Adoptees’ ‘lost language’ from infancy triggers brain response


Chinese children are lined up in Tiananmen Square in 2003 for photos with the overseas families adopting them. The children in the new study were adopted from China at an average age of 12.8 months and raised in French-speaking families.

You may not recall any memories from the first year of life, but if you were exposed to a different language at the time, your brain will still respond to it at some level, a new study suggests.

Brain scans show that children adopted from China as babies into families that don’t speak Chinese still unconsciously recognize Chinese sounds as language more than a decade later.

“It was amazing to see evidence that such an early experience continued to have a lasting effect,” said Lara Pierce, lead author of the study just published in the journal Proceedings of the National Academy of Sciences, in an email to CBC News.

The adopted children, who were raised in French-speaking Quebec families, had no conscious memory of hearing Chinese.

“If you actually test these people in Chinese, they don’t actually know it,” said Denise Klein, a researcher at McGill University’s Montreal Neurological Institute who co-authored the paper.

But their brains responded to Chinese language sounds the same way as those of bilingual children raised in Chinese-speaking families.


Children exposed to Chinese as babies display similar brain activation patterns as children with continued exposure to Chinese when hearing Chinese words, fMRI scans show.

“In essence, their pattern still looks like people who’ve been exposed to Chinese all their lives.”

Pierce, a PhD candidate in psychology at McGill University, working with Klein and other collaborators, scanned the brains of 48 girls aged nine to 17. Each participant lay inside a functional magnetic resonance imaging machine while she listened to pairs of three-syllable phrases. The phrases contained either:

■Sounds and tones from Mandarin, the official Chinese dialect.
■Hummed versions of the same tones but no actual words.

Participants were asked to tell if the last syllables of each pair were the same or different. The imaging machine measured what parts of the brain were active as the participants were thinking.

“Everybody can do the task — it’s not a difficult task to do,” Klein said. But the sounds are processed differently by people who recognize Chinese words — in that case, they activate the part of the brain that processes language.

Klein said the 21 children adopted from China who participated in the study might have been expected to show patterns similar to those of the 11 monolingual French-speaking children. After all, the adoptees left China at an average age of 12.8 months, an age when most children can only say a few words. On average, those children had not heard Chinese in more than 12 years.

The fact that their brains still recognized Chinese provides some insight into the importance of language learning during the first year of life, Klein suggested.

Effect on ‘relearning’ language not known

But Klein noted that the study is a preliminary one and the researchers don’t yet know what the results mean.

For example, would adopted children exposed to Chinese in infancy have an easier time relearning Chinese later, compared with monolingual French-speaking children who were learning it for the first time?

Pierce said studies trying to figure that out have had mixed results, but she hopes the findings in this study could generate better ways to tackle that question.

She is also interested in whether the traces of the lost language affect how the brain responds to other languages or other kinds of learning. Being able to speak multiple languages has already been shown to have different effects on the way the brain processes languages and other kinds of information.

http://www.cbc.ca/news/technology/adoptees-lost-language-from-infancy-triggers-brain-response-1.2838001

Facial structure predicts goals, fouls among World Cup soccer players


World Cup soccer players with higher facial-width-to-height ratios are more likely to commit fouls, score goals and make assists, according to a study by a researcher at the University of Colorado Boulder.

The structure of a soccer player’s face can predict his performance on the field—including his likelihood of scoring goals, making assists and committing fouls—according to a study led by a researcher at the University of Colorado Boulder.

The scientists studied the facial-width-to-height ratio (FHWR) of about 1,000 players from 32 countries who competed in the 2010 World Cup. The results, published in the journal Adaptive Human Behavior and Physiology, showed that midfielders, who play both offense and defense, and forwards, who lead the offense, with higher FWHRs were more likely to commit fouls. Forwards with higher FWHRs also were more likely to score goals or make assists.

“Previous research into facial structure of athletes has been primarily in the United States and Canada,” said Keith Welker, a postdoctoral researcher in CU-Boulder Department of Psychology and Neuroscience and the lead author of the paper. “No one had really looked at how facial-width-to-height ratio is associated with athletic performance by comparing people from across the world.”

FWHR is the distance between the cheekbones divided by the distance between the mid-brow and the upper lip. Past studies have shown that a high FWHR is associated with more aggressive behavior, with both positive and negative results. For example, high FWHR correlates with greater antisocial and unethical behavior, but it also correlates with greater success among CEOs and achievement drive among U.S. presidents. However, some previous research has failed to find a correlation between FWHR and aggressive behavior in certain populations.

The new study adds weight to the argument that FWHR does correlate with aggression. Welker and his colleagues chose to look at the 2010 World Cup because of the quality and quantity of the data available. “There are a lot of athletic data out there,” Welker said. “We were exploring contexts to look at aggressive behavior and found that the World Cup, which quantifies goals, fouls and assists, provides a multinational way of addressing whether facial structure produces this aggressive behavior and performance.”

Scientists have several ideas about how FWHR might be associated with aggression. One possibility is that it’s related to testosterone exposure earlier in life. Testosterone during puberty can affect a variety of physical traits, including bone density, muscle growth and cranial shape, Welker said.

