The patient: An 18-year-old in Louisiana

The symptoms: The teenager, who was training to be a welder, developed a cough and was hospitalized with pneumonia and respiratory failure a week later. He was intubated at the hospital, meaning a tube was placed into his airway and attached to a machine to help him breathe.

The teen was six months into his welding apprenticeship, which involved working four hours per day, four days per week. He was otherwise healthy and reported being a nonsmoker with no history of excessive drinking.

What happened next: The doctors ordered a blood test, which revealed an infection with a bacterium in a related group of microbes known as the Bacillus cereus group. At that point, the doctors did not know which specific bacterial species within that group had caused the infection. But most often, B. cereus group bacteria cause intestinal infections, like food poisoning, not lung infections.

Although very rare, the teen's combination of symptoms, occupation and geographic location had previously been documented in cases involving welders in Louisiana and Texas. The knowledge of this rare phenomenon enabled the medical team to quickly identify the likely cause of his symptoms, they wrote in a report of the case.

The diagnosis: The patient was suspected to have welder's anthrax, an anthrax-toxin infection that presents as pneumonia in metalworkers. This severe respiratory disease is exceptionally rare, with only eight documented cases before this patient. All previous cases involved welders or metalworkers. Of those eight patients, only two recovered.

Anthrax is normally contracted following contact with the spores of Bacillus anthracis — a bacterium included within the B. cereus group. In the body, the spores produce anthrax toxin, thanks to anthrax-toxin genes they carry in their DNA.

Exposure to the spores can happen through a cut or scrape or if someone eats infected animal products or breathes contaminated air. The latter, known as inhalation anthrax, is the most lethal form of the condition, according to the Centers for Disease Control and Prevention (CDC).

Welder's anthrax is unusual in that it is caused by a different Bacillus species. Historically, it was thought that only B. antracis could produce anthrax toxin, but in recent years, it's been discovered that some other bacterial species within the B. cereus group share the disease-causing genes normally found in B. anthracis.

The fumes produced through welding are known to increase the risk of developing lung infections. The patient previously conducted shielded metal arc welding, which uses an electric current to join metal plates and produces more fumes than other welding types do.

The treatment: Before waiting for the final diagnosis, the doctors gave the patient four powerful antibiotics — vancomycin, meropenem, ciprofloxacin and doxycycline — that treat some of the most severe bacterial infections, including pneumonia.

Then, in partnership with the CDC, the medical team administered the anthrax antitoxin obiltoxaximab 34 hours after the initial diagnosis. This antitoxin, which in this case was obtained from the U.S. Strategic National Stockpile, targets the protective antigen of B. anthracis, the bacterium that causes the typical form of anthrax.

This case marked the first time obiltoxaximab had been used to treat welder's anthrax; a different antitoxin, raxibacumab, was administered in the one previous case where the patient received an anthrax antitoxin.

The patient recovered quickly after receiving obiltoxaximab, and his breathing tube was removed three days later. The doctors continued to treat him with antibiotics, and they also drained the fluid that had built up around his lungs — a common occurrence in patients with pneumonia.

The Louisiana State Public Health Laboratory tested the patient's blood and found he had been infected with Bacillus tropicus, a bacterium within the B. cereus group.

After 26 days of hospitalization, the patient was discharged with a personalized antibiotic regime. He had fully recovered by his three-month follow-up appointment.

What makes the case unique: There have been only nine known instances of welder's anthrax since the first recognized case in 1994. Only three patients have survived the illness, of which two received an anthrax antitoxin.

This new case is also unique because of the patient's young age; the age range of all previous patients was 34 to 56 years old. Additionally, the patient had been welding for only six months, whereas some individuals who had contracted the disease in the past had been welding for a decade or longer.

In an investigation of the case, the Louisiana Department of Health collected 245 soil and surface samples from the man's workplace and found that 11.4% were positive for anthrax-toxin genes. Limited airflow and ventilation, inconsistent use of personal protective equipment and eating in the work area were risk factors for the patient contracting the disease, the authors wrote in the case report.

However, notably, no one else at the patient's worksite became ill.

"The reason that this previously healthy young man was the only worker to become ill, despite the detection of anthrax toxin genes in multiple environmental samples from his worksite, is unclear," the authors wrote.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Bacteria and the viruses that infect them, called phages, are locked in an evolutionary arms race. But that evolution follows a different trajectory when the battle takes place in microgravity, a study conducted aboard the International Space Station (ISS) reveals.

As bacteria and phages duke it out, bacteria evolve better defenses to survive while phages evolve new ways to penetrate those defenses. The new study, published Jan. 13 in the journal PLOS Biology, details how that skirmish unfolds in space and reveals insights that could help us design better drugs for antibiotic-resistant bacteria on Earth.

In the study, researchers compared populations of E. coli infected with a phage known as T7. One set of microbes was incubated aboard the ISS, while identical control groups were grown on Earth.

The analysis of the space-station samples revealed that microgravity fundamentally altered the speed and nature of phage infection.

While the phages could still successfully infect and kill the bacteria in space, the process took longer than it did in the Earth samples. In an earlier study, the same researchers had hypothesized that infection cycles in microgravity would be slower because fluids don't mix as well in microgravity as they do in Earth's gravity.

"This new study validates our hypothesis and expectation," said lead study author Srivatsan Raman, an associate professor in the Department of Biochemistry at the University of Wisconsin-Madison.

On Earth, the fluids bacteria and viruses exist within are constantly being stirred by gravity — warm water rises, cold water sinks, and heavier particles settle at the bottom. This keeps everything moving and bumping into each other.

In space, there is no stirring; everything just floats. So because the bacteria and phages weren't bumping into each other as often, phages had to adapt to a much slower pace of life and become more efficient at grabbing onto passing bacteria.

Experts think understanding this alternative form of phage evolution could help them develop new phage therapies. These emerging treatments for infections use phages to kill bacteria or make the germs more vulnerable to traditional antibiotics.

"If we can work out what phages are doing on the genetic level in order to adapt to the microgravity environment, we can apply that knowledge to experiments with resistant bacteria," Nicol Caplin, a former astrobiologist at the European Space Agency who was not involved in the study, told Live Science in an email. "And this can be a positive step in the race to optimise antibiotics on Earth."

Whole-genome sequencing revealed that both the bacteria and the phages on the ISS accumulated distinctive genetic mutations not observed in the samples on Earth. The space-based viruses accumulated specific mutations that boosted their ability to infect bacteria, as well as their ability to bind to bacterial receptors. Simultaneously, the E. coli developed mutations that protected against the phages' attacks — by tweaking their receptors, for instance — and enhanced their survival in microgravity.

Then, the researchers used a technique called deep mutational scanning to examine the changes in the viruses' receptor-binding proteins. They found that the adaptations driven by the unique cosmic environment may have practical applications back home.

When the phages were transported back to Earth and tested, the space-adapted changes in their receptor-binding protein resulted in increased activity against E. coli strains that commonly cause urinary tract infections. These strains are typically resistant to the T7 phages.

"It was a serendipitous finding," Raman said. "We were not expecting that the [mutant] phages that we identified on the ISS would kill pathogens on Earth."

"These results show how space can help us improve the activity of phage therapies," said Charlie Mo, an assistant professor in the Department of Bacteriology at the University of Wisconsin-Madison who was not involved in the study.

"However," Mo added, "we do have to factor in the cost of sending phages into space or simulating microgravity on Earth to achieve these results."

In addition to helping fight infections in Earthbound patients, the research could help yield more effective phage therapies for use in microgravity, Mo suggested. "This could be important for astronauts' health on long-term space missions — for example, missions to the moon or Mars, or prolonged ISS stays."

CRISPR kick-started a golden age of genetic research — but in nature, there are hundreds of similar systems with unexplored potential for gene editing. Now, scientists have made huge strides in explaining how an enigmatic system called SPARDA works.

CRISPR systems have enabled scientists to edit genetic information more easily than ever before. Although it's best known for its use in gene editing, CRISPR is actually an adapted bacterial immune defense system that was repurposed for human use.

A recent study in the journal Cell Research highlights another bacterial defense system, known as SPARDA (short prokaryotic Argonaute, DNase associated), and the advances raise the potential for SPARDA-derived biotechnology tools that could enhance diagnostics that currently use CRISPR.

Molecular argonautes

Study co-author Mindaugas Zaremba, a biochemist at Vilnius University in Lithuania, told Live Science that before the new work, researchers had conducted only limited studies of SPARDA systems. They had established that the proteins that make up the system adopt a kamikaze-like approach to cell defense, guarding the wider population of bacteria against foreign DNA, including free-floating DNA called plasmids and viruses called phages.

"SPARDA systems were demonstrated to protect bacteria from plasmids and phages by degrading the DNA of both infected cells and invaders, thereby killing the host cell but at the same time preventing further spread of the infection within the bacterial population," Zaremba said.

How SPARDA worked at a molecular level remained unclear, prompting Zaremba and his team to use the AI protein analysis tool AlphaFold, among a suite of other analysis techniques, to dig into SPARDA's setup. AlphaFold uses machine learning to predict the 3D shape of proteins based on the sequence of their underlying building blocks.

The SPARDA system is built from argonaute proteins, named for their resemblance to argonaut octopuses (Argonauta). The proteins were originally identified in plants, where seedlings affected by mutations in these proteins developed narrow leaves that reminded scientists of an octopus’s tentacles. These argonaute proteins are evolutionarily conserved and are present in cells across the three kingdoms of life.

Zaremba's analysis looked at SPARDA systems randomly selected from two different bacteria. The first, Xanthobacter autotrophicus, is a soil-dwelling microbe that shuns sunlight and builds its food from locally sourced nitrogen. The second, Enhydrobacter aerosaccus, was first found in Michigan's Wintergreen Lake and has built-in airbags that help it float around watery environments.

Zaremba's team chopped the SPARDA systems out of these bacteria and placed them in the reliable model organism E. coli for study. A molecular analysis revealed that each of their argonaute proteins included a critical "activating region." They called this area the beta-relay, because it resembled electrical relay switches that control machinery by flicking between "on" or "off" states.

When the SPARDA systems detected external threats, these switches changed shape. The new shape enabled the proteins to form complexes with other activated argonaute proteins. When that happens, the proteins line up like soldiers on parade, forming long, spiraling chains. These chains chop up any surrounding DNA that they encounter in an extreme reaction that spares neither the host nor the invader. This stops the infection from spreading to other cells.

Zaremba's team then used AlphaFold to scan for beta-relays in similar bacterial proteins. The same switches popped up repeatedly, suggesting that the relays are a universal feature of this protein type.

SPARDA in diagnostics

SPARDA is essential for bacterial defense, but Zaremba's team argues that the system could also help humans.

Activating SPARDA is a last-ditch maneuver for bacterial cells, to be used only when an infection is definitively present. Therefore, the system includes an incredibly accurate recognition system for spotting foreign DNA that would warrant self-destruction.

Researchers could repurpose the system for diagnostics, Zaremba suggested. In that scenario, the beta-relay could be altered to be activated only when a genetic sequence of interest is identified — so it would react only to the genetic material of a flu virus or SARS-CoV-2, for instance. This mechanism underlies existing CRISPR-based diagnostic tools.

The CRISPR diagnostics, however, are currently limited in their function — they recognize targets only when certain DNA sequences, called PAM sequences, flank them. These sequences are like the prongs on the end of a plug; if they don't match a socket, the system will have no power. This means choosing the right CRISPR protein to match a particular target is essential.

"We already know that SPARDA systems do not require a PAM sequence," Zaremba said. This means they could act like a universal adapter, giving future DNA diagnostics more flexibility and ultimately making the tests better at detecting a range of germs.

CRISPR research won a Nobel Prize and changed science forever. While SPARDA research is at a far earlier stage of research, its inner workings suggest that the design of tiny organisms could hold lessons for the biggest questions in science.

A postmortem examination has revealed that Cassius, an 18-foot-long (5.5 meters) captive crocodile that died last year in Australia at the age of about 120, succumbed to sepsis.

An infection from an injury that Cassius sustained in the wild more than 40 years ago burst out of a fibrous casing and "engulfed" the saltwater crocodile (Crocodylus porosus), killing him suddenly, Sally Isberg, the managing director of the Center for Crocodile Research in Darwin who conducted the examination, told ABC News.

Sealed, "dormant" infections are well documented in crocodiles, but Cassius had the longest reported existence of such an infection, Isberg said. "In mammals, it's known as an abscess," she said. "In reptiles, it's known as a fibrosis."

Cassius had a fibrosis lodged near his left lung that exploded last November, just a few months after Isberg conducted a health checkup and concluded that the crocodile was "happy and healthy." Just 17 days before Cassius's death, Isberg visited him and found no signs of disease. There had been no warning of an infection until the fibrosis ruptured, because the casing kept the infection neatly packaged and sealed, Isberg said.

The infection probably stemmed from when Cassius lost his front left leg as a youngster, before he was captured in the Northern Territory and brought into captivity in 1984.

"What we didn't know was that the rib cage had also been damaged in that injury," Isberg said. "Upon necropsy, his left rib was distended compared to his right one," because it housed the fibrosis.

The fibrosis finally burst because Cassius was growing too old, Isberg explained. "It's because the cells are breaking down, they're not able to renew themselves," she said. "He [Cassius] was not able to continue [making] that fibrous casing around that infection."

After Cassius died, Isberg removed one of his thigh bones to estimate his age more precisely. Staff at Marineland Crocodile Park, where Cassius lived for 40 years until his death, celebrated Cassius's 120th birthday in 2023 — but that age was a maximum estimate, given that the crocodile was between 30 and 80 years old when he was captured.

Isberg hoped that the thigh bone would show growth rings, but the tests didn't give a definitive result, because temperatures at Marineland Crocodile Park are very stable, she said. Growth rings on crocodile bones vary with metabolism fluctuations, which are partly dependent on temperature.

Cassius has now been taxidermied and returned to the crocodile park for an exhibit that will open Saturday (Dec. 12).

Crocodile quiz: Test your knowledge on the prehistoric predators

Scientists have used genetically engineered bacteria to simultaneously create and color fabrics in a one-pot method. Compared with current methods that rely on fossil fuels, the new technique offers a simpler and more sustainable way to produce colored textiles.

In a new study described Nov. 12 in the journal Trends in Biotechnology, the researchers created cellulose-based fabrics spanning the colors of the rainbow by altering the conditions used to grow the bacteria.

Synthetic fibers rely "heavily on chemical synthesis and post-treatment steps that are energy-intensive, laborious, and environmentally harmful," said study lead author Sang Yup Lee, a professor in the Department of Chemical and Biomolecular Engineering at the Korea Advanced Institute of Science and Technology. Such processes can generate large amounts of greenhouse gas emissions and contaminate water and soil with heavy metals and carcinogens, Lee told Live Science in an email.

Therefore, in recent years, there has been a growing trend to use an alternative method of producing natural fibers from the fermentation of bacteria. Cellulose is a promising target, as this material mimics the natural fibers found in fabrics such as cotton. A wide range of bacteria ordinarily convert glucose into fibers of cellulose to lend structural support and defend against other microbes. However, cellulose produced by bacteria is naturally white, which means it often needs to be dyed after processing.

Lee and his team have now simplified this process by growing cellulose-producing bacteria alongside microbes that produce natural colorants. The team used strains of color-producing Escherichia coli (E. coli) to create two classes of dyes: darker violaceins (which produced colors such as purple, blue and green) and warmer carotenoids (which produced colors such as red, orange and yellow).

Initially, the researchers genetically modified the metabolic pathway of a strain of Komagataeibacter xylinus bacteria to increase cellulose production during fermentation. Subsequently adding the violacein-producing E. coli to the reaction vessel resulted in purple-, blue- and green-dyed fabric.

However, the team was not able to use the same method to achieve the warmer tones, because the bacteria did not produce enough dye to stain the cellulose fabric, likely due to poor bacterial growth. To overcome this issue, they added pregrown and treated cellulose to a culture of carotenoid-producing E. coli. This co-culture method successfully led to red-, orange- and yellow-dyed fabrics, thereby completing the team's rainbow palette.

Overall, this method "eliminates the need for separate dying and washing processes," Lee said, adding that this helps to reduce chemical waste and water consumption.

The colored bacterial cellulose showed an overall strong stability against acids, bases, heat treatments, and washing. However, the team noted that further work is needed to fully test these materials — notably, to check their durability against industrial detergents and mechanical wear and tear.

Moving forward, Lee wants to "extend the current seven color platform to a broader spectrum" and scale up the process to an industrial level while maintaining consistent quality. Further altering the way bacteria produce the cellulose could open up other uses of the material, such as biodegradable packaging, he said.

The patient: A 3-year-old boy in San Antonio, Texas

What happened: The patient's mother worked as a microbiology lab technician, and part of her job involved visiting physicians' offices to gather lab dishes of clinical samples that had been collected from patients. One day, she had her son in the car while she was making these rounds, according to a report of the case, which was published in 1984.

While en route, she stopped at a grocery store and then drove home to drop off her purchases. Once home, she briefly left her son in the parked car as she brought the groceries inside. When she returned, she found that her son had crawled into the backseat where she'd placed the clinical cultures — and that he'd eaten most of the contents of one lab dish.

That dish contained "chocolate agar," a brownish medium used to grow bacteria that's made of split-open red blood cells. It's named for its color and contains no actual chocolate but nonetheless may have looked appetizing to the child, the report noted.

The diagnosis: The mother immediately brought her child to their family doctor, who found that the remaining material from the lab dish contained Neisseria gonorrhoeae, the bacteria that causes gonorrhea. Doctors decided to monitor the boy for signs of bacterial infection in his throat. Up to six days after he ate the agar, the boy's throat swabs tested negative for N. gonorrhoeae. No test was taken on the seventh day, but on the eighth day, he tested positive.

(The report didn't note whether the boy experienced any symptoms of the infection, and often, gonorrhea infections of the mouth and throat cause no symptoms. Possible symptoms include swollen lymph nodes and throat redness and soreness. Untreated gonorrhea can sometimes lead to dangerous complications, such as bloodstream infections or harmful immune system changes.)

The treatment: The doctors treated the infection following the Centers for Disease Control and Prevention's (CDC) guidelines at the time. This involved giving the patient intermuscular injections of an antibiotic called procaine penicillin G. (Nowadays, penicillin G is not recommended as a therapy for gonorrhea, in part because many strains of N. gonorrhoea circulating in the U.S. are now resistant to the drug's effects.)

The boy was also given probenecid mixed into ice cream. Probenecid helps boost the effect of some antibiotics by slowing the rate at which they're cleared from the body. This course of treatment "produced a prompt cure" and the boy tested negative for the bacteria on tests given afterward, the report said.

What makes the case unique: Gonorrhea most often spreads via sexual contact, through exposure to semen or vaginal fluid carrying the bacteria. As such, evidence of the infection in children can often point to sexual abuse taking place. In this case, however, doctors observed a very unusual instance of non-sexually transmitted gonorrhea related to exposure to laboratory cultures.

Cases of gonorrhea had been tied to laboratory exposures before — for example, a lab technician was once infected in the eye with N. gonorrhoeae while running experiments with the bacteria. When it comes to pediatric cases, though, this route of transmission is odd because children are not typically in environments where they could be inadvertently exposed to N. gonorrhoeae cultures.

Besides underscoring the importance of safety protocols in research, this case "reminds us of the risks involved in leaving children unattended in automobiles," the report authors added.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Scientists have discovered huge, mysterious pieces of DNA in the oral microbiome — the population of bacteria and other microbes living in our mouths — and they say this giant DNA might influence the human immune system.

It's well known that we have plenty of bacteria in our mouths and that these microbes can have both positive and negative impacts on our oral and overall health.

Now, in a study published Aug. 11 in the journal Nature Communications, researchers report a previously undiscovered feature of the oral microbiome: giant pieces of bacterial DNA that separate from the microbes' main genome. Moreover, these pieces of DNA are associated with changes in the body's immune system and even the occurrence of certain types of cancer, the team found.

The study provides a "new puzzle piece that is a step in understanding the oral microbiome, human health, and human disease," Floyd Dewhirst, a professor at the ADA Forsyth Institute who was not involved in the research, told Live Science in an email.

Microbiome studies, which have flourished in the past decade, have shown that the microbiomes across the body play major roles in human health and disease. Researchers have identified the types and proportions of different microbial species that live in places like our mouths and guts, and then used that data to see how differences in those features are linked to our health.

Over the years, the genomes of these species have been studied extensively but conventional genetic analyses have not yet been able to explain all of the links between our microbiome and overall health status.

Researchers in the Yutaka Suzuki lab at the University of Tokyo wanted to explore these missing data and were inspired by the recent discovery of giant extrachromosomal elements (ECEs) in bacteria living in soil. ECEs are pieces of DNA that are separate from an organism's main genome. In humans, our mitochondrial DNA — stored in the powerhouses of our cells — is an ECE. In bacteria, a commonly known small ECE is called a plasmid.

Lead study author Yuya Kiguchi, who is now a researcher at Stanford University, and his colleagues in the Suzuki lab predicted that giant ECEs could be found in bacteria living in places other than soil.

"Maybe many of these giant extra chromosomal elements are found in the environment, the microbiome field, or pathogens," Kiguchi told Live Science. "But we don't know any examples of this kind of giant extra chromosomal element from the commensal [human] microbiome." Commensal microbes are those that live symbiotically in or on the human body.

Using saliva samples from hundreds of people, the researchers found, for the first time, that giant ECEs also exist in our oral microbiome. The research team named these giant pieces of DNA "inocles;" the name stands for "insertion sequence encoded; oral origin; circle genomic structure." They also found that approximately 74% of people in their study possessed these inocles in their oral microbiome.

So why is this the first time inocles have been discovered? Most genetic experiments in bacteria use short-read DNA sequencing methods. This involves cutting a cell's DNA into smaller pieces, reading their code, and then assembling the bits into a full genome using a computer. While this method of sequencing can easily detect small ECEs, like typical bacterial plasmids, inocles are too large and complex for short-read sequencing to spot.

