Posts Tagged ‘microbiology’

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by BRET STETKA

Dr. Leslie Norins is willing to hand over $1 million of his own money to anyone who can clarify something: Is Alzheimer’s disease, the most common form of dementia worldwide, caused by a germ?

By “germ” he means microbes like bacteria, viruses, fungi and parasites. In other words, Norins, a physician turned publisher, wants to know if Alzheimer’s is infectious.

It’s an idea that just a few years ago would’ve seemed to many an easy way to drain your research budget on bunk science. Money has poured into Alzheimer’s research for years, but until very recently not much of it went toward investigating infection in causing dementia.

But this “germ theory” of Alzheimer’s, as Norins calls it, has been fermenting in the literature for decades. Even early 20th century Czech physician Oskar Fischer — who, along with his German contemporary Dr. Alois Alzheimer, was integral in first describing the condition — noted a possible connection between the newly identified dementia and tuberculosis.

If the germ theory gets traction, even in some Alzheimer’s patients, it could trigger a seismic shift in how doctors understand and treat the disease.

For instance, would we see a day when dementia is prevented with a vaccine, or treated with antibiotics and antiviral medications? Norins thinks it’s worth looking into.

Norins received his medical degree from Duke in the early 1960s, and after a stint at the Centers for Disease Control and Prevention he fell into a lucrative career in medical publishing. He eventually settled in an admittedly aged community in Naples, Fla., where he took an interest in dementia and began reading up on the condition.

After scouring the medical literature he noticed a pattern.

“It appeared that many of the reported characteristics of Alzheimer’s disease were compatible with an infectious process,” Norins tells NPR. “I thought for sure this must have already been investigated, because millions and millions of dollars have been spent on Alzheimer’s research.”

But aside from scattered interest through the decades, this wasn’t the case.

In 2017, Norins launched Alzheimer’s Germ Quest Inc., a public benefit corporation he hopes will drive interest into the germ theory of Alzheimer’s, and through which his prize will be distributed. A white paper he penned for the site reads: “From a two-year review of the scientific literature, I believe it’s now clear that just one germ — identity not yet specified, and possibly not yet discovered — causes most AD. I’m calling it the ‘Alzheimer’s Germ.’ ”

Norins is quick to cite sources and studies supporting his claim, among them a 2010 study published in the Journal of Neurosurgery showing that neurosurgeons die from Alzheimer’s at a nearly 2 1/2 times higher rate than they do from other disorders.

Another study from that same year, published in The Journal of the American Geriatric Society, found that people whose spouses have dementia are at a 1.6 times greater risk for the condition themselves.

Contagion does come to mind. And Norins isn’t alone in his thinking.

In 2016, 32 researchers from universities around the world signed an editorial in the Journal of Alzheimer’s Disease calling for “further research on the role of infectious agents in [Alzheimer’s] causation.” Based on much of the same evidence Norins encountered, the authors concluded that clinical trials with antimicrobial drugs in Alzheimer’s are now justified.

NPR reported on an intriguing study published in Neuron in June that suggested that viral infection can influence the progression of Alzheimer’s. Led by Mount Sinai genetics professor Joel Dudley, the work was intended to compare the genomes of healthy brain tissue with that affected by dementia.

But something kept getting in the way: herpes.

Dudley’s team noticed an unexpectedly high level of viral DNA from two human herpes viruses, HHV-6 and HHV-7. The viruses are common and cause a rash called roseola in young children (not the sexually transmitted disease caused by other strains).

Some viruses have the ability to lie dormant in our neurons for decades by incorporating their genomes into our own. The classic example is chickenpox: A childhood viral infection resolves and lurks silently, returning years later as shingles, an excruciating rash. Like it or not, nearly all of us are chimeras with viral DNA speckling our genomes.

But having the herpes viruses alone doesn’t mean inevitable brain decline. After all, up to 75 percent of us may harbor HHV-6 .

But Dudley also noticed that herpes appeared to interact with human genes known to increase Alzheimer’s risk. Perhaps, he says, there is some toxic combination of genetic and infectious influence that results in the disease; a combination that sparks what some feel is the main contributor to the disease, an overactive immune system.

The hallmark pathology of Alzheimer’s is accumulation of a protein called amyloid in the brain. Many researchers have assumed these aggregates, or plaques, are simply a byproduct of some other process at the core of the disease. Other scientists posit that the protein itself contributes to the condition in some way.

