defense happening within the microbial world that we’re not even fully aware of.”

    Source:

    Marine Biological Laboratory

    Journal reference:

    Vineis, J. H., et al. (2024). A novel conjugative transposon carrying an autonomously amplified plasmid. mBio. doi.org/10.1128/mbio.02787-23.

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  • Nerve overgrowth identified as cause of pain in recurring UTIs

    Nerve overgrowth identified as cause of pain in recurring UTIs

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    A perplexing problem for people with recurring urinary tract infections (UTIs) is persistent pain, even after antibiotics have successfully cleared the bacteria.

    Now Duke Health researchers have identified the likely cause – an overgrowth of nerve cells in the bladder.

    The finding, appearing March 1 in the journal Science Immunology, provides a potential new approach to managing symptoms of recurring UTIs that would more effectively target the problem and reduce unnecessary antibiotic usage.

    “Urinary tract infections account for almost 25% of infections in women,” said senior author Soman Abraham, Ph.D., professor in the departments of Pathology, Molecular Genetics and Microbiology, Integrative Immunobiology, and Cell Biology at Duke University School of Medicine.

    “Many are recurrent UTIs, with patients frequently complaining of chronic pelvic pain and urinary frequency, even after a round of antibiotics,” Abraham said. “Our study, for the first time, describes an underlying cause and identifies a potential new treatment strategy.”

    Abraham and colleagues collected bladder biopsies from recurrent UTI patients who were experiencing pain despite no culturable bacteria in their urine. Using biopsies from people without UTIs as a comparison, they found evidence that sensory nerves were highly activated in the UTI patients, explaining the persistent sense of pain and urinary frequency.

    Further studies in mice revealed the underlying events, with unique conditions in the bladder that prompt activated nerves in the lining to bloom and grow with each infection.

    “Typically, during every bout of UTI, epithelial cells laden with bacteria are sloughed off, and significant destruction of nearby nerve tissue occurs,” said Byron Hayes, lead author of the study and previously a postdoctoral fellow in Duke’s Department of Pathology. “These events trigger a rapid repair program in the damaged bladder involving massive regrowth of destroyed nerve cells.”

    This immune response, including repair activities, is led by mast cells – which are immune cells that fight infection and allergens. Mast cells release chemicals called nerve growth factor, which drive overgrowth and increase sensitivity of nerves. The result is pain and urgency.

    The researchers were able to address these symptoms by treating study mice with molecules that suppress production of the mast-cell generated nerve growth factor.

    This work helps illuminate a puzzling clinical condition that drives medical costs and affects the quality of life of millions of people, primarily women,” Abraham said. “Understanding the crosstalk between mast cells and nerves is an essential step toward effective treatments for people suffering repeat urinary tract infections.”


    Soman Abraham, Ph.D., Senior Author

    In addition to Abraham and Hayes, study authors include Hae Woong Choi, Abhay PS Rathore, Chunjing Bao, Jianling Shi, Yul Huh, Michael W Kim, Andrea Mencarelli, Pradeep Bist, Lai Guan Ng, Changming Shi, Joo Hwan Nho, Aram Kim, Hana Yoon, Donghoon Lim, Johanna L Hannan, J Todd Purves, Francis M Hughes Jr, and Ru-Rong Ji.

    The study received funding support from the National Institutes of Health (K12-DK100024, R01-DK121969, R01-DK121032, R01-GM144606), the National Research Foundation of Korea (2020R1C1C1003257), and a Korea University grant.

    Source:

    Duke University Medical Center

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  • Key link discovered between spread of antibiotic resistance genes and drug resistance evolution

    Key link discovered between spread of antibiotic resistance genes and drug resistance evolution

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    Biomedical engineers at Duke University have uncovered a key link between the spread of antibiotic resistance genes and the evolution of resistance to new drugs in certain pathogens.

    The research shows bacteria exposed to higher levels of antibiotics often harbor multiple identical copies of protective antibiotic resistance genes. These duplicated resistance genes are often linked to “jumping genes” called transposons that can move from strain to strain. Not only does this provide a mechanism for resistance to spread, having multiple copies of a resistance gene can also provide a handle for evolution to generate resistance to new types of drugs.

    The results appeared February 16 in the journal Nature Communications.

    Earlier work by the Lingchong You lab has shown that 25% of bacterial pathogens are capable of spreading antibiotic resistance through horizontal gene transfer. They have also shown that the presence of antibiotics does not speed up the rate of horizontal gene transfer, so there must be something else happening that pushes the genes to spread.

    “Bacteria are constantly evolving under many pressures, and elevated duplication of certain genes is like a fingerprint left at the crime scene that allows us to see what kinds of functions are evolving really rapidly,” said Rohan Maddamsetti, a postdoctoral fellow working in the laboratory of Lingchong You, the James L. Meriam Distinguished Professor of Biomedical Engineering at Duke.

    “We hypothesized that bacteria under attack from antibiotics would often have multiple copies of protective resistance genes, but until recently we didn’t have the technology to find the smoking gun.”