Using long-read DNA sequencing — a costlier and more time consuming method in which much larger pieces of DNA are sequenced and stitched together — the scientists could identify these large chunks of extrachromosomal DNA in the bacteria of human saliva samples. By correlating those results with blood samples from the same people, they also found that differences in the levels of inocles is associated with differences in the immune system, including the immune response to certain bacterial and viral infections.

Sixty-eight people in the study had either a type of head and neck or colorectal cancer, and these individuals had lower levels of inocles in their oral microbiomes compared with the people without these cancers. That raises the possibility of using these newly discovered giant chunks of DNA as future biomarkers for cancer, the study authors suggested.

As a next step, the researchers aim to grow these inocles in the lab so they can further investigate their function and how they can spread between bacteria and people.

"Now that we know that inocles exist, we can try and figure out their functions and potential roles in health and disease," Dewhirst said.

Scientists have released new images showing, in incredible detail, antibiotics defeating disease-causing bacteria by piercing the microbes' membranes and infiltrating their innards.

The antibiotics, called polymyxins, were observed forcing the armored membranes around Escherichia coli bacterial cells to grow bumps and bulges. The bacteria then shed their outer membranes, leaving space for the antibiotic to enter the cells.

"It was incredible seeing the effect of the antibiotic at the bacterial surface in real-time," study co-author Carolina Borrelli, a doctoral student studying biophysics and microbiology at University College London (UCL), said in a statement.

Gram-negative bacteria are a broad class of microorganisms that have two membranes surrounding each cell; the two membranes sandwich a cell wall. E. coli, Salmonella, and Shigella — a type of bacteria that causes dysentery — are all examples of gram-negative bacteria.

Polymyxins can help treat infections caused by gram-negative bacteria that have gained resistance to other antibiotic drugs; they work by targeting the outer of the bacteria's two membranes, which act as a kind of armor that keeps antibiotics out. But exactly how the antibiotics slip past this armor isn't well understood.

"Polymyxins are an important line of defense against Gram-negative bacteria, which cause many deadly drug-resistant infections," study co-author Bart Hoogenboom, a biophysicist at UCL, said in the statement. "It is important we understand how they work."

In the new study, published Sept. 29 in the journal Nature Microbiology, the team of researchers captured images of the antibiotic in action. Using a technique known as atomic force microscopy, the scientists passed a tiny needle back and forth over the bacteria to map out their shapes. This let them see how the bacteria changed as the polymyxin attacked.

Polymyxins forced E. coli to quickly grow tiny bumps and protrusions on its outer membrane, the team found. As these bumps grew, the bacterium shed its armor, leaving gaps in that outer membrane through which antibiotics could enter and kill the cell.

"Our images of the bacteria directly show how much polymyxins can compromise the bacterial armor," Borrelli said. "It is as if the cell is forced to produce 'bricks' for its outer wall at such a rate that this wall becomes disrupted, allowing the antibiotic to infiltrate."

Importantly, the polymyxins can only target bacteria that are actively growing, not those that have gone into a dormant state. Bacteria sometimes enter a state of dormancy to deal with difficult conditions, surviving years without eating, growing or reproducing, only to wake back up when conditions are more favorable. While dormant, bacteria can't grow their outer membrane armor, so the antibiotic couldn't ramp up production the same way it could in actively growing bacteria.

"Our next challenge is to use these findings to make the antibiotics more effective," Hoogenboom said. "One strategy might be to combine polymyxin treatment — counterintuitively — with treatments that promote armor production and/or wake up 'sleeping' bacteria so these cells can be eliminated too."

This article is for informational purposes only and is not meant to offer medical advice.

By adding a handful of live ants to warm milk, a group of anthropologists and food scientists investigated how to make "ant yogurt" — and they ended up learning that it has the same ingredient as a popular type of bread.

The bacteria in the "ant yogurt," which they made using a traditional Balkan method, is a strain that's commonly used as a sourdough starter today, the team found. They then served the yogurt to patrons at a restaurant to showcase historical methods of fermenting food.

The process behind concocting this ant delicacy is dramatically different from how the fermented dairy food is industrially made today, the researchers wrote in a study published Friday (Oct. 3) in the journal iScience.

"Today's yogurts are typically made with just two bacterial strains," study co-author Leonie Jahn, a researcher at the Technical University of Denmark, said in a statement. The strains, Lactobacillus bulgaricus and Streptococcus thermophilus, are introduced to warm milk as a bulk starter. The bacteria ferment the sugars in the milk, producing lactic acid, which lowers the pH and increases the acidity of milk, causing the milk to coagulate. This also gives yogurt its consistency and flavor.

"If you look at traditional yogurt, you have much bigger biodiversity," Jahn said, because various bacterial strains impart different flavors and textures to the food.

Study co-author Sevgi Mutlu Sirakova, a doctoral student at Ludwig Maximilian University of Munich, previously gathered oral histories from people in Turkey and Bulgaria that described different methods of creating yogurt, including the use of red wood ants (Formica sp.) to kick-start the process. The researchers visited Sirakova's family village in Bulgaria, where locals recalled the tradition of using ants to make yogurt.

"We dropped four whole ants into a jar of warm milk by the instruction of Sevgi's uncle and community members," study co-author Veronica Sinotte, a microbiologist at the University of Copenhagen, said in a statement. After keeping the jar of milk warm in the ant mound overnight, they tried the yogurt that had formed — and described it as "slightly tangy" and "herbaceous."

After making the ant yogurt, the team studied it to understand the role of the ant "holobiont," which includes both the ant and the microbial communities in and on the creature.

Chemical analysis of the yogurt revealed that the dominant bacterium responsible for fermentation was Fructilactobacillus sanfranciscensis, a species that is much better known as a key ingredient in sourdough bread. Additionally, they discovered abundant formic acid in the yogurt. Wood ants produce large amounts of formic acid in their venom gland, and they can spray it as a defense mechanism. The formic acid gave the yogurt a unique taste and texture.

"This study highlights ants as a reservoir of bacteria with potential for food fermentation, and the importance of both ant biodiversity and traditional practices in maintaining this potential," the researchers wrote in the study.

To further test the culinary possibilities of ant yogurt, the researchers partnered with Alchemist, a 2 Michelin-star restaurant in Copenhagen. The chefs created three new dishes from the ant yogurt: an ant-shaped ice cream sandwich, tangy cheeses, and a "milk wash cocktail" from a recipe dating back to the early 1700s.

But amateur cooks should not try this at home, the researchers warned, because ants can harbor parasites. The researchers used a microbiology-grade sieve to remove any potential parasites before passing the yogurt to the restaurant.

The use of ants in yogurt making remains widespread in Turkey and Bulgaria today, and now scientists understand exactly how the ants react with the milk to produce yogurt.

"I hope people recognize the importance of community and maybe listen a little closer when their grandmother shares a recipe or memory that seems unusual," Sinotte said.

Editor's Note: This story was updated at 10:05 a.m. ET on Oct. 6 to note that lactic acid lowers the pH and increases the acidity of milk, causing milk to coagulate.

On Sept. 28, 1928, Alexander Fleming woke up to check on his experiments investigating bacterial growth — and accidentally discovered the world's first antibiotic.

The Scottish physicist and microbiologist had been doing experiments in a cramped, roughly 12-square-foot (1 square meter) room in a turret inside London's St Mary's Hospital. The famously untidy scientist would culture bacteria from infected hospital patients; he would leave those cultures around for two or three weeks until his bench was crammed with 40 to 50 plates. Then, he would inspect each plate to see if anything interesting had grown in it, before tossing it out.

The discovery of penicillin occurred when Fleming returned from a two-week break. He looked at his plates of Staphylococcus aureus that had been cultured from an infected wound. On one of the plates, Fleming noticed a patch of green mold intersecting the golden-yellow bacterial colonies, according to an account from his assistant, V.D. Allison. Near the green patch, the bacteria were translucent, colorless and dead. The substance that killed the bacteria would form the basis of the first antibiotic, though the term wasn't coined until 1941.

"When I woke up just after dawn on September 28, 1928, I certainly didn't plan to revolutionize all medicine by discovering the world's first antibiotic, or bacteria killer," Fleming later said. "But I suppose that was exactly what I did."

Fleming determined that the "mold juice" came from a fungal species he eventually identified as Penicillium. When he described the discovery to his fellow doctors at a meeting the next year, he was met with almost total disinterest. Isolating the elusive "mold juice" also proved challenging, so the discovery languished for a decade, Allison wrote in personal recollections.

Then, in 1939, scientists Howard Florey and Ernst Chain took an interest in the substance. They created a research team and, along with scientists such as Margaret Jennings, Edward Abraham and Norman Heatley, managed to isolate penicillin from the mold, test it and use the yellowy, powdery substance to cure a handful of patients. However, the compound was still relatively impure.

In 1942, Fleming was treating a young patient who was seriously ill with meningitis. He found the powder killed the patient's bacterial infection, and he phoned Florey and Chain for some of their stash, even though it was not purified. After Fleming injected it into the boy's spinal cord, the patient recovered.

After this miraculous recovery, Fleming was convinced that penicillin needed to be mass-produced. He pitched it to the government, and soon there was a joint effort between the U.S. and the U.K. to mass-produce the substance. By 1945, the first antibiotic was widely available.

Fleming, Florey and Chain would win the 1945 Nobel Prize in medicine for their work on the discovery, isolation and production of penicillin. In 1964, Dorothy Hodgkin would earn the Nobel Prize in chemistry for elucidating its crystal structure, which helped chemists design later antibiotics.

It's estimated that since its discovery, penicillin has saved 500 million lives and, along with its derivatives, is still a mainstay in the treatment of myriad illnesses, including ear infections, strep throat, and urinary tract infections.

Penicillin also led to the development of hundreds of different antibiotics. But widespread use and misuse of these wonder drugs have meant that many bacterial strains have evolved resistance against common antibiotics, including penicillin. In the arms race against superbugs, scientists are now finding totally new ways to fight bacteria, from harnessing the power of viruses to attack bacteria to using the gene-editing tool CRISPR to design new drugs.

Scientists in Australia are deep-freezing the shoot tips of a critically endangered tree to preserve its DNA in case the species goes extinct.

Only 380 specimens of the angle-stemmed myrtle (Gossia gonoclada) remain in the wild, with about 300 of them concentrated in the City of Logan area in southeast Queensland. If scientists manage to cryopreserve a diverse collection of genes from the species, there is a good chance they could resurrect it if it ever dies out, researchers said.

"The most important thing is preventing its continuing decline in the wild as this is where the plant is providing ecological functions and potentially cultural significance," Alice Hayward, a plant molecular physiologist at the University of Queensland who supervises the project, told Live Science in an email. But "by capturing and keeping alive the remaining diversity of this species in cryobanks it effectively provides a back up storage device for the species," Hayward said.

The angle-stemmed myrtle is a small tree that grows along waterways in Australia's dry rainforests. It has glossy leaves, square stems and sweet, fleshy fruit that may be a food source for bats and birds, Hayward said. "There has been limited research on its ecological interactions but it likely aids in river bank stability and biodiversity," she said.

A combination of habitat loss, rising temperatures and a deadly fungal disease called myrtle rust has drastically reduced the number of angle-stemmed myrtle plants in Australia since 2010. Myrtle rust is caused by the exotic fungus Austropuccinia psidii, which attacks the newly grown parts of trees and shrubs in the Myrtaceae family, deforming the plants' leaves, stunting their growth and decreasing their fertility.

To save the angle-stemmed myrtle from extinction, scientists are designing a method to freeze plant tissues that can later regenerate a full tree whenever needed. Although seeds contain reproductive material, they are not suitable for this project, both because of their reduced fertility from myrtle rust infections and because they likely won't survive long-term cryopreservation, Hayward said.

Related: 'It is our obligation to future generations': Scientists want thousands of human poop samples for microbe 'doomsday vault'

So instead, Hayward and Jingyin Bao, a doctoral student at the University of Queensland, plan on preserving the angle-stemmed myrtle's shoot tips — the uppermost and actively growing parts of the plant — at ultra-low temperatures of minus 321 degrees Fahrenheit (minus 196 degrees Celsius).

This involves growing sterile shoots in a jelly and harvesting the tips before treating them with a cryoprotective solution and freezing them in liquid nitrogen, ABC News reported. Cryoprotective solutions protect plant cells during freezing by minimizing the formation of damaging ice crystals, Hayward said. Without these solutions, water inside the cells would expand, and the cells would burst; but with the solutions, the water turns "glassy" instead, she said.

The method already works for the sweet myrtle (Gossia fragrantissima), which is a small tree closely related to the angle-stemmed myrtle. After freezing sweet myrtle shoot tips, Bao achieved a 100% survival rate and managed to regrow all the plants, Hayward said. "We are transitioning this to gonoclada with some success and still working to improve the survival," she said.

Once the researchers land on a method for the angle-stemmed myrtle, they still need to make sure that they have enough genetic diversity in their samples to regrow a healthy population of trees.

"It is important that there is sufficient genetic diversity saved to provide the best chance of species survival in the future, especially if there happens to be any natural tolerance to myrtle rust or changing climate conditions," Hayward said. "Given the threats to this species in the wild due to habitat loss and invasive species including myrtle rust this needs to happen fast."

So far, Hayward and Bao haven't found any disease- or climate-resistant specimens in their sample, but City of Logan authorities and their partners are working to identify resistant individuals, Hayward said. "We want to preserve the most diverse individuals, whether tolerant or not, to provide a basis for future breeding," she explained.

And it's not just the angle-stemmed myrtle that needs preserving in this way, Hayward said. "We need Australia and the world to implement cryobanks to ensure we can bank the diversity of … foods and endangered plants for future generations," she said.

A person in Maryland has been confirmed to have an infection with the flesh-eating New World screwworm parasite — the first human case of the infection in the United States since the parasite was eradicated in the country over 60 years ago, according to the U.S. Department of Health and Human Services (HHS).

The Maryland patient had returned to the U.S. after traveling to El Salvador, HHS spokesperson Andrew G. Nixon told Reuters in an email, and the Centers for Disease Control and Prevention (CDC) confirmed the infection with the New World screwworm (Cochliomyia hominivorax) via images of the larvae on Aug. 4, according to Axios.

"This is the first human case of travel-associated New World screwworm myiasis (parasitic infestation of fly larvae) from an outbreak-affected country identified in the United States," Nixon said in an emailed statement to Axios. However, "the risk to public health in the United States from this introduction is very low," he added.

C. hominivorax is a species of parasitic fly that lays eggs inside the open wounds, eyes, noses or mouths of warm-blooded animals. Female screwworm flies can lay up to 300 eggs at a time. When the eggs hatch, screwworm larvae use their sharp mouths to burrow into the host's flesh, which causes a painful infestation called myiasis.

New World screwworms primarily affect cattle and other livestock, but they can also cause infestations in humans. An infestation can be fatal if left untreated, but a doctor can usually treat myiasis by removing the larvae. People who work with livestock, have weakened immune systems, open wounds, or who sleep outdoors are most at risk for developing an infection, according to the CDC. But because screwworm is an insect and not a virus, it’s not contagious, Max Scott, a professor of entomology and plant pathology at North Carolina State University, told NPR.

The New World screwworm is endemic to South America and the Caribbean, and it isn't typically found in the U.S., according to the CDC. No cases of screwworm infestation have been found in U.S. animals so far. In the 1960s, the U.S. eradicated New World screwworms within the country by releasing male sterile screwworm flies into infested areas. The sterile flies mated with wild female flies, but the eggs didn't hatch, which caused screwworm populations to decline.

Since 2023, screwworm populations have been increasing in Central America and slowly spreading northward. In November 2024, a screwworm infestation in Mexico prompted the U.S. to temporarily pause livestock imports at the southern border. Imports resumed in January, only to halt again in May. Ports are now reopening in stages, according to the U.S. Department of Agriculture, and a new sterile fly dispersal facility is being constructed in southern Texas.

Researchers have discovered the cause of a mysterious marine epidemic that has turned billions of sea stars into goo along the West Coast — and it's not what they expected.

Sea star wasting disease has been killing sea stars since 2013, causing catastrophic damage to ecosystems and driving the largest sea star species to the brink of extinction. Researchers thought a virus might be responsible for the disease, but after a four-year-long investigation, they've found that a strain of bacteria is to blame.

The pathogenic bacteria is Vibrio pectenicida, which is part of the same genus that causes cholera (V. cholerae) and produces strains that have devastated coral and shellfish populations, researchers said in a statement.

The researchers, who published their findings Monday (Aug. 4) in the journal Nature Ecology and Evolution, used DNA sequencing to identify microbes in infected sea stars that weren't in healthy individuals. Eventually, the team zeroed in on high levels of V. pectenicida in infected sea star "blood," known as coelomic fluid.

"When we looked at the coelomic fluid between exposed and healthy sea stars, there was basically one thing different: Vibrio," senior study author Alyssa Gehman, a marine disease ecologist at the Hakai Institute and the University of British Columbia (UBC), said in the statement. "We all had chills. We thought, That's it. We have it. That's what causes wasting."

Related: 'A disembodied head walking about the sea floor on its lips': Scientists finally work out what a starfish is

Sea star wasting disease has infected more than 20 different species, but it is particularly devastating for sunflower sea stars (Pycnopodia helianthoides). These giant sea stars, which can grow up to 39 inches (1 meter) in diameter, are now functionally extinct in much of their southern range in the continental U.S., while further north, they've suffered population losses of more than 87%. This decline has had disastrous consequences for the ecosystems they inhabit, according to the study.

Sunflower sea stars are predators that naturally keep sea urchins under control, which in turn stops the urchins from eating too much kelp. But with the sea stars sustaining heavy losses, scientists have seen urchin populations explode, leading to a major decline in kelp forests. That's a big problem because kelp forests provide habitat for thousands of species, support local economies through fishing and tourism, are important for coastal First Nations and tribal communities, protect coastlines from storms and store carbon dioxide, according to the statement.

"When we lose billions of sea stars, that really shifts the ecological dynamics," study first author Melanie Prentice, an evolutionary ecologist at the Hakai Institute and UBC, said in the statement. "Losing a sea star goes far beyond the loss of that single species."

Studying wasting disease

Scientists have had a hard time finding the cause of wasting disease. The disease starts as lesions on the sea star's body and then essentially melts tissues over the course of about two weeks, eventually reducing sea star bodies to goo. However, sea stars can present similar symptoms to other environmental stressors and diseases, making it difficult to figure out what's behind a specific ailment. The study authors investigated lots of pathogens that they thought could have been responsible for wasting disease, before identifying the strain of V. pectenicida, known as FHCF-3.

Once the researchers had identified the strain, they created cultures of V. pectenicida from infected sea stars and gave them to healthy sea stars. The result was death for almost all of the infected sea stars, indicating that FHCF-3 was to blame for the wasting disease, according to the study. The researchers still have a lot to learn about the disease, but they can now move on to investigating its drivers and how to best fight it.

"Understanding what led to the loss of the sunflower sea star is a key step in recovering this species and all the benefits that kelp forest ecosystems provide," Jono Wilson, the director of ocean science at the California chapter of The Nature Conservancy, which was involved in the study, said in the statement.

There's a secret, extra member of Crew-11 aboard the International Space Station right now: disease-causing bacteria.

Or, at least, such bacteria will be growing aboard the orbiting laboratory very soon. Scientists at the Sheba Medical Center in Israel, in partnership with U.S.-based space tech company SpaceTango, have developed a study that will examine how microgravity affects the growth of certain bacterial species that cause diseases in humans. To pull it off, researchers will grow different strains of bacteria under microgravity, freeze that bacteria at -80 degrees Celsius and then return the samples to Earth to see how they’ve grown differently than the same bacteria grown on the home planet.

The bacterial strains involved are E. Coli, Salmonella bongori and Salmonella typhimurium, and they were launched toward the International Space Station (ISS) aboard NASA's Crew-11 mission that SpaceX successfully launched on Friday, Aug. 1. (Editor's note: The Crew-11 team docked to the ISS on Aug. 2 and is now adjusting to life in orbit).

Scientists have already studied how a lack of gravity affects the way bacteria grows, and research from NASA is already underway to study bacteria in space in general. But researchers behind the current ISS-and-bacteria mission specifically hope to bring home data that will help curb the spread of infectious disease, or at least help experts find ways to stop bacteria from developing antibiotic resistance — a major public health problem that means some disease-causing bacteria is no longer wiped out by drugs that've been developed to clear the bacteria from people’s bodies and get them healthy again

"We know that space conditions affect bacterial behavior, including how they grow, express genes, and acquire traits like antibiotic resistance or virulence," Ohad Gal-Mor, Head of the Infectious Diseases Research Laboratory at Sheba Medical Center, said in a statement.

Related: Unknown strain of bacteria found on China's Tiangong Space Station

"This experiment will allow us, for the first time, to systematically and molecularly map how the genetic expression profile of several pathogenic bacteria changes in space."

The health of astronauts and microgravity's effect on the human body has been top of mind as people explore space and the idea of what life off Earth looks like. Human genes sometimes express themselves differently in microgravity conditions, and scientists have linked such an environment to the expedited loss of muscle seen in astronauts, and even their likelihood of developing skin rashes.

If examined on their own, however, genetic changes in bacteria will hopefully give researchers more clues about how they act once inside a human, whether it's how fast they spread or their likelihood of getting around our treatments: both in space and here on Earth.

An outbreak of a potentially fatal bacterial infection in Harlem, New York City has so far led to two deaths.

Overall, a total of 58 people have been diagnosed with the infection, according to a statement released Monday (Aug. 4) by the New York City Department of Health and Mental Hygiene. The outbreak, which started in late July, is affecting several communities in Central Harlem, specifically the ZIP codes 10027, 10030, 10035, 10037 and 10039.

