Tag: antibiotic resistance

Diabetes Can Drive the Evolution of Antibiotic Resistance

Photo by CDC on Unsplash

Staphylococcus aureus is a leading cause of antibiotic resistance associated infections and deaths. It is also the most prevalent bacterial infection among those with diabetes mellitus, a chronic condition that affects blood sugar control and reduces the body’s ability to fight infections.

Microbiologists at the UNC School of Medicine have just shown that people with diabetes are more likely to develop antibiotic-resistant strains of Staph, too. Their results, which were published in Science Advances, show how the diabetic microbial environment produces resistant mutations, while hinting at ways antibiotic resistance can be combatted in this patient population.

“We found that antibiotic resistance emerges much more rapidly in diabetic models than in non-diabetic models of disease,” said Brian Conlon, PhD, associate professor of immunology. “This interplay between bacteria and diabetes could be a major driver of the rapid evolution and spread of antibiotic resistance that we are seeing.”

 Staph feeds off the high levels of blood glucose in diabetes, allowing it to reproduce more rapidly. The bacterium can also grow without consequence, as diabetes also impairs the immune system’s ability to destroy cells and control infection.

As the numbers of bacteria increase in a diabetic infection, so does the likelihood of resistance. Random mutations appear and some build up resistance to external stressors, like antibiotics. Once a resistant mutant is present in a diabetic infection, it rapidly takes over the population, using the excess glucose to drive its rapid growth.

Staphylococcus aureus is uniquely suited to take advantage of this diabetic environment,” said Lance Thurlow, PhD, assistant professor of microbiology and immunology. “Once that resistant mutation happens, you have excess glucose and you don’t have the immune system to clear the mutant and it takes over the entire bacterial population in a matter of days.”

Conlon, an expert on antibiotic treatment failure, and Thurlow, an expert on Staph pathogenesis in diabetes, have long been interested in comparing the effectiveness of antibiotics in a model with and without diabetes. Using their connections within the Department of Microbiology and Immunology, the researchers brought their labs together to perform a study with antibiotics in a diabetic mouse model of S. aureus infection.

First, the team prepared a mouse model with bacterial infection in the skin and soft tissue. The mouse models were divided into two groups: one half was given a compound that selectively kills cells in the pancreas, rendering them diabetic, and the other half was not given the compound. Researchers then infected both diabetic and non-diabetic models with S. aureus and treated them with rifampicin, an antibiotic where resistance evolves at a high rate.

After five days of infection, it was time to observe the results.

Conlon and Thurlow were quick to notice that the rifampicin had practically no effect in diabetic models. So, they took some samples to investigate. Researchers were shocked to find that the bacteria had evolved to become resistant to rifampicin, with the infection harboring over a hundred million rifampicin resistant bacteria. There were no rifampicin resistant bacteria in the non-diabetic models.

Their new findings have left Conlon and Thurlow with many questions; however, they are certain that the evolution of antibiotic resistance in people with diabetes could spell trouble for the population at large.

And, even more surprisingly, the mutation had taken over the entire infection in just four days. They next inoculated diabetic and non-diabetic models with Staphylococcus aureus as before, but this time supplemented with a known number of rifampicin resistant bacteria. Again, these bacteria rapidly took over the diabetic infection, but remained as only a sub-population in non-diabetic models after 4 days rifampicin treatment.

Their new findings have left Conlon and Thurlow with many questions; however, they are certain that the evolution of antibiotic resistance in people with diabetes could spell trouble for the population at large. Antibiotic-resistant strains of bacteria spread from person to person in the same ways as other bacteria and viruses do – in the air, on doorknobs, and the food that we eat – which makes preventing these types of infections a major priority.

So, what can be done to prevent it? Well, the Conlon and Thurlow labs showed that reducing blood sugar levels in diabetic models (through administration of insulin) deprived bacteria of their fuel, keeping their numbers at bay, and reducing the chances of antibiotic-resistant mutations from occurring. Their findings suggest that controlling blood sugar through insulin use could be key in preventing antibiotic resistance.

