Shiga toxin is nasty stuff. If you are infected with a Shiga-producing bacterium, like Shigella dysenteriae or some E. coli strains, there is no clear treatment: if you are given antibiotics, your infected cells will explode, spraying the toxin all over neighboring cells and exacerbating your symptoms. Each year, 150 million people are infected with Shiga-producing bacteria, which cause dysentery and food poisoning, and a million of those die. The lack of effective treatment for such Shiga toxicosis infections is one of the main reasons this year’s outbreak of E. coli poisoning in Europe was so deadly, with more than 3,700 people infected and 45 dead. But now scientists studying how the toxin makes its way around the cell have discovered that treating mice with the metal element manganese makes them resistant to Shiga poisoning. Since manganese’s chemistry is already well understood and it’s readily available, the possibility of using it as a treatment is exciting.

Here’s how manganese blocks Shiga’s spread, according to the group’s experiments in cultured human cells:

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One of the most universally agreed upon facts in the world is that raw cookie dough is delicious. But it can also make you sick, though the ingredient to blame may be a surprise: In study published online in the journal Clinical Infectious Disease, researchers linked the 2009 outbreak of E. coli O157:H7  to tainted flour in Nestlé’s Toll House ready-to-bake cookie dough. Although they haven’t conclusively pinpointed the culprit, flour is the prime suspect after a detailed traceback investigation, since the other ingredients—including eggs—underwent a “kill step” to eliminate germs. In homemade cookie dough, eggs remain a possible source of contamination, particularly from Salmonella.

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E. coli.

Scientists have generally thought that superbugs are weaker than normal bacteria in drug-free environments because they expend more resources to maintain resistances, as seen by their slower cell-division rates. But researchers have now reported in the journal PLoS Genetics that some antibiotic-resistant superbugs can out-perform their normal cousins even when there are no drugs present. The results suggest that fighting these resilient bacteria will take more than just curbing antibiotic use.

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Fenugreek seeds

The European Food Safety Authority has released a scientific report on the deadly E. coli outbreak that has sickened more than 3,500 people and killed at least 44 in the last seven weeks, and the news is grim: the apparent source of the contamination, a shipment of fenugreek seeds from Egypt, has been scattered all across the continent, making recall tricky and new outbreaks likely until the seed packets reach their expiration date in three years. Maryn McKenna of Superbug expertly breaks down the report in all its chilling detail:

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What’s the News: A massive outbreak of E. coli is spreading through Europe, with 17 people dead in the last two weeks and 1,500 people sickened in Germany alone, where the outbreak began. Authorities are still trying to figure out where the outbreak originated and how it can be treated.

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Staphylococcus aureus

What’s the News: Adding sugar to certain antibiotics can boost their bacteria-battling ability, according to a study published today in Nature. In particular, sugar helps the drugs wipe out persisters, bacteria that evade antibiotics by essentially going dormant only to flare up again once the danger has passed. This technique could lead to the development of inexpensive, more effective treatments for bacterial infections.

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E. coli

What’s the News: Some bacteria can live in extreme “hypergravity,” found a new study published in the Proceedings of the National Academy of Sciences, surviving and reproducing in forces 400,000 times greater than what’s felt on Earth. These findings fit with the idea that microbes carried on meteorites or other debris—a ride that would have subjected them to hypergravity-strength forces—may be the ancestors of life on Earth.

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Cockroaches take advantage of our messy hospitality, skulking around in the cracks and holes of our houses and devouring the scraps we leave behind. Soon, though, maybe we’ll be the ones taking advantage of their fondness for filth.

The brains of these insects carry some serious antibiotics—strong enough to slaughter bacteria that have evolved resistance to the hospital antibiotics we use. The researchers presented their work at the Society for General Microbiology meeting this week in England, and say that while the finding is terrific, it’s no surprise given the roaches’ living circumstances:

“Some of these insects live in the filthiest places ever known to man,” says Naveed Khan, coauthor of the new study. “These insects crawl on dead tissue, in sewage, in drainage areas. We thought, ‘How do they cope with all the bacteria and parasites?’” [Science News]

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The antibiotics-resistant superbug that emerged in South Asia appears to have claimed its first life. According to doctors who treated a man in Belgium, he went to a hospital in Pakistan after a car accident, and there he picked up the bacterial infection. While the man died back in June, his doctors announced today that he carried the superbug.

This new health scare intensified this week after researchers published a study in The Lancet Infectious Diseases characterizing “a new antibiotic resistance mechanism” in the U.K., India, and Pakistan. How bad is this “mechanism?”