The infection, known as Legionnaires' disease, is a severe form of pneumonia caused by a genus of bacteria called Legionella, which thrives in fresh, warm water and can enter the body through the inhalation of water vapor carrying the bacteria. The illness cannot be transmitted between people.

People can be exposed when the bacteria grow in water systems, such as in shower heads, hot tubs, water features and cooling towers. In relation to the Harlem outbreak, 11 cooling towers tested positive for the disease-causing bacteria and have since undergone the remediation required by the NYC health department.

This outbreak does not change the safety of tap water in Harlem, the department emphasized. Residents can drink tap water, shower, bathe, cook and use air conditioners at home without concern.

Legionnaires' disease does not affect everyone who has been exposed to Legionella bacteria. People at highest risk of the infection include those with cancer, chronic lung disease, diabetes, kidney failure, liver failure or a weakened immune system, according to the U.S. Centers for Disease Control and Prevention. Adults ages 50 and older and current and former smokers also face an increased risk.

Related: Toilet flushes may spread Legionnaires' disease

The infection's flu-like symptoms include cough, fever, chills, muscle aches and difficulty breathing. These usually take two to 14 days to develop following Legionella exposure and severe symptoms and complications, such as lung failure, can become fatal if left untreated.

"Legionnaires' disease can be effectively treated if diagnosed early," Acting Health Commissioner Dr. Michelle Morse said in the statement. Antibiotics can effectively cure the infection. "Adults aged 50 and older and those who smoke or have chronic lung conditions should be especially mindful of their symptoms and seek care as soon as symptoms begin."

Complications from the disease are less likely if treatment begins early.

About 6,000 people develop Legionnaires' disease in the United States each year, although the true count might be higher due to missed cases or misdiagnoses. Between 200 and 800 cases are typically reported in New York state yearly. Outbreaks are most common in the summer, according to the New York State Department of Health.

This article is for informational purposes only and is not meant to offer medical advice.

On hot summer days, few things are more refreshing than a dip in the pool. But have you ever wondered if the pool is as clean as that crystal blue water appears?

As an immunologist and infectious disease specialist, I study how germs spread in public spaces and how to prevent the spread. I even teach a course called "The Infections of Leisure" where we explore the risks tied to recreational activities and discuss precautions, while also taking care not to turn students into germophobes.

Swimming, especially in public pools and water parks, comes with its own unique set of risks — from minor skin irritations to gastrointestinal infections. But swimming also has a plethora of physical, social and mental health benefits. With some knowledge and a little vigilance, you can enjoy the water without worrying about what might be lurking beneath the surface.

The reality of pool germs

Summer news headlines and social media posts often spotlight the "ick-factor" of communal swimming spaces. These concerns do have some merit.

The good news is that chlorine, which is widely used in pools, is effective at killing many pathogens. The not-so-good news is that chlorine does not work instantly — and it doesn't kill everything.

Every summer, the Centers for Disease Control and Prevention issues alerts about swimming-related outbreaks of illness caused by exposure to germs in public pools and water parks. A 2023 CDC report tracked over 200 pool-associated outbreaks from 2015 to 2019 across the U.S., affecting more than 3,600 people. These outbreaks included skin infections, respiratory issues, ear infections and gastrointestinal distress. Many of the outcomes from such infections are mild, but some can be serious.

Germs and disinfectants

Even in a pool that's properly treated with chlorine, some pathogens can linger for minutes to days. One of the most common culprits is Cryptosporidium, a microscopic germ that causes watery diarrhea. This single-celled parasite has a tough outer shell that allows it to survive in chlorine-treated water for up to 10 days. It spreads when fecal matter — often from someone with diarrhea — enters the water and is swallowed by another swimmer. Even a tiny amount, invisible to the eye, can infect dozens of people.

Another common germ is Pseudomonas aeruginosa, a bacterium that causes hot tub rash and swimmer's ear. Viruses like norovirus and adenovirus can also linger in pool water and cause illness.

Swimmers introduce a range of bodily residues to the water, including sweat, urine, oils and skin cells. These substances, especially sweat and urine, interact with chlorine to form chemical byproducts called chloramines that may pose health risks.

These byproducts are responsible for that strong chlorine smell. A clean pool should actually lack a strong chlorine odor, as well as any other smells, of course. It is a common myth that a strong chlorine smell is a good sign of a clean pool. In fact, it may actually be a red flag that means the opposite — that the water is contaminated and should perhaps be avoided.

How to play it safe at a public pool

Most pool-related risks can be reduced with simple precautions by both the pool staff and swimmers. And while most pool-related illnesses won't kill you, no one wants to spend their vacation or a week of beautiful summer days in the bathroom.

These 10 tips can help you avoid germs at the pool:

• Shower before swimming. Rinsing off for at least one minute removes most dirt and oils on the body that reduce chlorine's effectiveness.
• Avoid the pool if you're sick, especially if you have diarrhea or an open wound. Germs can spread quickly in water.
• Try to keep water out of your mouth to minimize the risk of ingesting germs.
• Don't swim if you have diarrhea to help prevent the spread of germs.
• If diagnosed with cryptosporidiosis, often called "crypto," wait two weeks after diarrhea stops before returning to the pool.
• Take frequent bathroom breaks. For children and adults alike, regular bathroom breaks help prevent accidents in the pool.
• Check diapers hourly and change them away from the pool to prevent fecal contamination.
• Dry your ears thoroughly after swimming to help prevent swimmer's ear.
• Don't swim with an open wound — or at least make sure it's completely covered with a waterproof bandage to protect both you and others.
• Shower after swimming to remove germs from your skin.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

If bacteria had a list of things to fear, phages would be at the top. These viruses are built to find, infect and kill them — and they have been doing it for billions of years. Now that ancient battle is offering clues for how we might fight back against antibiotic-resistant infections.

As more bacteria evolve to withstand our antibiotics, previously treatable infections are becoming harder — and in some cases, impossible — to cure. This crisis, known as antimicrobial resistance (AMR), already causes over a million deaths a year globally, and the number is rising fast. The World Health Organization has named AMR one of the top ten global public health threats.

Phage therapy — the use of phages to treat bacterial infections — is gaining attention as a potential solution. Phages are highly specific, capable of targeting even drug-resistant strains. In some compassionate-use cases in the U.K., they have cleared infections where every antibiotic had failed. But phages still face a challenge that is often overlooked: the bacteria themselves.

Bacteria have evolved sophisticated systems to detect and destroy phages. These defenses are diverse: some cut up viral DNA, others block entry, and a few launch a kind of intracellular shutdown to prevent viral takeover. In a new study published in Cell, my colleagues and I describe a system that works differently, called Kiwa. It acts like a sensor embedded in the bacterial membrane, detecting early signs of attack.

Exactly what Kiwa is sensing remains an open question, but our findings suggest it responds to the mechanical stress that occurs when a phage latches on to the cell and injects its DNA. Once triggered, Kiwa acts fast. It shuts down the phage's ability to make the components it needs to build new phages, stopping the infection before it can take over the cell.

But just as bacteria evolve ways to defend themselves, phages evolve ways to fight back. In our latest experiments, we saw two strategies in play.

Related: 'Medicine needed an alternative': How the 'phage whisperer' aims to replace antibiotics with viruses

Some phages developed small mutations in the proteins they use to attach to the bacterial surface — subtle changes that helped them avoid triggering Kiwa's detection system. Others took a different approach: they allowed themselves to be detected, but escaped the consequences.

These phages carried mutations in a viral protein that seems to be involved in how Kiwa shuts down the infection. We don't yet know exactly how this works, but the result is clear: with just a few changes, the virus keeps replicating, even after Kiwa has been activated.

This evolutionary flexibility is part of what makes phages so powerful, and why they hold such promise in treating infections. But it also highlights a key challenge: to make phage therapy effective, we need to understand how these microbial battles play out.

Rules of engagement

If a bacterial strain carries a defense like Kiwa, not all phages will succeed against it. Some might be blocked entirely. But others, with just the right mutations, might slip through. That means choosing or engineering the right phage for the job is not just a matter of trial and error — it is a matter of knowing the rules of engagement.

Studying bacterial defense systems like Kiwa gives us a deeper understanding of those rules. It helps explain why some phages fail, why others succeed, and how we might design better phage therapies in the future. In time, we may be able to predict which bacterial defenses a given strain carries, and select phages that are naturally equipped — or artificially tuned — to overcome them.

That is the idea behind our growing phage collection project. We are gathering phages from across the U.K. and beyond, including from public submissions — dirty water is often a goldmine — and testing them to see which ones can overcome the defenses carried by dangerous bacteria. With over 600 types already catalogued, we are building a resource that could help guide future phage therapy, pairing the right phage with the right infection.

Kiwa is just one piece of the puzzle. Bacteria encode many such defense systems, each adding a layer of complexity — and opportunity — to this microbial arms race. Some detect viral DNA directly, others sense damage or stress, and some even coordinate responses with neighbouring cells. The more we learn, the more precisely we can intervene.

This is not a new war. Bacteria and phages have been locked in it for billions of years. But for the first time, we are starting to listen in. And if we learn how to navigate the strategies they have evolved, we might find new ways to treat the infections our antibiotics can no longer handle.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

A Salmonella outbreak that sickened over 160 people in California and a handful of individuals in other states was caused by raw milk products from a single dairy farm, a new report explains.

The outbreak — described Thursday (July 24) in the Morbidity and Mortality Weekly Report (MMWR), which is published by the Centers for Disease Control and Prevention — took place between September 2023 and March 2024. The California Department of Public Health was first notified of the outbreak when nine people fell ill after consuming a specific brand of raw milk produced by the same dairy. This prompted an investigation by state and federal officials.

This outbreak is notable because it was "one of the largest foodborne outbreaks linked to raw milk in recent U.S. history," the report authors emphasized. Between 2009 and 2021, there have been 16 Salmonella outbreaks tied to raw milk consumption and those were comparatively small, involving between two and 33 people.

Additionally, last year's outbreak was notable because it disproportionately affected young children, as the median age of those sickened was 7 years old, the report says.

"Commercially distributed raw dairy products have the potential to cause large and widespread infectious disease outbreaks," the report writers cautioned. "Public health authorities should continue to raise awareness of the risks associated with consuming raw dairy products, especially by persons at increased risk for severe disease from enteric [intestinal] pathogens, including children."

In addition to Salmonella, raw milk can contain a range of other disease-causing germs, including bird flu viruses, Campylobacter, Cryptosporidium, Escherichia coli, Listeria and Brucella. That's because raw milk, also called unpasteurized milk, isn't heated to a high temperature to kill off those germs prior to being sold. Children under 5 years old, pregnant people, and people with weakened immune systems face particularly high risks from consuming raw milk products because the germs listed above can make them severely ill.

Related: How does E. coli get into food?

The Salmonella outbreak described in the report affected 171 people in total, including 159 confirmed and 12 probable cases. Most cases occurred in California, but there was one case each in New Mexico, Pennsylvania, Texas and Washington state.

Of the total cases, 67 occurred in children under 5, 40 were in children ages 5 to 12, and 13 were in teens under 18. That means about 70% of the total cases affected kids and teens. Out of 22 known cases that required hospitalization, 18 were in children under 18. No deaths were reported.

"The distribution of the cases was consistent with a continuous common source outbreak," the report authors wrote. This was also confirmed by genetic analyses of Salmonella samples gathered from the affected patients and found in products from the dairy.

That said, the source of infection in the four cases outside California is not 100% certain. Raw milk products intended for human consumption are not allowed to be sold across state lines, per federal law. However, "federal law does not prohibit the interstate sale of raw milk intended for pet consumption or interstate sale of raw cheese aged for ≥60 days," the report authors noted.

As such, it's possible that these four cases involved local sales of products that were originally produced in California — namely, raw cheese or raw milk marketed for pets.

"Other possible explanations for the non-California outbreak cases are that patients could not recall or did not accurately report travel history or were infected through unrecognized secondary transmission," the authors speculated.

The MMWR doesn't name the dairy implicated in the outbreak. But in 2024, The Fresno Bee reported that officials had linked the outbreak to Raw Farm LLC, based in Fresno County, and that this led to a recall of some of the company's products and inspections of its facilities. Separately, the same company also detected bird flu in some of its products in late 2024, prompting another recall.

Live Science contacted Raw Farm prior to publication, but the company declined to comment for this story.

Meanwhile, this month, the Allegheny County Health Department in Pennsylvania is urging people to discard all Family Cow brand raw milk products after locals became sick with Salmonella infections after consuming the products. The Family Cow is based in Chambersburg. "Anyone who consumed raw milk products from The Family Cow should consult a healthcare provider if they become ill," the department advises.

This article is for informational purposes only and is not meant to offer medical advice.

After 15 years of debate, a study that announced the alleged discovery of an arsenic-eating microbe has been retracted by the journal Science due to contaminated and flawed data. However, the original study authors disagree with the move.

The microbe strain, labeled GFAJ-1, was recovered from the salty water of arsenic-rich Mono Lake in California by a research team led by Felisa Wolfe-Simon of NASA's Astrobiology Institute.

Wolfe-Simon and colleagues grew GFAJ-1 in petri dishes while replacing phosphorus — a crucial component of DNA — with arsenic, which is usually highly toxic to living organisms, they reported. The team published their findings in the journal Science in 2010.

Before the paper came out, NASA hyped the finding by telling the media it would hold a news conference "to discuss an astrobiology finding that will impact the search for evidence of extraterrestrial life." Soon after, the GFAJ-1 microbe discovery quickly went viral, and it was hailed as a breakthrough in astrobiology. It upended biologists' understanding of the basic requirements for life, ostensibly proving that "arsenic life" was possible.

"What we've found is a microbe doing something new — building parts of itself out of arsenic," Wolfe-Simon said in a 2010 NASA statement. "If something here on Earth can do something so unexpected, what else can life do that we haven't seen yet?"

But critiques of the study quickly flowed in, and by the time Science published the paper in a 2011 print issue, the original study was accompanied by eight technical comments from outside experts pointing out key scientific flaws in the methods and interpretations.

Related: What's the best evidence we've found for alien life?

In 2012, two studies published in Science tried to replicate the arsenic-eating findings of Wolfe-Simon and colleagues. Both studies determined that GFAJ-1 could tolerate high levels of arsenic but could not use it instead of phosphorus as a building block for life.

Although the controversial "arsenic life" study was never replicated, it was not retracted because there was no deliberate fraud or misconduct. But in the past five years, Science has begun retracting papers for reasons other than fraud and misconduct. On Thursday (July 24), Science decided to officially retract the study by Wolfe-Simon and colleagues.

"One of the Technical Comments had pointed out that the nucleic acids that were analyzed were not sufficiently purified," Valda Vinson, executive editor of the Science journals, and Holden Thorp, editor-in-chief of the Science journals, wrote in a blog post. "Given the evidence that the results were based on contamination, Science believes that the key conclusion of the paper is based on flawed data."

The study's authors, however, do not support the retraction.

"Disputes about the conclusions of papers, including how well they are supported by the available evidence, are a normal part of the process of science," they wrote in an eLetter, also published Thursday. "While our work could have been written and discussed more thoroughly, we stand by the data as reported."

Periodic table of elements quiz: How many elements can you name in 10 minutes?

Diseases started jumping from animals to humans at least 6,500 years ago, researchers found in a new study of ancient DNA.

After analyzing ancient DNA from 1,313 prehistoric humans from Europe and Asia, researchers charted a map and timeline of human infectious disease that spans 37,000 years. Within that long history, they uncovered the earliest-known evidence of zoonotic disease — in which pathogens in animals transfer to humans — dated to 6,500 years ago.

The researchers described their findings in a study published Wednesday (July 9) in the journal Nature, noting that cases of zoonotic disease probably occurred before that point. But they said the risk and extent of the transmission of such diseases probably increased as humans interacted with animals more frequently, namely through farming and animal husbandry.

Migration likely also played a role, as individuals may have carried zoonotic diseases to new populations that had not yet been exposed to them.

"Today, zoonoses account for more than 60% of newly emerging infectious diseases," the researchers wrote.

The researchers found a peak in evidence of zoonosis in samples that are around 5,000 years old. They argue this coincides with the period when livestock domestication became more widespread. (Evidence suggests animal domestication began around 8,000 to 10,000 years ago and then likely took time to spread to various geographies.)

Related: 32 diseases you can catch from animals

Until now, questions remained about where and when known human pathogens first emerged and how they were distributed around the world. Thanks to new technology that can capture genomic evidence of such diseases in ancient DNA, some of these questions are beginning to be answered.

In total, 214 known human pathogens were detected in the study's DNA samples, which were gathered from the bones and teeth of ancient human remains. The oldest case with a known pathogen uncovered in the study involved Corynebacterium diphtheriae, the bacterium behind diphtheria. The microbe's DNA was discovered in a sample from the Mesolithic period and dated back as far as 11,400 years.

Twelve cases involved the Yersinia enterocolitica bacterium behind the zoonotic disease yersiniosis, which causes various symptoms including fever and diarrhea. The oldest remains showing evidence of this pathogen were found in Denmark and are about 6,500 years old.

The researchers also found evidence of some more well-known pathogens — including 42 suspected cases of the plague-causing bacterium Yersinia pestis — in about 3% of their samples. However, they did not detect the pathogen responsible for tuberculosis: Mycobacterium tuberculosis.

The team suspects that they didn't detect M. tuberculosis because it is typically a low-load bloodstream infection. Due to the dataset they used, they were most likely to detect bugs that accumulate in high concentrations in the blood during an infection.

The samples from the human remains consisted of a mixture of human, germ and other DNA. After excluding any human DNA, the team then identified which DNA belonged to human pathogens and which came from other sources, such as bacteria involved in the decomposition process, the soil or from the human microbiome.

One limitation of the study is that the technology used does not detect RNA, a cousin of DNA that forms the basis of many germs. Flu viruses contain RNA, for instance, so analyzing RNA could have provided evidence of different influenza pandemics throughout history.

"There are many epidemic-type pathogens that are RNA viruses that we would like to study from the past. But the problem with those is that RNA is not as stable a molecule as DNA," study lead author Martin Sikora, an associate professor who studies human and pathogen evolution at the University of Copenhagen, told Live Science. "So far, we haven't really been successful at extracting this type of information from archaeological remains."

This is "the largest study to date on the history of infectious diseases," the researchers said in a statement, adding that it could potentially have implications for the future of medicine, including the development of vaccines.

Sikora said that while reconstructing the genomes of these ancient pathogens, sometimes they got enough data to recover the whole genome sequence of a particular germ. In theory, new vaccines could be developed based on this information and would be available to protect humans against viruses that are not around now but could emerge again in the future, he suggested.

Researchers have identified gut bacteria that can absorb toxic "forever chemicals" in lab mice, according to a new study, potentially offering up a way to control PFAS levels in humans.

PFAS, or perfluoroalkyl and polyfluoroalkyl substances, are synthetic chemicals used in a variety of products, from non-stick cooking pans to cosmetics. These substances are often nicknamed "forever chemicals" because they have strong chemical bonds that don't easily break down in nature and, in some cases, stick around for thousands of years. As a result, these chemicals pose a major pollution concern, both in our environment and in our own bodies.

Our drinking water and agricultural systems are already contaminated with PFAS to some degree, and as some of these chemicals can be absorbed through the skin and into our blood, there's no keeping them out of our bodies. Scientists are still untangling the health implications of PFAS, but exposure has been linked to various potential harms, including an increased risk of some cancers and disruptions to our immune system.

However, our bodies may also have a way of protecting themselves from these chemicals. The new study, published Tuesday (July 1) in the journal Nature Microbiology, investigated how human gut bacteria interacted with PFAS and found that nine species could effectively fend off the chemicals, at least in lab mice. The bacteria absorbed a good chunk of common PFAS that the mice were exposed to, which was then excreted in the mice's feces.

While there's a lot more work to be done, these findings suggest that we may be able to employ some bacterial species to control forever chemicals.

"The reality is that PFAS are already in the environment and in our bodies, and we need to try and mitigate their impact on our health now," study co-author Indra Roux, a researcher in the Medical Research Council (MRC) Toxicology Unit at the University of Cambridge, said in a statement. "We haven’t found a way to destroy PFAS, but our findings open the possibility of developing ways to get them out of our bodies where they do the most harm."

Related: How worried should we be about PFAS, the 'forever chemicals'?

PFAS resist water, oil and heat, making them useful in many different products. Today, there are thousands of different chemicals under the PFAS umbrella. While they are being phased out of some industries, like food packaging, many already exist in the environment and aren't going anywhere anytime soon.

To explore how gut bacteria interact with PFAS, the researchers first identified nine bacterial species that could absorb these chemicals and then gave those species to lab mice. The mice were then exposed to PFAS, including the common perfluorooctanoic acid (PFOA) and perfluorononanoic acid (PFNA). The bacteria absorbed between 25% and 74% of PFNA and 23% to 58% of PFOA, according to the study.

Accumulated PFAS didn't seem to affect the bacteria much. The PFAS aggregated (grouped together) in dense clusters within the bacteria, which appeared to minimize their impact on vital cell processes, according to the study.

"We found that certain species of human gut bacteria have a remarkably high capacity to soak up PFAS from their environment at a range of concentrations, and store these in clumps inside their cells," senior study author Kiran Patil, an investigator within the University of Cambridge’s MRC Toxicology Unit, said in the statement. "Due to aggregation of PFAS in these clumps, the bacteria themselves seem protected from the toxic effects."

The researchers noted in the study that their experiments involved giving mice a one-time dosage of PFAS, while humans — and other animals — typically experience low but chronic exposure to the chemicals.

Lawrence Wackett, a professor of biochemistry at the University of Minnesota Twin Cities who wasn't involved in the study, told Live Science in an email that the research was "particularly interesting" in light of another study published June 13 in the journal PNAS, which found that human gut microbial enzymes can break down carbon–fluorine bonds — the strong bonds present in PFAS.

"Taken together, there might be both sequestration and degradation of certain fluorinated compounds in the human gut," Wackett said.

