How Germy Are Airplanes?

By Susanne Rust

Plane: My Good Images/Shutterstock. Bacteria from left: National Institute of Allergy and Infectious Diseases; CDC/Janice Haney Carr; CDC/Melissa Brower

Viruses and bacteria can persist on airplane surfaces for days, researchers find.

Missed connections and lost bags might not be your biggest worry when traveling. Researchers have found that nasty, contagious bacteria can last for days on airplane surfaces.

James Barbaree, a pathologist at Alabama’s Auburn University, and colleague Kiril Vaglenov were curious about how long bacteria could last under typical air travel conditions. They applied smears of methicillin-resistant Staphylococcus aureus(MRSA) and the virulent E. coli strain O157:H7 to six airplane surface types — armrests, plastic tray tables, metal toilet buttons, window shades, seat pocket cloths and leather — which were supplied by an unnamed major airline.

What they found was disturbing. MRSA lasted for 168 hours, or seven days, on seat pockets (where travelers reach for magazines and store their iPads), while E. coli samples thrived for up to four days on armrests. Barbaree and Vaglenov rubbed pig skin on the tainted surfaces to mimic contact with human flesh. They found that the less porous the surface, the more transmissible the bug.

Bacteria survived longer, however, on more porous surfaces, such as seat pockets, though they were much less transmissible than those on, say, a tray table.

The researchers are now performing the same tests on Streptococcus pyogenes, which causes strep throat. They also are testing cleaning agents that might help prevent bacterial stowaways.

For now, Barbaree says regular hand-washing is probably the best way to prevent the spread of disease. He says he and his wife now take alcohol wipes with them on flights.

And the next time you’re waiting to get on a plane, ponder this: There are no federal cabin-cleaning regulations.

How microbes contribute to heart disease

Taken from: http://dx.doi.org/10.1016/j.cell.2016.02.011

The role of gut microbes in cardiovascular disease

RESEARCHERS HAVE SHOWN BACTERIA MAY ADD TO HEART-RELATED ISSUES

By Jason Tetro

Cardiovascular disease can take many forms and numerous causes have been identified. Most of these have been associated with genetics and behavior. Yet there may be one other reason for heart troubles although it may seem highly unlikely.

Back in 2011, a large group of American researchers made a highly controversial postulate. In addition to human causes of cardiovascular disease, there may be a microbial one as well. They based their assumption on the creation of a particular chemical, trimethylamine-N-oxide, or TMAO.

In mice, an increase in TMAO concentration ultimately leads to cardiovascular troubles including atherosclerotic lesions. This molecule is formed only in individuals with a rare genetic disorder known as trimethylaminuria. Yet, microbes are also able to form TMAO and release it into the body. By 2013, the formation of TMAO in the human body by bacteria was confirmed.

The news of microbial TMAO shook both the cardiology and microbiology fields leading to a variety of studies examining the link between this chemical and the potential for cardiovascular disease. While the connections were established, one question was left unanswered. No one could quite explain what TMAO was doing inside the body.

Now there may be an answer, thanks to further investigations by American researchers including some of the authors of the original 2011 paper. Last week, they revealed a possible mechanism behind the detrimental effects of TMAO. It turns out the chemical sparks an even greater cascade of problems inside the body leading to cardiovascular disease and an increased risk for heart attack and stroke.

The team first wanted to determine whether there was any correlation between TMAO and a cardiovascular event. They looked at more than 4,000 individuals and found a possible link between concentrations of the chemical and a risk for thrombotic events such as heart attack and stroke. Although this didn't offer a mechanism, it did offer a path for further analysis.

The next step was to identify whether the major players in thrombosis,platelets, were affected at all by the presence of TMAO. Platelets are responsible for patching up lesions in blood vessels by aggregating together in clots. In normal people, this clotting is well regulated, but in those with thrombosis, platelets can form clots without the presence of injury. If TMAO was indeed a risk factor for thrombosis, platelets would have to react accordingly.

