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.”
Researchers from the University of Kent’s School of Biosciences have combined computational and microbiology laboratory approaches to identify existing drugs that can be repurposed to combat antibiotic-resistant bacterial infections, instead of developing new ones.
This research, which has been published in the Journal of Infectious Diseases, revealed that a class of steroid drugs currently used in hormone replacement therapy (HRT) can also stop the growth of antibiotic-resistant E. coli and effectively kill MRSA.
These drugs are particularly good at binding to a protein complex, cytochrome bd, which is important for the growth and survival of a range of disease-causing bacterial species. The researchers made an in silico screening for drugs that could inhibit bd activity, and identified quinestrol, ethinyl estradiol and mestranol, then evaluated their effectiveness in vitro.
The steroid drugs ethinyl estradiol and quinestrol inhibited E. coli bd-I activity. The IC50 of quinestrol for inhibiting oxygen consumption in E. coli bd-I-only membranes as 0.2µg/mL, although residual activity remained at around 20% at higher concentrations Quinestrol exhibited potent bactericidal effects against S. aureus but not E. coli.
It is expected that steroids may provide an alternative to conventional antibiotics that are becoming increasingly ineffective.
Dr Mark Shepherd, Reader in Microbial Biochemistry at Kent and the corresponding author on the paper, said: “These exciting developments will help to advance research into new antimicrobials, and we are enthusiastic to use our powerful experimental approach to discover drugs that can target other bacterial proteins and combat a wide range of antibiotic-resistant infections.”
A virulent strain of Staphylococcus aureus produces proteins that trigger toxic shock syndrome (TSS), a disease characterised by the quick onset of fever, a telltale rash, and, without treatment, multi organ failure. In the vagina, TSS is associated with a life-threatening reaction from the immune system. Research published in the journal Microbiology Spectrum shows that probiotics may help prevent the disease before the cytokine cascade ever begins.
Probiotics may help prevent the disease before the cytokine cascade ever begins. This study reports that strains of two bacteria, Lactobacillus acidophilus and Lacticaseibacillus rhamnosus, successfully inhibited the production of the superantigens that cause TSS, in lab experiments. L. acidophilus, in addition, inhibited the growth of the S. aureus strains that produce the problematic proteins.
A combination of the two could both prevent growth and inhibit the immune response. “It’s kind of a double whammy against S. aureus,” said microbiologist Patrick Schlievert, Ph.D., at the University of Iowa Carver College of Medicine, in Iowa City. “If any toxin is made, the probiotics still prevent inflammation.”
He noted that adding these probiotics to tampons or other menstrual products could reduce the risk of TSS associated with menstruation. Such a preventive measure has the potential to benefit millions of vulnerable people, Schlievert said. “We know that 20% of people over age 12 cannot make antibodies and never will make antibodies against toxic shock syndrome,” he said.
Schlievert has been studying TSS and its prevention for decades. In the early 1980s, he was the first researcher to identify the toxin that triggers an overreaction of the immune system, and to show how high-absorbency tampons facilitated production of that toxin if S. aureus was present.
The new work, he said, was motivated by observations made during an earlier study. A few years ago, he and his colleagues recruited 205 women to test whether a novel molecular mixture, when added to tampons, would inhibit pathogenic bacteria. That molecule proved effective against E. coli and other pathogens, but the researchers noticed an unexpected consequence.
“Some of the women in the treatment group had this tremendous growth of Lactobacilli,” Schlievert said.
Researchers have developed a new method that combines palmitoleic acid, gentamicin, and non-invasive ultrasound to help improve drug delivery in chronic wounds that have been infected with Staphylococcus aureus and protected by thick biofilms. Their results were published in Cell Chemical Biology.
Chronic wounds are notoriously challenging to treat because of bacterial infections like S. aureus, which can also be resistant to antibiotics.
To defend itself from the immune system and other threats, S. aureus can band together, creating a slick, slimy biofilm around itself. The biofilm barrier is so thick that neither immune cells nor antibiotics can penetrate through and neutralise the harmful bacteria.