Two men were left riddled with parasitic worms after they received infected kidney transplants at two U.S. hospitals, a new case report reveals.

The two kidneys had come from the same organ donor, who had resided in the Caribbean before death, according to the report, published June 18 in the New England Journal of Medicine.

The first of the two kidney recipients, a 61-year-old man, had undergone transplant surgery at Massachusetts General Hospital (MassGen). Ten weeks after receiving the transplant, he was transferred back to MassGen after an initial admission to a different hospital.

He had developed nausea, vomiting, excessive thirst, abdominal discomfort, back pain and a fever. At the first hospital, doctors found fluid building up in his lungs, and the man began breathing quickly, feeling as though he couldn't get enough air, and his oxygen levels dropped.

As he entered respiratory failure and shock — meaning he had dangerously low blood pressure — he was transferred to the intensive care unit of MassGen, where doctors documented a purple rash, like a constellation of bruises, spreading across the skin of his stomach.

The doctors began an extensive investigation into the patient's medical history and ran a battery of tests to pinpoint the cause of his symptoms.

Related: 32 scary parasitic diseases

The patient was on immunosuppressive medications to prevent his body from rejecting his new kidney, making him more susceptible to infections. The medical team, including infectious disease and organ transplant expert Dr. Camille Kotton, had the challenge of whittling down a lengthy list of possible infections to find the most likely cause.

They could rule out bacterial infections, because the man had been given antibiotics and wasn't improving. He was also taking an antiviral and had tested negative for SARS-CoV-2, the virus behind COVID-19. That left some kind of parasite as a likely culprit. This was backed up by the fact that levels of eosinophils, a type of white blood cell that fights parasitic infections, had also spiked in the man's blood. These cells can also spike due to drug reactions or transplant rejection, but those causes were unlikely given the man's symptoms, Kotton noted.

Kotton had heard of cases in which transplanted organs infected their recipients with a small roundworm called Strongyloides stercoralis. She contacted New England Donor Services, a regional organ-procurement organization, about the potential contamination. Although the kidney donor was deceased, they were able to test a vial of the donor's blood, which had antibodies for Strongyloides, meaning the donor's immune system had at some point encountered the worm.

Tests of the patient's blood samples showed that he did not have antibodies to Strongyloides before the transplant, but he did afterward. When the medical team sampled various sites across the man's body, they found that the worms had spread far and wide, invading his abdomen, lungs and skin.

Infections from transplants are rare — in over 10 years of transplants in the U.S., donor-derived infections affected only 14 out of every 10,000 organ transplants, a review found. U.S. doctors cannot use organs from people with certain active infections, such as tuberculosis, and donated organs are tested for infectious diseases, but these tests don't always catch everything.

The review noted 13 proven or probable Strongyloides infections over a decade, accounting for 42% of all parasitic infections transmitted by organ transplants. Prior to this review, fewer than 1 in 4 organ transplant organizations regularly screened for Strongyloides, but in 2023, the Organ Procurement and Transplantation Network called for universal testing for this parasite.

The MassGen medical team treated the man with ivermectin, a powerful antiparasitic drug. They received special permission to administer the drug directly underneath his skin to combat the full body infection, which ultimately cured him.

Meanwhile, other medical centers that had transplanted organs from the same deceased donor were notified. This flagged a 66-year-old man who was being treated at Albany Medical Center for fatigue, low white blood cells and worsening kidney function following a transplant operation.

Sharing notes with the MassGen team, the doctors were able to successfully treat this second patient, who had received the donor's other kidney.

"Organ transplants save lives," a spokesperson for Albany Medical Center told Live Science in an email. "In rare cases like this, the communication and coordination between our hospitals and the involvement of infectious disease physicians at both hospitals was critically important, as was the alert our regional organ procurement organization provided us."

Live Science have contacted MassGen for comment.

U.S. health officials are investigating a multistate outbreak of Salmonella in contaminated cucumbers after nine people were hospitalized, according to the U.S. Centers for Disease Control and Prevention (CDC).

As of May 20, 26 cases had been reported across 15 states after Bedner Growers, Inc. of Boynton Beach, Florida voluntarily recalled whole cucumbers sold at its Farm Fresh Market retail outlets between April 29 and May 14, according to the U.S. Food and Drug Administration (FDA). The recalled cucumbers were also sold to wholesale distributor, Fresh Start Produce Sales, Inc.

The FDA is still working to determine where the potentially contaminated products were distributed, but cases have been reported in Alabama, California, Colorado, Florida, Illinois, Kansas, Kentucky, Michigan, North Carolina, New York, Ohio, Pennsylvania, South Carolina, Tennessee and Virginia.

Salmonella are a group of food-borne bacteria that infect roughly 1.35 million people in the U.S. every year, according to the CDC. Salmonella infections can cause diarrhea, fever and stomach cramps, and symptoms usually develop between six hours and six days of exposure.

While most patients will recover without treatment, some — especially young children, pregnant women, those with weakened immune systems, and those over age 65 — may require medical intervention or hospitalization. In severe cases, the infection may spread beyond the intestines, which can be life-threatening.

Related: How does E. coli get into food?

There are more than 2,500 different types of Salmonella bacteria, roughly 100 of which cause human illness. The FDA reported that the strain involved in the current incident is called Salmonella Montevideo, a subtype of the species Salmonella enterica.

"Salmonella is a serious health concern. Bedner Growers is extremely concerned about the safety of the products it grows," a spokesperson for Bedner Growers said in a statement. "This recall has been undertaken by us voluntarily. Safety first."

The contaminated cucumbers were identified during an inspection in April in response to a similar outbreak of salmonella in 2024 linked to cucumbers grown by Bedner Growers, Inc., the FDA reports.

The CDC has urged customers to wash cucumbers before eating them and to throw away cucumbers if they don't know where they are from. The recall does not include cucumbers sold at Bedner's Farm Fresh Market after May 14, the FDA noted.

A spokesperson from Fresh Start Produce said that "after learning of the farm's recall, the company contacted its wholesale and regional distribution center customers to ask that they provide their customers with recall instructions, including notifying any consumer point-of-purchase locations."

Dozens of never-before-seen species of "extremophile" bacteria were hiding in a NASA clean room used to quarantine a Mars lander before it was successfully launched to the Red Planet more than 17 years ago, a new study reveals.

Some of the hardy microbes may be capable of surviving the vacuum of space. However, there is no evidence that the spacecraft or Mars were contaminated.

NASA's Phoenix Mars lander touched down on the Red Planet on May 25, 2008, and spent 161 days (156 Martian days) collecting a variety of data, before suddenly going offline. Around 10 months before arriving on Mars, the lander spent several days inside a clean room at the Payload Hazardous Servicing Facility at Kennedy Space Center in Florida, before being launched from neighboring Cape Canaveral Space Force Station (then known as Cape Canaveral Air Force Station) on Aug. 4, 2007, according to Live Science's sister site Space.com.

Clean rooms are spaces where spacecraft and their payloads are quarantined before launches and upon reentry to Earth, in order to prevent environmental contamination by microbes and keep them free of potentially damaging particles, according to NASA. These spaces are sterilized, pressurized, constantly vacuumed and supplied with air via special filters that keep out 99.97% of all airborne particles. Anybody entering the room must wear an all-in-one "bunny suit" and have an air shower before entering.

But all of these measures still can't keep everything out. When researchers reanalyzed samples collected from the Phoenix lander clean room before, during and after the spacecraft was quarantined there, they found DNA from 26 novel species of bacteria. The team reported their findings in a study published May 12 in the journal Microbiome.

Related: Alien organisms could hitch a ride on our spacecraft and contaminate Earth, scientists warn

Most of the newly described microbes displayed at least some characteristics that made them resistant to harsh environmental conditions, such as extreme temperatures, pressures and levels of radiation. Some had genes associated with DNA repair, detoxification of harmful molecules, and improved metabolism, and may even be able to survive the vacuum of space, the researchers wrote.

"Our study aimed to understand the risk of extremophiles being transferred in space missions and to identify which microorganisms might survive the harsh conditions of space," study co-author Alexandre Rosado, a microbiologist at the King Abdullah University of Science and Technology in Saudi Arabia, said in a statement. "This effort is pivotal for monitoring the risk of microbial contamination and safeguarding against unintentional colonization of exploring planets."

The newly described species made up just under a quarter of all the species identified in the room, most of which also had extremophile properties. This suggests spacecraft clean rooms could be an excellent place to search for more of these hardy microbes.

Finding new extremophiles is important because it can help researchers predict what potential extraterrestrial microbes might look like and how we can prevent them from contaminating Earth. Some of them also produce substances, such as biofilms, that have potential applications in medicine, food preservation and biotechnologies.

"Together, we are unraveling the mysteries of microbes that withstand the extreme conditions of space — organisms with the potential to revolutionize the life sciences, bioengineering, and interplanetary exploration," study co-author Kasthuri Venkateswaran, a retired senior research scientist at NASA's Jet Propulsion Laboratory, said in the statement.

Scientists have discovered a new microbe never-before-seen on Earth inside China's Tiangong space station.

The new strain of bacteria, named Niallia tiangongensis after the space station, is a variant of a soil-dwelling terrestrial microbe that can cause sepsis, and was found inside one of the station's cabins.

Now, a new analysis of the strain has revealed that the bacterium isn't only one of a kind, but has also picked up some key adaptations that could be helpful in future space missions. The researchers published their findings March 3 in the journal International Journal of Systematic and Evolutionary Microbiology.

"Understanding the characteristics of microbes during long-term space missions is essential for safeguarding the health of astronauts and maintaining the functionality of spacecraft," the researchers wrote in the study.

The new strain was found in samples collected in 2023 by the crew of the Shenzhou-15 mission, who swabbed the space station's modules with sterile wipes before freezing them for transport.

Related: Purple bacteria could be key to finding extraterrestrial life on exoplanets

After being sent back to Earth, analysis revealed that the bacteria was closely related to Niallia circulans, a rod-shaped, spore-propagating bacteria that typically dwells in soil, sewage and food, and can cause sepsis in immunocompromised patients.

However, the new strain had also picked up a few new adaptations to survive the harsh conditions of space. These include genes that code responses to oxidative stress, repair the bacteria from radiation damage, and enable it to form biofilms by breaking down gelatin to extract carbon and nitrogen.

It's not yet clear if the new strain could cause harm to humans, but the researchers hope that by studying it further they could learn more about how it, and others, survive; as well as the best ways to prevent human astronauts from any risks associated with space-adapted bugs.

This isn't the first microbe to have made the evolutionary leap to survive beyond our planet, either. In 2018, NASA scientists discovered four previously unknown strains of antibiotic-resistant bacteria hiding inside the International Space Station's toilets, each with a suite of new adaptations to help them survive in outer space.

A superbug that commonly causes infections in hospitals can feed on plastic used for medical interventions, potentially making it even more dangerous, a world-first study has found.

The bug is a bacteria species called Pseudomonas aeruginosa, which is commonly found in hospital environments and can cause potentially deadly infections in the lungs, urinary tract and blood.

Now, scientists have analyzed a strain of this bacteria from a hospital patient's wound, which revealed a surprising trick that could enable it to persist on surfaces and in patients for longer — its ability to break down the biodegradable plastics used in stints, sutures and implants. The researchers published their findings May 7 in the journal Cell Reports.

"It means we need to reconsider how pathogens exist in the hospital environment," study lead author Ronan McCarthy, a professor in biomedical sciences at Brunel University of London, said in a statement. "Plastics, including plastic surfaces, could potentially be food for these bacteria. Pathogens with this ability could survive for longer in the hospital environment. It also means that any medical device or treatment that contains plastic could be susceptible to degradation by bacteria."

The team's laboratory study raises the need for further research to better understand how this plastic-eating ability affects the bug in realistic hospital environments, in which specific cleaning protocols are in place to help prevent exposing patients and medical instruments to bacteria.

P. aeruginosa is thought to have rapidly evolved over the last 200 years to infect humans as they began living in densely populated areas, especially among those with weakened lungs due to air pollution.

Related: Dangerous 'superbugs' are a growing threat, and antibiotics can't stop their rise. What can?

Since then, many strains of the bug have acquired resistance to a wide variety of antibiotics. These resistant microbes can contaminate catheters and ventilation devices, making P. aeruginosa a common cause of hospital-acquired infections, especially among vulnerable patients. P. aeruginosa is tied to roughly 559,000 deaths per year globally, the majority of which are associated with antimicrobial resistance.

Yet how the bacteria can thrive in ostensibly sterile hospital environments has remained unclear.

To investigate, the researchers took a swab from a patient's wound in a British hospital and analyzed it, which revealed the bug can make an enzyme named Pap1. This enzyme is able to break down the plastic polycaprolactone (PCL) — commonly used in sutures, wound dressings, surgical meshes and other medical equipment — and release the plastic's carbon, which P. aeruginosa can then feed on.

To test whether this enzyme is really responsible for breaking down plastic, the scientists inserted the gene that codes for Pap1 into Escherichia coli bacteria, and found that when that bacteria expressed the enzyme, it too was able to break down PCL. The team further confirmed the enzyme's plastic-eating role when they deleted the gene that codes for it in a P. aeruginosa variant, finding that the microbe was no longer able to dissolve the plastic.

The bug's plastic-chewing power doesn't just seem to be granting it a food source: It is also making it more dangerously resistant to treatment. This is because the bacteria uses plastic fragments to form hardier biofilms — structures with protective coatings that shield superbugs from antibiotics — the researchers found.

The scientists also identified similar enzymes in other bacteria, meaning that other widely used medical plastics could be providing sustenance and improved resilience to additional superbugs, possibly contributing to hospital-acquired infections.

To follow up on this, the researchers have called for urgent research on the prevalence of the plastic-eating enzymes among other pathogens, and for experts to reconsider the plastics they use in medical settings, and the ways that they monitor hospital environments.

"Plastic is everywhere in modern medicine, and it turns out some pathogens have adapted to degrade it," McCarthy said. "We need to understand the impact this has on patient safety."

This article is for informational purposes only and is not meant to offer medical advice.

While analyzing an 18th-century Austrian mummy, researchers discovered that the man died from tuberculosis and was preserved in a very unusual way: with wood chips, twigs and fabric packed into his abdomen through his anus.

The mummified body was located in a church crypt in St. Thomas am Blasenstein, a small village in Austria near the Danube River. Known locally as the "air-dried chaplain," the mummy was assumed to have been the preserved remains of a parish vicar named Franz Xaver Sidler von Rosenegg, who died in 1746.

Over the years, Sidler's body has been associated with various healing miracles. But his cause of death remained a mystery, heightened by an X-ray analysis in 2000 that suggested his mummy contained a poison capsule.

In a study published Friday (May 2) in the journal Frontiers in Medicine, researchers conducted a new analysis, using multiple techniques to quash rumors about Sidler's puzzling death. In the process, they discovered a remarkable embalming method missing from historical records.

"Our investigation uncovered that the excellent preservation status came from an unusual type of embalming, achieved by stuffing the abdomen through the rectal canal with wood chips, twigs and fabric, and the addition of zinc chloride for internal drying," study lead author Andreas Nerlich, a researcher at Ludwig-Maximilians University in Munich who specializes in mummy research, said in a statement.

Related: 'Pregnant' ancient Egyptian mummy with 'cancer' actually wasn't pregnant and didn't have cancer, new study finds

Following a macroscopic observation of the body, which revealed male external genitalia, the research team performed a CT scan of the mummy to identify the organs and other material inside the body. They also took samples of skin, tissue and dental enamel for chemical analyses, to establish when the man died, what he ate and whether he had been poisoned.

The CT scan revealed a minor-but-chronic infection in the man's nasal sinuses, and several of his front teeth were worn in a semicircular pattern, both of which suggested long-term pipe smoking. Additionally, the researchers discovered calcifications and cysts in his lungs, both of which are common in people with chronic tuberculosis. These lung issues may have resulted in acute pulmonary hemorrhage, the researchers noted in the study. This was his likely cause of death, the research team said, since the toxicology analysis did not reveal any evidence of poisoning.

But the afterlife of the mummy and the way it was created have baffled the researchers.

After making a small incision in the chest wall, the team closely examined the foreign material found inside the body of the mummy. This material included mud, wood chips from spruce and fir trees, and branches from unidentified tree species. Intermingled in this mixture were swatches of hemp, flax and silk fabric, along with wooden buttons that presumably adorned the fabric. The round, hollow object that researchers previously believed was a poison capsule was extracted and found to be a glass bead from a rosary.

Historically, mummies have often been created by opening the body's abdominal wall, removing the organs, and inserting packing material. But in this case, the mummy's abdomen was intact, leading the researchers to conclude that his pelvis was packed via his anus, which they found to be somewhat enlarged.

Based on the radiocarbon date from the mummy's skin, the age at death determined from the skeleton, and historical records, the researchers concluded that the mummy could indeed be positively identified as Franz Xaver Sidler, who died in St. Thomas in 1746 at only 37 years old. Because most people at that time were not mummified, however, it is still unclear why Sidler merited this treatment.

"We have some written evidence that cadavers were 'prepared' for transport or elongated laying-out of the dead," Nerlich said. "Possibly, the vicar was planned for transportation to his home abbey, which might have failed for unknown reasons."

Mummy quiz: Can you unwrap these ancient Egyptian mysteries?

Germ theory was never a given. This now-commonplace idea — the notion that human diseases can be sparked by tiny pathogens infiltrating the body — emerged on the backs of discoveries made by people over time. Those discoveries steadily slotted together to form a bigger picture, revealing both the wonders and terrors of the microbial world around us.

Thomas Levenson, a professor of science writing at MIT and author, traces the history of germ theory from its inception to the present day in a new book called "So Very Small: How Humans Discovered the Microcosmos, Defeated Germs — and May Still Lose the War Against Infectious Disease" (Random House, 2025). In the book, Levenson also tackles the larger question of how and why new ideas are pursued, accepted or ignored.

In the following passage from "So Very Small," he highlights how, despite our modern understanding of germs, we're still locked in an ongoing struggle with them and with our own hubris. The rise of antibiotic-resistant superbugs is a prescient example of that, he argues.

Related: Superbugs are on the rise. How can we prevent antibiotics from becoming obsolete?

Autumn, 1945. The war in Europe has been over for five months. Something resembling normal life is sputtering into shape. In Stockholm, for the first time since 1938, the Nobel Foundation is getting ready to award its full catalog of prizes. The deliberations reach a familiar intensity as the committees for each scientific discipline struggle to apportion credit to no more than three people for discoveries to which dozens or more had contributed. Finally, on October 25, telegrams go out to the winners of the Nobel Prize for Physiology and Medicine: Alexander Fleming for discovering penicillin, and Howard Florey and Ernst Chain

for turning Fleming's mold juice into a world-changing medicine.

The prize ceremony takes place on December 10. At the traditional after-party there is plenty of drink on tap, and rumors of dancing. The usually buttoned-down Fleming keeps going until three a.m. The next day, hungover or not, the three new laureates deliver their Nobel lectures. Fleming goes first, devoting most of his talk to retelling the details of his serendipitous encounter with the penicillium mold. As he draws to a close, though, he abandons memory to deliver a sermon, complete with the command that his audience go forth and sin no more:

"The time may come when penicillin can be bought by anyone in the shops. Then there is the danger that the ignorant man may easily underdose himself and by exposing his microbes to non-lethal quantities of the drug make them resistant. Here is a hypothetical illustration. Mr. X has a sore throat. He buys some penicillin and gives himself, not enough to kill the streptococci but enough to educate them to resist penicillin. He then infects his wife. Mrs. X gets pneumonia and is treated with penicillin. As the streptococci are now resistant to penicillin the treatment fails. Mrs. X dies. Who is primarily responsible for Mrs. X's death? Why Mr. X whose negligent use of penicillin changed the nature of the microbe. Moral: If you use penicillin, use enough."

This was no mere parable. What Fleming prophesied as he stood before Sweden's great and good had already come to pass. The first of four cases of gonorrhea "resistant to 'large' amounts of penicillin" appeared in the medical literature in 1946. Even earlier, as far back as 1940, Edward Abraham and co-workers in Florey's laboratory had been able to train cultured colonies of staphylococcus to resist penicillin in their petri dishes. And, of course, the wartime erosion of the effectiveness of sulfa drugs against gonorrhea was a very public demonstration of the problem.

And yet, despite Fleming's warning, the dynamic that killed Mrs. X has recurred again and again throughout the antibiotic era. The first drug effective against TB, streptomycin, was isolated in 1944. Resistant strains of M. tuberculosis emerged no later than 1948. It's been the same story in disease after disease, bug after bug, drug to drug to drug. Staphylococcus aureus, the ubiquitous killer of World War I's wounded, has shrugged off penicillin, erythromycin, the tetracyclines, and what was seen as the big gun, methicillin.

Related: Dangerous 'superbugs' are a growing threat, and antibiotics can't stop their rise. What can?

Methicillin came on the market in 1959. Its effectiveness began to erode almost immediately. The first staph strain immune to the new drug showed up later in 1961, marking the appearance of what we now know as MRSA, or Methicillin-resistant Staphylococcus aureus. MRSA flourishes in hospitals, where microbes and plentiful antibiotics meet, but over time has emerged in the broader population. This pattern has been repeated across the spectrum of diseases around the world. About 1.3 million people die of TB each year. As of 2020, XDR-TB, extensively drug-resistant tuberculosis, has been reported in 123 nations. For those infected with XDR-TB, all front-line antibiotics have failed, along with at least one of the three break-glass-in-case-of-emergency backup drugs.

Taken together, there were nearly 3 million antibiotic-resistant infections in the United States in 2019, the most recent numbers available as of this writing. Some 35,000 Americans died that year of once-treatable microbial diseases. Since 1945, we have failed both to anticipate the speed with which microbes would gain the ability to evade our best drugs, and to come up with a satisfactory response to their resistance — to the point where the single greatest gift of germ theory may not be wholly ours much longer.