    Traditional DNA-reading technology copies short snippets of genes and counts them up, making it hard to determine whether high counts of specific sequences are actually in the sample or if they are being artificially amplified by the reading process. In the past five years, however, complete genome sequencing with long-read technology has become more common, allowing researchers to spot high levels of genetic repetition.

    In the study, Maddamsetti and coauthors counted the repetitions of resistance genes present in samples of bacterial pathogens taken from a variety of environments. They discovered that those living in places with higher levels of antibiotic use -; humans and livestock -; are enriched with multiple identical copies of antibiotic resistance genes, while such duplications are rare in bacteria living in wild plants, animals, soil and water.

    Most bacteria have some basic antibiotic resistance genes in them, but we rarely saw them being duplicated out in nature. By contrast, we saw lots of duplication happening in humans and livestock where we’re likely hammering them with antibiotics.”


    Lingchong You, the James L. Meriam Distinguished Professor of Biomedical Engineering at Duke University

    The researchers also found that the levels of resistance duplication were even higher in samples taken from clinical datasets where patients are likely taking antibiotics. This is an important point, they say, because the increase in copying antibiotic resistance genes also increases the likelihood of bacteria evolving resistance to new types of treatments.

    “Constantly creating copies of genes for resistance to penicillin, for example, may be the first step toward being able to break down a new kind of drug,” Maddamsetti said. “It gives evolution more rolls of the dice to find a special mutation.”

    “Everyone recognizes there is a growing antibiotic resistance crisis, and the knee jerk reaction is to develop new antibiotics,” You added. “But what we find time and again is that, if we can figure out how to use antibiotics more efficiently and effectively, we can potentially address this crisis much more effectively than simply developing new drugs.”

    “The majority of antibiotics used in the United States are not used on patients, they’re used in agriculture,” You added. “So this is an especially important message for the livestock industry, which is a major driver of why antibiotic resistance is always out there and becoming more serious.”

    This work was supported by the National Institutes of Health (R01AI125604, R01GM098642, R01EB031869).

    Source:

    Journal reference:

    Maddamsetti, R., et al. (2024). Duplicated antibiotic resistance genes reveal ongoing selection and horizontal gene transfer in bacteria. Nature Communications. doi.org/10.1038/s41467-024-45638-9.

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  • Maternal antibiotic use during childbirth tied to higher risk of autoimmune diseases in children

    Maternal antibiotic use during childbirth tied to higher risk of autoimmune diseases in children

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    Children whose mothers have received antibiotic treatment during childbirth are more likely to develop autoimmune diseases compared to their counterparts, according to a recent registry-based study conducted at the University of Oulu, Finland, involving nearly 46,000 children. The most common autoimmune diseases in children include type 1 diabetes, celiac disease, and rheumatic diseases. However, the study found that administration of antibiotics during childbirth showed no association with allergic diseases or asthma in the child.

    Antibiotic treatment given to mothers during delivery effectively prevents rare serious infections caused by Group B streptococcus in newborns, thereby reducing associated mortality. In Finland, antibiotics are administered to mothers during childbirth if Group B streptococcus is detected in the birth canal before delivery, and almost one in four women delivering vaginally receives antibiotic treatment.

    The research findings play a crucial role in assessing the potential drawbacks of perinatal antibiotic use and investigating the underlying mechanisms of immune-related diseases. Previous knowledge indicated that antibiotics given to mothers during childbirth affect the development of the child’s intestinal microbiota. The study supports the idea that a normal gut microbiota may have implications for a child’s long-term health.

    This is an observational study that does not directly establish a cause-and-effect relationship between the antibiotics given to mothers during childbirth and the child’s later health. The result is a statistical association possibly influenced by other factors as well.”


    Sofia Ainonen, lead author of the article and doctoral researcher at the University of Oulu

    According to Professor Terhi Ruuska, who led the study, the findings encourage the development of precise prevention methods for Group B streptococcus infections. One potential method could be a vaccine administered to mothers that does not impact the child’s normal microbiota.

    The study followed children born vaginally in Oulu University Hospital (OYS) and Oulaskangas hospital in Northern Ostrobothnia, Finland, between 2007 and 2018. The study utilised national registers from the National Institute for Health and Welfare, the Social Insurance Institution of Finland (Kela) and Statistics Finland, as well as high-quality electronic patient records from the hospitals in the OYS region, which provided comprehensive information on maternal antibiotic exposure.

    The pre-approved version of the study was published in the American Journal of Obstetrics and Gynecology on February 16th.

    Source:

    Journal reference:

    Ainonen, S., et al. (2024) Risk of Immune-related Diseases in Childhood after Intrapartum Antibiotic Exposure. ​​American Journal of Obstetrics and Gynecology. doi.org/10.1016/j.ajog.2024.02.020.

