Escherichia Coli Infections

It is the world's first AI-Powered sepsis alert system to save more lives TAICHUNG, Taiwan, April 3, 2024 /PRNewswire/ -- In conventional practice, a blood culture report wouldn't be available until 18 to 72 hours later, rendering it non-feasible to facilitate rapid response. Led by Superintendent Der-Yang Cho, CMUH's team developed "Intelligent Sepsis Early Prediction System (ISEPS)", the world's first AI-powered sepsis alarm system. The AI model of ISEPS takes only one minute for the early detection of sepsis and bacteremia to help clinicians identify patients at higher risk and provide early intervention with antibiotics to improve patient outcome and prevent it from progressing to sepsis. When compared to conventional blood cultures, it doesn't require additional blood collection or device operation, reducing the demands on healthcare labor while keeping the timeliness and quality of management. Mrs. Qu, 60, experienced serious vomiting and chills. Her vital signs showed a heart rate of 158bpm, ECG analysis suggested suspected acute myocardial infarction, and Troponin-I value was 13.91 (normal range: <0.0875). Dr. Hong-Mo Shih, Deputy Director of CMUH Emergency Department, immediately activated cardiac catheterization team and ordered a routine complete blood count test. The ISEPS alerted that Mrs. Qu was at high risk of bacteremia. Therefore, Dr. Shih initiated infection evaluation immediately, including two sets of blood bacterial cultures, and concurrent treatment of antibiotics. During the cardiac catheterization procedure, vascular obstruction wasn't found and hence ruled out acute myocardial infarction. The blood culture report then showed the presence of Gram-negative bacteria in circulation. She was then confirmed to be a case of E. coli infection. Dr. Shih stated that Mrs. Qu's bacteremia was secondary to urinary tract infection (UTI), and she was also one of the much rarer cases of bacteremia-induced cardiac reaction resembling myocardial infarction. Through physician's clinical judgment with ISEPS support, Mrs. Qu received immediate and proper treatment and was discharged healthy a week later. Dr. Shih notes that bacteremia is a relatively common acute condition, occurring in about 30% of UTI patients. Without prompt intervention, bacteremia can escalate to septic shock, resulting in a mortality rate exceeding 40%. For each hour delayed for antibiotic administration, the mortality risk increases linearly by 7-9%. With the ability to provide immediate bacteremia risk prediction, ISEPS provides the physicians timely and precisely assistance against infectious disease. It is currently regular used in CMUH and is expected to be a topic of future collaborations with more medical institutions to enhance the timeliness and quality of infection management. Media Contact: Carolyn Chen 100709@tool.caaumed.org.tw View original content to download multimedia: SOURCE China Medical University Hospital

Infectious diseases specialists call the medical field to be ready to deal with the impact of climate change on spreading diseases, such as malaria, Valley fever, E. coli and Lyme disease. A team of infectious diseases experts called for more awareness and preparedness in the medical field to deal with the impact of climate change on the spread of diseases. Their article, published today in JAMA raises the alarm about the emergence and spread of harmful pathogens. The authors also urge the medical community to update their education and training and take steps to combat global warming. "Clinicians need to be ready to deal with the changes in the infectious disease landscape," said lead author George R. Thompson. Thompson is a professor at the UC Davis School of Medicine in the Department of Internal Medicine, Division of Infectious Diseases, and the Department of Medical Microbiology and Immunology. "Learning about the connection between climate change and disease behavior can help guide diagnoses, treatment and prevention of infectious diseases." Thompson encouraged physicians and practitioners to maintain "a high index of suspicion of diseases on the move." "I think with improvements in our understanding of the disease, there will be more testing and we'll miss fewer cases that way," he said. Changing infectious diseases landscape Infectious diseases can be caused by viruses, bacteria, fungi or parasites. Many of these diseases are transmitted from animal to human or from human to human. One type of infectious disease is vector-borne diseases. They are caused by pathogens carried by vectors like mosquitoes, fleas and ticks. Some diseases caused by vectors aredengue, malaria and Zika. Changing rain patterns are expanding vectors' range and their active periods. Shorter, warmer winters and longer summers are also linked to more vector-borne diseases. For example, diseases caused by ticks (like babesiosis and Lyme disease) are now occurring in the winter too. They're also being found in regions farther west and north than in the past. "We're seeing cases of tick-borne diseases in January and February," said first author of the study Matthew Phillips. Phillips is an infectious diseases fellow at Massachusetts General Hospital and Harvard Medical School. "The tick season is starting earlier and with more active ticks in a wider range. This means that the number of tick bites is going up and with it, the tick-borne diseases." Another concern is malaria. The mosquitos that transmit the disease are expanding northward, a climate-induced change. Changing rain patterns have led to more mosquitos and a higher disease transmission rate. "As an infectious disease clinician, one of the scariest things that happened last summer was the locally acquired cases of malaria. We saw cases in Texas and Florida and then all the way north in Maryland, which was really surprising. They happened to people who didn't travel outside the U.S.," Phillips said. Zoonotic diseases, such as plague and hantavirus (carried by rodents), are also showing changes in incidence and location. The experts noted changes in animal migration patterns and natural ranges. Due to their habitat loss, wild animals are coming closer to humans. With that comes a higher risk of animal diseases spilling over to humans and for new pathogens to develop. The study also pointed to the emergence of new fungal infections, such as Candida auris (C. auris), and changes in the location of some fungal pathogens. For example, the fungal infection Coccidioides (also known as Valley fever) was endemic to hot, dry areas in California and Arizona. But Valley fever was recently diagnosed as far north as Washington State. Changes in rain patterns and coastal water temperature can also affect the spread of waterborne diseases, such as E. coli and Vibrio. According to the team, the sea level is rising, and storm surges and coastal flooding that used to be rare or extreme events are happening more frequently. Call for medical community to take steps Over the last few years, infectious diseases, such as COVID-19, impacted the world enormously. "They can spring up and cause absolute chaos for the whole world and then we kind of forget about them for a while. Yet, the epidemic and pandemic potential of infections really mandates that we stay involved with federal funding agencies and advisory groups to make sure that infectious diseases don't slip back too far on the public's radar," Thomspon explained. The team called for stronger measures for infectious disease surveillance and urged medical educators to train clinicians to anticipate the changes in infectious disease patterns. "It's not a hopeless situation. There are distinct steps that we can take to prepare for and help deal with these changes. Clinicians see first-hand the impact of climate change on people's health. As such, they have a role in advocating for policies that can slow climate change," Phillips said. Regina C. LaRocque, associate professor of medicine at Harvard Medical School and infectious diseases physician at Harvard Medical School, is a coauthor of this study. This study was partially supported by National Institutes of Health grants T32AI007061 and 5U19AI166798.