Shards of that future are already here. What are sometimes called superbugs — microbes resistant to every available drug — are not merely the stuff of nightmares. They are taking lives right now. A report published by the U.S. Centers for Disease Control and Prevention described the case of a woman in her seventies who had been traveling across the Indian subcontinent. They did not release her name but reported that somewhere on her travels she fractured her femur. She was taken to one hospital, then another, and then on to more in India. In August 2016, she returned to her home in Washoe County, Nevada. She went back to the hospital, presenting with systemic inflammatory response syndrome, a characteristic immune response to an unresolved infection. So her doctors looked for the microbe that could have engendered her increasingly perilous condition.

They found it in Klebsiella pneumoniae, a bacterium that occurs naturally in soils and can live quite peaceably in human guts, mouths, or skin. If it makes its way elsewhere, though, it can cause disease, often pneumonia, but several other conditions as well. Until recently, treating a K. pneumoniae infection was simple. Any one of several common antibiotics could do the job. So her medical team tested the patient's bacterial samples to see which drug would be most effective. The answer came back: none of them. The woman's microbes were resistant to the fourteen antibiotics available in Reno. The hospital sent samples to the federal Centers for Disease Control and Prevention, and the tests there showed that these bugs were resistant to twelve more medicines — which is to say, all the remaining possibilities. There was nothing available in the United States that could knock out her singular infection.

Within weeks the woman was dead, slain by a superbug for which there was no cure. She wasn't the first such casualty and she certainly has not been the last. But this one life lost to an infection that so recently was trivially easy to cure forces the question: How could this happen? How could it have been allowed to happen?

Gynecologists should be informed of the signs of rare, "flesh-eating" infections, doctors warn, because these dangerous infections can sometimes infiltrate the vulva.

In a new case report published April 8 in the journal BMJ Case Reports, U.K. doctors describe three patients who were found to have necrotizing fasciitis of the vulva. The vulva includes the external female genitalia, such as the labia majora and labia minora, for example.

"Necrotizing fasciitis (NF), also known as flesh-eating disease, can arise when certain bacteria enter the skin through a wound — a cut, abrasion, burn, surgical wound, or even an insect bite," Bill Sullivan, a professor of microbiology and immunology at Indiana University, who was not involved in the case report, told Live Science in an email. "NF can occur anywhere skin or tissue is breached, including genitalia."

In necrotizing fasciitis, bacteria infiltrate the fascia, which is the connective tissue surrounding muscles, nerves, fat and blood vessels. The infection rapidly causes soft tissues to die, or "necrotize," and spreads through the body very quickly.

Related: Scientists are building an ultimate atlas of the vagina. Here's why.

The case report authors, who are affiliated with the Shrewsbury and Telford Hospital in England, shared these three cases to notify other gynaecologists of the possibility of vulvar involvement in necrotizing fasciitis cases.

They noted that their hospital has seen a significant uptick in flesh-eating infections in recent years, with 20 cases seen between 2022 and 2024 when only 18 had been reported in the preceding decade. In addition, several EU states and the U.S. have reported increases in invasive group A streptococcus, an infection that can lead to necrotizing fasciitis.

If the infection is becoming more common, doctors should know the importance of rapid treatment, the case report authors emphasized.

"It's an extremely aggressive infection that can advance to a life-threatening situation in 24-48 hours," Sullivan said. "After these bacteria get into the skin, they release potent toxins that lead to rapid tissue destruction, liquefying muscle, nerves, and blood vessels."

The subsequent loss of blood supply to the affected body parts makes treating necrotizing fasciitis with antibiotics difficult, Sullivan explained; infected areas sometimes need to be surgically cut out of the body. Additionally, once the bacteria get into the bloodstream, they can cause sepsis, a dangerous, body-wide immune reaction, potentially leading to organ failure and death.

In the case report, the doctors described the cases of two patients who came to the emergency room with necrotising fasciitis of the vulva, as well as a third who developed the infection following a postoperative wound.

The first patient was alerted to the infection when she found a small spot on her mons pubis — the fatty tissue over the pubic bone. She initially went to her primary care doctor, who prescribed antibiotics. However, the spot worsened over the next five days, which resulted in necrotizing fasciitis that spread to her labia majora, left hip and lower abdomen.

At the ER, the infected tissue was surgically removed, or "debrided." But "despite intensive care unit (ICU) management for systemic infection," the patient died of sepsis only 28 hours after diagnosis.

The second patient came to the ER with a one-week history of having a lump on her labia majora, which turned out to be an infected abscess. Over the next 12 hours, the upper third of her labia majora broke down from necrotizing fasciitis. The patient ultimately needed three debridements to control the infection, after which she underwent reconstructive surgery for the lost tissue. "The wound has since healed well," her doctors noted.

The third patient suffered necrotizing fasciitis after a surgical wound got infected; she had gotten a hysterectomy as a treatment for fibroids. This patient ultimately survived after having the infected tissue surgically removed and being given broad-spectrum antibiotics.

"NF is very rare," and it most often arises in people with conditions that weaken the immune system, such as diabetes or cancer, Sullivan explained. An estimated 700 to 1,200 cases are seen in the U.S. each year. About 500 cases are reported annually in the U.K., or about 0.4 to 0.53 cases per 100,000 people, the case report authors noted.

Vaginal necrotizing fasciitis is even more rare, as people are more likely to have skin injuries on more exposed parts of the body.

"Vaginal NF could be contracted through rough sex, a piercing, or cosmetic and surgical procedures," Sullivan said. "The mortality rate of vaginal NF is estimated to be up to 50%."

The case report authors urged other gynecologists to keep an eye out for any signs of an infection that could develop into necrotizing fasciitis, and they also emphasized that "time is of the essence" when treating the condition.

"Vaginal NF could be considered more dangerous in the sense that it might be more difficult to diagnose in time, " Sullivan said. "Gynecologists may not have NF on their diagnostic radar, and surgical interventions, which are usually required to stop NF from spreading and remove dead tissue, may be limited."

Recognizing the disease quickly is key to saving patients' lives. "Delayed diagnosis can lead to delayed treatment, increasing the odds of sepsis and death," Sullivan said.

This article is for informational purposes only and is not meant to offer medical advice.

Disease name: Hantavirus disease

Affected populations: Hantavirus disease is an uncommon but potentially deadly infection caused by a family of viruses called hantaviruses. These viruses are found worldwide and are typically carried and spread by rodents, such as rats and mice. Different types of hantaviruses are associated with specific rodent species, which can carry the viruses without overt signs of illness.

Most hantaviruses cannot spread from person to person, but one type — the Andes virus, found in South America — can do so.

The United States began tracking hantavirus disease in 1993, and between then and 2023, 890 cases were reported within the country. The states with the highest number of reported cases include Washington, California, Arizona, Colorado and New Mexico. An imported case of Andes virus was reported in 2018 in Delaware after a traveler had been exposed in South America.

"Worldwide, it is estimated that from 10,000 to over 100,000 infections occur each year, with the largest burden in Asia and Europe," the World Health Organization (WHO) says. Historically, the Americas have reported hundreds of cases each year.

Given that rodents spread hantaviruses, people who are more likely to encounter these animals have a greater chance of developing hantavirus disease. So forestry workers, farmers and trappers are at higher risk than the general population.

Causes: Humans can develop hantavirus disease after being exposed to the urine, droppings or saliva of infected rodents. This can happen if a person rubs their eyes after touching bodily fluids or poop carrying the virus. Additionally, if someone disrupts debris containing infected animal droppings — while cleaning a barn, for instance — hantaviruses can be released into the air and then inhaled. On rare occasions, people may develop hantavirus disease after being bitten by an infected rodent.

The Andes virus, which can transmit between people, has been associated with several clusters of infection in recent years, including the 2026 cluster associated with the cruise ship MV Hondius.

Once inside the body, hantaviruses can cause two types of serious infections: hantavirus cardiopulmonary syndrome (HCPS) and hemorrhagic fever with renal syndrome (HFRS). (Note that HCPS is sometimes called hantavirus pulmonary syndrome; these two terms refer to the same condition.)

Hantaviruses in the Americas are known to cause HCPS, while those in Europe and Asia cause HFRS.

Symptoms: Early symptoms of HCPS include fever, muscle aches and fatigue, which can take one to eight weeks to develop following exposure to a hantavirus. Additional symptoms include chills, headaches, dizziness and gastrointestinal issues. Within four to 10 days of the first symptoms, the disease can progress to cause coughing, shortness of breath, shock and fluid buildup in the lungs.

Approximately 38% of patients who develop these respiratory symptoms die from the disease, the U.S. Centers for Disease Control and Prevention (CDC) states. Case fatality rates up to 50% have been reported in some contexts, the WHO says.

By contrast, HFRS is less deadly, with case fatality rates between 1% and 15% depending on the virus at fault. Symptoms usually emerge within one to two weeks after exposure to a hantavirus, but they can take up to eight weeks to appear. Early symptoms include intense headaches, back and abdominal pain, fever, chills, nausea and blurred vision. Later stages of the disease involve low blood pressure, lack of blood flow, internal bleeding and kidney failure.

Treatments: There is no cure for hantavirus disease. Instead, treatment aims to manage a patient's symptoms and stabilize their vitals. Doctors may provide a patient breathing support if they have respiratory issues, or dialysis if their kidneys are too damaged to filter blood properly.

Prevention: To reduce exposure to hantaviruses in the first place, the U.S. Centers for Disease Control and Prevention (CDC) recommends that people eliminate or minimize their contact with wild rodents. They can do this by storing food securely, sealing any holes or gaps in their houses or garages to prevent rodents from entering, and using traps when rodents have already infiltrated, for example.

Tips for safely cleaning up rodent droppings can be found on the CDC website.

When it comes to the Andes virus, which can spread between people, healthcare providers caring for infected patients should wear personal protective equipment and employ other standard safety procedures, such as hand hygiene, environmental cleaning, and safe handling of blood and bodily fluids.

"During outbreaks or when cases are suspected, early identification and isolation of cases, monitoring of close contacts, and application of standard infection prevention measures are important to limit further spread," the WHO says.

For people outside healthcare, the precautions recommended to avoid Andes virus infection are similar to those recommended to avoid more common illnesses like the flu or common cold. These include avoiding kissing or sexual contact with potentially infected people, as well as avoiding sharing drinks and eating utensils. It's also advisable to wash hands frequently and maintain distance from potentially infected people.

Recent cases: In February 2025, the American classical pianist and businesswoman Betsy Arakawa, who was also the wife of actor Gene Hackman, reportedly died from HCPS.

In April 2026, the cruise ship MV Hondius was struck by a cluster of hantavirus cases that were later confirmed to be caused by the Andes virus, the only hantavirus known to spread from person to person.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 60-year-old man in Chicago who worked in a laboratory

The symptoms: The man visited a clinic after experiencing body aches, fever and a three-day cough. At that point, his doctors suspected a respiratory infection, like the flu, and they referred the patient to emergency care. However, the man opted against further evaluation and went home.

What happened next: But three days later, the man's existing symptoms hadn't improved, and he also developed shortness of breath. An ambulance was called, and when the paramedics arrived they found low levels of oxygen in his blood. They administered oxygen through a mask and then rushed the man to the emergency room.

Despite the man's breathing difficulties, emergency room doctors found nothing abnormal when they scanned his lungs using chest radiography. They performed blood tests to probe what else might be driving his symptoms. By examining a blood sample under the microscope, they counted his white blood cells and found he had an elevated level, suggesting he was fighting an infection.

The clinicians also saw bacteria in his blood sample; the exact bacterial species was not known right away, but the presence of any bacteria in blood signals a serious infection.

Related: Earliest known strain of plague could have come from a beaver bite

The treatment: The doctors put the patient on three intravenous antibiotics to treat the bloodstream infection. But his labored breathing worsened after about 12 hours, so the doctors placed a breathing tube in his airway. Despite these interventions, he died of cardiac arrest one hour later.

The diagnosis: After the patient died, clinicians tried to work out which species of bacteria were present in his blood. That was when the physicians were informed that the patient had worked in a lab and had handled a weakened strain of Yersinia pestis, the bacterium that causes the plague.

The hospital used a lab technique to produce multiple copies of genes from the patient’s bacteria in a dish and then conducted DNA sequencing to determine the species and strain. Although the weakened Y. pestis was considered noninfectious, the patient had somehow contracted it, they confirmed.

What makes the case unique: Before this case, this weakened strain of plague bacteria had never caused infections in humans. As such, the Centers for Disease Control and Prevention (CDC) had not deemed it threatening to work with, according to a report of the case.

The weakened bacteria lack an important gene for absorbing iron, which they need to produce energy and fuel processes such as growth and cell division. The CDC independently confirmed that the patient's infection had been caused by this weakened strain and not by a virulent one.

Concerned that the weakened strain might be more hazardous than thought, the CDC and other regulatory bodies investigated the laboratory where the patient worked. This inspection revealed no signs that safety protocols were being breached, and no infections were reported among any of the patient's colleagues, although all of them were given antibiotics as a precaution after the man's infection became known.

No one knew for sure how the patient was exposed to the bacteria, but his colleagues noted that he did not always wear lab gloves while handling the microbes.

To determine if the weakened strain had evolved or had been engineered to cause disease, the CDC exposed lab mice to either the patient's strain or the original, weakened strain from laboratory stocks. Neither proved lethal to the rodents.

This hinted that the man was unusually susceptible to the bacteria. Though the patient had type 1 diabetes, which can affect the immune system, the doctors did not believe this was relevant. Then, a postmortem analysis on the patient revealed abnormally high levels of iron in his liver. He also had between three and 13 times more iron in his blood than an average person.

DNA testing revealed the patient had hereditary hemochromatosis, a genetic condition in which the body absorbs excessive amounts of iron from food. Rates of this rare disorder differ between demographics; for instance, it affects an estimated 1 in 300 people of European ancestry and 1 in 25,000 African Americans.

The report authors theorized that this excess iron in the man's blood may have compensated for the reduced iron-absorbing capacity of the weakened bacteria. In other words, that enabled the microbes to sequester enough iron and generate the energy needed to multiply and establish an infection.

"Researchers should adhere to recommended biosafety practices when handling any live bacterial cultures, even attenuated strains," the report cautioned. That's because people may vary in their susceptibility to biological agents, including plague bacteria, due to genetic traits that safety personnel cannot always account for when determining risk.

Since then, at least three other reports have been published about people with hereditary hemochromatosis who developed sepsis, a dangerous immune reaction, after contracting another, more common Yersinia species. This species, called Y. enterocolitica, typically causes only mild symptoms in people with normal iron levels.

This article is for informational purposes only and is not meant to offer medical advice.

Disease name: Nocardiosis

Affected populations: Nocardiosis is a rare but potentially deadly infectious disease caused by bacteria in the genus Nocardia. Nocardiosis is an opportunistic infection, meaning it doesn't typically affect healthy people but may seize the chance to infect people with weakened immune systems, such as people with cancer or HIV/AIDS, as well as organ transplant recipients who are taking immunosuppressive drugs.

However, around 20% to 30% of patients with nocardiosis have no known pre-existing conditions, so the infection doesn't exclusively affect people with immune deficits. People over the age of 40, especially men, are also more likely to develop the disease than other demographics.

Between 500 and 1,000 new cases of nocardiosis are reported in the United States every year.

Related: Scientists have found a secret 'switch' that lets bacteria resist antibiotics — and it's been evading lab tests for decades

Causes: Nocardia bacteria are found in soil, standing water and decaying plant material. Around 100 Nocardia species have been identified so far, of which 12 are known to infect humans.

People may become infected with Nocardia bacteria when they inhale dust containing the microbes or they have a cut or scrape that comes in contact with contaminated soil or water.

Nocardiosis is not known to spread from one person to another; people pick it up directly from the environment.

Symptoms: The symptoms of nocardiosis vary depending on which part of the body is infected by Nocardia bacteria.

Most cases of nocardiosis start out as lung infections, in which pus-filled cavities, or abscesses containing the bacteria, form in the lungs. This can cause symptoms such as chest pain, a cough (including coughing up blood), sweats, chills and general weakness.

Nocardia bacteria can then travel in the bloodstream and form abscesses in other regions of the body, including the brain, kidneys and intestines. Infections of the brain can cause headache, weakness, confusion and seizures.

Approximately one-third of all patients infected with nocardiosis develop skin ulcers or sores, instead of an internal infection. These skin lesions typically form across the hands, chest wall or buttocks. They may look like open wounds or bumps under the skin.

Without treatment, nocardiosis can rapidly lead to death, often by causing organ failure or sepsis, a dangerous body-wide immune reaction. Between 16% and 40% of patients with nocardiosis die as a result of their infection. If the disease spreads to the brain, death rates jump to more than 80%.

Treatments: Nocardiosis can be treated with common antibiotics, although these bacteria are normally resistant to penicillin. The antibiotic treatment usually takes between six and 12 months to complete, and some patients may need to take antibiotics for even longer to prevent the disease from coming back.

Surgery may sometimes also be required to remove specific abscesses from the body, especially if a patient is not responding to antibiotic treatment.

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A man in his 70s in Japan

The symptoms: The patient was initially brought to the emergency room after he was found collapsed in his home. Tests showed he had severe metabolic acidosis, in which too much acid builds up in the blood. Further labs, as well as CT scans and a review of the patient's medical history, suggested the buildup was caused by a lung infection, kidney injury and, potentially, heavy drinking, as the patient had a history of alcohol dependence.

The patient later tested positive for COVID-19 and a bacterial infection. Given the complexity of the case, he ultimately spent over a month in the intensive care unit (ICU) before being transferred to a general hospital ward to fully recover. Toward the end of his ICU stay, he had started having diarrhea. His doctors put him on a probiotic that they thought would ease the symptoms, and he continued taking that probiotic in the general ward.

But then, after nearly two months of treatment, the man suddenly developed swelling and "severe, continuous" pain in his abdomen. Tests again revealed a high level of acid in his blood, and scans showed signs of nonocclusive mesenteric ischemia, a dangerous condition in which the intestines don't get enough blood.

What happened next: While investigating the man's symptoms, the medical team took a blood sample that tested positive for a bacterium called Clostridium butyricum — the same bacteria contained in the probiotic supplement he'd been taking. A genetic test confirmed that the strain in the man's blood perfectly matched the probiotic strain.

The diagnosis: The man had contracted a blood infection from the bacteria in his probiotic — a condition known as probiotic-related bacteremia.

The treatment: Unfortunately, the patient's condition rapidly progressed to multiorgan failure, and he became too unstable for the doctors to consider surgical treatment options. "His treatment was transitioned to palliative care and he died on the 60th hospital day," his doctors wrote in a report of the case.

What makes the case unique: Probiotic-related bacteremia is a known risk of taking probiotics, but it is rare. Having a weakened immune system or abnormalities in the gastrointestinal tract can raise the risk of these blood infections.

When they do occur, the infections are seen most often in older adults with multiple medical conditions. In the man's case, he had a history of alcohol dependence, smoking, colon cancer, high blood pressure and chest pain due to heart disease, along with the conditions that caused his initial trip to the ER. The report didn't note how recently the man had had cancer or if he'd undergone chemotherapy, which can suppress the immune system.

While being treated, he'd also been given a steroid to tamp down the inflammation driven by his COVID-19 infection, and steroidal drugs suppress the immune system. This may have further increased the likelihood of developing a bloodstream infection from a probiotic.

Notably, this is not the only case of this particular strain of C. butyricum causing probiotic-related bacteremia.

The probiotic is widely used, especially in Japan, and generally has a good safety profile. It's given in hospital settings as a diarrhea treatment, in part because it's thought to make the gut less favorable to pathogens and more favorable to bacteria that aid digestion and help mitigate inflammation.

Antibiotics, which the man was given for his bacterial infection, can also deplete the gut of bacteria, and probiotics can help restore some of those lost microbes. But in medically unstable and immunocompromised patients, these probiotics can occasionally go rogue, the doctors warned in the case report.

This article is for informational purposes only and is not meant to offer medical advice.

Author John Green has been obsessed with tuberculosis (TB) since 2019, when he first visited Lakka Government Hospital in Sierra Leone and met a young TB patient named Henry Reider. In his latest book Everything Is Tuberculosis: The History and Persistence of Our Deadliest Infection (Crash Course Books, 2025), Green explores the history of the bacterial disease, highlighting its impact in different eras of history. And he calls attention to the present reality of TB, a curable disease that nonetheless kills over a million people each year due to stark health care inequities around the globe.

In this day and age, Green argues that injustice is the root cause of TB cases and deaths, and that we can collectively choose to correct that injustice and finally snuff out the deadly disease.

Related: 'We have to fight for a better end': Author John Green on how threats to USAID derail the worldwide effort to end tuberculosis

At the time, I knew almost nothing about TB. To me, it was a disease of history — something that killed depressive 19th-century poets, not present-tense humans. But as a friend once told me, "Nothing is so privileged as thinking history belongs to the past."

When we arrived at Lakka, we were immediately greeted by a child who introduced himself as Henry. "That's my son's name," I told him, and he smiled. Most Sierra Leoneans are multilingual, but Henry spoke particularly good English, especially for a kid his age, which made it possible for us to have a conversation that could go beyond my few halting phrases of Krio. I asked him how he was doing, and he said, "I am happy, sir. I am encouraged." He loved that word. Who wouldn't? Encouraged, like courage is something we rouse ourselves and others into.

My son Henry was 9 then, and this Henry looked about the same age — a small boy with spindly legs and a big, goofy smile. He wore shorts and an oversized rugby shirt that reached nearly to his knees. Henry took hold of my T-shirt and began walking me around the hospital. He showed me the lab where a technician was looking through a microscope. Henry looked into the microscope and then asked me to, as the lab tech, a young woman from Freetown, explained that this sample contained tuberculosis even though the patient had been treated for several months with standard therapy. The lab tech began to tell me about this "standard therapy," but Henry was pulling on my shirt again. He walked me through the wards, a complex of poorly ventilated buildings that contained hospital rooms with barred windows, thin mattresses, and no toilets. There was no electricity in the wards, and no consistent running water. To me, the rooms resembled prison cells. Before it was a TB hospital, Lakka was a leprosy isolation facility — and it felt like one.

