Tag: hospital-acquired infections

Categories : Hospitals Respiratory DiseasesTags :

More Often than Not, Hospital Pneumonia Diagnoses are Revised

On By ModernMedia
Photo by engin akyurt on Unsplash

Pneumonia diagnoses are marked by pronounced uncertainty, according to an AI-based analysis of over 2 million hospital visits. The study, published in Annals of Internal Medicine, found that more than half the time, a pneumonia diagnosis made in the hospital will change from a patient’s entrance to their discharge – either because someone who was initially diagnosed with pneumonia ended up with a different final diagnosis, or because a final diagnosis of pneumonia was missed when a patient entered the hospital (not including cases of hospital-acquired pneumonia).

Understanding that uncertainty could help improve care by prompting doctors to continue to monitor symptoms and adapt treatment accordingly, even after an initial diagnosis. 

Barbara Jones, MD, pulmonary and critical care physician at University of Utah Health and the first author on the study, found the results by searching medical records from more than 100 VA medical centres across the country, using AI-based tools to identify mismatches between initial diagnoses and diagnoses upon discharge from the hospital. More than 10% of all such visits involved a pneumonia diagnosis, either when a patient entered the hospital, when they left, or both.

“Pneumonia can seem like a clear-cut diagnosis,” Jones says, “but there is actually quite a bit of overlap with other diagnoses that can mimic pneumonia.” A third of patients who were ultimately diagnosed with pneumonia did not receive a pneumonia diagnosis when they entered the hospital. And almost 40% of initial pneumonia diagnoses were later revised.

The study also found that this uncertainty was often evident in doctors’ notes on patient visits; clinical notes on pneumonia diagnoses in the emergency department expressed uncertainty more than half the time (58%), and notes on diagnosis at discharge expressed uncertainty almost half the time (48%). Simultaneous treatments for multiple potential diagnoses were also common.

When the initial diagnosis was pneumonia, but the discharge diagnosis was different, patients tended to receive a greater number of treatments in the hospital, but didn’t do worse than other patients as a general rule. However, patients who initially lacked a pneumonia diagnosis, but ultimately ended up diagnosed with pneumonia, had worse health outcomes than other patients.

A path forward

The new results call into question much of the existing research on pneumonia treatment, which tends to assume that initial and discharge diagnoses will be the same. Jones adds that doctors and patients should keep this high level of uncertainty in mind after an initial pneumonia diagnosis and be willing to adapt to new information throughout the treatment process. “Both patients and clinicians need to pay attention to their recovery and question the diagnosis if they don’t get better with treatment,” she says.

Source: University of Utah

Categories : Diseases, Syndromes and Conditions HospitalsTags :

Klebsiella Thrives in Nutrient-deprived Hospital Environments

On By ModernMedia
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

Categories : Dentistry Respiratory DiseasesTags :

Can Toothbrushing Reduce Rates of Hospital-acquired Pneumonia?

On By ModernMedia
Photo by Towfiqu barbhuiya: https://www.pexels.com/photo/a-toothbrush-with-toothpaste-on-a-white-surface-12065623/

A new study by investigators from Brigham and Women’s Hospital examined whether daily toothbrushing among hospitalised patients is associated with lower rates of hospital-acquired pneumonia and other outcomes. Their analysis of 15 randomised clinical trials found that hospital-acquired pneumonia rates were lower among patients who received daily toothbrushing compared to those who did not. The results were especially compelling among patients on mechanical ventilation. Their results are published in JAMA Internal Medicine.

“The signal that we see here towards lower mortality is striking – it suggests that regular toothbrushing in the hospital may save lives,” said corresponding author Michael Klompas, MD, MPH, hospital epidemiologist and an infectious disease physician in the Department of Medicine at BWH and Professor of Population Medicine at Harvard Pilgrim Health Care Institute.

“It’s rare in the world of hospital preventative medicine to find something like this that is both effective and cheap. Instead of a new device or drug, our study indicates that something as simple as brushing teeth can make a big difference.”