It’s bad:

The problem isn’t a particular kind of bacteria. It’s a gene that encodes an enyzme called New Delhi metallo-lactamase-1 (NDM-1). Bacteria that carry it aren’t bothered by traditional antibiotics, or even the drugs known as carbapenems deployed against antibiotic-resistant microbes.

The NDM-1 gene is a special worry because it is found in plasmids — DNA structures that can easily be copied and then transferred promiscuously among different types of bacteria. These include Escherichia coli, the commonest cause of urinary tract infections, and Klebsiella pneumoniae, which causes lung and wound infections and is generated mainly in hospitals [AFP].

It’s no worse than what we had before:

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One might think that identical-twin bacteria—clones of each other—would grow up and live very similarly. But a study published today in Science that examined individual bacterial cells in detail found that genetically identical E. Coli cells actually seem to express their genes quite differently, simply because of the random accidents of how their molecular machinery happens to operate.

“The paper is quite rich,” said Sanjay Tyagi, a molecular biologist at New Jersey Medical School who was not involved in the research [but published a perspectives piece on it]. “People think that if an organism has a particular genotype, it determines its phenotype [observable characteristics]–that there’s a one-to-one relationship,” said Tyagi. “But as it turns out, [differences in gene expression] can arise just from chance.” [The Scientist]

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Most of us associate the bacteria E. coli with nasty stomach ailments. But a new study published in Nature magazine suggests E. coli can not just turn stomachs, but could potentially turn the wheels of your car, since a genetically engineered strain of the bacteria has produced clean, road-ready biodiesel.

The bacteria can work on any type of biomass, including wood chip, switchgrass, and the plant parts that are left behind after a harvest–all contain cellulose, a structural material that comprises much of a plant’s mass. Study coauthor Jay Keasling and his colleagues report engineering E. coli bacteria to synthesize and excrete the enzyme hemicellulase, which breaks down cellulose into sugars. The bacteria can then convert those sugars into a variety of chemicals–diesel fuel among them. The final products are excreted by the bacteria and then float to the top of the fermentation vat before being siphoned off [Technology Review].

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Eating red meat could make your body more vulnerable to a dangerous bacterial toxin, according to a new study. A sugar molecule, Neu5Gc, found in beef, lamb, pork, and unpasteurized milk can attach itself to the cells lining the human intestines and act as a magnet for toxins produced by certain strains of E. coli, often carried in the same meats. The result is bloody diarrhea and sometimes death. “This uncovered the first example of bacterium causing disease in humans by targeting a molecule which is incorporated into our bodies through what we eat,” [ABC Science] says researcher Travis Beddoe.

The study, published in Nature [subscription required], was conducted in petri dishes using mouse tissues and human cells. The scientists tested human gut and kidney cells steeped in these sugar molecules and discovered that the toxin was about seven times more likely to bind to these cells if the sugar was present. It is still “not clear how to extrapolate this precisely to the human body,” [Science News] says co-author Ajit Varki. That is, researchers don’t know exactly what it means for human health yet. (more…)

A “sustainable chemical” company called Genomatica has developed a way to use sugar and genetically engineered bacteria to produce a common industrial chemical that’s usually produced using petroleum, and which is found in everything from Spandex to car bumpers. By using sugar from sugar cane as a feedstock, industrial chemical companies can get a cheaper alternative to petroleum-derived chemicals, while investing in processes that are less polluting and nontoxic, said Genomatica CEO Chris Gann [CNET].

Genomatica produces the chemical, 1,4-butanediol (BDO), by feeding pure glucose derived from sugarcane to E. coli bacteria, which has been engineered to produce BDO. “We have engineered the organism such that it has to secrete that product in order for it to grow,” says [company president] Christophe Schilling…. “The interests of the organism are aligned with our interests: It grows faster when it produces more” [Scientific American].

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Villagers living deep in the Guyanese rain forest have developed resistance to an antibiotic they’ve never taken, and a malaria drug may be to blame. Researchers say the malaria drug is chemically similar to a type of widely used antibiotic, and they believe that the E. coli bacteria in the villagers’ guts evolved a broad resistance to both medications.

Antibiotic resistance is a major problem in Western countries, where strains of disease-causing bacteria such as Staphylococcus have adapted to beat some of the most commonly-used drugs. However, for a resistant strain to develop, bacteria usually need to be exposed to the drug involved [BBC News]. In this case, researchers say that a cheap malaria medication called chloroquine is similar enough to the antibiotic ciprofloxacin to allow the E. coli to develop defenses to the unknown drug.

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