Co-authors of the study were Stefan Goetz, Shyneth Galicia and Jordan Liphardt of Wayne State University in Michigan and Justin Carré of Nipissing University in Ontario, Canada. –

See more at: http://www.colorado.edu/news/releases/2014/11/11/facial-structure-predicts-goals-fouls-among-world-cup-soccer-players#sthash.mAvOP9oO.dpuf

Watch A Bowling Ball And Feather Falling In A Vacuum

Here is the perfect example of how any two objects will fall at the same rate in a vacuum, brought to us by physicist Brian Cox. He checked out NASA’s Space Simulation Chamber located at the Space Power Facility in Ohio. With a volume of 22,653 cubic meters, it’s the largest vacuum chamber in the world.

In this clip from the BBC, Cox drops a bowling ball and a feather together, first in normal conditions, and then after virtually all the air has been sucked out of the chamber. We know what happens, but that doesn’t stop it from being awesome, especially with the team’s ecstatic faces.

http://www.iflscience.com/physics/dropping-bowling-ball-and-feather-vacuum

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

Scientists propose existence and interaction of parallel worlds: Many Interacting Worlds theory challenges foundations of quantum science

Academics are challenging the foundations of quantum science with a radical new theory on parallel universes. Scientists now propose that parallel universes really exist, and that they interact. They show that such an interaction could explain everything that is bizarre about quantum mechanics.

Griffith University academics are challenging the foundations of quantum science with a radical new theory based on the existence of, and interactions between, parallel universes.

In a paper published in the journal Physical Review X, Professor Howard Wiseman and Dr Michael Hall from Griffith’s Centre for Quantum Dynamics, and Dr Dirk-Andre Deckert from the University of California, take interacting parallel worlds out of the realm of science fiction and into that of hard science.
The team proposes that parallel universes really exist, and that they interact. That is, rather than evolving independently, nearby worlds influence one another by a subtle force of repulsion. They show that such an interaction could explain everything that is bizarre about quantum mechanics.

Quantum theory is needed to explain how the universe works at the microscopic scale, and is believed to apply to all matter. But it is notoriously difficult to fathom, exhibiting weird phenomena which seem to violate the laws of cause and effect.

As the eminent American theoretical physicist Richard Feynman once noted: “I think I can safely say that nobody understands quantum mechanics.”

However, the “Many-Interacting Worlds” approach developed at Griffith University provides a new and daring perspective on this baffling field.

“The idea of parallel universes in quantum mechanics has been around since 1957,” says Professor Wiseman.

“In the well-known “Many-Worlds Interpretation,” each universe branches into a bunch of new universes every time a quantum measurement is made. All possibilities are therefore realised — in some universes the dinosaur-killing asteroid missed Earth. In others, Australia was colonised by the Portuguese.

“But critics question the reality of these other universes, since they do not influence our universe at all. On this score, our “Many Interacting Worlds” approach is completely different, as its name implies.”

Professor Wiseman and his colleagues propose that:

•The universe we experience is just one of a gigantic number of worlds. Some are almost identical to ours while most are very different;
•All of these worlds are equally real, exist continuously through time, and possess precisely defined properties;
•All quantum phenomena arise from a universal force of repulsion between ‘nearby’ (i.e. similar) worlds which tends to make them more dissimilar.
Dr Hall says the “Many-Interacting Worlds” theory may even create the extraordinary possibility of testing for the existence of other worlds.

“The beauty of our approach is that if there is just one world our theory reduces to Newtonian mechanics, while if there is a gigantic number of worlds it reproduces quantum mechanics,” he says.

“In between it predicts something new that is neither Newton’s theory nor quantum theory.

“We also believe that, in providing a new mental picture of quantum effects, it will be useful in planning experiments to test and exploit quantum phenomena.”

The ability to approximate quantum evolution using a finite number of worlds could have significant ramifications in molecular dynamics, which is important for understanding chemical reactions and the action of drugs.

Professor Bill Poirier, Distinguished Professor of Chemistry at Texas Tech University, has observed: “These are great ideas, not only conceptually, but also with regard to the new numerical breakthroughs they are almost certain to engender.”

Journal Reference:

1.Michael J. W. Hall, Dirk-André Deckert, Howard M. Wiseman. Quantum Phenomena Modeled by Interactions between Many Classical Worlds. Physical Review X, 2014; 4 (4) DOI: 10.1103/PhysRevX.4.041013

http://www.sciencedaily.com/releases/2014/10/141030101654.htm

Brain decoder can eavesdrop on your inner voice

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Talking to yourself used to be a strictly private pastime. That’s no longer the case – researchers have eavesdropped on our internal monologue for the first time. The achievement is a step towards helping people who cannot physically speak communicate with the outside world.

“If you’re reading text in a newspaper or a book, you hear a voice in your own head,” says Brian Pasley at the University of California, Berkeley. “We’re trying to decode the brain activity related to that voice to create a medical prosthesis that can allow someone who is paralysed or locked in to speak.”

When you hear someone speak, sound waves activate sensory neurons in your inner ear. These neurons pass information to areas of the brain where different aspects of the sound are extracted and interpreted as words.