Using a new strategy, researchers at the UNC School of Medicine and the UNC-NC State Joint Department of Biomedical Engineering were able to reduce the challenging MRSA infection in the wounds of diabetic mice by 94%. They were able to completely sterilise the wounds in several of the mice, and the rest had significantly reduced bacterial burden.
“When bacteria are not completely cleared from chronic wounds, it puts the patient at high risk for the infection recurring or of developing a secondary infection,” said senior author Sarah Rowe-Conlon, PhD. “This therapeutic strategy has the potential to improve outcomes and reduce relapse of chronic wound infections in patients. We are excited about the potential of translating this to the clinic, and that’s what we’re exploring right now.”
Biofilms act as a physical barrier to many classes of antibiotics. Virginie Papadopoulou, PhD, was curious to know if non-invasive cavitation-enhanced ultrasound could create enough agitation to form open spaces in the biofilm to facilitate drug-delivery.
Liquid droplets which can be activated by ultrasound, called phase change contrast agent (PCCA), are applied topically to the wound. An ultrasound transducer is focused on the wound and turned on, causing the liquid inside the droplets to expand and turn into microscopic gas-filled microbubbles, when then move rapidly.
The oscillation of these microbubbles agitates the biofilm, both mechanically disrupting it as well as increasing fluid flow. Ultimately, the combination of the biofilm disruption and the increased permeation of the drugs through the biofilm allowed the drugs to come in and kill the bacterial biofilm with very high efficiency.
“Microbubbles and phase change contrast agents act as local amplifiers of ultrasound energy, allowing us to precisely target wounds and areas of the body to achieve therapeutic outcomes not possible with standard ultrasound,” said Dayton. “We hope to be able to use similar technologies to locally delivery chemotherapeutics to stubborn tumours or drive new genetic material into damaged cells as well.”
When the bacterial cells are trapped inside the biofilm, they are left with little access to nutrients and oxygen. To conserve their resources and energy, they transition into a dormant or sleepy state. The bacteria, which are known as persister cells in this state, are extremely resistant to antibiotics.
Researchers chose gentamicin, a topical antibiotic typically ineffective against S. aureus due to widespread antibiotic resistance and poor activity against persister cells. The researchers also introduced a novel antibiotic adjuvant, palmitoleic acid, to their models.
Palmitoleic acid, an unsaturated fatty acid, is a natural product of the human body that has strong antibacterial properties. The fatty acid embeds itself into the membrane of bacterial cells, and the authors discovered that it facilitates the antibiotic’s successful entry into S. aureus cells and is able to kill persistent cells and reverse antibiotic resistance.
Overall, the team is enthusiastic about the new topical, non-invasive approach because it may give scientists and doctors more tools to combat antibiotic resistance and to lessen the serious adverse effects of taking oral antibiotics.
“Systemic antibiotics, such as oral or IV, work very well, but there’s often a large risk associated with them such as toxicity, wiping out gut microflora and C. difficile infection,” said Rowe-Conlon. “Using this system, we are able to make topical drugs work and they can be applied to the site of infection at very high concentrations, without the risks associated with systemic delivery.”
Methicillin-resistant Staphylococcus aureus (MRSA). Image by CDC on Unsplash
Researchers reported in Cell Host & Microbe that early tests of a bioengineered drug candidate were successful in countering Staphylococcus aureus, a bacteria particularly dangerous to hospitalised patients.
Experiments demonstrated that SM1B74, an antibacterial biologic agent, was superior to a standard antibiotic drug at treating mice infected with S. aureus, including its treatment-resistant form known as MRSA.
The researchers tested mAbtyrins, a combination molecule based on an engineered version of a human monoclonal antibody (mAb), a protein that clings to and marks S. aureus for uptake and destruction by immune cells. Attached to the mAb are centyrins, small proteins that prevent these bacteria from boring holes into the human immune cells in which they hide. As the invaders multiply, these cells die and burst, eliminating their threat to the bacteria.
Together, the experimental treatment targets ten disease-causing mechanisms employed by S. aureus, but without killing it, say the study authors. This approach promises to address antibiotic resistance, say the researchers, where antibiotics kill vulnerable strains first, only to make more space for others that happen to be less vulnerable until the drugs no longer work.