Hospital-acquired pneumonia occurs when bacteria in the mouth enter a patient’s airways and infect their lungs.

Patients experiencing frailty or patients with a weakened immune system are particularly susceptible to developing hospital-acquired pneumonia during their hospital stay.

However, adopting a daily toothbrushing regimen can decrease the amount of bacteria in the mouth, potentially lowering the risk of hospital-acquired pneumonia from occurring.

The team conducted a systematic review and meta-analysis to determine the association between daily toothbrushing and hospital-acquired pneumonia.

Using a variety of databases, the researchers collected and analysed randomised clinical trials from around the world that compared the effect of regular oral care with toothbrushing versus oral care without toothbrushing on the occurrence of hospital-acquired pneumonia and other outcomes.

The team’s analysis found that daily toothbrushing was associated with a significantly lower risk for hospital-acquired pneumonia and ICU mortality.

In addition, the investigators identified that toothbrushing for patients in the ICU was associated with fewer days of mechanical ventilation and a shorter length of stay in the ICU.

Most of the studies in the team’s review explored the role of a teeth-cleaning regimen in adults in the ICU.

Only two of the 15 studies included in the authors’ analysis evaluated the impact of toothbrushing in non-ventilated patients.

The researchers are hopeful that the protective effect of toothbrushing will extend to non-ICU patients but additional studies focusing on this population are needed to clarify if in fact this is the case.

“The findings from our study emphasise the importance of implementing an oral health routine that includes toothbrushing for hospitalised patients. Our hope is that our study will help catalyse policies and programs to assure that hospitalised patients regularly brush their teeth. If a patient cannot perform the task themselves, we recommend a member of the patient’s care team assist,” said Klompas.

Source: Brigham and Women’s Hospital

Categories : Diseases, Syndromes and Conditions HospitalsTags :

The Greater Clostridioides Difficile Threat may Come from Within

On By ModernMedia
Clostridioides difficile. Credit: CDC

Despite strenuous control efforts, hospital-acquired infections still occur – the most common of which is caused by the bacterium Clostridioides difficile, which creates lingering spores and resists alcohol-based hand sanitisers. Surprising findings from a new study in Nature Medicine suggest that the burden of C. diff infection may be less a matter of hospital transmission and more a result of characteristics associated with the patients themselves.

The study team, led by Evan Snitkin, PhD; Vincent Young, MD, PhD; and Mary Hayden, MD, leveraged ongoing epidemiological studies focused on hospital-acquired infections that enabled them to analyse daily faecal samples from every patient within the intensive care unit at Rush University Medical Center over a nine-month period.

Arianna Miles-Jay, a postdoctoral fellow in Dr Snitkin’s lab, analysed 1141 eligible patients, and found that a little over 9% were colonised with C. diff. Using whole genome sequencing at U-M of 425 C. difficile strains isolated from nearly 4000 faecal specimens, she compared the strains to each other to analyse spread. But she found that, based on the genomics, there was very little transmission.

Essentially, there was very little evidence that the strains of C. diff from one patient to the next were the same, which would imply in-hospital acquisition. In fact, there were only six genomically supported transmissions over the study period. Instead, people who were already colonised were at greater risk of transitioning to infection.

“Something happened to these patients that we still don’t understand to trigger the transition from C. diff hanging out in the gut to the organism causing diarrhoea and the other complications resulting from infection,” said Snitkin.

Hayden notes this doesn’t mean hospital infection prevention measures are not needed. In fact, the measures in place in the Rush ICU at the time of the study – high rates of compliance with hand hygiene among healthcare personnel, routine environmental disinfection with an agent active against C. diff, and single patient rooms were likely responsible for the low transmission rate. The current study highlights, though that more steps are needed to identify patients who are colonised and try to prevent infection in them.

Where did the C. diff come from? “They are sort of all around us,” said Young. “C. diff creates spores, which are quite resistant to environmental stresses including exposure to oxygen and dehydration…for example, they are impervious to alcohol-based hand sanitiser.”