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  • Missing gut microbes after antibiotics and a high-fat diet may be to blame for sugar-free candy and gum giving you gas

    Missing gut microbes after antibiotics and a high-fat diet may be to blame for sugar-free candy and gum giving you gas

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    In high-income countries, carbohydrate intolerance affects about 30% of the population. The exact mechanism of sorbitol intolerance remains unresolved. A recent Cell study showed how a high-fat diet and antibiotic exposure could trigger sorbitol intolerance by depleting Clostridia from the gut microbiota.

    Study: High fat intake sustains sorbitol intolerance after antibiotic-mediated Clostridia depletion from the gut microbiota. Image Credit: liveostockimages/Shutterstock.com
    Study: High fat intake sustains sorbitol intolerance after antibiotic-mediated Clostridia depletion from the gut microbiota. Image Credit: liveostockimages/Shutterstock.com

    Background

    Sorbitol is poorly absorbed by the small intestine, which results in food items having fewer calories. It is a naturally occurring polyol present in fruits like apples, apricots, and pears, as well as sugar-free gum. Excessive consumption of sorbitol can lead to symptoms of carbohydrate intolerance, including flatulence, abdominal distention, and diarrhea. This is especially true in irritable bowel syndrome (IBS) patients or patients with quiescent inflammatory bowel disease (IBD).

    Antibiotic treatment can temporarily raise polyol intolerance by altering the gut microbiota. This alteration could hamper metabolic functions that clear osmotically active solutes. Since this effect is temporary, it cannot explain the prolonged carbohydrate intolerance in IBD and IBS patients. Therefore, the treatment of sustained polyol intolerance centers around dietary interventions reducing polyol intake and other poorly absorbed oligosaccharides.

    About this study

    For this study, male C57BL6/J mice were obtained from The Jackson Laboratory. These animals were aged about six weeks. Furthermore, by mating Ppargfl/fl with Villincre/- mice, researchers were able to generate littermate Ppargfl/flVillin-/ mice and C57BL/6 Ppargfl/flVillincre/- mice. Animals were fed either a (sorbitol-free) 45% fat (HF) diet or a (sorbitol-free) 10% control (LF) diet. To study antibiotic-induced sorbitol intolerance, 20 mg/animal of streptomycin was used.

    Study findings

    This study developed a mice model for prolonged sorbitol intolerance and shed light on the pathophysiology of this condition. It was noted that the abundance of Clostridia was lowered by a combination of HF diet and antibiotic exposure. This observation challenges a commonly held view that malabsorption causes prolonged sorbitol intolerance. HF intake and sustained antibiotic exposure are also environmental risk factors for the pathophysiology of IBD.

    In this mouse model, it was shown that a reduced abundance of Clostridia in the fecal microbiota and muted butyrate production could be functionally related to sustained sorbitol intolerance. These findings align well with clinical trials that demonstrate a correlation between gastrointestinal symptoms in IBD patients and carbohydrate intake.

    An environment conducive to the growth of Clostridia is fostered by epithelial hypoxia, which lowers the diffusion of oxygen into the intestinal lumen. When colonic microbiota is disrupted by antibiotics, short-chain fatty acids are depleted. This alters epithelial metabolism and enhances the availability of host-derived oxygen.

    Oxidative stress is triggered in host cells by an HF diet by raising the production of hydrogen peroxide by the mitochondria. This is how an HF diet hampers mitochondrial bioenergetic recovery post-antibiotic treatment. Subsequently, this interferes with microbiota recovery. The results presented here suggest that prophylaxis with 5-ASA could promote microbiota recovery and reestablish epithelial hypoxia post-exposure to antibiotics. This is true even when the subject is consuming a HF diet. Therefore, to treat prolonged sorbitol intolerance, a potential target could be the intestinal epithelium.

    The findings also suggest that the microbiota could be a second treatment target. This is motivated by the observation that impaired microbial sorbitol catabolism could lead to prolonged sorbitol intolerance. Probiotics that consume sorbitol, such as L. plantarum or E. coli Nissle 1917, could be another treatment option, but the concentration of probiotics in the feces should govern the protective effect.

    The data documented here suggest that A. caccae could be a second-generation probiotic targeting the microbes and the host to protect against sorbitol intolerance. Importantly, A. caccae was seen to protect against prolonged sorbitol intolerance even in a low abundance of probiotics. A. caccae was less effective when microbiota recovery was complete.

    Limitations of the study

    The limitations of the study center around the use of a mouse model and the extension to humans. Antibiotic-naive mice were seen to tolerate up to 5% sorbitol. In humans, this is equivalent to a daily intake of 20–30 g. This is a high dose that can potentially induce symptoms of carbohydrate intolerance among healthy control volunteers. Mice can tolerate a higher sorbitol intake compared to because humans possess an enlarged cecum in order to slow digestive flow. This aids in the catabolism of carbohydrates in the gut microbiota.

    The difference in morphology and function between the gastrointestinal tracts of humans and mice presents the main limitations of rodent models. More studies are needed to assess whether probiotics or proliferator-activated receptor-γ (PPAR-γ) agonists could potentially treat or prevent sorbitol intolerance.

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