In a previous study, Pasley and his colleagues recorded brain activity in people who already had electrodes implanted in their brain to treat epilepsy, while they listened to speech. The team found that certain neurons in the brain’s temporal lobe were only active in response to certain aspects of sound, such as a specific frequency. One set of neurons might only react to sound waves that had a frequency of 1000 hertz, for example, while another set only cares about those at 2000 hertz. Armed with this knowledge, the team built an algorithm that could decode the words heard based on neural activity alone (PLoS Biology, doi.org/fzv269).

The team hypothesised that hearing speech and thinking to oneself might spark some of the same neural signatures in the brain. They supposed that an algorithm trained to identify speech heard out loud might also be able to identify words that are thought.

Mind-reading

To test the idea, they recorded brain activity in another seven people undergoing epilepsy surgery, while they looked at a screen that displayed text from either the Gettysburg Address, John F. Kennedy’s inaugural address or the nursery rhyme Humpty Dumpty.

Each participant was asked to read the text aloud, read it silently in their head and then do nothing. While they read the text out loud, the team worked out which neurons were reacting to what aspects of speech and generated a personalised decoder to interpret this information. The decoder was used to create a spectrogram – a visual representation of the different frequencies of sound waves heard over time. As each frequency correlates to specific sounds in each word spoken, the spectrogram can be used to recreate what had been said. They then applied the decoder to the brain activity that occurred while the participants read the passages silently to themselves.

Despite the neural activity from imagined or actual speech differing slightly, the decoder was able to reconstruct which words several of the volunteers were thinking, using neural activity alone (Frontiers in Neuroengineering, doi.org/whb).

The algorithm isn’t perfect, says Stephanie Martin, who worked on the study with Pasley. “We got significant results but it’s not good enough yet to build a device.”

In practice, if the decoder is to be used by people who are unable to speak it would have to be trained on what they hear rather than their own speech. “We don’t think it would be an issue to train the decoder on heard speech because they share overlapping brain areas,” says Martin.

The team is now fine-tuning their algorithms, by looking at the neural activity associated with speaking rate and different pronunciations of the same word, for example. “The bar is very high,” says Pasley. “Its preliminary data, and we’re still working on making it better.”

The team have also turned their hand to predicting what songs a person is listening to by playing lots of Pink Floyd to volunteers, and then working out which neurons respond to what aspects of the music. “Sound is sound,” says Pasley. “It all helps us understand different aspects of how the brain processes it.”

“Ultimately, if we understand covert speech well enough, we’ll be able to create a medical prosthesis that could help someone who is paralysed, or locked in and can’t speak,” he says.

Several other researchers are also investigating ways to read the human mind. Some can tell what pictures a person is looking at, others have worked out what neural activity represents certain concepts in the brain, and one team has even produced crude reproductions of movie clips that someone is watching just by analysing their brain activity. So is it possible to put it all together to create one multisensory mind-reading device?

In theory, yes, says Martin, but it would be extraordinarily complicated. She says you would need a huge amount of data for each thing you are trying to predict. “It would be really interesting to look into. It would allow us to predict what people are doing or thinking,” she says. “But we need individual decoders that work really well before combining different senses.”

http://www.newscientist.com/article/mg22429934.000-brain-decoder-can-eavesdrop-on-your-inner-voice.html

Scientists learn that mice nest together to confuse paternity and reduce infanticide

mice

It is a cruel world out there, particularly for young animals born into social groups where infanticide occurs. This dark side of evolution is revealed when adults – often males – kill offspring to promote their own genes being passed on, by reducing competition for resources or making females become sexually receptive more quickly.

This behaviour proves expensive for females, who have evolved strategies to avoid this fate. One strategy is to join forces with other females to physically ward off killer males. A more interesting strategy is to mate with several males, known as “polyandry”, so fathers can’t distinguish their young from others’, which means they avoid killing pups so that they don’t accidently kill their own.

Now, researchers at the University of Zurich have found a new type of infanticide counter-strategy: mothers can achieve paternity confusion even if they don’t mate with multiple males, through nesting with other females, which they call “socially mediated polyandry”. And such a strategy might be happening close to home, in the unassuming house mouse.

Yannick Auclair and his colleagues put their theory to the test on a wild population of mice living in an old agricultural building outside Zurich. They measured the genetic relationships within litters and found a complex picture of female social relationships and mating patterns. These allowed them to identify mothers nesting alone or with others and those who mated with one or more males. To examine the risk of infanticide for pups born into these different types of litters, they assessed survival until just before weaning, which is about two weeks after birth.

Direct observations of infanticide are extremely rare in natural systems. But studying an enclosed population without the presence of a predator meant that infanticide becomes the most likely cause of death for young pups. And indeed, from the corpses of pups that were recovered, most gave direct evidence – missing limbs or holes in the skull – of this harsh fate.

The results of the study were published in the journal Behavioral Ecology. The researchers found that pups born to females nesting alone and who had only one mate had the lowest survival rate (50% surviving, the rest presumably killed by males who were confident they were not the father). Meanwhile, those born to females nesting together were better off (80% surviving).