They did. In the presence of TMAO, lab cultures of platelets were far more active and began to form clots. When the platelets were introduced to another factor in clotting, collagen, the clot itself was stronger and more resistant to liquid flow similar to that of blood in the body. Essentially, TMAO was responsible for making and solidifying clots.

The next step was to prove this effect inside an actual mammal--in this case, mice. The researchers injected TMAO directly into mice and observed the levels of thrombosis. Just as it was in the culture dish, TMAO raised the activity of platelets and increased the chances for cardiovascular troubles. What made this part of the study even more useful was the actual amount of TMAO used, which was within the identified range found in humans.

With this information at hand, the researchers eventually found the molecular mechanism behind platelet activation. When the cell is stimulated with TMAO, it becomes overly alert and ready to act. Once it comes into contact with collagen, the platelet goes into overdrive and begins to form a cascade of clotting action. Other TMAO-stimulated platelets will do the same increasing the chance for a troublesome clot. Over a long period of time, this could eventually lead to a blockage and resultant heart attack and stroke.

Though the information was sufficient to provide a mechanism, the authors wanted to prove that the trouble was indeed caused by bacteria. To do this, they took fecal bacteria from a mouse suffering from thrombosis and transplanted it into a normal, healthy mouse. Within 6 weeks, the normal mouse began to suffer from similar TMAO-related troubles. The team went as far as to define particular bacterial genera responsible for the condition.

The results of this study come close to proving microbes may act as a risk factor for cardiovascular disease. Unfortunately, this information may initially be more problematic than helpful. Because of the nature of cardiovascular disease treatment, addressing the bacterial contribution will require a change in focus and tact.

The authors themselves suggest there may be a route forward by trying to target the TMAO pathway in microbes. Or, there may be another route in which probiotics and prebiotics may be used as heart helpers. In this way, the level of TMAO-forming microbes will be reduced as will the risk. The most influential benefit of this path would be a lack of any pharmaceutical intervention. The risk would be reduced simply by shifting the microbial population through diet and exercise.

Year in review: Microbe discoveries spur rethink of treetop of life

LIFE STORIES  DNA samples of microbes discovered near hydrothermal vents like this one in the Arctic Mid-Ocean Ridge may be the closest kin yet known to complex life.

Scientists consider deep history of eukaryotes

BY 

SUSAN MILIUS

Microbes discovered in Arctic mud could be the closest relatives yet found to the single-celled ancestor that swallowed a bacterium and made life so complicated. Biologists have proposed that this swallowing event, perhaps 1.8 billion years ago, led to complex cells with membrane-wrapped organelles, the hallmark of all eukaryotes from amoebas to zebras.

Researchers discovered the new phylum of microbes, dubbed Lokiarchaeota, by screening DNA from sediment (SN: 5/30/15, p. 6). Though no one has identified an actual cell yet, the new phylum appears to mingle genes similar to those in modern eukaryotes and genes from archaea, the sister group to bacteria. Analyses suggest the cells have dynamic structures that could have engulfed bacteria long ago. (Biologists have proposed representing that merger as a ring of life, rather than a tree.) What happened next in the tale is clearer but still a puzzle.

Forget the split

Unlike the three-domain tree, the ring conveys that bacteria and archaea merged to give rise to eukaryotes.

SOURCE: W. MARTIN AND T.M. EMBLEY/NATURE 2004, J.O. MCINERNEY ET AL/NATURE REVIEWS MICROBIOLOGY 2014

“We don’t have all the existing pieces right now because a lot of the diversity of microbial eukaryotes remains unexplored,” says Patrick Keeling of the University of British Columbia in Vancouver, who studies early eukaryote history. But what scientists have found has radically reshaped the old multicellular-biased tree of life learned by generations of schoolchildren.

This year marked the 10th anniversary of a paper, in the Journal of Eukaryotic Microbiology, that served as an obituary for that tree (SN: 8/8/15, p. 22). Old textbooks had drawn a eukaryote treetop that branched into three kingdoms of mostly multicellular organisms (plants, animals and fungi) and one hodgepodge kingdom of single-celled beasts called Protista. Beginning in the late 1980s, though, new genetic studies relegated the multicelled kingdoms to mere side branches on five to seven much bigger branches of mostly single-celled protists.