The theory that amyloid is the root cause of Alzheimer’s is losing steam. But the protein may still contribute to the disease, even if it winds up being deemed infectious.

Work by Harvard neuroscientist Rudolph Tanzi suggests it might be a bit of both. Along with colleague Robert Moir, Tanzi has shown that amyloid is lethal to viruses and bacteria in the test tube, and also in mice. He now believes the protein is part of our ancient immune system that like antibodies, ramps up its activity to help fend off unwanted bugs.

So does that mean that the microbe is the cause of Alzheimer’s, and amyloid a harmless reaction to it? According to Tanzi it’s not that simple.

Tanzi believes that in many cases of Alzheimer’s, microbes are probably the initial seed that sets off a toxic tumble of molecular dominoes. Early in the disease amyloid protein builds up to fight infection, yet too much of the protein begins to impair function of neurons in the brain. The excess amyloid then causes another protein, called tau, to form tangles, which further harm brain cells.

But as Tanzi explains, the ultimate neurological insult in Alzheimer’s is the body’s reaction to this neurotoxic mess. All the excess protein revs up the immune system, causing inflammation — and it’s this inflammation that does the most damage to the Alzheimer’s-afflicted brain.

So what does this say about the future of treatment? Possibly a lot. Tanzi envisions a day when people are screened at, say, 50 years old. “If their brains are riddled with too much amyloid,” he says, “we knock it down a bit with antiviral medications. It’s just like how you are prescribed preventative drugs if your cholesterol is too high.”

Tanzi feels that microbes are just one possible seed for the complex pathology behind Alzheimer’s. Genetics may also play a role, as certain genes produce a type of amyloid more prone to clumping up. He also feels environmental factors like pollution might contribute.

Dr. James Burke, professor of medicine and psychiatry at Duke University’s Alzheimer’s Disease Research Center, isn’t willing to abandon the amyloid theory altogether, but agrees it’s time for the field to move on. “There may be many roads to developing Alzheimer’s disease and it would be shortsighted to focus just on amyloid and tau,” he says. “A million-dollar prize is attention- getting, but the reward for identifying a treatable target to delay or prevent Alzheimer’s disease is invaluable.”

Any treatment that disrupts the cascade leading to amyloid, tau and inflammation could theoretically benefit an at-risk brain. The vast majority of Alzheimer’s treatment trials have failed, including many targeting amyloid. But it could be that the patients included were too far along in their disease to reap any therapeutic benefit.

If a microbe is responsible for all or some cases of Alzheimer’s, perhaps future treatments or preventive approaches will prevent toxin protein buildup in the first place. Both Tanzi and Norins believe Alzheimer’s vaccines against viruses like herpes might one day become common practice.

In July of this year, in collaboration with Norins, the Infectious Diseases Society of America announced that they plan to offer two $50,000 grants supporting research into a microbial association with Alzheimer’s. According to Norins, this is the first acknowledgement by a leading infectious disease group that Alzheimer’s may be microbial in nature – or at least that it’s worth exploring.

“The important thing is not the amount of the money, which is a pittance compared with the $2 billion NIH spends on amyloid and tau research,” says Norins, “but rather the respectability and more mainstream status the grants confer on investigating of the infectious possibility. Remember when we thought ulcers were caused by stress?”

Ulcers, we now know, are caused by a germ.

https://www.npr.org/sections/health-shots/2018/09/09/645629133/infectious-theory-of-alzheimers-disease-draws-fresh-interest?ft=nprml&f=1001

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A team of American and Russian computer scientists has developed an algorithm that can rapidly search databases to discover novel variants of known antibiotics — a potential boon in fighting antibiotic resistance.

In just a few hours, the algorithm, called VarQuest, identified 10 times more variants of peptidic natural products, or PNPs, than all previous PNP discovery efforts combined, the researchers report in the latest issue of the journal Nature Microbiology. Previously, such a search might have taken hundreds of years of computation, said Hosein Mohimani, assistant professor in Carnegie Mellon University’s Computational Biology Department.

“Our results show that the antibiotics produced by microbes are much more diverse than had been assumed,” Mohimani said. VarQuest found more than a thousand variants of known antibiotics, he noted, providing a big picture perspective that microbiologists could not obtain while studying one antibiotic at a time.