Key evidence supporting their theory was that some of these communal litters were composed of pups whose mothers had actually only mated once, but the different females had different mates. These litters had similar survival to those where paternity was mixed for individual mothers, suggesting that mothers can achieve the same survival benefits of communal nesting without mating with multiple males.

There were also a few communal litters (nine of the 90 studied) where the different females had mated with the same male and, as such, featured multiple mothers but no paternity confusion. These litters had worse survival rate (40% surviving) suggesting that – as predicted by the theory – paternity confusion is a more important driving factor of communal nesting than the physical warding off of males.

According to Elise Huchard of CNRS Montpelier: “This study presents an interesting idea, and an interesting system to test it.” Yet the data raise more questions than they answer – and additional experiments or comparative work would be insightful.

For example, it is not clear whether higher survival in litters with multiple fathers might actually reflect variation among females if, as in the case of mouse lemurs, higher-quality females have more mates. Dieter Lukas of Cambridge University concurs that the theory is interesting, but believes it is too early to assess its generality.

Infanticide occurs across diverse mammal systems – from meerkats and rabbits, to lions and gorillas – and comparative analyses could help assess how this theory fares among the many hypotheses about the evolution of infanticide.

Communal nesting may have evolved as an alternative to mating with multiple mates (which is costly when males harass females during mating or transmit disease) as a strategy to avoid infanticide through paternity confusion. “We don’t know whether other social behaviours may have evolved through similar ways,” said Auclair.

Comparative analyses will lead to new insights and future research on the nest-box population will also address such interesting questions as how females choose their nesting partners – and why some still nest alone even if this comes at a cost to offspring survival.

http://theconversation.com/whos-your-daddy-mice-nest-together-to-confuse-paternity-and-reduce-infanticide-31796

Ebola’s Family Tree: Disease May Have Existed For 23 Million Years, Much Longer Than Previously Believed

A family of viruses that Ebola belongs to may have existed over 20 million years ago, according to a new study published in the journal PeerJ.

Researchers from the University of Buffalo found that Filoviruses did not begin appearing 10,000 years ago as previously thought, but in fact have been around for much longer. The Ebola virus belongs to the family of filoviruses, also known as the Filoviridae family. “Filoviruses are far more ancient than previously thought,” said Derek Taylor, lead author of the study and a professor of biological sciences at the University of Buffalo, in the press release. “These things have been interacting with mammals for a long time, several million years.”

Despite the fact that scientists around the world are frantically searching for a cure and better treatment for Ebola, there’s still much to learn about the deadly virus. The authors of the study argue that better understanding Ebola’s evolutionary roots could “affect design of vaccines and programs that identify emerging pathogens.”

The study focused not on Ebola specifically, but the ancestors and family of Ebola to better understand where it may have come from. Both the Ebola virus and Marburg virus — also a hemorrhagic fever virus that belongs to the Filoviridae family — were found to be tied to ancient evolutionary lines, and they shared a common ancestor 16 to 23 million years ago. The authors discovered this by examining viral fossil genes, which are bits of genetic material that animals acquire from viruses during infection. They found Filovirus-like genes in rodents, particularly hamsters and voles, which means that the filovirus family is likely as old as these rodents’ common ancestor. The genetic material in these fossils were more closely related to Ebola than Marburg, meaning the two lines had already begun to diverge during the Miocene Epoch, a time period that occurred five to 23 million years ago. During this time, there were also warmer climates, as well as the first appearances of kelp forests and grasslands on Earth.

“These rodents have billions of base pairs in their genomes, so the odds of a viral gene inserting itself at the same position in different species at different times are very small,” Taylor said. “It’s likely that the insertion was present in the common ancestor of these rodents.”

The Filoviridae family is defined by viruses that form virions, or filamentous infectious viral particles. The Ebola virus and Marburg virus are the most well-known among this group, and they are both severe viruses that cause hemorrhagic fevers in both animals and humans (essentially, they’re deadly diseases that lead to fever and bleeding).

Taylor believes that the study may help in the fight against Ebola by widening our knowledge about its history, and identifying what species are most likely to be hosts of the virus. “When they first started looking for reservoirs for Ebola, they were crashing through the rainforest, looking at everything — mammals, insects, other organisms,” Taylor said. “The more we know about the evolution of filovirus-host interactions, the more we can learn about who the players might be in the system.”

Source: Taylor D, Ballinger M, Zhan J, Hanzly L, Bruenn J. Evidence that ebolaviruses and cuevaviruses have been diverging from marburgviruses since the Miocene. PeerJ. 2014.

http://www.medicaldaily.com/ebolas-family-tree-disease-may-have-existed-23-million-years-much-longer-previously-307958

Scientists publish new evidence of that awareness may persist several minutes after clinical death, which was previously thought impossible

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The largest ever medical study into near-death and out-of-body experiences has discovered that some awareness may continue even after the brain has shut down.

Scientists at the University of Southampton spent four years examining more than 2000 people who suffered cardiac arrest from 15 hospitals in the UK, US and Austria. They found that of 360 people who had been revived after experiencing cardiac arrest, about 40 percent of them had some sort of “awareness” during the period when they were “clinically dead.”