Inside each room, one or two patients lay on cots, generally on their side or back. A few sat on the edges of their beds, leaning forward. All these men (the women were in a separate ward) were thin. Some were so emaciated that their skin seemed wrapped tightly around bone. As we walked down a hallway between buildings, Henry and I watched a young man drink water from a plastic bottle, and then promptly vomit a mix of bile and blood. I instinctively turned away, but Henry continued to stare at the man.

I figured Henry was someone's kid — a doctor, maybe, or a nurse, or one of the cooking or cleaning staff. Everyone seemed to know him, and everyone stopped their work to say hello and rub his head or squeeze his hand. I was immediately charmed by Henry — he had some of the mannerisms of my son, the same paradoxical mixture of shyness and enthusiastic desire for connection.

Henry eventually brought me back to the group of doctors and nurses who were meeting in a small room near the entrance of the hospital, and then one of the nurses lovingly and laughingly shooed him away.

"Who is that kid?" I asked.

"Henry?" answered a nurse. "The sweetest boy."

"He's one of the patients we're worried about," said a physician who went by Dr. Micheal.

"He's a patient?" I asked.

"Yes."

"He's such a cute little kid," I said. "I hope he's going to be okay."

Dr. Micheal told me that Henry wasn't a little boy. He was seventeen. He was only so small because he'd grown up malnourished, and then the TB had further emaciated his body.

"He seems to be doing okay," I said. "Lots of energy. He walked me all around the hospital."

"This is because the antibiotics are working," Dr. Micheal explained. "But we know they are not working well enough. We are almost certain they will fail, and that is a big problem." He shrugged, tight-lipped.

There was a lot I didn't understand.

After I first met Henry, I asked one of the nurses if he would be okay. "Oh, we love our Henry!" she said. She told me he had already gone through so much in his young life. Thank God, she said, that Henry was so loved by his mother, Isatu, who visited him regularly and brought him extra food whenever she could. Most of the patients at Lakka had no visitors. Many had been abandoned by their families; a tuberculosis case in the family was a tremendous mark of shame. But Henry had Isatu.

I realized none of this was an answer to whether he would be okay.

He is such a happy child, she told me. He cheers everyone up. When he'd been able to go to school, the other kids called him pastor, because he was always offering them prayers and assistance.

Still, this was not an answer.

"We will fight for him," she told me at last.

Editor's note: This excerpt, from Chapter 1 of "Everything is Tuberculosis," has been shortened for the purpose of this reprinting.

Did you know that tuberculosis (TB) brought us the Adirondack chair? TB patients used to recline, completely immobile, upon that now-iconic piece of furniture on the orders of their doctors. TB also brought about the cities of Pasadena, California, and Colorado Springs, Colorado, which were founded as places for TB patients to seek fresh air. And did you know that before penning "Sherlock Holmes," Sir Arthur Conan Doyle debunked a supposed cure for TB that had been overhyped in the press in the 19th century?

In "Everything Is Tuberculosis: The History and Persistence of Our Deadliest Infection" (Crash Course Books, 2025), John Green recounts these unsung ways in which TB shaped history. He also highlights how public perception of the disease has shifted through time. TB was once seen as a romantic condition that rendered people with the illness "beautiful," "waiflike" and "sensitive," but the illness later became seen as a stigmatizing disease of poverty.

And while we now have a cure for TB, "the disease is where the cure is not," Green notes, paraphrasing a Ugandan doctor who said the same about HIV/AIDS treatments. Annually, there are more than 10 million cases of TB and 1 million TB deaths worldwide, and most of these cases and fatalities occur in low- and middle-income countries.

Green is one-half of the vlogbrothers on YouTube, co-creator of the educational series Crash Course, and author of the bestselling books "The Fault in Our Stars" (Penguin Books, 2012) and "The Anthropocene Reviewed" (E. P. Dutton, 2021), among others. Live Science spoke with him about his latest book, its featured subject, TB survivor Henry Reider, and the uncertain future of efforts to end TB worldwide.

Nicoletta Lanese: In the book, you say that you initially thought of TB as a disease of the past — of "19th-century poets." How was it to have that idea dispelled through writing the book?

John Green: If you'd asked me in 2018, "What are the biggest infectious health problems facing the world," I would have said, "I don't know, malaria, HIV, typhoid, cholera." I would have been so far down the list before I said tuberculosis, even though it turns out tuberculosis is the deadliest infectious disease in the world and sickens over 10 million people every year.

To some extent, that's been a throughline throughout history — when Robert Koch was declaring that he'd discovered that TB was infectious, he almost seemed defensive. He said, "I know we're more afraid of cholera and plague, but actually tuberculosis is a much bigger deal."

I just had no idea that tuberculosis was a crisis until I visited a TB hospital in Sierra Leone in 2019. … [There] I met a young boy named Henry Reider, and that kind of changed the course of my life.

NL: Henry is a big focus of the book. For those who haven't read it yet, could you share a bit about him?

JG: Henry and I met at that hospital in Sierra Leone, and when we arrived, he just grabbed me by the T-shirt and started walking me around the hospital. He seemed to be about the same age as my son, who was 9 at the time, and he also shares a name with my son. They [now] call each other "the namesakes."

He walked me all around the hospital, showed me the lab, showed me the wards where patients were staying. I was really astonished by how many people were sick and how sick they were. And we finally made our way back to where the doctors were, and they sort of shooed Henry away and I said, "Whose kid is that?" And they said, "He's a patient, and he's one of the patients we're most concerned about."

It turns out, he wasn't 9. He was 17 — just he'd been stunted by malnutrition and by TB.

He and I have become really good friends and through the process of reporting this — like, I'm not a good reporter. I don't know how to have a distance between the reporter and the subject, as I try to acknowledge in the book. He inspired the book in many ways because I think if I hadn't met Henry that day, I probably wouldn't have become obsessed with tuberculosis.

NL: And how is Henry doing now?

JG: He's very excited about the book. He's a junior at the University of Sierra Leone, Sierra Leone's best university, and he's studying human resources and management and doing really, really well.

However, it is also true that like so many people whose lives are marginalized, his life is made much more fragile by the recent cuts to USAID, and his life is made much more challenging by the recent cuts to USAID. That's been a constant topic of conversation between him and me over the last few weeks.

Related: 'It is a dangerous strategy, and one for which we all may pay dearly': Dismantling USAID leaves the US more exposed to pandemics than ever

[Although Henry has now been cured of TB], Henry also has other health problems, and he has some long-term consequences from having lived with such serious tuberculosis. Like a lot of people, he depends upon USAID-funded medication in order to survive, and that funding has been canceled.

He and I had a conversation recently where I said, "Look, you know, we'll make sure that you and your mom have access to the medication that you need." And he said, "Thank you, but what about everyone else?"

NL: From your description of him, that seems like a question he would ask.

JG: Yeah, he's an extraordinarily empathetic person. He's a poet. He has what used to be called spes phthisica [meaning "consumptive spirit"], the "tubercular personality." We used to think that people who had this tuberculous personality tended to be sensitive and alive to the suffering in the world and generous and beautiful and lots of other romantic ideals.

NL: In the book, you explore how the perception of TB has changed through time, starting with that romantic, idealized vision of the disease. Could you sum up what you learned?

JG: It's almost like they're two different diseases. It's almost like the disease of consumption [a past name for TB] is different from the disease of tuberculosis. Because at least in Northern Europe and the U.S., consumption was an inherited disease that was associated with being beautiful and having certain personality traits that were desirable. Tuberculosis is seen as a disease of poverty, a disease of filth, a disease of infection. They're very different diseases in the way they're imagined, even though they have the same cause and the same course.

You see this all over the history of tuberculosis, but I think you especially see it in the way the disease was racialized. It was widely believed in the 18th and 19th centuries that only white people could get tuberculosis. And then in the 20th and 21st centuries, it was believed white people were insulated from tuberculosis in some ways and that it's a disease primarily of people of color.

The way that I think about it sometimes is that Charles Dickens wrote that tuberculosis was the "disease that wealth never warded off," and, of course, now it's a disease that wealth entirely wards off.

NL: We've touched on this already, but could you expand on how USAID factors into TB efforts worldwide and what it means for that funding to be disrupted?

JG: We did have ongoing projects I would have liked to highlight. I would have liked to highlight our work in the Philippines with USAID to bring TB down to zero in specific communities to offer a blueprint for how we eliminate TB from the planet. [Beyond our own work], I'd like to highlight the work that has been done to reduce TB death by over 50% in the last 25 years. I'd like to highlight the efforts that are being made by the U.S. government and others to radically reduce the burden of tuberculosis in the most impoverished countries in the world. But we've just abandoned all of those.

The project that we've been working on in the Philippines with Partners In Health and USAID and the Philippine government will continue in some way, thanks to the generosity of the Philippine government. But it won't accomplish its biggest dreams, and that's entirely because of the decision to stop funding essentially all global health services.

I'm confused as to how all of this is happening, but I'm just also heartbroken. I'm hearing every day from people who are having to make horrible decisions about how to ration care.

Related: 10 of the deadliest superbugs that scientists are worried about

NL: And in tuberculosis, continuity of care is very important.

JG: Continuity of care is essential for curing tuberculosis. If someone has even a couple of weeks without access to their medication, it's vastly more likely that their disease will become drug resistant, which is a personal catastrophe because it means that they are much more likely to die of tuberculosis. It's also a societal catastrophe because it means there's much more drug-resistant tuberculosis floating around, having the opportunity to evolve ever more drug resistance.

I think it's important to understand that we've never done anything like this before; we've never suddenly interrupted the treatment of thousands or tens of thousands or hundreds hundreds of thousands. We don't even know how many people's treatment is being interrupted right now because we have no way to count it. … What we're doing to the future of tuberculosis is unconscionable to me.

NL: In a moment when the situation feels so bleak, is there anything bringing you hope?

JG: It's inevitable for me to feel like I live at the end of history because today is the most recent day I've ever experienced, you know, and so this feels like the culmination of everything that came before, but I don't live at the end of history. I live in the middle of history, and this is not the end of the story; this is the middle of the story, and we have to fight for a better end.

That's what gives me hope, and working with people I love. In this work, you get to work with people you care about and whose love and attention is focused in the same direction as yours, and there's a lot of comfort in that for me.

Editor's note: This interview was conducted on Feb. 28, 2025, so it may not reflect recent developments with USAID. The transcript has been lightly edited for length and clarity.

Google's new artificial intelligence (AI) tool has cracked a problem that took scientists a decade to solve in just two days.

José Penadés and his colleagues at Imperial College London spent 10 years figuring out how some superbugs gain resistance to antibiotics — a growing threat that claims millions of lives each year.

But when the team gave Google's "co-scientist" — an AI tool designed to collaborate with researchers — this question in a short prompt, the AI's response produced the same answer as their then-unpublished findings in just two days.

Astonished, Penadés emailed Google to check if they had access to his research. The company responded that it didn't. The researchers published their findings Feb. 19 on the preprint server bioRxiv, so they have not been peer reviewed yet.

"What our findings show is that AI has the potential to synthesise all the available evidence and direct us to the most important questions and experimental designs," co-author Tiago Dias da Costa, a lecturer in bacterial pathogenesis at Imperial College London, said in a statement. "If the system works as well as we hope it could, this could be game-changing; ruling out 'dead ends' and effectively enabling us to progress at an extraordinary pace."

Using AI to fight superbugs

Antimicrobial resistance (AMR) occurs when infectious microbes — such as bacteria, viruses, fungi and parasites — gain resistance to antibiotics, rendering essential drugs ineffective. Dubbed a "silent pandemic," AMR represents one of the biggest health threats facing humanity as the overuse and misuse of antibiotics in both medicine and agriculture accelerate its prevalence.

According to a 2019 report by the Centers for Disease Control and Prevention (CDC), drug-resistant bacteria killed at least 1.27 million people globally that year. About 35,000 of those deaths were in the U.S. alone, meaning that U.S. fatalities from the issue had spiked by 52% since the CDC's last AMR report, in 2013.

To investigate the problem, Penadés and his team began searching for ways one type of superbug — a family of bacteria-infecting viruses known as capsid-forming phage-inducible chromosomal islands (cf-PICIs) — acquire their ability to infect diverse species of bacteria.

Related: Dangerous 'superbugs' are a growing threat, and antibiotics can't stop their rise. What can?

The scientists hypothesized that these viruses did this by taking tails, which are used to inject the viral genome into the host bacterial cell, from different bacteria-infecting viruses. Experiments proved their hunch to be correct, revealing a breakthrough mechanism in horizontal gene transfer that the scientific community was previously unaware of.

Before anyone on the team shared their findings publicly, the researchers posed this same question to Google's AI co-scientist tool. After two days, the AI returned suggestions, one being what they knew to be the correct answer.

"This effectively meant that the algorithm was able to look at the available evidence, analyse the possibilities, ask questions, design experiments and propose the very same hypothesis that we arrived at through years of painstaking scientific research, but in a fraction of the time," Penadés, a professor of microbiology at Imperial College London, said in the statement.

The researchers noted that using the AI from the start wouldn't have removed the need to conduct experiments but that it would have helped them come up with the hypothesis much sooner, thus saving them years of work.

Despite these promising findings and others, the use of AI in science remains controversial. A growing body of AI-assisted research, for example, has been shown to be irreproducible or even outright fraudulent. To minimize these problems and maximize the benefits AI could bring to research, scientists are proposing tools to detect AI misconduct and establishing ethical frameworks to assess the accuracy of findings.

Multiple sclerosis is a disease that results when the immune system mistakenly attacks the brain and spinal cord. It affects nearly one million people in the U.S. and over 2.8 million worldwide. While genetics play a role in the risk of developing multiple sclerosis, environmental factors such as diet, infectious disease and gut health are major contributors.

The environment plays a key role in determining who develops multiple sclerosis, and this is evident from twin studies. Among identical twins who share 100% of their genes, one twin has a roughly 25% chance of developing MS if the other twin has the disease. For fraternal twins who share 50% of their genes, this rate drops to around 2%.

Scientists have long suspected that gut bacteria may influence a person's risk of developing multiple sclerosis. But studies so far have had inconsistent findings.

To address these inconsistencies, my colleagues and I used what researchers call a bedside-to-bench-to-bedside approach: starting with samples from patients with multiple sclerosis, conducting lab experiments on these samples, then confirming our findings in patients.

In our newly published research, we found that the ratio of two bacteria in the gut can predict multiple sclerosis severity in patients, highlighting the importance of the microbiome and gut health in this disease.

Related: Twin study reveals signs of MS that might be detectable before symptoms

Bedside to bench

First, we analyzed the chemical and bacterial gut composition of patients with multiple sclerosis, confirming that they had gut inflammation and different types of gut bacteria compared with people without multiple sclerosis.

Specifically, we showed that a group of bacteria called Blautia was more common in multiple sclerosis patients, while Prevotella, a bacterial species consistently linked to a healthy gut, was found in lower amounts.

In a separate experiment in mice, we observed that the balance between two gut bacteria, Bifidobacterium and Akkermansia, was critical in distinguishing mice with or without multiple sclerosis-like disease. Mice with multiple sclerosis-like symptoms had increased levels of Akkermansia and decreased levels of Bifidobacterium in their stool or gut lining.

Bench to bedside

To explore this further, we treated mice with antibiotics to remove all their gut bacteria. Then, we gave either Blautia, which was higher in multiple sclerosis patients; Prevotella, which was more common in healthy patients; or a control bacteria, Phocaeicola, which is found in patients with and without multiple sclerosis. We found that mice with Blautia developed more gut inflammation and worse multiple sclerosis-like symptoms.

Even before symptoms appeared, these mice had low levels of Bifidobacterium and high levels of Akkermansia. This suggested that an imbalance between these two bacteria might not just be a sign of disease, but could actually predict how severe it will be.

We then examined whether this same imbalance appeared in people. We measured the ratio of Bifidobacterium adolescentis and Akkermansia muciniphila in samples from multiple sclerosis patients in Iowa and participants in a study spanning the U.S., Latin America and Europe.

Our findings were consistent: Patients with multiple sclerosis had a lower ratio of Bifidobacterium to Akkermansia. This imbalance was not only linked to having multiple sclerosis but also with worse disability, making it a stronger predictor of disease severity than any single type of bacteria alone.

How "good" bacteria can become harmful

One of the most interesting findings from our study was that normally beneficial bacteria can turn harmful in multiple sclerosis. Akkermansia is usually considered a helpful bacterium, but it became problematic in patients with multiple sclerosis.

A previous study in mice showed a similar pattern: Mice with severe disease had a lower Bifidobacterium-to-Akkermansia ratio. In that study, mice fed a diet rich in phytoestrogens — chemicals structurally similar to human estrogen that need to be broken down by bacteria for beneficial health effects — developed milder disease than those on a diet without phytoestrogens. Previously we have shown that people with multiple sclerosis lack gut bacteria that can metabolize phytoestrogen.

Although the precise mechanisms behind the link between the Bifidobacterium-to- Akkermansia ratio and multiple sclerosis is unknown, researchers have a theory. Both types of bacteria consume mucin, a substance that protects the gut lining. However, Bifidobacterium both eats and produces mucin, while Akkermansia only consumes it. When Bifidobacterium levels drop, such as during inflammation, Akkermansia overconsumes mucin and weakens the gut lining. This process can trigger more inflammation and potentially contribute to the progression of multiple sclerosis.

Our finding that the Bifidobacterium-to-Akkermansia ratio may be a key marker for multiple sclerosis severity could help improve diagnosis and treatment. It also highlights how losing beneficial gut bacteria can allow other gut bacteria to become harmful, though it is unclear whether changing levels of certain microbes can affect multiple sclerosis.

While more research can help clarify the link between the gut microbiome and multiple sclerosis, these findings offer a promising new direction for understanding and treating this disease.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

We often forget how wonderful it is that life exists, and what a special and unique phenomenon it is. As far as we know, ours is the only planet capable of supporting life, and it seems to have arisen in the form of something like today's single-celled prokaryotic organisms.

However, scientists have not given up hope of finding what they call LUCA (Last Universal Common Ancestor, the ancestral cell from which all living things we know are descended) beyond the confines of our planet.

Related: 12 strange reasons humans haven't found alien life yet

Where are we looking?

Since humans started dreaming about Martians, scientific understanding has changed significantly. The most recent vehicles to have traversed the Red Planet's surface — the Perseverance and Curiosity rovers — have identified compounds and minerals that suggest its conditions may once have been habitable, but that is the extent of it.

Right now, Mars is a reddish desert landscape — attractive but dead, and certainly not home to any little green men.

Other nearby planets offer even less hope. Mercury is a scorched rock too close to the Sun, Venus' atmosphere is dry and toxic, and the others in our solar system are either made of gas or very far from the Sun. So, apart from Mars, the search for other forms of life is focused on satellites, especially those orbiting Jupiter and Saturn.

Europa and Enceladus — moons of Jupiter and Saturn, respectively — appear to have large oceans of water under a thick crust of ice that could potentially harbour organic molecules, the building blocks for the origin of life as we know it. These would be nothing like E.T. — they would look more like the simplest terrestrial single-celled organisms.

Looking further afield, more than 5,500 planets have been detected orbiting stars other than the Sun. Only a few are considered potentially habitable and are currently being researched, but as Carl Sagan said in Contact, "the universe is a pretty big place. If it's just us, seems like an awful waste of space."

Looking for life in inhospitable places

Before the 1960s, the conditions on the solar system's most promising satellites would have seemed impossible for life.

The prevailing belief until then was that life could only occur under the conditions where we saw multi-cellular organisms survive. Water, mild temperatures between 0⁰ C and 40⁰ C, pH in neutral ranges, low salinity, and sunlight or an equivalent energy source were considered essential for life.

However, in the mid-20th century, microbiologist Thomas D. Brock discovered bacteria living in the hot springs of Yellowstone National Park, where temperatures exceed 70⁰C. Though unrelated to the search for extraterrestrial life at the time, his discovery broadened its scientific possibilities.

Since then, organisms known as extremophiles have been found inhabiting a range of extreme conditions on Earth, from the cold of cracks in polar ice to the high pressures of the deep ocean. Bacteria have been found attached to small suspended particles in clouds, in extremely saline environments such as the Dead Sea, or extremely acidic ones, such as Rio Tinto. Some extremophiles are even resistant to high levels of radiation.

What was most surprising, however, was finding them inside ourselves.

Martians in your stomach

In the 1980s, two Australian doctors, Barry Marshall and Robin Warren, began studying gastroduodenal ulcers. Until then, the condition had been attributed to stress or excess gastric acid secretion, which did little to help cure the condition.

Warren was a pathologist, and having identified bacteria in gastric biopsy samples from patients, he realised that they had to be considered a cause of the disease. However, he had to fight against the dogma that microorganisms could not grow in the highly acidic environment of the human stomach.

Warren conducted his research alone until 1981, when he met Barry Marshall, a fellow of the Royal Australasian College of Physicians. He approached Marshall and asked if he would like to work alongside "that crackpot Warren who's trying to turn gastritis into an infectious disease".

In 2005, Barry Marshall and Robin Warren received the Nobel Prize in Physiology or Medicine for their discovery of Helicobacter pylori and its role in gastric diseases, a discovery that revolutionised the field of gastroenterology.

H. pylori has an amazing array of factors that help it survive in hostile environments, such as flagella that allow it to surf stomach fluids to get close to the stomach wall, breaking through the protective mucus layer and attaching itself to it.

Using the enzyme urease, H. pylori degrades urea in the stomach into ammonia and CO₂, creating a higher pH microclimate that allows it to reproduce. As its numbers increase, it releases exotoxins that inflame and damage gastric tissue in the stomach. This is how ulcers eventually develop, as the underlying connective tissue is exposed to the acidity of the stomach.