However, only about 5% of the population outside of a healthcare setting has C. diff in their gut – where it typically causes no issues.

“We need to figure out ways to prevent patients from developing an infection when we give them tube feedings, antibiotics, proton pump inhibitors – all things which predispose people to getting an actual infection with C. diff that causes damage to the intestines or worse,” said Young.

The team next hopes to build on work on AI prediction for patients at risk of C. diff infection to identify patients more likely to be colonised and who could benefit from more focused intervention.

Said Snitkin, “A lot of resources are put into gaining further improvements in preventing the spread of infections, when there is increasing support to redirect some of these resources to optimise the use of antibiotics and identify other triggers that lead patients harbouring C. diff and other healthcare pathogens to develop serious infections.”

Source: Michigan Medicine – University of Michigan

Categories : Diseases, Syndromes and Conditions HospitalsTags :

How the Hospital Pathogen Acinetobacter Baumannii can Adapt so Quickly

On By ModernMedia
Photo by National Cancer Institute on Unsplash

Acinetobacter baumannii is a notorious hospital pathogen, and there is great pressure to devise novel therapeutic approaches to combat this growing threat. German researchers have now detected an unexpectedly wide diversity of certain cell appendages known as pili in A. baumannii that are associated with pathogenicity. This finding, published in PLOS Genetics, could lead to treatment strategies that are specifically tailored to a particular pathogen.

Each year, over 670 000 people in Europe fall ill because of antibiotic-resistant pathogens, and 33 000 die from the infections. Especially feared are pathogens with resistances against multiple, or even all, known antibiotics. One of these is the bacterium Acinetobacter baumannii, feared today above all as the “hospital superbug”: According to estimates, up to five percent of all hospital-acquired and one tenth of all bacterial infections resulting in death can be attributed to this pathogen alone. This puts A. baumannii right at the top of WHO’s list of pathogens for which there is an urgent need to develop new therapies.

Understanding which characteristics make A. baumannii a pathogen is one of the prerequisites for this. To this end, bioinformaticians led by Professor Ingo Ebersberger of Goethe University Frankfurt and the LOEWE Center for Translational Biodiversity Genomics (LOEWE-TBG) are comparing the genomes and the proteins encoded therein across a wide range of different Acinetobacter strains. Conclusions about which genes contribute to pathogenicity can be drawn above all from the differences between dangerous and harmless strains.

Due to a lack of suitable methods, corresponding studies have so far concentrated on whether a gene is present in a bacterial strain or not. However, this neglects the fact that bacteria can acquire new characteristics by modifying existing genes and thus also the proteins encoded by them. That is why Ebersberger’s team has developed a bioinformatics method to track the modification of proteins along an evolutionary lineage and has now applied this method for the first time to Acinetobacter in collaboration with microbiologists from the Institute for Molecular Biosciences and the Institute of Medical Microbiology and Infection Control at Goethe University Frankfurt.

In the process, the researchers concentrated on hair-like cell appendages, known as type IVa (T4A) pili, which are prevalent in bacteria and that they use to interact with their environment. The fact that they are present in harmless bacteria on the one hand and have even been identified as a key factor for the virulence of some pathogens on the other suggests that the T4A pili have repeatedly acquired new characteristics associated with pathogenicity during evolution.

The research team could show that the protein ComC, which sits on the tip of the T4A pili and is essential for their function, shows conspicuous changes within the group of pathogenic Acinetobacter strains. Even different strains of A. baumannii have different variants of this protein. This leads bioinformatician Ebersberger to compare the T4A pili to a multifunctional garden tool, where the handle is always the same, but the attachments are interchangeable. “In this way, drastic functional modifications can be achieved over short evolutionary time spans,” Ebersberger is convinced. “We assume that bacterial strains that differ in terms of their T4A pili also interact differently with their environment. This might determine, for example, in which corner of the human body the pathogen settles.”