One man’s memory of what he saw “after death” was spot-on in describing what actually happened during his resuscitation. The 57-year-old recalled leaving his body and watching his resuscitation from the corner of the room. He reported hearing two beeps come from a machine that went off every three minutes — indicating that his conscious experience during the time he had no heartbeat lasted for around three minutes. According to the researchers, that suggests the man’s brain may not have shut down completely, even after his heart stopped.

“This is paradoxical, since the brain typically ceases functioning within 20-30 seconds of the heart stopping and doesn’t resume again until the heart has been restarted,” study co-author Dr. Sam Parnia, a professor of medicine at Stony Brook University and former research fellow at Southampton University, said in a written statement.

Parnia added that it’s possible even more patients in the study had mental activity following cardiac arrest but were unable to remember events during the episode as a result of brain injury or the use of sedative drugs.

“We know the brain can’t function when the heart has stopped beating,” said Dr Sam Parnia, a former research fellow at Southampton University, now at the State University of New York, who led the study.

“But in this case, conscious awareness appears to have continued for up to three minutes when the heart wasn’t beating, even though the brain typically shuts down within 20 to 30 seconds after the heart has stopped.

Although many could not recall specific details, some themes emerged. One in five said they had felt an unusual sense of peace while nearly one third said time had slowed down or speeded up.

Some recalled seeing a bright light and others recounted feelings of fear, drowning or being dragged through deep water.

Dr Parnia believes many more people may have experiences when they are close to death but drugs or sedatives used in resuscitation may stop them remembering.

“Estimates have suggested that millions of people have had vivid experiences in relation to death but the scientific evidence has been ambiguous at best.

“Many people have assumed that these were hallucinations or illusions but they do seem to have corresponded to actual events.

“These experiences warrant further investigation.”

Dr David Wilde, a research psychologist at Nottingham Trent University, is currently compiling data on out-of-body experiences in an attempt to discover a pattern that links each episode.

“There is some good evidence here that these experiences are happening after people have medically died.

“We just don’t know what is going on. We are still in the dark about what happens when you die.”

The study was published in the journal Resuscitation.

http://www.resuscitationjournal.com/article/S0300-9572(14)00739-4/abstract

Infectious disease specialists from University of Illinois make first recommendation that health workers need optimal respiratory protection for Ebola, due to possible transmission in the air.

Lisa M Brosseau, ScD, and Rachael Jones, PhD

The authors are national experts on respiratory protection and infectious disease transmission. In May they published a similar commentary on MERS-CoV. Dr Brosseau is a Professor and Dr Jones an Assistant Professor in the School of Public Health, Division of Environmental and Occupational Health Sciences, at the University of Illinois at Chicago.

Healthcare workers play a very important role in the successful containment of outbreaks of infectious diseases like Ebola. The correct type and level of personal protective equipment (PPE) ensures that healthcare workers remain healthy throughout an outbreak—and with the current rapidly expanding Ebola outbreak in West Africa, it’s imperative to favor more conservative measures.

The precautionary principle—that any action designed to reduce risk should not await scientific certainty—compels the use of respiratory protection for a pathogen like Ebola virus that has:

•No proven pre- or post-exposure treatment modalities
•A high case-fatality rate
•Unclear modes of transmission

We believe there is scientific and epidemiologic evidence that Ebola virus has the potential to be transmitted via infectious aerosol particles both near and at a distance from infected patients, which means that healthcare workers should be wearing respirators, not facemasks (1).

The minimum level of protection in high-risk settings should be a respirator with an assigned protection factor greater than 10. A powered air-purifying respirator (PAPR) with a hood or helmet offers many advantages over an N95 filtering facepiece or similar respirator, being more protective, comfortable, and cost-effective in the long run.

We strongly urge the US Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) to seek funds for the purchase and transport of PAPRs to all healthcare workers currently fighting the battle against Ebola throughout Africa—and beyond.

There has been a lot of on-line and published controversy about whether Ebola virus can be transmitted via aerosols. Most scientific and medical personnel, along with public health organizations, have been unequivocal in their statements that Ebola can be transmitted only by direct contact with virus-laden fluids (2,3) and that the only modes of transmission we should be concerned with are those termed “droplet” and “contact.”

These statements are based on two lines of reasoning. The first is that no one located at a distance from an infected individual has contracted the disease, or the converse, every person infected has had (or must have had) “direct” contact with the body fluids of an infected person.

This reflects an incorrect and outmoded understanding of infectious aerosols, which has been institutionalized in policies, language, culture, and approaches to infection control. We will address this below. Briefly, however, the important points are that virus-laden bodily fluids may be aerosolized and inhaled while a person is in proximity to an infectious person and that a wide range of particle sizes can be inhaled and deposited throughout the respiratory tract.

The second line of reasoning is that respirators or other control measures for infectious aerosols cannot be recommended in developing countries because the resources, time, and/or understanding for such measures are lacking (4).