Their discovery showed that even tucked away in our innards — in the walls of our stomachs, subjected to vinegar-like pH levels, total darkness, the violent movements of our digestive systems, harmful enzymes and churning tides of food — life is able to resist and proliferate.

The study of extremophile micro-organisms offers the hope that on other bodies in the solar system, or on one of the 5,500 known exoplanets, even in extreme conditions, the extraordinary phenomenon of life may be present. The Martians we dream of today might look more like H. pylori than anything else.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

A painful burning sensation in a woman's legs turned out to be the result of a parasite burrowing into her brain, her doctors have revealed.

The 30-year-old, from New England, likely contracted the parasite while travelling in Hawaii, according to a case report published Feb. 13 in The New England Journal of Medicine.

Her symptoms began with a strange burning sensation in her feet. Over the coming days, the pain spread up her legs, and the impacted areas became sensitive to even the lightest touch. She was also fatigued, but she initially attributed that to jet lag following a three-week trip to Thailand, Japan and Hawaii.

She went to an emergency department about the sensations in her legs, but her exams came back normal and she was ultimately discharged. Days later, the sensations spread to her truck and arms and she developed a headache. So she went to a second emergency department, and again, her exams were "reportedly normal," although her immune-cell count was up. She received medications that relieved her headache before being discharged.

Related: 32 scary parasitic diseases

After about a week of these symptoms, the woman developed confusion and her partner brought her to hospital once again. Her blood tests and kidney function were still normal, and microscopic examination of her blood showed no obvious signs of parasites. However, one thing that did stand out was an elevated level of a type of white blood cell called eosinophils; these cells help the body fight off foreign invaders, including parasites.

The medical team then performed a lumbar puncture, or spinal tap, to draw out a sample of cerebrospinal fluid. This fluid surrounds the spinal cord and brain. This test also revealed a very high level of eosinophils.

Her results were consistent with a condition known as eosinophilic meningitis, a rare form of inflammation in the brain and spinal cord often caused by parasites.

According to the case report, the most common cause of eosinophilic meningitis is rat lungworm (Angiostrongylus cantonensis), a parasite that lives in many tropical and subtropical regions in Southeast Asia and the Pacific Islands, including Hawaii.

After ruling out other culprits, the team determined A. cantonensis was behind the woman's case. While the parasite was not detected in the patient's blood, further testing of her cerebrospinal fluid revealed genetic traces of the parasite.

The adult form of the parasite primarily lives inside rodents. Their larvae then pass out through the rodent's feces, at which point they are eaten by slugs and snails. These larvae mature inside the mollusks until their host is eventually eaten by a rat or other rodent, and the life cycle starts again.

If a human eats an infected mollusk that's raw or undercooked, or a raw vegetable that has been contaminated with their slime, they can also become infected. Shellfish, including land crabs and freshwater prawns, may also become contaminated if they eat an infected slug or snail.

Not all people who ingest A. cantonensis experience symptoms, according to the U.S. Centers for Disease Control and Prevention (CDC). However, in some cases the larvae migrate to the host's central nervous system and reach the brain — in some lab animals, this can happen within four hours of ingestion, the case report notes.

Once in the human brain, the parasite can trigger headaches, a stiff neck, vomiting, confusion, tingling or burning sensations and eventually, seizures and vision problems.

In many cases, A. cantonensis infections resolve on their own as the parasites die off, even in cases of meningitis, the CDC says. In those cases, supportive treatments might include painkillers and antiinflammatories. That said, these infections can sometimes be fatal.

In the woman's case, the patient was given a 14-day course of antiparasitic medication, together with a steroid drug to help bring down inflammation in her nervous system. She was discharged from hospital after six days.

To prevent infection with rat lungworms like A. cantonensis , the CDC recommends that people not eat raw or undercooked snails or slugs, frogs, shrimp or prawns. They should wear gloves and wash hands after handling snails or slugs in the garden. The agency also adds that people should always wash fresh produce thoroughly and avoid eating uncooked vegetables in areas where the parasite is endemic.

This article is for informational purposes only and is not meant to offer medical advice.

Health officials are raising the alarm over a large and ongoing tuberculosis (TB) outbreak in Kansas.

According to data from the Kansas Department of Health and Environment (KDHE), the cases have all occurred in Wyandotte County and Johnson County, both part of the greater Kansas City metro area. So far, 67 "active" TB infections and 79 "latent," or "inactive" infections have been linked to the outbreak.

In latent TB, the immune system suppresses the bacteria — called Mycobacterium tuberculosis — behind the infection. Although they're inside the body, the bacteria don't cause any symptoms and can't spread to additional people. While many people with latent TB never develop active TB, about 5% to 10% do. This is more likely to happen to people with malnourishment, a history of smoking or tobacco use, or who have weakened immune systems, due to diabetes, immune-suppressing drugs or infections like HIV/AIDS.

"This outbreak is still ongoing, which means that there could be more cases," Jill Bronaugh, the KDHE communications director, told Live Science by email. The earliest cases linked to the ongoing outbreak took place in January 2024. Two deaths in 2024 were connected to the outbreak.

Related: 1st known tuberculosis cases in Neanderthals revealed in prehistoric bone analysis

With 67 active cases reported between January 2024 and the present, Bronaugh added that the outbreak is "largest outbreak in the U.S. at this time over the span of one year since the CDC began reporting TB cases in the 1950's."

That national recordkeeping started after the first effective treatments for TB were developed in the 1940s and 1950s, when improvements in housing and nutrition had already been helping drive down cases nationwide.

"According to CDC, a TB outbreak is generally defined as a situation where there are more TB cases than expected within a geographic area or population during a particular time period, AND [there is] evidence of recent transmission of M. tuberculosis among those cases," Bronaugh clarified. "Recent" transmission is often defined as happening within the past two years, she added.

The annual rate of active TB cases and TB-related deaths currently remains low in the U.S., especially compared to countries where the disease is widespread. However, cases have been on the rise in recent years. In 2023, the Centers for Disease Control and Prevention (CDC) recorded over 9,600 active TB cases nationwide, or about 2.9 per 100,000 people. That's about 15% more than reported in 2022, and the most reported since 2013.

Notably, in 2021, Kansas experienced an outbreak of multidrug-resistant TB that affected just over a dozen people. These infections are trickier to treat because the bacteria show resistance to common first-line antibiotics used to cure TB. Live Science asked KDHE if any of the cases in the current outbreak are drug-resistant but did not receive a response by the time of publication.

The health department is currently working with infected patients to identify close contacts who may have been exposed. Anyone who tests positive will be further examined to see if they have active or latent TB, since that dictates which treatment they receive. Although there is a vaccine for TB, it is generally not used in the U.S. because the risk of infection is so low, according to the CDC.

Treatments for TB typically involve taking multiple antibiotics for months at a time. Local health departments will provide these treatments to the patients in Kansas, and they will be free for those who are underinsured or uninsured, KGHE said.

TB-causing bacteria spread through the air, and are released when a person with active TB in their lungs speaks, sings or coughs. Once in the body, the bacteria can also spread beyond the lungs to other organs, such as the kidneys, spinal cord or brain. The symptoms a person experiences depend on which body parts are infected, but active TB in the lungs causes cough (including coughing up blood), chest pain, weakness, weight loss and fever, for example.

"TB is spread person-to-person only through prolonged contact with someone who has active TB," Bronaugh emphasized.

As of Jan. 28, KDHE is managing 384 individuals linked to the outbreak who are in various stages of testing, diagnostics and treatment. Its case counts are being updated weekly.

"While there is a very low risk of infection to the general public in these communities, KDHE is working to ensure that patients are receiving appropriate treatment, which will limit the ability to spread this disease and prevent additional cases from occurring," Bronaugh told Live Science.

"KDHE and public health professionals from the CDC are working together to mitigate the risk of TB in the community and ensure the safety of all individuals," she said.

Editor's note: Live Science originally published this article on Jan. 28, 2025, after receiving initial comments from KGHE. The department then sent out new information on Jan. 29, and the article was updated the same day.

This article is for informational purposes only and is not meant to offer medical advice.

Laser beams powered by the sun are one small step closer to becoming a reality after researchers received funding to develop the pioneering technology. These lasers could eventually help power lunar bases and missions to Mars, and contribute to sustainable energy solutions on Earth, scientists say.

In June, the international team of researchers announced it had received a roughly €4 million ($1.2 million) grant from the European Innovation Council and Innovate UK to develop solar-powered laser technology inspired by photosynthetic bacteria.

"In my group, we spend a lot of time thinking about artificial light harvesting and what we can learn from nature," Erik Gauger, a quantum theorist at Heriot-Watt University in Scotland who is involved in the collaboration, told Live Science in an interview. "If it's possible in nature, we should be able to utilize similar effects in artificial systems."

Sunlight-powered lasers aren't a new concept — the first one was demonstrated in 1963, just three years after the first laser was built. But regular sunlight is too dilute to power a laser effectively. Solar-powered lasers typically require complex, heavy-duty optics to intensify sunlight at least a thousand-fold. The weight of these components means it's challenging to send them to space.

Related: 'It invites us to reconsider our notion of shadow': Laser beams can actually cast their own shadows, scientists discover

To overcome these challenges, Gauger and his colleagues will turn to bacteria that live in darkness deep in the ocean. These bacteria have extremely sensitive light-harvesting structures that can pick up nearly every photon they encounter. These structures enable the bacteria to photosynthesize even in very low-light conditions. By extracting these light-harvesting structures and replicating them in the lab, the team hopes to concentrate ambient sunlight enough to power a laser, Gauger said.

Powering lunar bases and interplanetary missions

He and his colleagues described how such a system might work in a 2021 paper. In the proposed system, the structures capture incoming sunlight, then funnel the light into a solid material, such as a crystal. The electrons in the atoms of that material absorb energy from the light and then release that extra energy as laser light.

With the new grant, the team plans to develop new laser-emitting materials that can interface with the bacteria's photosynthetic structures.

Once the laser system is online, it could help power satellites, lunar bases and even missions to Mars, according to a statement. Because laser beams remain narrow and tightly focused over long distances, they can transmit energy to faraway systems. For example, a solar laser built on a space station could power that station or send power to a nearby satellite, or even to Earth. At the receiving site, the energy from the laser light could then be converted into heat or electricity.

The solar-powered lasers could also support a shift toward renewable energy on Earth, Gauger said.

"They could, for example, help you split water, drive chemistry, synthesize fertilizers, and help with processes which require a significant fraction of the energy we currently produce, including from fossil sources," Gauger said. "They're not going to solve all our problems directly, but they might play a small part in the challenge we face to move to clean, sustainable energies."

The team plans to develop a prototype laser within the next three years.

Each year, Escherichia coli, or E. coli, causes about 265,000 infections and 100 deaths in the United States. Many of those infections result in foodborne illness. Notably, E. coli contamination has historically caused large and notable food recalls. In 2023 alone, the U.S. Food and Drug Administration (FDA) recalled 72,858 pounds (33,048 kilograms) of E. coli-contaminated food.

But how does E. coli get into food in the first place?

First off, it's important to understand that not all strains of E. coli are the same.

"E. coli are a group of common bacteria that are found naturally in many places including the environment, food, water and in the intestines of people and certain animals," Janell Goodwin, a spokesperson for the FDA, told Live Science in an email. "Most E. coli are harmless and contribute to intestinal health."

However, certain E. coli strains are dangerous because they produce Shiga toxins, harmful substances that can damage the digestive tract. These strains are called Shiga-toxin-producing E. coli (STEC). People can become sick if they eat or drink food or water contaminated by STEC, and children under 5 and adults over 65 typically face the greatest risk of severe infections.

How dangerous bacteria contaminate food

There are a number of ways STEC can end up in food. "Food goes through several steps from where it is grown or made to the dining table," a spokesperson for the U.S. Centers for Disease Control and Prevention (CDC) told Live Science in an email. "Contamination can occur at any point along the chain — during production, processing, distribution or preparation."

Goodwin noted that one major route of infection occurs through animals, including both livestock and wildlife. Animals may carry STEC in their intestines and then shed it through their feces. Even a tiny amount of feces present on a livestock carcass can lead to E. coli contamination in the resulting products made from that flesh. Ground beef is at particularly high risk of contamination, for instance, because cattle are the main carrier of E. coli O157, an especially dangerous strain of STEC. The bacteria can spread around when the meat is ground, and this has resulted in major recalls.

Bacteria from livestock or wildlife feces can also contaminate produce. For example, runoff from livestock farms can shepherd E. coli into water used to irrigate crops. Improperly treated manure used as fertilizer can also carry the harmful bacteria.

In addition, farmworkers who come into contact with livestock or produce may unknowingly transfer E. coli during planting, harvesting or processing if they don't carefully follow safety protocols aimed at preventing the transfer of bacteria from fecal contamination.

Harmful E. coli strains can also taint food on the other end of the food processing chain, such as at a restaurant. "Carriers [who shed the bacteria in their feces] can spread infections when food handlers do not use proper hand washing hygiene after using the restroom," Goodwin said.

Related: Bacteria from meat may cause a half-million UTIs a year

Stopping the spread

The FDA recommends that people wash their hands with warm water and soap for at least 20 seconds before and after handling any raw food. The agency also emphasizes the importance of handwashing before, during and after changing a baby's diaper, and when making contact with livestock.

Countertops and cutting boards can be another source of contamination, so the FDA advises washing those carefully as well.

Certain foods are more likely to be contaminated with harmful E. coli than others. A 2021 report from the CDC found that beef — particularly raw or undercooked ground beef — and vegetable row crops, such as leafy greens, were the source of 80% of O157 infections in the U.S. from 1998 to 2021. Raw and undercooked poultry; raw sprouts such as alfalfa; and products made with unpasteurized, or raw, milk are also common culprits, Goodwin added.

Researchers are still working to gain a better understanding of the factors that contribute to E. coli contamination in the food supply. One recent study found that seasonal changes in temperature may influence the likelihood of E. coli outbreaks tied to lettuce grown in California, while another study from Arizona found that STEC can spread through the air, traveling from large livestock facilities to nearby produce farms.

Goodwin also noted that, while it can be alarming to see more regular E. coli recalls and advisories in the news, it doesn't necessarily mean that the food safety system is failing.

"The occurrence of recalls and advisories means that manufacturers, importers, and distributors are monitoring for issues and taking action when they detect a problem," she said. "Consumers should know that recalls and outbreak advisories indicate that the problem has been identified and is being addressed. "

This article is for informational purposes only and is not meant to offer medical advice.

When you look in a mirror, the reflection is fundamentally you, but with a perfect reversal of all your features. This illustrates a phenomenon we also see in the tiny world of molecules.

Some molecules exist as mirror images of themselves, known as "enantiomers", that can't be superimposed on one another. This concept is known as chirality, or "handedness". It's important because mirror images of the same molecules can have completely different effects and functions in biology.

Writing in the journal Science, a group of 40 renowned scientists have warned that within the next decade, it may be possible to create entire mirror-image life forms made up of these enantiomers — specifically, microbial life such as bacteria. This poses real dangers, they argue.

"Mirror bacteria" could evade people's immune systems, they suggest, causing deadly infections. Such infections could also lead to a substantial proportion of plant and animal species being displaced, completely disrupting the environment.

Mirror-image molecules are structurally identical, just as your left and right hands are structurally identical and can perform exactly the same functions. These molecules also have exactly the same chemical properties — but for unknown reasons, nature has a preference for building life from just one version of such molecules.

For example, amino acids — the building blocks of proteins — are left-handed, while sugars are right-handed. The DNA molecule is a right-handed screw thread.

This selective chirality defines how molecules interact in living systems. It influences how drugs and enzymes (biological catalysts that speed up reactions) function in our body, as well as how we perceive flavours and smells. For example, the molecule carvone can smell of either spearmint or caraway seeds, depending which "mirror" version of the molecule you get this scent from.

Related: Scientists discover once-in-a-billion-year event — 2 lifeforms merging to create a new cell part

Other mirror molecules have much more profound implications. The drug thalidomide exists in two forms. One is a powerful treatment for morning sickness; the mirror version causes devastating birth defects.

This begs the question: what if we could make biological molecules that exist on the other side of the mirror? The drive behind this research is partly from curiosity, but it also has practical applications.

Medical treatments are increasingly derived from biological molecules such as peptides (small fragments of proteins), which can be used for treating cancer. But despite their effectiveness, natural proteins and peptides face a significant limitation: they degrade quickly in the body.

This is because the enzymes in our bodies, which evolved to break down biological molecules for recycling, are highly efficient at targeting natural peptides. So, these cancer treatments may require frequent dosing to ensure they work.

However, similar peptides built from mirror amino acids probably wouldn't be recognised by these degradation systems, yet could still be designed to target cancers. And building these mirror biological molecules is already achievable: we've made reflections of DNA, fully functional "mirror enzymes", and more.

The risks of mirror life

The potential benefits of mirror molecules are tantalising. The obvious next step would be to create full mirror organisms, made entirely from molecules that are the reflections of natural versions.

There are already research groups working on building bacteria "from the ground up". In other words, they are trying to synthesise biological molecules and assemble them into functional cells.

While making mirror bacteria from the ground up is still probably a decade away, there are already real concerns about where this research might lead. The 40 scientists writing in Science fear that mirror life, if it were to escape from labs (and there are plenty of examples of this happening), could have devastating consequences.

The most immediate concern is that mirror bacteria could evade the immune systems of humans, animals and plants. Our immune defenses rely on recognising conserved molecular patterns found in natural pathogens (an organism or other agent — such as a virus — that causes disease), all of which are built from left-handed amino acids. Mirror bacteria would lack these recognisable patterns, rendering our immune systems blind to their presence.

Mirror bacteria could also disrupt ecosystems in unpredictable ways. For example, they would probably be able to evade biological controls such as viral infection and bacterial antibiotics, allowing them to proliferate unchecked.

This could result in invasive populations of mirror bacteria that displace native species, disrupt food webs and alter nutrient cycles, potentially leading to cascading ecological consequences.

The scientists' warning about mirror life is striking — in part because it appears in such a prestigious academic journal, but also because it is underpinned by a rigorous 300-page technical analysis.

Their stark message, emphasising the extraordinary risks of mirror organisms, might sound like the plot of a sci-fi thriller, but the concerns are grounded in valid scientific reasoning.

Mirror bacteria present a unique and unprecedented challenge. However, this is not a crisis that will unfold tomorrow. The technical barriers to creating full mirror life remain significant, providing the global community with ample time to consider its response. And the scientists also acknowledge that, beyond research driven purely by curiosity, they struggle to conceive of any compelling justification for developing full mirror organisms.

By acting now — through robust governance, careful oversight and international collaboration — we can guide the development of mirror biomolecules responsibly, while ensuring that the creation of full mirror life is prevented — unless its risks are unequivocally understood and mitigated.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Antarctica's Lake Enigma certainly lives up to its name. The permanently ice-covered lake, named for the peculiar cone of debris at its center, was until recently thought to be frozen solid. But scientists have discovered a layer of fresh water hidden beneath the ice-covered surface — and it's populated by a diverse cast of microorganisms.

During an expedition to Antarctica from November 2019 to January 2020, researchers surveyed the lake with ground-penetrating radar and detected at least 40 feet (12 meters) of liquid water under the ice. The researchers then drilled into the ice and sent a camera to explore the lake's depths.

The team first tested the water to determine where it came from. This was important to establish because the area has low precipitation, high winds and intense solar evaporation, so any water in Lake Enigma should have dried up long ago.

Based on the chemical composition of salts in the water, the researchers hypothesized that the lake's water is consistently replenished by the nearby Amorphous Glacier through an unknown underground pathway.

Hidden ecosystem beneath Antarctic ice

The scientists found that, despite being isolated from the atmosphere, the waters of Lake Enigma are home to several kinds of microbial life, which cover the bottom of the lake in blobs known as microbial mats. Many of these organisms are photosynthetic, giving the lake a high concentration of dissolved oxygen.

Some of the mats formed thin, spiky coatings on the lakebed. Others resembled "a crumpled thick carpet, sometimes forming large amorphous tree-like structures up to 40 cm [centimeters, or 16 inches] high and up to 50 to 60 cm [20 to 24 inches] in diameter," the researchers wrote in the study, published Dec. 3 in the journal Communications Earth and Environment.

The microbial residents included several species of Patescibacteria — tiny, single-celled organisms that attach themselves to larger host cells to form either mutually beneficial or predatory relationships. These organisms had never before been found in ice-covered lakes and don't normally thrive in high-oxygen conditions, suggesting that these Patescibacteria may have developed unique metabolic tricks to survive.

"This finding highlights the complexity and diversity of food webs in Antarctic permanently ice-covered lakes, with symbiotic and predatory lifestyles a possibility not previously recognized," the researchers wrote in the study.

Environments similar to Lake Enigma exist on icy moons like Europa or Enceladus. The lake's extreme ecosystem could therefore offer insights into conditions in places where microbial life might be found on other worlds, study co-author Stefano Urbini, a geophysicist at the National Institute of Geophysics and Volcanology in Italy, wrote in a translated statement.

Antarctica quiz

Two men in New York state have died of a rare fungal lung infection that they caught from bat poop — specifically, poop they were using or planned to use as fertilizer to grow cannabis.

Both men, based in Rochester, shared a love of "Mary Jane" and cultivated their own cannabis plants for personal use. They each developed a condition called histoplasmosis after breathing in spores of a harmful fungus known as Histoplasma capsulatum from bat poop, or guano.

The first man, who was 59-years-old, had purchased guano online to use as fertilizer for his cannabis plants. The other man, 64, was intending to fertilize his cannabis plants with guano he'd found in his attic following a "heavy" bat infestation.

The men developed an array of symptoms from their infections, including fever, chronic cough, extensive weight loss, blood poisoning and respiratory failure. Despite being hospitalized and treated with antifungal medication, both men died of their illnesses, according to a report of their cases, published Dec. 4 in the journal Open Forum Infectious Diseases.