Mohimani and Pavel A. Pevzner, professor of computer science at the University of California, San Diego, designed and directed the effort, which included colleagues at St. Petersburg State University in Russia.

PNPs have an unparalleled track record in pharmacology. Many antimicrobial and anticancer agents are PNPs, including the so-called “antibiotics of last resort,” vancomycin and daptomycin. As concerns mount regarding antibiotic drug resistance, finding more effective variants of known antibiotics is a means for preserving the clinical efficacy of antibiotic drugs in general.

The search for these novel variants received a boost in recent years with the advent of high-throughput methods that enable environmental samples to be processed in batches, rather than one at a time. Researchers also recently launched the Global Natural Products Social (GNPS) molecular network, a database of mass spectra of natural products collected by researchers worldwide. Already, the GNPS based at UC San Diego contains more than a billion mass spectra.

The GNPS represents a gold mine for drug discovery, Mohimani said. The VarQuest algorithm, which employs a smarter way of indexing the database to enhance searches, should help GNPS meet its promise, he added.

“Natural product discovery is turning into a Big Data territory, and the field has to get prepared for this transformation in terms of collecting, storing and making sense of Big Data,” Mohimani said. “VarQuest is the first step toward digesting the Big Data already collected by the community.”

Reference: Gurevich, A., Mikheenko, A., Shlemov, A., Korobeynikov, A., Mohimani, H., & Pevzner, P. A. (2018). Increased diversity of peptidic natural products revealed by modification-tolerant database search of mass spectra. Nature Microbiology, 1. https://doi.org/10.1038/s41564-017-0094-2

https://www.technologynetworks.com/informatics/news/algorithm-unearths-over-1000-antibiotic-proteins-in-a-few-hours-296639?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=60184554&_hsenc=p2ANqtz-9YDsGiTl44CBfQpgNtYgc43xBeVKpAbPZym9Lh_GzlHoEVts0rAwMhHHXIDam3Jit0D3aTqKGhCceUREgr6sZfLGMWpQ&_hsmi=60184554

BR3GWM bacteria streaked and grows on an agar plate in the lab

BR3GWM bacteria streaked and grows on an agar plate in the lab

by SARAH ZHANG

THE WOMAN HARBORING E. coli resistant to colistin did not know it, and it’s only luck that we do. Her doctor would have never prescribed that last-resort antibiotic for a routine urinary tract infection—it can cause serious kidney damage. But her doctor did take a urine sample, which ended up at the Walter Reed National Military Medical Center, where researchers had recently started testing for colistin resistance. The test came back positive. Then the came scary headlines about a new superbug in the US.

Superbugs are bacteria with genetic mutations that let them survive humanity’s harshest weapons in germ warfare: antibiotics. The gene behind this E. coli’s colistin resistance is called mcr-1. It first emerged last year when Chinese researchers found it in samples from hospital patients and raw pork. Why pork? Colistin’s serious side effects mean it’s no longer used as a human antibiotic in many countries. But in China, farmers have been adding it by the pound into feed to fatten animals up.

Once epidemiologists knew to look for mcr-1, they found it in Malaysia, England and then the rest of Europe. It was only a matter of time before colistin resistance turned up in the US. On the same day news came out about this woman’s colistin-resistant UTI, the Department of Health and Human Services also announced it found mcr-1 in a sample from a pig intestine.

Colistin is not used in animal feed in the US, so it’s unclear how colistin-resistant bacteria ended up infecting that woman—or that pig. But food and people move freely across borders. And more even seriously, US animal farmers do use other antibiotics—even human ones—on chicken, pigs, and cows. A growing body of research has linked antibiotic use in food animals to drug-resistant bouts of food poisoning from salmonella, campylobacter, and MRSA. Even more interesting is a possible link between antibiotics on meat and urinary tract infections, which science journalist Maryn McKenna has covered extensively. The Food and Drug Administration issued a guidance last year for farms to phase out medically important antibiotics, though only voluntarily.


The Rise of the Drug-Resistant UTI

Urinary tract infections are damn common—annoyingly common if you ask many women. And antibiotic resistant UTIs are on the rise, too: From 2000 to 2010, the number of UTIs resistant to the antibiotic Cipro went from 3 percent to 17.1 percent. Because UTIs afflict so many people, they’re fairly representative antibiotic resistance out there in people community—especially compared to the resistant infections that epidemiologists tend to study most intensely, like ones that kill already sick hospital patients. “UTIs are a good picture of what people are being exposed to on a daily basis” says Amee Manges, an epidemiologist at the University of British Columbia. Case in point: That colistin-resistant bacteria in the woman from Philadelphia.

