Illness-inducing bacteria, meet nano-engineered cotton–and a quick death. Researchers have created a new “filter” that zaps bacteria with electric fields to clean drinking water. They say their system may find use in developing countries since it requires only a small amount of voltage (a couple of car batteries, a stationary bike, or a solar panel could do the job) and cleans water an estimated 80,000 times faster than traditional devices.

Instead of trapping bacteria in small pores like many slow-going traditional filters, the cotton and silver nanowire combo uses small electric currents running through the nanowires to kill the bacteria outright. In a paper to appear in the journal Nano Letters researchers say that 20 volts and 2.5 inches worth of the material killed 98 percent of Escherichia coli in the water they tested in their lab setup.

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From Ed Yong:

In 8 May 1980, the World Health Organisation declared that “the world and its peoples have won freedom from smallpox.” Through decades of intense vaccination, this once fatal disease had been wiped out. It was a singular victory and having won it, countries around the world discontinued the vaccination programmes. After all, why protect against a disease that no longer exists (save in a few isolated stocks)?

Unfortunately, this is not a rhetorical question. The smallpox vaccine did more than protect against smallpox. It also reduced the risk of contracting a related illness called monkeypox, which produces the same combination of scabby bumps and fever. It’s milder than smallpox but it’s still a serious affliction. In Africa, where monkeypox originates from, it kills anywhere from 1-10% of those who are infected. And more and more people are becoming infected.

Read the rest of this post at Not Exactly Rocket Science.

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Image: U.S. Air Force

In this week’s Nature Medicine, a study brings a ray of success in researchers’ quest to fight the deadly viruses Ebola and Marburg. Testing a new approach on monkeys, scientists at the U.S. Army Medical Research Institute of Infectious Diseases saw most of the monkeys survive a normally fatal Ebola infection—and all of them who had Marburg lived.

Within an hour of infecting the primates, researchers gave them antisense phosphorodiamidate morpholino oligomers, or PMOs.

The morpholino oligomers are a new class of drugs in a family of what is known as antisense nucleotides. Antisense nucleotides are designed to bind tightly to specific areas of viral messenger RNA, blocking replication. Such compounds already are being used to treat certain types of cancer and cytomegalovirus infections, and they are being tested against HIV [Los Angeles Times].

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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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You can’t defeat what you can’t identify. That’s part of the human body’s problem with HIV–a virus that mutates constantly. Most antibodies can identify, latch onto, and neutralize only certain variants of the virus, or none at all. But two new studies published in Science yesterday point to two antibodies that almost always hits their targets--neutralizing some 90 percent of the most common HIV strains.

Scientists hope to eventually use their knowledge of these antibodies to develop a vaccine, but this is not an easy task.

“The path forward isn’t as clear as we’d like it to be, but we are turning a corner, I think,” says David Montefiori, a viral immunologist at Duke University Medical Center in Durham, N.C., who was not involved in the research. [Science News]

But first, how did they find these antibodies?

Step 1: Learning from a Survivor

Researchers at the National Institute of Allergy and Infectious Diseases looked at the blood of a 60-year-old African American man who had survived with HIV for 20 years.

The HIV antibodies were discovered in the cells of a 60-year-old African-American gay man, known in the scientific literature as Donor 45, whose body made the antibodies naturally…. Donor 45′s antibodies didn’t protect him from contracting HIV. That is likely because the virus had already taken hold before his body produced the antibodies. He is still alive, and when his blood was drawn, he had been living with HIV for 20 years. [Wall Street Journal]

Something about Donor 45′s antibodies were keeping the virus at bay or, more specifically, keeping it from binding with certain white blood cells to infect and destroy them.

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A rare but potentially life-threatening tropical fungus is spreading through the Pacific Northwest, researchers have reported.

The culprit is a new strain of the Cryptococcus gatti fungus, and is known to have been lethal in 25 percent of the reported human infections. C. gatti usually only infects transplant and AIDS patients and people with otherwise compromised immune systems, but the new strain is genetically different, the researchers said. “This novel fungus is worrisome because it appears to be a threat to otherwise healthy people” [Reuters], says lead researcher Edmond Byrnes.

However, scientists aren’t sounding a public health alert because the death toll is still very small–in the United States, five of the 21 people who contracted the fungus in the have died.

The new strain of the C. gatti fungus has been found in both humans and animals like cats, dogs, and sheep, researchers write in the journal PLoS Pathogens. Because its such a rare infection, researchers warn that physicians could potentially miss diagnosing it.

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It’s a big year for South Africa: Less than four months remain until the first matches of the World Cup, when much of the planet’s attention will turn to the country. But being under the spotlight of international sport makes it difficult to hide a country’s less glamorous bits, as China and Canada have found out trying to shield pollution and addiction problems from the glare of the last couple Olympiads. In June, the microscope will turn to South Africa and its ongoing AIDS crisis.