Related: New cause of asthma lung damage revealed

The doctors who treated them said that their deaths should serve as a warning about the potential dangers of using bat guano as a fertilizer for any plants. This may be a particular issue for cannabis growers.

"Given the recent legalization and an expected increase in home cultivation of cannabis, along with the promotion of bat guano for this purpose, it is important to raise public awareness about the potential risk of using bat guano as fertilizer," the case report authors wrote. The authors added that they found numerous articles calling bat guano a "natural superfood" for cannabis plants due to its high concentration of nitrogen and phosphorus.

These recent deadly cases also "emphasize the need for protective measures, such as wearing masks when handling it," the authors added.

Histoplasmosis is a type of pneumonia caused by breathing in spores of H. capsulatum, a fungus found in soil and bird and bat droppings. In the lungs, H. capsulatum spores transform into mature yeast that can spread to other regions of the body via the bloodstream. However, the disease cannot spread between people or between people and their pets.

Each year, around 1 to 2 per 100,000 people in the U.S. are infected with histoplasmosis. Infections mainly occur in the Mississippi and Ohio River valleys, although cases have been reported in 14 states, according to the U.S. Centers for Disease Control and Prevention (CDC).

Only about 1% of people exposed to H. capsulatum develop symptoms. When symptoms do emerge, they usually occur within three to 17 days after exposure, and include fever, chills, muscle aches and chest pain.

People who have had a lung disease prior to being infected and those with weakened immune systems are more likely to develop severe forms of histoplasmosis, which can last for months or longer, and be deadly. Between 5% and 7% of patients hospitalized with histoplasmosis die as a result of their infection.

The men in Rochester had other existing diseases when they caught histoplasmosis, which may have worsened their infections. The first, for instance, had a condition known as emphysema, where the air sacs in the lungs are damaged, which restricts breathing. And both patients had histories of tobacco use, in addition to smoking marijuana.

The authors of the new case report say that commercial fertilizers containing bat guano should be tested for H. capsulatum before being put on the market. If that is not possible, products should be labeled with warning signs and provide instructions on how to use them safely, they said.

To minimize the risk of infection, the CDC additionally recommends that people avoid engaging in activities that may increase their chances of being exposed to H. capsulatum, such as cleaning chicken coops or exploring caves. Large amounts of bird and bat droppings, which may be found in an infested attic, should be removed by professional companies, the agency states.

This article is for informational purposes only and is not meant to offer medical advice.

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New insight into how unique bacteria resist damage from radiation could lead to better protection for humans — both on Earth and among the stars.

Deinococcus radiodurans is an extremophile, a bacterium that can withstand conditions that would kill off most life-forms. D. radiodurans' ability to resist radiation thousands of times stronger than the lethal dose for humans has earned the microbe the nickname "Conan the Bacterium."

"Ionizing radiation — such as X-rays, gamma rays, solar protons and galactic cosmic radiation — is highly toxic to both bacteria and humans," Michael Daly, a geneticist and D. radiodurans expert at Uniformed Services University in Maryland, told Live Science.

"In bacteria, radiation can cause DNA damage, protein oxidation and membrane disruption, leading to cell death," he explained. "In humans, radiation exposure can result in acute radiation syndrome, increased cancer risk, and damage to tissues and organs."

Related: Super space sunblock made from skin pigment could shield astronauts from radiation

Ionizing radiation removes electrons from atoms. This results in reactive molecules called free radicals, which are unstable, and in large enough numbers, can damage DNA, proteins and cells.

D. radiodurans' ability to resist this damage comes from a unique combination of factors: a protective cell wall, efficient repair mechanisms to fix radiation-induced DNA damage, and a collection of antioxidants that diffuse free radicals.

In a new study, published Dec. 12 in the journal PNAS, Daly and his colleagues took inspiration from a powerful antioxidant made by D. radiodurans to design their own version of the antioxidant.

Complexes inside the bacterium that contain manganese protect its proteins from radiation by removing the free radicals that can damage them. This leaves those proteins free to perform vital cellular functions, such as DNA repair. The researchers created a lab-made version of the complex by combining charged manganese particles, or ions, with a phosphate ion and a specially designed peptide, or short chain of amino acids. The peptide was based on the amino acids that are most common in D. radiodurans.

The researchers dubbed their new antioxidant manganese-dependent peptide (MDP).

"I started as a skeptic," said study co-author Brian Hoffman, a professor of chemistry and molecular biosciences at Northwestern University. "I suspected that MDP's efficacy was nothing more than the 'sum of its parts.'"

However, Hoffman said he was surprised to discover that the parts interacted to form a more powerful whole. "This is the 'secret sauce,'" he said.

Experiments that measured how strongly the parts of the complex bound together showed that manganese alone didn't form strong enough bonds with the designed peptide to be protective. Adding the phosphate ion strengthened the bonds and produced a complex that could withstand over 12,000 times the human lethal dose of ionizing radiation.

Related: How radioactive is the human body?

Now, the researchers are using special techniques to examine the structure of MDP, in hopes of understanding how it's put together, why it works so well, and how to make it even more effective. The results could have wide-reaching applications.

"Astronauts on deep-space missions are exposed to chronic high-level ionizing radiation, primarily from cosmic rays and solar protons," Daly said. "MDP — a simple, cost-effective, nontoxic and highly effective radioprotector — could be administered orally to mitigate these space radiation risks."

He added that, "for manned missions to Mars, which may extend over a year, radioprotection will be essential for the crew's safety."

Closer to home, Daly and Hoffman want to explore MDP's potential for improving health on Earth.

"Acute radiation syndrome, which involves severe immunological complications, might be preventable with MDP," Daly said. "There's also a well-recognized link between radiation resistance and aging." So perhaps MDP could be a potential treatment to combat metabolic aging.

However, more research is needed to develop safe, effective forms of MDP for use in humans. With time, though, Hoffman, Daly and their colleagues foresee MPD's potential in everything from health care to space travel.

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The first antibiotics made once-deadly infections curable, and their early developers were lauded with a Nobel. But these miracle drugs soon revealed their Achilles heel: When antibiotics are overused, they grow less effective as the bacteria they're designed to kill evolve to have escape strategies. This flaw has prompted scientists to seek alternative solutions.

One alternative to antibiotics is phage therapy, which harnesses viruses to attack bacterial cells. Conceived over a century ago, phage therapy fell to the wayside as antibiotics rose to prominence, but recently, the field has seen a resurgence. In "The Living Medicine: How a Lifesaving Cure Was Nearly Lost — and Why It Will Rescue Us When Antibiotics Fail" (St. Martin's Press, 2024), science journalist Lina Zeldovich recounts the complex history of phage therapy and its proponents while also highlighting how the treatment could save humanity in the future.

Related: Dangerous 'superbugs' are a growing threat, and antibiotics can't stop their rise. What can?

The Phage Whisperer

Biswajit Biswas drew a syringe full of phage and injected it into his laboratory mice, one after another. The mice weren't sick, so he wasn't using phages as medicine. He just wanted to know how long the phages would persist inside the mice — an experiment similar to what [Giorgi] Eliava and [Félix] d'Hérelle once carried out to understand how far phages could travel in rodents' bodies. In about a day, Biswas would test the mice's blood to see if the phages were still floating inside them. Typically, most phages would be gone because they were quickly filtered by the liver and spleen, but sometimes a tiny fraction remained. Biswas would harvest the survivors, grow them — and inject them into the mice again.

Biswas was working on this unconventional project in the mid-1990s, in the laboratory of Carl Merril, an NIH scientist and an early phage enthusiast who was playing around with the idea of using them to treat disease. Their mice were getting blood tests right about the same time that [Alexander] Sandro [Sulakvelidze] and [Glenn] Morris were having their first phage conversations and putting together their VRE [vancomycin-resistant enterococcus] proposals. Geographically, the two teams weren't far from each other. Both were located in Maryland. Both understood phages as medicinal agents, which the rest of the medical field viewed as nonsensical.

Merril, however, approached the problem from a different angle. Rather than treating sick mice with phages, he wanted to know how long living medicines could survive inside a creature. In humans and animals, the liver, spleen, and immune system tackle foreign invaders and filter them out quickly. Merril wanted to know how long phages could persist before they got gobbled up by the body's natural defense mechanisms. He also wanted to know if phages could evolve to avoid being devoured. By handpicking surviving phages and reinjecting them again, Biswas and Merril hoped to find answers.

"It was a selection process," Biswas explains. "I was growing phages and injecting them intravenously and intraperitoneally in mice, and the next day, after thirteen or eighteen hours, I would bleed the mice and take those phages and grow it again — passage after passage." It was a method akin to what d'Hérelle outlined in his book "The Bacteriophage and the Phenomenon of Recovery," which Eliava translated.

Originally from India, Biswas followed his family's tradition and earned a degree in veterinary medicine. Working in animal husbandry in the mid-1980s, he watched with growing concern the increasing use of antibiotics — both to battle infections and to fatten up the animals. While looking for possible alternatives, he came across intriguing scientific literature dating back to the early 20th century, when d'Hérelle's successful phage experiments prompted doctors to first use them to treat disease.

Between 1930 and 1935, British medical officer Lieutenant Colonel J. Morison, who was inspired by d'Hérelle's work, used phages during cholera epidemics in India, for treatment and prevention. In 1932, he reported few cholera deaths in the phage-treated Naogaon region, compared to 474 deaths in the Habiganj region that declined to utilize the treatment.

Related: 10 of the deadliest superbugs that scientists are worried about

"I read a paper that the British actually used bacteriophage from River Ganges to treat cholera," says Biswas. "They inoculated a water well in a village, and that reduced the incidences of cholera."

As a veterinarian in India, Biswas didn't have a way to experiment with phages. But then, like Sandro, he came to the United States in the 1990s to work on his PhD. He landed in the same place as Sandro, the University of Maryland. There, he found an ally in Merril, who was equally fascinated with bacteria eaters. As an NIH scientist, Merril watched antibiotics lose their punch and knew medicine needed an alternative. "When I started my career in the 1970s, we thought antibiotics were doing fine. By the 1990s, it was clear that we were going to have a problem. I thought phages were worth trying."

Merril had become interested in bacteriophages after taking a summer course at Cold Spring Harbor back in the 1970s. The course focused on phages' basic biology, but for Merril, it left two big unanswered questions.

"Why don't we use them for treating infectious diseases?" Merril asked his professor. The man told him to go read "Arrowsmith" by Sinclair Lewis — the very book that left d'Hérelle excited in the spring of 1925, shortly before he so spectacularly cured plague in Egypt. The professor's intention was to show Merril why phages had become discredited, but that wasn't what he found. In fact, Merril realized that his professor likely skimmed the book, if he read it at all. "He didn't read 'Arrowsmith,' because if you read it really carefully, it's not an indictment of phage," Merril says. "It's an indictment of human beings and their greed and their misuse of things."

Merril's other big question was about what happens to phages once they enter the human body — in particular, the circulatory system. Does the immune system destroy them? How quickly? Can some persist? From initial experiments with injecting phages into mice, he found that even before the immune system cells gobbled up bacteriophages as foreign organisms, the liver and spleen filtered them out. "My next question was, can we find a phage strain that wouldn't be taken up by the liver?" he recalls. "Such a strain would be more effective."

Merril happened to be on a committee that oversaw Biswas's PhD research, and one day, they started talking. "I told him that I used phages before in my graduate studies to make a phage library mainly for molecular biology work," Biswas recalls. Merril was interested. "I'd like to try to use bacteriophages to overcome antibiotic resistance problems," he told Biswas. "Would you come work in my lab?" Biswas was intrigued. "I said, 'It's an interesting idea. I can work in that field.'"

For a while after he joined Merril's lab, Biswas's days revolved around injecting mice with phages against E. coli and Salmonella typhimurium and then taking their blood tests to see how quickly the bacteria eaters were eaten themselves, disappearing from circulation. About a day later, most phages would be gone, except for a tiny fraction. Biswas would filter them — and repeat the process again.

The first few rounds didn't exhibit much success. But then Biswas noticed that the survivors' numbers increased. "Surprisingly, after the eleventh round, we saw that the phage titer from the blood was getting higher," he recalls. "So we isolated those long-circulating or long-swimming phages." Similarly to d'Hérelle, they also turned to Greek mythology, naming their newfound potent creatures after Jason and the Argonauts, who sailed on the ship called Argo to retrieve the Golden Fleece. Although technically speaking phages can't swim on their own, they merely float, Biswajit and Merril liked the term. "We called them Argo1 and Argo2 phages because they were good swimmers."

The two types of Argo phages Biswas and Merril selected weren't just good swimmers — they were exceptional. Argo1's 18-hour survival numbers were 16,000-fold higher than the strain Biswas started with. Argo2's was 13,000-fold higher. Notably, these Argo phages also made better medicines than their original brethren. "Mice would survive when you treat with either phage," Biswas says. "But when we treated them with the Argo phages, they would recover much faster because the phages persisted longer in their bodies."

From "The Living Medicine: How a Lifesaving Cure Was Nearly Lost — and Why It Will Rescue Us When Antibiotics Fail" by Lina Zeldovich. Copyright © 2024 by the author and reprinted by permission of St. Martin's Publishing Group.

Colds and the flu are two incredibly common respiratory infections. Each calendar year, the average American adult gets around two to three colds, while approximately 8% of the population catches the flu as it circulates between about October and May.

In some ways, it is easy to confuse the common cold with the flu. After all, they're both contagious respiratory illnesses, and they share many symptoms, such as headache, sore throat and cough. However, there are important distinctions between these two illnesses, and the differences affect how each is diagnosed and treated.

So how is the common cold different from the flu?

First, colds and the flu are caused by different viruses. More than 200 respiratory viruses can cause colds. These include rhinoviruses, adenoviruses and non-rhinovirus enteroviruses, as well as some types of coronaviruses. The flu, in contrast, is caused only by influenza viruses. Most commonly, it's caused by the two main types of viruses that cause seasonal flu epidemics in humans: influenza A and B.

The commonly used nickname for the infection — "the flu" — is short for "influenza."

Related: How do people die of the flu?

The viruses that cause colds and the flu also vary slightly in the regions of the body they infect. A cold is a type of upper respiratory infection, Dr. Angela Branche, an associate professor of medicine at the University of Rochester, told Live Science. This means it affects the top portion of the respiratory system: the nose, mouth, sinuses and throat.

When you get a cold, you'll most likely experience a blocked or runny nose, a cough and sneezing. These symptoms are generally mild, and they come on gradually and often go away on their own within a week, without the need for medication. During that time, you may feel unwell but you can usually continue with daily activities. That said, the Centers for Disease Control and Prevention advises avoiding other people while your symptoms persist, to avoid spreading your cold to them.

Flu, on the other hand, usually affects both the upper respiratory tract and the lower respiratory tract, which includes the windpipe and the lungs, and it can also impact other organs. Symptoms of the flu are generally more intense than those associated with colds, and they come on more abruptly.

Patients with the flu may experience additional symptoms, such as fever, chills and body aches, and in severe cases, the infection can lead to serious health problems, including pneumonia and other complications that require hospitalization. Such complications can also happen with colds, but they are much less likely.

Colds and the flu also differ in the way they're diagnosed. Typically, doctors only need to conduct a physical exam and gather the medical history of a patient to determine if they have a cold. A specific test, such as one that requires a nasal swab, is needed to definitively diagnose the flu. In this case, samples of fluid from the nose are analyzed to see if they are laden with influenza viruses.

What's more, some products can now test for the flu and the virus behind COVID-19 at the same time. This is useful because COVID-19 and the flu can also cause some of the same symptoms, but they require different treatments.

Neither the flu nor a cold can be cured with medicine. However, specific drugs can help alleviate a patient's symptoms and shorten the length of time a person has them.

People with a cold may take nasal decongestants or pain relievers, such as ibuprofen (Advil or Motrin) or acetaminophen (Tylenol), Branche said. For the flu, antivirals like oseltamivir (Tamiflu) can reduce the duration of infection by about a day. For people with very severe flu infections, Tamiflu can also lower the risk of death if provided early in the infection.

There is no vaccine against colds, but there is a seasonal vaccine against the flu. With rare exceptions, the CDC recommends that everyone ages 6 months and older get vaccinated every flu season. This vaccination reduces the risk of developing serious complications or dying from the disease, especially for groups vulnerable to the illness, such as very young children, older adults and pregnant people.

This article is for informational purposes only and is not meant to offer medical advice.

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The patient: A 56-year-old woman in Maryland

The symptoms: The woman was hospitalized after experiencing fever, cough and chest pain for about two days.

What happened next: Scans of the patient's chest revealed signs of pneumonia, and lab results suggested she had a higher-than-normal number of immune cells in her blood. Suspecting an infection, doctors tested the patient's blood for bacteria and found Burkholderia pseudomallei, a species that's widespread in Australia and Southeast Asia. However, the woman hadn't been out of the country.

The diagnosis: The woman had melioidosis, a bacterial infection caused by a microbe that lives in soil and water in tropical and subtropical regions. People can become infected by breathing in dust or water contaminated with B. pseudomallei, or by touching contaminated soil or water, especially with broken skin.

The treatment: The patient was given antibiotics that resolved her fever and normalized her immune cell count. She was discharged after 11 days but continued getting antibiotics via IV at an outpatient clinic. A few weeks later, though, the patient's fever returned, and she was readmitted for a more extensive antibiotic regimen. She was discharged a week later but ultimately had to remain on antibiotics for months to completely clear the infection.

What makes the case unique: Historically, most melioidosis cases detected in the U.S. have been connected to international travel. In this case, though, the woman was exposed to the bacteria much closer to home.

The patient had never traveled outside the continental U.S., but she owned two fish tanks. While looking for the source of the bacteria in her home, scientists gathered samples of water, gravel, filters and artificial plants from both tanks and found that several samples from one tank tested positive for B. pseudomallei. The patient had purchased the tank and supplies from a large retail store, and the water in the contaminated tank was "persistently cloudier" than the other, she said. Several sets of fish that she had kept in that tank had died, and she recalled reaching her bare hands and arms into the water to clean the tank.

The scientists concluded that this case marked the first time someone caught melioidosis from a fish tank, potentially due to imported aquarium supplies or the fish themselves being contaminated.

In the years since this case, scientists have found B. pseudomallei in soil and water samples from the Gulf Coast region of Mississippi, and data suggest that nearby states, like Texas, may also harbor the bacteria. Therefore, these states could see more local cases of melioidosis in the future. Recent cases have also been tied to contaminated, imported products, including an aromatherapy spray.

This article is for informational purposes only and is not meant to offer medical advice.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

Infectious diseases make up three of the ten slots in the World Health Organization's top 10 causes of death and account for millions of deaths annually across the globe. Despite these high numbers, however, diseases like COVID-19 and tuberculosis don't kill the majority of people they affect: COVID-19 kills an estimated 1% of those infected, based on totals reported by the World Health Organization (WHO), and tuberculosis kills fewer than 15%, according to WHO reports.

But do any infectious diseases have a 100% fatality rate? And if so, what makes them so deadly?

Infectious diseases are caused by pathogens, including viruses, bacteria, fungi and parasites. According to Dr. Amesh Adalja, an infectious disease physician at the Johns Hopkins Center for Health Security, nearly all the infections that once had a 100% fatality rate can now be prevented with vaccination or treated with modern medicine.

For example, HIV infections can now be treated with medications that extend people's lives and stop the disease from progressing to AIDS. Smallpox, some rare variants of which were nearly 100% fatal, is now eradicated across the globe. Death from rabies, which is nearly 100% fatal once symptoms appear, can be almost entirely prevented with immediate medical care after exposure. This care includes washing the wound, getting a rabies vaccine and, sometimes, getting antibodies against the rabies virus.

"Things that are 100% fatal [if left untreated] have become manageable because of human ingenuity," Adalja told Live Science.

However, there are a few fatal infectious diseases that we still haven't cracked. Some of these are always or nearly always deadly, while others just have very high fatality rates.

Related: Why do we develop lifelong immunity to some diseases, but not others?

For example, amoebic meningitis — better known as a "brain-eating" amoeba infection — is a rare infection that is nearly always fatal. Amoebic meningitis spreads to the brain through the nose, usually after a person is submerged in contaminated water. In rare cases, these infections have been successfully treated but scientists are hunting for better solutions.

And there are other, rare diseases that still remain a mystery, such as prion diseases. These diseases are caused by misfolded proteins in the brain — called prions — which cause other proteins to misfold in a chain reaction that ultimately causes brain damage and death.

Most prion disease cases would not be considered infectious; they stem from genetic mutations that are inherited or arise spontaneously. However, people can rarely develop them after eating meat contaminated with prions or being exposed to them during medical procedures. Examples include variant Creutzfeldt-Jakob Disease (vCJD), which people can get after consuming beef from cows with "mad cow disease," and Kuru, which famously affected the Fore people in Papua New Guinea.

"Prions have been looked at for decades, but I think they're still trying to figure out what the ultimate trigger is there," said Rodney E. Rohde, an infectious disease specialist at Texas State University. Although they are extremely rare, prion diseases all have one thing in common: Once you get them, there is no cure, and death can often occur within weeks of symptoms beginning to show.

What makes diseases like these so fatal? One factor is the disease's evolutionary history. If a disease has infected human hosts for tens of thousands of years, our bodies have the opportunity to try to build up a defense to it, which increases our odds of survival. However, if humans are an accidental, or dead-end host — as is the case for diseases like rabies — the disease isn't built to keep us alive, as we aren't its main hosts. In those cases, we usually haven't developed a suitable immune response to fight it without the help of medical treatment.

Rabies, for example, does engender an immune response in humans, but the response is not fast enough to defeat the virus before it infects the brain and kills the host. "Some pathogens have way more of a diabolical and notorious nature," Rohde told Live Science. "They flood the immune system so the body can't adapt quick enough."