Manges has spent the past fifteen years studying the link between antibiotic use in meat production, especially poultry, and UTIs. Back when she was working on her doctoral thesis at the University of California, Berkeley, she kept seeing young, otherwise healthy students with UTIs. Originally, she thought she was going to track sexual transmission of the E. coli that caused such infections. With that kind of sporadic sexual transmission, she should have seen many different strains. But when she DNA fingerprinted the bacteria, she found they were all the same strain—the same pattern you’d see from a single source, like if the campus cafeteria gave everyone food poisoning. She was never able to trace those UTI cases back to the original source, but she’s been working on the question ever since.

UTIs are so hard to trace because the infection might not set in until long after a patient first acquired to bacteria. Say a woman eats some undercooked chicken. “The bacteria just hangs out in your intestine for months or possibly years,” says Manges. Then you get risk factor for UTI—sex or a catheter insertion—and that bacteria makes its way from, ahem, the end of your gut to the urethra. But getting people to remember what they ate a week ago is hard. Getting people to remember what they ate a year ago? Hahaha.

The Surveillance Net
Nevertheless, Manges and others have found that strains on meat match strains found in UTIs. Because of the difficulty in tracing UTIs, that evidence is not as ironclad as the evidence for antibiotics use and antibiotic-resistant food poisoning. With routine surveillance of UTIs though, epidemiologists could get a better handle of not only resistant bacteria that come from meat—but also other sources like drinking water or travel or family members being in the hospital. But that surveillance doesn’t happen. “There’s no organized infrastructure to get a good handle about resistance rates across communities,” says Kalpana Gupta, an infectious disease specialist at Boston University.

When patients walk in with UTIs, doctors will often hand out antibiotics without doing a urine culture. Growing the bacteria takes two days—testing for antibiotic-resistance a third—and by that time the patient is usually on the mend already. The fact that the women in Philadelphia got tested was unusual. The fact that her sample was tested against colistin even more so. As Gupta says, “Colistin is not something we would even use to treat UTIs.” (Resistance to another class of antibiotics triggered that extra test in this case.)

The Centers for Disease Control and Prevention is now following up with the woman in Philadelphia to find out she ended up with that colistin-strain of E. coli, which has never been found in the US before. Her infection was fortunately not resistant to all antibiotics. But what makes the colistin-resistance gene mcr-1 so worrisome is that it’s on a small loop of DNA that different bacteria easily swap back and forth. Someday, another bacteria already immune to all other antibiotics will pick up mcr-1, too. It’s only a matter of time.

The wider the surveillance net though, the more quickly we’ll find it.

A 2015 report found that 60 percent of Americans report eating out at least once a week. Restaurant dining can be easy, enjoyable, even decadent — but are you prepared for the germs you may be exposed to along with your side of fries?

Here are eight things you should never touch at a restaurant.

The table

Charles Gerba, a professor of microbiology at the University of Arizona, found significant numbers of E. coli and coliform bacteria on restaurant tabletops — enough to present a danger to the public — particularly young children, the elderly, and people with compromised immune systems. And the bacteria numbers were even higher after the tables were wiped down, suggesting a direct connection between dirty rags and bacteria. The solution? Ask your server not to wipe your table before you sit down.

The menu

It’s hard to avoid touching a menu — which is probably why they’re some of the germiest things in any restaurant. Think about how many hands touch them on a daily basis, and how infrequently the menus are cleaned (or replaced). Also, restaurant staff may wipe down laminated menus with a rag. (Remember how filthy those are?)

A 2013 study found that menus are an ideal vehicle for different types of bacteria. E. coli can survive on a laminated menu for as long as 24 hours, and salmonella for as long as 72 hours. Donna Duberg, an assistant professor of clinical laboratory science from Saint Louis University, suggests paying attention to how your menu feels. “If there is visible food on the outside or if it feels ‘sticky,’” she tells Yahoo Health, “it is most likely harboring germs, bacteria, and viruses from everyone who has sat there or worked there over the last few days.” Be safe and give your hands a good wash after ordering (and before eating).