This new scheme has held up “pretty well,” says Sina Adl of the University of Saskatchewan in Saskatoon, a coauthor on the 2005 paper. In the May 22 Science, for example, the Tara Oceans consortium, which surveyed plankton worldwide, classified diversity using the new divisions: SAR, Amoebozoa, Archaeplastida, Excavata and Opisthokonta (to which humans belong). These aren’t exactly house-hold names, though — at least not yet.

Microbes show up on schedule after death

MICROBIAL CLOCK  Telltale crews of microbes (including bacteria from a group called Enterobacteria, shown here) colonize the soil beneath a decomposing body during different stages of decay.

BY MEGHAN ROSEN

Dead people tell no tales — but dead people’s microbes do.

Bacteria, fungi and worms living in the soil beneath a decomposing body can help reveal the time — and place — of death, scientists report December 10 in Science.

Researchers have tracked the comings and goings of cadaver microbes before, but the new study is the mostcomprehensive survey yet. For months, microbial ecologist Jessica Metcalf of the University of Colorado Boulder and colleagues tallied up microbes on and near dead mice and humans.

As bodies decayed, similar microbes cropped up like clockwork, even on different soil types and during different seasons of the year, the team found. The microbes were so predictable that researchers could estimate the time of death (within a few days) of a body that had been dead for about a month.

And because telltale microbes stayed in the soil long after a body had been moved, they could offer investigators clues about potential crime scenes, the team suggests.  

MICROBES ARE PARTLY TO BLAME FOR ARCTIC’S MELTING PERMAFROST

By Mary Beth Griggs

Qajaa Archaeological Site, Greenland

Bo Elberling

One of the best preserved settlements in the region, dating back to 4,000 BC is under threat from climate change

The whole idea behind the term permafrost, is that it is a permanently frozen layer of soil. Perma = Permanent, Frost = Brrr. Perma + Frost = You aren't getting warm again anytime soon. But in Greenland, that equation is starting to look a little less definitive. With temperatures on the rise in the Arctic, permafrost is melting, and scientists might have just found something that could make it all worse.

Microbes. Rising temperatures were always going to deal a huge blow to permafrost in the Arctic, but adding insult to injury, a new paper published inNature Climate Change shows that microbes might accelerate the loss of permafrost by the year 2100.

Because permafrost is so cold, it has a lot of organic matter that just never breaks down, because microbes can't get to it. When the permafrost starts to thaw, microbes move in, breaking down the organic matter. The process of breaking down the organic matter produces heat, the heat melts more permafrost, and the cycle continues melting downward.

This is terrible for a few reasons, most prominently: archaeology and climate change.

Unlike China or Egypt, Greenland isn't exactly known for its archaeology, but it does have some of the best-preserved evidence of human occupation in the Arctic, with sites like Qajaa (seen above) dating back thousands of years. These sites often feature settlements and garbage heaps. They're not as pretty as more elaborate sites, but are still incredibly valuable sources of information for archeologists, containing details about the diet, environment, and culture of the people who lived there before. Because Greenland is so remote, many sites haven't been fully documented or explored. As the permafrost melts, the artifacts will decay faster, meaning a clock is ticking for archaeologists to get to them.

The second, more urgent aspect of this finding is the fact that huge amounts of carbon are trapped in organic matter the Arctic permafrost. When microbes eat that organic matter from long-dead plants and animals, the microbes produce carbon dioxide--a greenhouse gas with the potential to raise temperatures even more. The amount by which the microbes affect the permafrost varied by area, but in some places the change was dramatic. In one location, Disko Bay, the researchers found that without accounting for the microbes, the area would lose between one and five kilograms of carbon per square meter of permafrost, but when they accounted for the microbes, that number skyrocketed to between 20 and 52 kilograms of carbon per square meter.