“To our knowledge, this is the first report showing that mAbtyrins can drastically reduce the populations of this pathogen in cell studies, and in live mice infected with drug-resistant strains so common in hospitals,” said lead study author Victor Torres, PhD, the C.V. Starr Professor of Microbiology and director of the NYU Langone Health Antimicrobial-Resistant Pathogen Program.”Our goal was to design a biologic that works against S. aureus inside and outside of cells, while also taking away the weapons it uses to evade the immune system.”
Inside Out
The new study is the culmination of a five-year research partnership between scientists at NYU Grossman School of Medicine and Janssen to address the unique nature of S. aureus.
The NYU Langone team together with Janssen researchers, published in 2019 a study that found that centyrins interfere with the action of potent toxins used by S. aureus to bore into immune cells. They used a molecular biology technique to make changes in a single parental centyrin, instantly creating a trillion slightly different versions of it via automation. Out of this “library,” careful screening revealed a small set of centyrins that cling more tightly to the toxins blocking their function.
Building on this work, the team fused the centyrins to a mAb originally taken from a patient recovering from S. aureus infection. Already primed by its encounter with the bacteria, the mAb could label the bacterial cells such that they are pulled into bacteria-destroying pockets inside of roving immune cells called phagocytes. That is unless the same toxins that enable S. aureus to drill into immune cells from the outside let it drill out of the pockets to invade from the inside.
In a “marvel of bioengineering,” part of the team’s mAbtyrin serves as the passport recognised by immune cells, which then engulf the entire, attached mAbtyrin, along with its centyrins, and fold it into the pockets along with bacteria. Once inside, the centyrins block the bacterial toxins there. This, say the authors, sets their effort apart from antibody combinations that target the toxins only outside of cells.
The team made several additional changes to their mAbtyrin that defeat S. aureus by, for instance, activating chain reactions that amplify the immune response, as well by preventing certain bacterial enzymes from cutting up antibodies and others from gumming up their action.
The researchers tracked the growth of S. aureus strains commonly occurring in US communities in the presence of primary human immune cells (phagocytes). Bacterial populations grew almost normally in the presence of the parental antibody, slightly less well in the presence of the team’s engineered mAb, and half as fast when the mAbtyrin was used.
In another test, 98% of mice treated with a control mAb (no centyrins) developed bacteria-filled sores on their kidneys when infected with a deadly strain of S. aureus, while only 38% of mice did so when treated with the mAbtyrin. Further, when these tissues were removed and colonies of bacteria in them counted, the mice treated with the mAbtyrin had one hundred times (two logs) fewer bacterial cells than those treated with a control mAb.
Finally, the combination of small doses of the antibiotic vancomycin with the mAbtyrin in mice significantly improved the efficacy of the mAbtyrin, resulting in maximum reduction of bacterial loads in the kidneys and greater than 70% protection from kidney lesions.
“It is incredibly important,” said Torres, “that we find new ways to boost the action of vancomycin, a last line of defence against MRSA.”
A new study published in eLife has found that a highly antibiotic-resistant strain of methicillin resistant Staphylococcus aureus (MRSA) has emerged in livestock in the last 50 years, likely a result of widespread antibiotic use in pig farming.
The strain, CC398, has become the dominant type of MRSA in European livestock in the past fifty years. It is also a growing cause of human MRSA infections.
The study found that CC398 has maintained its antibiotic resistance over decades in pigs and other livestock. And it is capable of rapidly adapting to human hosts while maintaining this antibiotic resistance. Increasing numbers of humans have been infected with the strain.
“Historically high levels of antibiotic use may have led to the evolution of this highly antibiotic resistant strain of MRSA on pig farms,” said Dr Gemma Murray, a lead author of the study.
She added: “We found that the antibiotic resistance in this livestock-associated MRSA is extremely stable – it has persisted over several decades, and also as the bacteria has spread across different livestock species.”
Antibiotic use in European livestock is much lower than it has been in the past. But despite policy changes reducing antibiotic use on pig farms, this strain of MRSA in pigs is unlikely to be impacted because it is so stable.