This month one of the country’s health leaders has renewed his call for blanket HIV testing and anti-retroviral drug dispersal to all patients, which he says can stop the AIDS epidemic once and for all–without having to find a vaccine against the virus or a cure for the disease.

Brian Williams’s idea isn’t new. The former World Health Organization figure, who is now one of South Africa’s top health officials, came out with a paper more than a year ago explaining his model for how effective universal testing and immediate therapy could be. But this week at the American Association for the Advancement of Science meeting in San Diego he expounded on his proposal: “The epidemic of HIV is really one of the worst plagues of human history…. I hope we can get to the starting line in one to two years and get complete coverage of patients in five years. Maybe that’s being optimistic, but we’re facing Armageddon” [The Guardian].

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An estimated three in 1,000 people suffers from the mysterious affliction chronic fatigue syndrome. Those people were probably enthusiastic in October when a team of U.S. medical researchers released a study arguing that not only is the syndrome real (some doctors dismissed it as purely psychological “yuppie flu”), but also that they’d connected it to a specific virus. DISCOVER covered the hubbub after the paper came out in the journal Science.

But now, in a study in PLoS One, a British research team has cast doubt on the American team’s findings, saying there’s no conclusive link between the virus and chronic fatigue syndrome, which is also known as myalgic encephalomyelitis.

The U.S. team’s findings sounded robust when they came out. They found the murine leukaemia virus-related virus (XMRV) in blood samples of 68 of 101 patients diagnosed with chronic fatigue syndrome. Just eight out of 101 healthy “controls” drawn at random from the same parts of the US also tested positive, suggesting that XMRV played a key role in triggering the condition [The Independent]. When the scientists from Imperial and Kings colleges in London attempted to replicate these findings, however, they found nothing of the sort. Of the 186 people with the syndrome that this team tested, not one showed signs of XMRV, or of any related virus.

Study coauthor Myra McClure of the Imperial College also criticized the U.S. team and the journal Science for rushing the findings into print in October. “When you’ve got such a stunning result you want to be absolutely clear that you are 1,000 per cent right and there are things in that [previous study] I would not have done. I would have waited. I would have stalled a little” [The Independent], she said.

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The mysterious and deadly facial cancer that has sent populations of Tasmanian devils crashing now has a known source, according to findings published last week in the journal Science. The ailment originated in nerve cells of the devils themselves.

A genetic analysis of tumors from Tasmanian devils widely separated geographically shows that all the tumors are virtually identical and distinct from the animals’ own genomes…. The tumors probably arose from Schwann cells, which normally play a role in protecting and cushioning nerves [Los Angeles Times]. Tasmanian devils have a lot of nerves on their faces near their whiskers, the researchers note, and therefore have Schwann cells there. Team member Jenny Graves says the tumor could have arisen in one cell in one animal two decades ago, and then passed from devil to devil as they bit each other. The disease has already killed 60 percent of the population.

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Last week, seemingly out of nowhere, Oklahoma State University president Burns Hargis pulled the plug on a federally funded research project that would have tested anthrax vaccines on baboons, and euthanized the primates at the experiment’s end. This week more details are beginning to come out regarding why Hargis made his call. Basically, his office says, they didn’t want to deal with possibly violent animal rights protesters.

The plan was to expose the animals to the spores of the attenuated Sterne strain of anthrax and eventually advance to the Ames strain — the fully encapsulated and virulent form of the bacterium that was used in the anthrax attacks of 2001 — and observe the pathobiology of infection. It was part of a collaborative multi-institutional NIH grant originally awarded for $12 million in 2004, and renewed in September of this year for another $14.3 million [The Scientist]. Oklahoma State would have hosted only a small part of the research, and the university’s animal testing committee approved the project unanimously.

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News that an Iowa cat has been diagnosed with swine flu has sparked a new round of concerns, as pet-owners worry both that their furry companions could get sick, and that their pets could pass the virus on to other humans. The 13-year-old, mixed-breed cat showed the symptoms of lethargy, sneezing and coughing typical to sick cats [ABC News]. The veterinarians who treated him say that several people in the cat’s home had been experiencing flu-like symptoms, and lab work confirmed that the feline had the H1N1 virus.

Happily, the cat is expected to make a full recovery. But both vets and public health officials are rushing to reassure the public that one sick cat probably does not indicate a coming crisis. While it’s possible that more cats will be diagnosed with the swine flu, vets point out that the virus was circulating for more than six months before the first cat case was discovered, indicating that the virus probably doesn’t jump from species to species very easily. Doctors also note that there’s very little chance that a cat will spread the virus to humans: Even when inter-species transmissions do occur, the H1N1 virus seems more likely to move from humans to animals, rather than the other way around [HealthDay News].