“Resistance and its spread are not only associated with the prescription of drugs, but also the health status of those that are taking antibiotics,” said Conlon. “Controlling blood glucose then becomes really important. When we gave our mice insulin, we were able to bring their blood sugar back to normal and we didn’t get this rapid proliferation of resistant bacteria.”

Now, Conlon and Thurlow are expanding their efforts to study the evolution of resistance in humans (with and without diabetes) and other antibiotic-resistant bacteria of interest, including Enterococcus faecalisPseudomonas aeruginosa, and Streptococcus pyogenes. Recognizing how large a role the host plays a role in the evolution of antibiotic resistance, the researchers plan to perform similar studies in patients undergoing chemotherapy and recent transplant recipients to see if those populations are also prone to antibiotic resistant infections.

Source: University of North Carolina Health Care

Study Finds Three New Safe, Effective Ways to Treat Drug-resistant TB

Tuberculosis bacteria. Credit: CDC

An international clinical trial has found three new safe and effective drug regimens for tuberculosis that is resistant to rifampin, the most effective of the first-line antibiotics used to treat TB. The research, published in the New England Journal of Medicine, was led by researchers at Harvard Medical School and other members of the endTB project.

The newly identified regimens take advantage of recently discovered drugs to expand the treatment arsenal and give physicians new ways to shorten and personalise treatment, minimise side effects, and treat patients using only pills instead of daily injections. They also offer alternatives in case of drug intolerance, medication shortages or unavailability, or drug resistance, the researchers said.

The endTB trial is one of four recent efforts to use randomised controlled trials to test new, shorter, less toxic regimens for drug-resistant TB. endTB uses two new drugs – bedaquiline and delamanid — which, when brought to market in 2012-2013, were the first new TB medicines developed in nearly 50 years.

To find shorter, injection-free drug combinations for people infected with TB resistant to rifampin, endTB tested five new, all-oral 9-month regimens using the two new drugs in combination with older medications.

A third drug, pretomanid, received emergency authorisation from the FDA for specific use within a regimen against highly drug-resistant TB in 2019, after the endTB clinical trial was underway, and is not included in the regimens used in these trials.

Trial regimens were considered effective if they performed at least as well as the control group, which received a well-performing standard of care composed in accordance with a stringent interpretation of World Health Organization (WHO) recommendations.

The three successful new regimens were successful for between 85 and 90% of patients, compared with 81% success for people in the control group. The control group was treated with longer treatments, which also included the recently discovered medicines.

The trial launched in 2017 and enrolled 754 patients across seven countries: Georgia, India, Kazakhstan, Lesotho, Pakistan, Peru, and South Africa. The goal was to improve treatment for patients with tuberculosis resistant to rifampin. The WHO estimates that some 410 000 people become sick with rifampin-resistant TB each year, including people who have multidrug-resistant TB (MDR-TB). Only 40% are diagnosed and treated, 65%of them successfully.

The study population included children as well as people infected with HIV or hepatitis C, both common in populations with high rates of TB. In another innovation, women who became pregnant while on treatment were included in the endTB trial. These groups are often excluded from clinical trials. In a special report published in August 2024, the WHO added the three noninferior regimens from the endTB trial to the list of treatment options for rifampin-resistant and multidrug-resistant TB (MDR-TB) treatment; the recommendations extend to these neglected groups as well as to pregnant women.

With recent efforts to end patent exclusivity on bedaquiline, two of the endTB regimens and the WHO-recommended pretomanid-containing regimen can all be purchased for less than $500, an access target set by activists more than 10 years ago, which has only just now been achieved. All of these innovations together mean the new shortened, all-oral regimens are available to more people than ever.

Source: Harvard Medical School

The Spread of a Highly Drug-resistant Cholera Strain

Scanning electron micrograph image of cholera bacteria.

Scientists from the National Reference Center for Vibrios and Cholera at the Institut Pasteur, in collaboration with the Centre hospitalier de Mayotte, have revealed the spread of a highly drug-resistant cholera strain from Yemen down through Africa. The study was published in the New England Journal of Medicine.