The ice in your drink

Like a cold drink? Restaurant ice makers aren’t cleaned nearly as often as they should be (ideally once a month), and may harbor bacteria. The bottom line? Ask for your soda without ice — your stomach will thank you.

The lemon and lime wedges in your drink

Whether you request it or not, restaurant drinks often come with a slice of lemon or lime. But a 2007 study found that 69.7 percent of lemon wedges tested showed some type of microbial growth — either on the rind or the flesh. Why? By the time it reaches your drink, that piece of fruit may have been handled by multiple people — plus, there’s no way to ensure proper handwashing practices have been followed. Although it won’t be as tasty, it’s wise to take that beverage straight up.

The ketchup bottle and salt and pepper shakers

“These are most likely never wiped off — and if they are, it is with a cloth that has been used to wipe off the table, chairs, trays, and has been ‘rinsed’ in a tub of dirty water,” Duberg says. Beyond that, it’s impossible to know who touched these before you (and whether they washed their hands). You’ve got your antibacterial wipes, right? If you need that ketchup, give the bottle a once-over before squeezing.

The tray

Just like the condiment bottles and menus, trays are rarely wiped down (and when they are, it’s with that same rag — yuck). Duberg suggests you avoid touching your tray as much as possible. “When eating in a fast-food establishment with trays,” she says, “I use hand sanitizer before touching my food, and never touch the tray after I sit down until after I am done eating.”

The buffet

Yes, buffets are as dirty as you thought they were. “It is a rare day when I will eat at a buffet or a salad bar,” Duberg says. “There are very few assurances that the food has been kept at the proper temperature (hot or cold); the remaining food from the container being replaced is often scooped into the container of fresh food, and the serving utensils are usually reused over and over again.” These latter two actions can carry bacteria, which have been multiplying all day, from one batch of food to the next. All you can eat? It may not be worth it.

The bathroom

It seems obvious, but the bathroom is often a reflection of how clean the rest of a restaurant is. Duberg suggests checking to see whether there’s a cleaning schedule posted on the door. “And use the sniff test,” she says. “If it smells dirty, it most likely is — wash your hands with lots of soap and water, dry with a paper towel, use the paper towel to open the door, and use hand sanitizer at the table before eating your food. Reminder: People who are not feeling well often go into the bathroom to vomit or have diarrhea, and may not wash their hands as well as I do.”

Thanks to Pete Cuomo for bringing this to the It’s Interesting community.

The five-second rule is based on the not-entirely-scientific belief that bacteria cannot contaminate food within five seconds, so you won’t get sick eating things you have picked up from the floor.

The first person to investigate this urban myth scientifically was Jillian Clarke, an American high-school student, during an apprenticeship in a microbiology laboratory at the University of Illinois in 2003. Clarke and her colleagues inoculated rough and smooth tiles with the bacterium E coli (certain strains of which cause stomach cramps, diarrhoea and vomiting) and put gummy bears or cookies on the tiles for five seconds. She found that E coli was transferred to gummy bears within five seconds, more so from smooth than rough tiles. As a side issue, Clarke also established in her work that university floors are remarkably clean and that people are more likely to pick up cookies from the floor than cauliflower.

Paul Dawson, professor of food science at Clemson University in South Carolina is a five-second-rule expert. His 2007 study, published in the Journal of Applied Microbiology, found that the dirtiness of the floor was more important than how long the food lay on it. His study was a progression from Clarke’s because it measured the amount of contamination. Using bread or bologna, he showed that it was better to drop either of them on carpet inoculated with salmonella, where less than 1% of the bacteria were transferred, than on tiles or wood, where up to 70% got on to the food. A similar study from Aston University found that, as soon as food hit the floor, it became contaminated – especially on smooth surfaces – but that the number of bacteria on the food increased up to 10 times between lying from three seconds to 30 seconds on the floor.

Dawson says that the five-second rule is simply not true because, if food hits a virulent brand of E coli, even the small number of bacteria it attracts immediately will make you sick. He doesn’t eat food when it falls on the floor. The very young or old shouldn’t use the five-second rule as their immune systems may not cope with even tiny amounts of bacteria. If the floor is filthy, then the rule is invalid on the grounds of grossness anyway. But the likelihood is that, for most of us, eating food off the floor isn’t going to hurt us. So if you are very hungry and you must pick food off the floor, then do it quickly, and preferably off a carpet.

http://www.theguardian.com/lifeandstyle/2015/sep/28/is-the-five-second-food-rule-really-true?channel=us

Have you ever been on the subway and seen something that you did not quite recognize, something mysteriously unidentifiable?