Although there are some important barriers to the use of respirators, especially PAPRs, in developing countries, healthcare workers everywhere deserve and should be afforded the same best-practice types of protection, regardless of costs and resources. Every healthcare worker is a precious commodity whose well-being ensures everyone is protected.

If we are willing to offer infected US healthcare workers expensive treatments and experimental drugs free of charge when most of the world has no access to them, we wonder why we are unwilling to find the resources to provide appropriate levels of comparatively less expensive respiratory protection to every healthcare worker around the world.

How are infectious diseases transmitted via aerosols?

Medical and infection control professionals have relied for years on a paradigm for aerosol transmission of infectious diseases based on very outmoded research and an overly simplistic interpretation of the data. In the 1940s and 50s, William F. Wells and other “aerobiologists” employed now significantly out-of-date sampling methods (eg, settling plates) and very blunt analytic approaches (eg, cell culturing) to understand the movement of bacterial aerosols in healthcare and other settings. Their work, though groundbreaking at the time, provides a very incomplete picture.

Early aerobiologists were not able to measure small particles near an infectious person and thus assumed such particles existed only far from the source. They concluded that organisms capable of aerosol transmission (termed “airborne”) can only do so at around 3 feet or more from the source. Because they thought that only larger particles would be present near the source, they believed people would be exposed only via large “droplets” on their face, eyes, or nose.

Modern research, using more sensitive instruments and analytic methods, has shown that aerosols emitted from the respiratory tract contain a wide distribution of particle sizes—including many that are small enough to be inhaled (5,6). Thus, both small and large particles will be present near an infectious person.

The chance of large droplets reaching the facial mucous membranes is quite small, as the nasal openings are small and shielded by their external and internal structure. Although close contact may permit large-droplet exposure, it also maximizes the possibility of aerosol inhalation.

As noted by early aerobiologists, liquid in a spray aerosol, such as that generated during coughing or sneezing, will quickly evaporate (7), which increases the concentration of small particles in the aerosol. Because evaporation occurs in milliseconds, many of these particles are likely to be found near the infectious person.

The current paradigm also assumes that only “small” particles (less than 5 micrometers [mcm]) can be inhaled and deposited in the respiratory tract. This is not true. Particles as large as 100 mcm (and perhaps even larger) can be inhaled into the mouth and nose. Larger particles are deposited in the nasal passages, pharynx, and upper regions of the lungs, while smaller particles are more likely to deposit in the lower, alveolar regions. And for many pathogens, infection is possible regardless of the particle size or deposition site.

It’s time to abandon the old paradigm of three mutually exclusive transmission routes for a new one that considers the full range of particle sizes both near and far from a source. In addition, we need to factor in other important features of infectivity, such as the ability of a pathogen to remain viable in air at room temperature and humidity and the likelihood that systemic disease can result from deposition of infectious particles in the respiratory system or their transfer to the gastrointestinal tract.

We recommend using “aerosol transmissible” rather than the outmoded terms “droplet” or “airborne” to describe pathogens that can transmit disease via infectious particles suspended in air.

Is Ebola an aerosol-transmissible disease?

We recently published a commentary on the CIDRAP site discussing whether Middle East respiratory syndrome (MERS) could be an aerosol-transmissible disease, especially in healthcare settings. We drew comparisons with a similar and more well-studied disease, severe acute respiratory syndrome (SARS).

For Ebola and other filoviruses, however, there is much less information and research on disease transmission and survival, especially in healthcare settings.

Being at first skeptical that Ebola virus could be an aerosol-transmissible disease, we are now persuaded by a review of experimental and epidemiologic data that this might be an important feature of disease transmission, particularly in healthcare settings.

What do we know about Ebola transmission?

No one knows for certain how Ebola virus is transmitted from one person to the next. The virus has been found in the saliva, stool, breast milk, semen, and blood of infected persons (8,9). Studies of transmission in Ebola virus outbreaks have identified activities like caring for an infected person, sharing a bed, funeral activities, and contact with blood or other body fluids to be key risk factors for transmission (10-12).

On the basis of epidemiologic evidence, it has been presumed that Ebola viruses are transmitted by contaminated hands in contact with the mouth or eyes or broken skin or by splashes or sprays of body fluids into these areas. Ebola viruses appear to be capable of initiating infection in a variety of human cell types (13,14), but the primary portal or portals of entry into susceptible hosts have not been identified.

Some pathogens are limited in the cell type and location they infect. Influenza, for example, is generally restricted to respiratory epithelial cells, which explains why flu is primarily a respiratory infection and is most likely aerosol transmissible. HIV infects T-helper cells in the lymphoid tissues and is primarily a bloodborne pathogen with low probability for transmission via aerosols.

Ebola virus, on the other hand, is a broader-acting and more non-specific pathogen that can impede the proper functioning of macrophages and dendritic cells—immune response cells located throughout the epithelium (15,16). Epithelial tissues are found throughout the body, including in the respiratory tract. Ebola prevents these cells from carrying out their antiviral functions but does not interfere with the initial inflammatory response, which attracts additional cells to the infection site. The latter contribute to further dissemination of the virus and similar adverse consequences far beyond the initial infection site.