Cholera is caused by the bacteria Vibrio cholerae and in its most severe forms, it is one of the most rapidly fatal infectious diseases: in the absence of treatment, patients can die within hours. Treatment primarily involves replacing lost water and electrolytes, but antibiotics are also used in addition to rehydration therapy. They are essential in reducing the duration of infection and breaking chains of transmission as quickly as possible.

A strain resistant to ten antibiotics – including azithromycin and ciprofloxacin, two of the three recommended for treating cholera – was identified for the first time in Yemen during the cholera outbreak in 2018-2019[1].

Scientists have now been able to trace the spread of this strain by studying the bacterial genomes. After Yemen, it was identified again in Lebanon in 2022[2], then in Kenya in 2023, and finally in Tanzania and the Comoros Islands – including Mayotte, a French département off the south-east coast of Africa – in 2024. Between March and July 2024, the island of Mayotte was affected by an outbreak of 221 cases caused by this highly drug-resistant strain.

“This study demonstrates the need to strengthen global surveillance of the cholera agent, and especially to determine how it reacts to antibiotics in real time. If the new strain that is currently circulating acquires additional resistance to tetracycline, this would compromise all possible oral antibiotic treatment,” concludes Professor François-Xavier Weill, Head of the Vibrios CNR at the Institut Pasteur and lead author of the study.

[1] Press release 19/08/2023 – Genes fuelling antibiotic resistance in Yemen cholera outbreak uncovered

[2] https://www.nature.com/articles/s41467-024-51428-0

Source: Institut Pasteur

Research Shines a Light on Emerging Virulent Streptococcus Subspecies

This illustration depicts a 3D computer-generated image of a group of Gram-positive, Streptococcus pneumoniae bacteria. The artistic recreation was based upon scanning electron microscopic (SEM) imagery. Credit: CDC on Unsplash

A concerning increase in global rates of severe invasive infections becoming resistant to key antibiotics has a team of infectious disease researchers at the Houston Methodist Research Institute studying a recently emerged strain of bacteria, Streptococcus dysgalactiae subspecies equisimilis (SDSE). SDSE infects humans via the skin, throat, gastrointestinal tract and female genital tract to cause infections ranging in severity from pharyngitis to necrotising fasciitis. The findings of this study are described in a paper appearing in the journal mBio

Though closely related to group A streptococcus (also commonly known as Streptococcus pyogenes), which has been very well studied, little is known about SDSE.

“Given its great emerging importance to human health, our limited understanding of SDSE molecular pathogenesis is remarkable,” said Jesus M. Eraso, PhD, an assistant research professor of pathology & genomic medicine with Houston Methodist and lead author on the study.

To close this knowledge gap, the Houston Methodist team used a sophisticated integrative approach to study 120 human isolates of a particular SDSE subtype, called stG62647. They analysed the subtype’s genome, where the information of its DNA is stored, its transcriptome, which provides a snapshot of the complete gene expression profile at the time the SDSE cells were collected, and its virulence, which refers to the degree of damage it causes to its host. The stG62647 SDSE strains are important to study because they have been reported to cause unusually severe infections, and understanding the relationships and interplay between these three entities gave the researchers a richer understanding of how it causes disease.

The data from this integrative analysis provided much new data about this important emerging human bacterial pathogen and are useful in vaccine research. It also raised many new questions and generated new hypotheses to be studied in this ongoing line of investigation.

Source: Houston Methodist Research Institute

Bacteria able to Overcome Cost of Vancomycin Resistance in Lab Setting

Compensatory mutations enabled vancomycin resistance to persist through several generations

Methicillin resistant Staphylococcus aureus (MRSA) – Credit: CDC

Staphylococcus aureus has the potential to develop durable vancomycin resistance, according to a study published August 28, 2024, in the open-access journal PLOS Pathogens by Samuel Blechman and Erik Wright from the University of Pittsburgh, USA.