CC398 is found in a range of livestock but mostly in pigs. Its rise has been particularly evident in Danish pig farms where the proportion of MRSA-positive herds has increased from less than 5% in 2008 to 90% in 2018. MRSA doesn’t cause disease in pigs.
“Understanding the emergence and success of CC398 in European livestock – and its capacity to infect humans – is vitally important in managing the risk it poses to public health,” said Dr Lucy Weinert in the University of Cambridge’s Department of Veterinary Medicine, senior author of the paper.
The success of CC398 in livestock and its ability to infect humans is linked to three mobile genetic elements in the MRSA genome. These are chunks of genetic material that give the MRSA certain characteristics, including its resistance to antibiotics and its ability to evade the human immune system.
The researchers reconstructed the evolutionary history of two particular mobile genetic elements called Tn916 and SCCmec that confer antibiotic resistancein MRSA, and found they have persisted in a stable way in CC398 in pigs over decades. They also persist when CC398 jumps to humans — carrying with them high levels of resistance to antibiotics commonly used in farming.
In contrast, a third mobile genetic element called ?Sa3, which enables the CC398 strain of MRSA to evade the human immune system, was found to have frequently disappeared and reappeared over time, in both human-associated and livestock-associated CC398. This suggests that CC398 can rapidly adapt to human hosts.
“Cases of livestock-associated MRSA in humans are still only a small fraction of all MRSA cases in human populations, but the fact that they’re increasing is a worrying sign,” said Weinert.
Intensification of farming, combined with high levels of antibiotic use in livestock, has led to particular concerns about livestock as reservoirs of antibiotic-resistant human infections.
Zinc oxide has been used for many years on pig farms to prevent diarrhoea in piglets. Due to concerns about its environmental impact and its potential promotion of antibiotic resistance in livestock, the European Union will ban its use from this month. But the authors say this ban may not help reduce the prevalence of CC398 because the genes conferring antibiotic resistance are not always linked to the genes that confer resistance to zinc treatment.
Globally, infections by antimicrobial-resistant (AMR) bacteria caused more than 1.2 million deaths worldwide in 2019, according to a study published in The Lancet. It is the largest and most comprehensive one to date of this critical issue.
Lower-income countries are worst affected but antimicrobial resistance remains a global threat, the researchers wrote.
The researchers emphasised that investment in new drugs is urgently needed, as well as vaccination and better antimicrobial stewardship.
The estimate of global deaths from AMR, is based on the researchers’ analysis of 204 countries, assuming the counterfactual that the bacteria responsible would be antibiotic-susceptible.
Of the 4.95 million deaths in which AMR played a role, 1.27 million were directly attributable to it. In 2019, 860 000 deaths were estimated from HIV and 640 000 from malaria.
Most of the AMR-related deaths resulted from lower respiratory infections, such as pneumonia, and bloodstream infections, which can lead to sepsis.
Deaths from AMR were estimated to be highest in sub-Saharan Africa at 23.7 deaths per 100 000, and lowest in North Africa and the Middle East at 11.2 per 100 000. Young children are at most risk, with about one in five deaths linked to AMR being among the under-fives.
The researchers also noted that “resistance is high for multiple classes of essential agents, including beta-lactams and fluoroquinolones.”
MRSA (methicillin-resistant Staphylococcus aureus) was particularly deadly, while E. coli, K. pneumoniae, S. pneumoniae, A. baumannii, and P. aeruginosa were associated with high levels of resistance. The researchers wrote that “each of these leading pathogens is a major global health threat that warrants more attention, funding, capacity building, research and development, and pathogen-specific priority setting from the broader global health community.”
They also recommend that immunity to these pathogens be built up by vaccination, and since currently only S. pneumoniae has a vaccine readily available, these will need to be developed and deployed as a matter of urgency. They noted several limitations to their study, the first being the sparsity of data drawn from low- and middle-income countries, which may in fact lead to an underestimate of the prevalence of AMR. Secondly, there is the possibility of multiple sources of bias inherent in combining datasets from different providers. Finally, there may be bias in surveillance, eg if cultures are drawn only if a patient is unresponsive to antibiotics, leading to an overestimate.