The potential for transmission via inhalation of aerosols, therefore, cannot be ruled out by the observed risk factors or our knowledge of the infection process. Many body fluids, such as vomit, diarrhea, blood, and saliva, are capable of creating inhalable aerosol particles in the immediate vicinity of an infected person. Cough was identified among some cases in a 1995 outbreak in Kikwit, Democratic Republic of the Congo (11), and coughs are known to emit viruses in respirable particles (17). The act of vomiting produces an aerosol and has been implicated in airborne transmission of gastrointestinal viruses (18,19). Regarding diarrhea, even when contained by toilets, toilet flushing emits a pathogen-laden aerosol that disperses in the air (20-22).

Experimental work has shown that Marburg and Ebola viruses can be isolated from sera and tissue culture medium at room temperature for up to 46 days, but at room temperature no virus was recovered from glass, metal, or plastic surfaces (23). Aerosolized (1-3 mcm) Marburg, Ebola, and Reston viruses, at 50% to 55% relative humidity and 72°F, had biological decay rates of 3.04%, 3.06%. and 1.55% per minute, respectively. These rates indicate that 99% loss in aerosol infectivity would occur in 93, 104, and 162 minutes, respectively (23).

In still air, 3-mcm particles can take up to an hour to settle. With air currents, these and smaller particles can be transported considerable distances before they are deposited on a surface.

There is also some experimental evidence that Ebola and other filoviruses can be transmitted by the aerosol route. Jaax et al (24) reported the unexpected death of two rhesus monkeys housed approximately 3 meters from monkeys infected with Ebola virus, concluding that respiratory or eye exposure to aerosols was the only possible explanation.

Zaire Ebola viruses have also been transmitted in the absence of direct contact among pigs (25) and from pigs to non-human primates (26), which experienced lung involvement in infection. Persons with no known direct contact with Ebola virus disease patients or their bodily fluids have become infected (12).

Direct injection and exposure via a skin break or mucous membranes are the most efficient ways for Ebola to transmit. It may be that inhalation is a less efficient route of transmission for Ebola and other filoviruses, as lung involvement has not been reported in all non-human primate studies of Ebola aerosol infectivity (27). However, the respiratory and gastrointestinal systems are not complete barriers to Ebola virus. Experimental studies have demonstrated that it is possible to infect non-human primates and other mammals with filovirus aerosols (25-27).

Altogether, these epidemiologic and experimental data offer enough evidence to suggest that Ebola and other filoviruses may be opportunistic with respect to aerosol transmission(28). That is, other routes of entry may be more important and probable, but, given the right conditions, it is possible that transmission could also occur via aerosols.

Guidance from the CDC and WHO recommends the use of facemasks for healthcare workers providing routine care to patients with Ebola virus disease and respirators when aerosol-generating procedures are performed. (Interestingly, the 1998 WHO and CDC infection-control guidance for viral hemorrhagic fevers in Africa, still available on the CDC Web site, recommends the use of respirators.)

Facemasks, however, do not offer protection against inhalation of small infectious aerosols, because they lack adequate filters and do not fit tightly against the face (1). Therefore, a higher level of protection is necessary.

Which respirator to wear?

As described in our earlier CIDRAP commentary, we can use a Canadian control-banding approach to select the most appropriate respirator for exposures to Ebola in healthcare settings (29). (See this document for a detailed description of the Canadian control banding approach and the data used to select respirators in our examples below.)

The control banding method involves the following steps:

1.Identify the organism’s risk group (1 to 4). Risk group reflects the toxicity of an organism, including the degree and type of disease and whether treatments are available. Ebola is in risk group 4, the most toxic organisms, because it can cause serious human or animal disease, is easily transmitted, directly or indirectly, and currently has no effective treatments or preventive measures.

2.Identify the generation rate. The rate of aerosol generation reflects the number of particles created per time (eg, particles per second). Some processes, such as coughing, create more aerosols than others, like normal breathing. Some processes, like intubation and toilet flushing, can rapidly generate very large quantities of aerosols. The control banding approach assigns a qualitative rank ranging from low (1) to high (4) (eg, normal breathing without coughing has a rank of 1).

3.Identify the level of control. Removing contaminated air and replacing it with clean air, as accomplished with a ventilation system, is effective for lowering the overall concentration of infectious aerosol particles in a space, although it may not be effective at lowering concentration in the immediate vicinity of a source. The number of air changes per hour (ACH) reflects the rate of air removal and replacement. This is a useful variable, because it is relatively easy to measure and, for hospitals, reflects building code requirements for different types of rooms. Again, a qualitative ranking is used to reflect low (1) versus high (4) ACH. Even if the true ventilation rate is not known, the examples can be used to select an appropriate air exchange rate.

4.Identify the respirator assigned protection factor. Respirators are designated by their “class,” each of which has an assigned protection factor (APF) that reflects the degree of protection. The APF represents the outside, environmental concentration divided by the inside, facepiece concentration. An APF of 10 means that the outside concentration of a particular contaminant will be 10 times greater than that inside the respirator. If the concentration outside the respirator is very high, an assigned protection factor of 10 may not prevent the wearer from inhaling an infective dose of a highly toxic organism.