Despite decades of widespread treatment with the antibiotic vancomycin, vancomycin resistance among the bacterium S. aureus is extremely uncommon – only 16 such cases have reported in the US to date. Vancomycin resistance mutations enable bacteria to grow in the presence of vancomycin, but they do so at a cost. Vancomycin-resistant S. aureus (VRSA) strains grow more slowly and will often lose their resistance mutations if vancomycin is not present. The reason behind vancomycin’s durability and the potential for VRSA strains to further adapt have not been adequately explored.

In this study, researchers took four VRSA strains and grew them in the presence and absence of vancomycin to see how the strains would evolve. They found that strains grown in the presence of vancomycin developed additional mutations in the ddl gene, which has previously been associated with vancomycin dependence. These mutations enabled VRSA strains to grow faster when vancomycin was present. Unlike the original strains, which quickly lost vancomycin resistance, the evolved strains maintained resistance through several generations, even when vancomycin was no longer present.

The study shows that durability of vancomycin susceptibility to date should not be taken for granted. The trade-off that often comes with vancomycin resistance can be overcome if the bacteria is allowed to grow in the presence of vancomycin. As antibiotic resistance continues to grow as a public health threat, studies like this underscores the importance of developing new antibiotics.

The authors add: “The superbug MRSA has been held off by the antibiotic vancomycin for decades. A new study shows we will not be able to count on vancomycin forever.”

Provided by PLOS

Klebsiella Thrives in Nutrient-deprived Hospital Environments

Photo by Hush Naidoo Jade Photography on Unsplash

Scientists at ADA Forsyth Institute (AFI) have identified a critical factor that may contribute to the spread of hospital-acquired infections (HAIs), shedding light on why these infections are so difficult to combat. Their study reveals that the dangerous multidrug resistant (MDR) pathogen, Klebsiella, thrives under nutrient-deprived polymicrobial community conditions found in hospital environments.

According to the World Health Organization, HAIs pose significant risks to patients, often resulting in prolonged hospital stays, severe health complications, and a 10% mortality rate. One of the well-known challenging aspects of treating HAIs is the pathogens’ MDR. In a recent study published in Microbiome, AFI scientists discovered that Klebsiella colonising a healthy person not only have natural MDR capability, but also dominate the bacterial community when starved of nutrients.

“Our research demonstrated that Klebsiella can outcompete other microorganisms in its community when deprived of nutrients,” said Batbileg Bor, PhD, associate professor at AFI and principal investigator of the study. “We analysed samples of saliva and nasal fluids to observe Klebsiella‘s response to starvation conditions. Remarkably, in such conditions, Klebsiella rapidly proliferates, dominating the entire microbial community as all other bacteria die off.”

Starvation environments

Klebsiella is one of the top three pathogens responsible for HAIs, including pneumonia and irritable bowel disease. As colonising opportunistic pathogens, they naturally inhabit the oral and nasal cavities of healthy individuals but can become pathogenic under certain conditions. “Hospital environments provide ideal conditions for Klebsiella to spread,” explained Dr Bor. “Nasal or saliva droplets on hospital surfaces, sink drains, and the mouths and throats of patients on ventilators, are all starvation environments.”

Dr Bor further elaborated, “When a patient is placed on a ventilator, they stop receiving food by mouth, causing the bacteria in their mouth to be deprived of nutrients and Klebsiella possibly outcompete other oral bacteria. The oral and nasal cavities may serve as reservoirs for multiple opportunistic pathogens this way.”

Additionally, Klebsiella can derive nutrients from dead bacteria, allowing it to survive for extended periods under starvation conditions. The researchers found that whenever Klebsiella was present in the oral or nasal samples, they persisted for over 120 days after being deprived of nutrition.

Other notable findings from the study include the observation that Klebsiella from the oral cavity, which harbours a diverse microbial community, was less prevalent and abundant than those from the nasal cavity, a less diverse environment. These findings suggest that microbial diversity and specific commensal (non-pathogenic) saliva bacteria may play a crucial role in limiting the overgrowth of Klebsiella species. 

The groundbreaking research conducted by AFI scientists offers new insights into the transmission and spread of hospital-acquired infections, paving the way for more effective prevention and treatment strategies.

Source: Forsyth Institute

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