The aim is to use this knowledge of the unexpectedly high diversity within the pathogen to improve the treatment of A. baumannii infections, as Ebersberger explains: “Building on our results, it might be possible to develop personalised therapies that are tailored to a specific strain of the pathogen.” However, the study by Ebersberger and his colleagues also reveals something else: Previous studies on the comparative genomics of A. baumannii have presumably only unveiled the tip of the iceberg. “Our approach has gone a long way towards resolving the search for possible components that characterize pathogens,” says Ebersberger.

Source: Goethe University Frankfurt

Categories : Antibiotics HospitalsTags :

Patients Themselves may be the Source of New Strains of HAIs

On By ModernMedia
E. Coli bacteria. Image by CDC
E. Coli bacteria. Image by CDC

Despite stringent infection-control efforts around the world, hospital-acquired infections (HAIs)keep on popping up from new strains of bacteria. In Science Translational Medicine, researchers report evidence pointing to an unexpected source of such bacteria: the hospitalised patients themselves.

From experiments with mice, researchers at Washington University School of Medicine in St. Louis discovered that urinary tract infections (UTIs) can arise after sterile tubes, called catheters, are inserted into the urinary tract, even when no bacteria are detectable in the bladder beforehand. Such tubes are commonly used in hospitals to empty the bladders of people undergoing surgery. In the mice, inserting the tubes activated dormant Acinetobacter baumannii bacteria hidden in bladder cells, triggering them to emerge, multiply and cause UTIs, the researchers said.

The findings suggest that screening patients for hidden reservoirs of dangerous bacteria could supplement infection-control efforts and help prevent deadly HAIs.

“You could sterilise the whole hospital, and you would still have new strains of A. baumannii popping up,” said co-senior author Mario Feldman, PhD, a professor of molecular microbiology. “Cleaning is just not enough, and nobody really knows why. This study shows that patients may be unwittingly carrying the bacteria into the hospital themselves, and that has implications for infection control. If someone has a planned surgery and is going to be catheterised, we could try to determine whether the patient is carrying the bacteria and cure that person of it before the surgery. Ideally, that would reduce the chances of developing one of these life-threatening infections.”

The notoriously multidrug-resistant A. baumannii is a major threat to patients, causing many cases of UTIs in people with urinary catheters, pneumonia in people on ventilators, and bloodstream infections in people with central-line catheters into their veins.

The researchers set out to investigate why so many A. baumannii UTIs develop after people receive catheters.

Most UTIs among otherwise healthy people are caused by the bacterium Escherichia coli. Research has shown that E. coli can hide out in bladder cells for months after a UTI seems to have been cured, and then re-emerge to cause another infection.

The researchers investigated whether A. baumannii can hide inside cells like E. coli can. They studied mice with UTIs caused by A. baumannii. They used mice with weakened immune systems because, like people, healthy mice can fight off A. baumannii.

Once the infections had resolved and no bacteria were detected in the mice’s urine for two months, the researchers inserted catheters into the mice’s urinary tracts with a sterile technique. Within 24 hours, about half of the mice developed UTIs caused by the same strain of A. baumannii as the initial infection.

“The bacteria must have been there all along, hiding inside bladder cells until the catheter was introduced,” said co-senior author Scott J. Hultgren, PhD, a professor and expert on UTIs. “Catheterisation induces inflammation, and inflammation causes the reservoir to activate, and the infection blooms.”

Since A. baumannii rarely causes symptoms in otherwise healthy people, many people who carry the bacteria may never know they’re infected, the researchers said. According to the researchers’ literature search, 2% of healthy people carry A. baumannii in their urine.

“I wouldn’t put much weight on the precise percentage, but I think we can say with certainty that some percentage of the population is walking around with A. baumannii,” Feldman said. “As long as they’re basically healthy, it doesn’t cause any problems, but once they’re hospitalised, it’s a different matter. This changes how we think about infection control. We can start considering how to check if patients already have Acinetobacter before they receive certain types of treatment; how we can get rid of it; and if other bacteria that cause deadly outbreaks in hospitals, such as Klebsiella, hide in the body in the same way. That’s what we’re working on figuring out now.”

Source: Washington University School of Medicine