Well, there is a good chance scientists do not know what it is either.

Researchers at Weill Cornell Medical College released a study on Thursday that mapped DNA found in New York’s subway system — a crowded, largely subterranean behemoth that carries 5.5 million riders on an average weekday, and is filled with hundreds of species of bacteria (mostly harmless), the occasional spot of bubonic plague, and a universe of enigmas. Almost half of the DNA found on the system’s surfaces did not match any known organism and just 0.2 percent matched the human genome.

“People don’t look at a subway pole and think, ‘It’s teeming with life,’ ” said Dr. Christopher E. Mason, a geneticist at Weill Cornell Medical College and the lead author of the study. “After this study, they may. But I want them to think of it the same way you’d look at a rain forest, and be almost in awe and wonder, effectively, that there are all these species present — and that you’ve been healthy all along.”

Dr. Mason said the inspiration for the study struck about four years ago when he was dropping off his daughter at day care. He watched her explore her new surroundings by happily popping objects into her mouth. As is the custom among tiny children, friendships were made on the floor, by passing back and forth toys that made their way from one mouth to the next.

“I couldn’t help thinking, ‘How much is being transferred, and on which kinds of things?’ ” Dr. Mason said. So he considered a place where adults can get a little too close to each other, the subway.

Thus was the project, called PathoMap, born. Over the past 17 months, a team mainly composed of medical students, graduate students and volunteers fanned out across the city, using nylon swabs to collect DNA, in triplicate, from surfaces that included wooden benches, stairway handrails, seats, doors, poles and turnstiles.

In addition to the wealth of mystery DNA — which was not unexpected given that only a few thousand of the world’s genomes have been fully mapped — the study’s other findings reflected New York’s famed diversity, both human and microbial.

The Bronx was found to be the most diverse borough in terms of microbial species. Brooklyn claimed second place, followed by Manhattan, Queens and Staten Island, where researchers took samples on the Staten Island Railway.

On the human front, Dr. Mason said that, in some cases, the DNA that was found in some subway stations tended to match the neighborhood’s demographic profile. An area with a high concentration of Hispanic residents near Chinatown in Manhattan, for example, yielded a large amount of Hispanic and Asian genes.

In an area of Brooklyn to the south of Prospect Park that roughly encompassed the Kensington and Windsor Terrace neighborhoods, the DNA gathered frequently read as British, Tuscan, and Finnish, three groups not generally associated with the borough. Dr. Mason had an explanation for the finding: Scientists have not yet compiled a reliable database of Irish genes, so the many people of Irish descent who live in the area could be the source of DNA known to be shared with other European groups. The study produced some less appetizing news. Live, antibiotic-resistant bacteria were discovered in 27 percent of the collected samples, though among all the bacteria, only 12 percent could be associated with disease. Researchers also found three samples associated with bubonic plague and two with DNA fragments of anthrax, though they noted that none of those samples showed evidence of being alive, and that neither disease had been diagnosed in New York for some time. The presence of anthrax, Dr. Mason said, “is consistent with the many documented cases of anthrax in livestock in New York State and the East Coast broadly.”

The purpose of the study was not simply to satisfy scientific curiosity, the authors said. By cataloging species now, researchers can compare them against samples taken in the future to determine whether certain diseases, or even substances used as bioterrorism weapons, had spread.

City and transit officials did not sound grateful for the examination.

“As the study clearly indicates, microbes were found at levels that pose absolutely no danger to human life and health,” Kevin Ortiz, a spokesman for the Metropolitan Transportation Authority, said in an email. And the city’s health department called the study “deeply flawed” and misleading.

Dr. Mason responded by saying he and his team had simply presented their complete results.

“For us to not report the fragments of anthrax and plague in the context of a full analysis would have been irresponsible,” he said. “Our findings indicate a normal, healthy microbiome, and we welcome others to review the publicly available data and run the same analysis.”

http://www.nytimes.com/2015/02/06/nyregion/among-the-new-york-city-subways-millions-of-riders-a-study-finds-many-mystery-microbes.html?hp&action=click&pgtype=Homepage&module=mini-moth&region=top-stories-below&WT.nav=top-stories-below

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.