There have been no reported cases of dogs catching the virus, but there is one type of pet that is known to be vulnerable. Ferrets are generally susceptible to the seasonal flu, and the AP reported Wednesday that H1N1 infection has been confirmed in two ferrets, one in Nebraska and the other in Oregon. “Not only can they be infected with the flu but they are clearly able to transmit the flu back to people,” Treanor said [HealthDay News]. But the bottom line appears to be: Unless you’re a ferret-owner, you probably have nothing to worry about.

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Image: flickr / theogeo

As swine flu is now prevalent in 41 states, doctors are getting plenty of chances to study the workings of the disease. They now know that in severely ill patients, intense inflammation in the lungs prevents oxygen from being tranfered to the blood stream. Says physician Robert Fowler: “Most patients are still able to take breaths, but these breaths are ineffective” [Science News]. That oxygen deprivation can cause widespread organ damage.

The speed with which swine flu patients can go downhill marks the H1N1 virus as strikingly different from the seasonal flu virus, doctors say. “In severe cases, patients generally begin to deteriorate around three to five days after symptom onset. Deterioration is rapid, with many patients progressing to respiratory failure within 24 hours, requiring immediate admission to an intensive care unit” [Reuters], says World Health Organization doctor Nikki Shindo.

Doctors say that severely ill patients should promptly be put on breathing machines and given antiviral drugs like Tamiflu. In cases where patients’ respiratory systems have already crashed, some doctors are trying a treatment called extracorporeal membrane oxygenation, in which blood is extracted from each patient and passed through a machine that adds oxygen [Science News].

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Sufferers of the baffling ailment known as chronic fatigue syndrome, take hope: For the first time, there’s good evidence that the symptoms aren’t just in your head, and experimental treatments may be coming soon.

Over the past few decades, the syndrome has been a source of intense frustration both to patients diagnosed with it and doctors who try to treat it. The diffuse collection of symptoms can include incapacitating fatigue, muscle aches, headaches, problems with concentration. Doctors, meanwhile, have been mystified by the cause of the symptoms, and some have suggested that it’s a psychiatric problem, leading to the coining of the dismissive label “yuppie flu.”

Now, researchers report that 68 of 101 patients with the syndrome, or 67 percent, were infected with an infectious virus, xenotropic murine leukemia virus-related virus, or XMRV. By contrast, only 3.7 percent of 218 healthy people were infected. Continuing work after the paper was published has found the virus in nearly 98 percent of about 300 patients with the syndrome, said Dr. Judy A. Mikovits, the lead author of the paper [The New York Times]. While it hasn’t been proven that the virus causes the syndrome, the link opens new avenues of research and treatment.

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Swine flu vaccines have arrived! Or more accurately, limited amounts of the first available vaccine, a nasal spray, have been delivered to distribution points around the country, and several states began vaccinating health care workers and young children on Monday. It’s not a moment too soon: The Centers for Disease Control and Prevention have announced that flu is now widespread in most of the United States. The infections are “overwhelmingly” pandemic H1N1 influenza, commonly known as swine flu. The flu season generally lasts well into May, so many months of uncertainties lie ahead [Los Angeles Times].

CDC director Thomas Frieden says that so far, vaccine “demand is outstripping supply, but we expect that fairly soon supply will be outstripping demand.” … Over the next two to three weeks, tens of millions of additional doses will become available [Los Angeles Times]. The injectable form of the vaccine will be ready for distribution next week.

Now that the vaccines have been successfully hustled off the assembly lines, the next daunting challenge for public health officials is convincing people to go get vaccinated. Myths and worries about the vaccine have spread on talk radio and anti-vaccine Web sites [The New York Times], with even celebrities like Bill Maher unhelpfully chiming in via Twitter. At a Tuesday press conference, Frieden strongly refuted one of the most commonly voiced concerns: that in rushing the vaccine through production, it wasn’t properly tested for safety.

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A team of researchers recently discovered that Tamiflu, the leading flu-fighting drug,  is accumulating in rivers downstream from sewage-treatment plants in Kyoto. How is this possible? Tamiflu’s active ingredient, oseltamivir phosphate, is excreted in the urine of people taking the medication. Concerns are now building that birds, which are natural influenza carriers, are being exposed to waterborne residues of Tamiflu’s active form and might develop and spread drug-resistant strains of seasonal and avian flu [Science News]. The resistant virus strains would be of the conventional seasonal or avian flu variety, not the H1N1 swine flu strain that is currently pandemic in humans. Seasonal flu, however, kills thousands of people each year.

Study coauthor Gopal Ghosh explains that the team took measurements during normal flu season, and found concentrations that seem “high enough to lead to antiviral resistance in waterfowl” [Science News]. Computer models show that oseltamivir phosphate will survive sewage treatment, but it should break down when exposed to sunlight and its concentrations should decrease by half every three weeks. The high concentrations were found during a period where 1,738 flu cases were reported in Kyoto, according to the study, published in the journal Environmental Health Perspectives. In the United States, Tamiflu is only recommended for the very sick or those with compromised immune system, while Japan has a more liberal policy.

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Image: flickr / law_keven