Gut bacteria and a diet rich in the amino acid tryptophan can play a protective role against pathogenic E. coli, which can cause severe stomach upset, cramps, fever, intestinal bleeding and renal failure. Gut bacteria and a diet rich in the amino acid tryptophan can play a protective role against pathogenic E. coli, which can cause severe stomach upset, cramps, fever, intestinal bleeding and renal failure, according to a study published March 13 in Nature. The research reveals how dietary tryptophan -- an amino acid found mostly in animal products, nuts, seeds, whole grains and legumes -- can be broken down by gut bacteria into small molecules called metabolites. It turns out a few of these metabolites can bind to a receptor on gut epithelial (surface) cells, triggering a pathway that ultimately reduces the production of proteins that E. coli use to attach to the gut lining where they cause infection. When E. coli fail to attach and colonize the gut, the pathogen benignly moves through and passes out of the body. The research describes a previously unknown role in the gut for a receptor, DRD2. DRD2 has otherwise been known as a dopamine (neurotransmitter) receptor in the central and peripheral nervous systems. "It's actually two completely different areas that this receptor could play a role in, which was not appreciated prior to our findings," said Pamela Chang, associate professor of immunology in the College of Veterinary Medicine and of chemical biology in the College of Arts and Sciences. "We essentially think that DRD2 is moonlighting in the gut as a microbial metabolite sensor, and then its downstream effect is to help protect against infection." Samantha Scott, a postdoctoral researcher in Chang's lab, is first author of the study, "Dopamine Receptor D2 Confers Colonization Resistance via Microbial Metabolites." Now that Chang, Scott and colleagues have identified a specific pathway to help prevent E. coli infection, they may now begin studying the DRD2 receptor and components of its downstream pathway for therapeutic targets. In the study, the researchers used mice infected with Citrobacter rodentium, a bacterium that closely resembles E. coli, since certain pathogenic E. coli don't infect mice. Through experiments, the researchers identified that there was less pathogen and inflammation (a sign of an active immune system and infection) after mice were fed a tryptophan-supplemented diet. Then, to show that gut bacteria were having an effect, they gave the mice antibiotics to deplete microbes in the gut, and found that the mice were infected by C. rodentium in spite of eating a tryptophan diet, confirming that protection from tryptophan was dependent on the gut bacteria. Then, using mass spectrometry, they ran a screen to find the chemical identities of tryptophan metabolites in a gut sample, and identified three such metabolites that were significantly increased when given a tryptophan diet. Again, based on pathogen levels and inflammation, when these three metabolites alone were fed to the mice, they had the same protective effect as giving the mice a full tryptophan diet. Switching gears, the researchers used bioinformatics to find which proteins (and receptors) might bind to the tryptophan metabolites, and from a long list they identified three related receptors within the same family of dopamine receptors. Using a human intestinal cell line in the lab, they were able to isolate receptor DRD2 as the one that had the protective effect against infection in the presence of tryptophan metabolites. Having identified the metabolites and the receptor, they analyzed the downstream pathway of DRD2 in human gut epithelial cells. Ultimately, they found that when the DRD2 pathway was activated, the host's ability to produce an actin regulatory protein was compromised. C. rodentium (and E. coli) require actin to attach themselves to gut epithelial cells, where they colonize and inject virulence factors and toxins into the cells that cause symptoms. But without actin polymerization they can't attach and the pathogen passes through and clears. The experiments revealed a new role of dopamine receptor DRD2 in the gut that controls actin proteins and affects a previously unknown pathway for preventing a pathogenic bacteria's ability to colonize the gut. Jingjing Fu, a former postdoctoral researcher in Chang's lab, is a co-author. The study was supported by the Arnold and Mabel Beckman Foundation, a President's Council of Cornell Women Affinito-Stewart Grant, the National Institutes of Health and a Cornell Institute of Host-Microbe Interactions and Disease Postdoctoral Fellowship.