A surprising discovery in hedgehogs showed that a variant of the MRSA superbug appeared in nature well before antibiotics use in humans and livestock, which has traditionally been blamed for its emergence.
Staphylococcus aureus first developed resistance to the antibiotic methicillin around 200 years ago, according to a large international study which has traced the genetic history of the bacteria.
The finding comes from research showing that up to 60% of hedgehogs in Denmark and Sweden carry a type of MRSA called mecC-MRSA. The new study also found high levels of MRSA in swabs taken from hedgehogs across their range in Europe and New Zealand. Their findings were published in the journal Nature.
The researchers believe that antibiotic resistance evolved in S. aureus as an adaptation to having to exist on hedgehog skin next to the fungus Trichophyton erinacei, which produces its own antibiotics. The discovery of this centuries-old antibiotic resistance predates antibiotic use in medical and agricultural settings.
“Using sequencing technology we have traced the genes that give mecC-MRSA its antibiotic resistance all the way back to their first appearance, and found they were around in the nineteenth century,” said Dr Ewan Harrison, a senior author of the study.
He added: “Our study suggests that it wasn’t the use of penicillin that drove the initial emergence of MRSA, it was a natural biological process. We think MRSA evolved in a battle for survival on the skin of hedgehogs, and subsequently spread to livestock and humans through direct contact.”
Antibiotic resistance in human pathogens was previously thought to be a modern phenomenon, driven by the clinical use of antibiotics. Antibiotic misuse is now accelerating the process, with antibiotic resistance rising dangerously worldwide.
Since nearly all antibiotics used today arose in nature, the researchers say it is likely that resistance to them already exists in nature too. Overuse of any antibiotic in humans or livestock will favour resistant strains of the bacteria, causing it to lose effectiveness over time.
“This study is a stark warning that when we use antibiotics, we have to use them with care. There’s a very big wildlife ‘reservoir’ where antibiotic-resistant bacteria can survive – and from there it’s a short step for them to be picked up by livestock, and then to infect humans,” said Professor Mark Holmes, a senior author of the report.
In 2011, mecC -MRSA was identified in human and dairy cow populations, which was assumed to have arisen due to the large number of antibiotics cows are routinely given.
MRSA was first identified in patients in 1960, and around 1 in 200 of all MRSA infections are caused by mecC-MRSA. Due to its resistance to antibiotics, MRSA is much harder to treat than other bacterial infections. The World Health Organization now considers MRSA one of the world’s greatest threats to human health.
Human infections are rare with mecC-MRSA however, even though it has been present in hedgehogs for more than 200 years.
Scanning electron micrograph of methicillin-resistant Staphylococcus aureus and a dead human neutrophil. Credit: NIAID
Researchers have uncovered a novel trick employed by the bacterium Staphylococcus aureus — MRSA uses toxins to ‘fight dirty’ and stifle the immune response. This finding is a step towards one day producing a vaccine against MRSA.
Every year, there are some 700 000 deaths due to the emerging global threat of antimicrobial resistance (AMR). Turning the tables against AMR requires immediate action, and the development of novel vaccines to prevent such infections in the first place, are an attractive and potentially very effective option.
Staphylococcus aureus is the causative agent of the infamous MRSA ‘superbug’, one of the chief concerns of AMR. Immunologists from Trinity College Dublin, working with scientists at GSK, discovered the deadly bacteria’s new trick to foil the immune system. They found that the bacterium interferes with the host immune response by causing toxic effects on white blood cells, preventing them from carrying out their infection-fighting jobs.
The study also showed that the toxicity could be lessened following vaccination with a mutated version of a protein specifically engineered to throw a spanner in the MRSA works. This could one day lead to a vaccine for humans.
Rachel McLoughlin, Professor in Immunology in Trinity’s School of Biochemistry and Immunology and the Trinity Biomedical Sciences Institute (TBSI), said: “As a society we are witnessing first-hand the powerful impact that vaccination can have on curbing the spread of infection. However, in the backdrop of the COVID epidemic we must not lose sight of the fact that we are also waging war on a more subtle epidemic of antimicrobial resistant infection, which is potentially equally deadly.
“In this study we have identified a mechanism by which a protein made by the bacterium – known as Staphylococcal Protein A (SpA) – attacks and rapidly kills white blood cells. This protein has been widely studied for its immune evasion capacity and has a well-documented role in rendering antibodies raised against the bacterium non-functional.
“Here we uncover a previously undocumented strategy by which SpA forms immune complexes through its interaction with host antibodies, that in turn exert toxic effects on multiple white blood cell types. This discovery highlights how important it will be for effective vaccines to be capable of disarming the effects of protein A.”
Dr Fabio Bagnoli, Director, Research & Development Project Leader, GSK, said: “Our collaboration with Trinity College Dublin and in particular with Professor Rachel McLoughlin, a worldwide recognised expert on staphylococcal immunology, is critical for increasing our knowledge on protective mechanisms against S. aureus.”
The study documents the latest discovery made by this group at Trinity under an ongoing research agreement with GSK Vaccines (Siena, Italy). Overall, this collaboration aims to increase understanding of the immunology of Staphylococcus aureus infection to advance development of next-generation vaccines to prevent MRSA infections.
Journal information: Fox, P. G., et al. (2021) Staphylococcal Protein A Induces Leukocyte Necrosis by Complexing with Human Immunoglobulins. Scientific Reports. doi.org/10.1128/mBio.00899-21.
Adults middle-aged or older who carry methicillin-resistant Staphylococcus aureus (MRSA) ‘superbug’ on their skin are twice as likely to die within the next decade as people who do not, according to a study by the University of Florida (UF).
“Very few people who carry MRSA know they have it, yet we have found a distinct link between people with undetected MRSA and premature death,” said lead author Arch Mainous, PhD, a professor in the department of health services research, management and policy at UF.
The findings suggest that routine screening for undetected MRSA may be warranted in older people to prevent deaths from infection.
A third of Americans carry Staphylococcus aureus, or staph, on their skin or in nasal passages, and of these about 1% carry MRSA, the notorious antibiotic resistant staph strain.
MRSA carriers may not even be aware that they carry the bacteria unless they develop an infection or are tested for it. A quarter of people who carry MRSA without an active infection, known as colonised MRSA for at least a year, eventually develop a MRSA infection.
“MRSA can be part of normal body flora, but it can lead to infection when immune systems are compromised, especially in people who are hospitalized, have underlying disease, or after antibiotic use,” said Prof Mainous, also vice chair for research in the UF College of Medicine’s department of community health and family medicine.
According to a 2017 Centers for Disease Control and Prevention report, 119 000 Americans experienced a staph bloodstream infection and nearly 20 000 died. Hospitalised patients with colonised MRSA may be particularly vulnerable to infection in hospital or after discharge. Among carriers, wounds, surgical incisions and use of medical devices, such as catheters, may also lead to MRSA infection.
In this study, researchers analysed data from the 2001-2004 National Health and Nutrition Examination Survey, a nationally representative study combining survey questions with laboratory testing, which includes nasal swabs for detecting MRSA.
Adjusting for risk factors including gender and ethnicity, the researchers linked data on participants ages 40-85 with data from the National Death Index to track deaths over an 11-year period.
The mortality rate among participants without MRSA was about 18% compared with 36% among those with colonised MRSA. There was no increased mortality risk for those with non-MRSA staph bacteria on their skin.
Although some states and hospital systems require MRSA testing for patients before hospital admission, policies for testing and treatment of colonised MRSA, which may include antibiotics use, vary widely betweens hospitals, Prof Mainous said.
“Without a uniform strategy, we are missing an opportunity to help prevent deaths caused by MRSA,” he said. “Maybe we should know who is carrying MRSA.”
Journal information: Mainous, A. G., et al. (2021) Methicillin-Resistant Staphylococcus Aureus Colonization and Mortality Risk Among Community Adults Aged 40-85. Journal of the American Board of Family Medicine.