Practical examples

Two examples follow. These assume that infectious aerosols are generated only during vomiting, diarrhea, coughing, sneezing, or similar high-energy emissions such as some medical procedures. It is possible that Ebola virus may be shed as an aerosol in other manners not considered.

Caring for a patient in the early stages of disease (no bleeding, vomiting, diarrhea, coughing, sneezing, etc). In this case, the generation rate is 1. For any level of control (less than 3 to more than 12 ACH), the control banding wheel indicates a respirator protection level of 1 (APF of 10), which corresponds to an air purifying (negative pressure) half-facepiece respirator such as an N95 filtering facepiece respirator. This type of respirator requires fit testing.

Caring for a patient in the later stages of disease (bleeding, vomiting, diarrhea, etc). If we assume the highest generation rate (4) and a standard patient room (control level = 2, 3-6 ACH), a respirator with an APF of at least 50 is needed. In the United States, this would be equivalent to either a full-facepiece air-purifying (negative-pressure) respirator or a half-facepiece PAPR (positive pressure), but standards differ in other countries. Fit testing is required for these types of respirators.

The control level (room ventilation) can have a big effect on respirator selection. For the same patient housed in a negative-pressure airborne infection isolation room (6-12 ACH), a respirator with an assigned protection factor of 25 is required. This would correspond in the United States to a PAPR with a loose-fitting facepiece or with a helmet or hood. This type of respirator does not need fit testing.

Implications for protecting health workers in Africa

Healthcare workers have experienced very high rates of morbidity and mortality in the past and current Ebola virus outbreaks. A facemask, or surgical mask, offers no or very minimal protection from infectious aerosol particles. As our examples illustrate, for a risk group 4 organism like Ebola, the minimum level of protection should be an N95 filtering facepiece respirator.

This type of respirator, however, would only be appropriate only when the likelihood of aerosol exposure is very low. For healthcare workers caring for many patients in an epidemic situation, this type of respirator may not provide an adequate level of protection.

For a risk group 4 organism, any activity that has the potential for aerosolizing liquid body fluids, such as medical or disinfection procedures, should be avoided, if possible. Our risk assessment indicates that a PAPR with a full facepiece (APF = 50) or a hood or helmet (APF = 25) would be a better choice for patient care during epidemic conditions.

We recognize that PAPRs present some logistical and infection-control problems. Batteries require frequent charging (which requires a reliable source of electricity), and the entire ensemble requires careful handling and disinfection between uses. A PAPR is also more expensive to buy and maintain than other types of respirators.

On the other hand, a PAPR with a loose-fitting facepiece (hood or helmet) does not require fit testing. Wearing this type of respirator minimizes the need for other types of PPE, such as head coverings and goggles. And, most important, it is much more comfortable to wear than a negative-pressure respirator like an N95, especially in hot environments.

A recent report from a Medecins Sans Frontieres healthcare worker in Sierra Leone30 notes that healthcare workers cannot tolerate the required PPE for more than 40 minutes. Exiting the workplace every 40 minutes requires removal and disinfection or disposal (burning) of all PPE. A PAPR would allow much longer work periods, use less PPE, require fewer doffing episodes, generate less infectious waste, and be more protective. In the long run, we suspect this type of protection could also be less expensive.

Adequate protection is essential

To summarize, for the following reasons we believe that Ebola could be an opportunistic aerosol-transmissible disease requiring adequate respiratory protection:
•Patients and procedures generate aerosols, and Ebola virus remains viable in aerosols for up to 90 minutes.
•All sizes of aerosol particles are easily inhaled both near to and far from the patient.
•Crowding, limited air exchange, and close interactions with patients all contribute to the probability that healthcare workers will be exposed to high concentrations of very toxic infectious aerosols.
•Ebola targets immune response cells found in all epithelial tissues, including in the respiratory and gastrointestinal system.
•Experimental data support aerosols as a mode of disease transmission in non-human primates.

Risk level and working conditions suggest that a PAPR will be more protective, cost-effective, and comfortable than an N95 filtering facepiece respirator.

Acknowledgements

We thank Kathleen Harriman, PhD, MPH, RN, Chief, Vaccine Preventable Diseases Epidemiology Section, Immunization Branch, California Department of Public Health, and Nicole Vars McCullough, PhD, CIH, Manager, Global Technical Services, Personal Safety Division, 3M Company, for their input and review.

References
1.Oberg L, Brosseau LM. Surgical mask filter and fit performance. Am J Infect Control 2008 May;36(4):276-82

2.CDC. Ebola hemorrhagic fever: transmission. 2014 Aug 13

3.ECDC. Outbreak of Ebola virus disease in West Africa: third update, 1 August 2014. Stockholm: ECDC 2014 Aug 1

4.Martin-Moreno JM, Llinas G, Hernandez JM. Is respiratory protection appropriate in the Ebola response? Lancet 2014 Sep 6;384(9946):856

5.Papineni RS, Rosenthal FS. The size distribution of droplets in the exhaled breath of healthy human subjects. J Aerosol Med 1997;10(2):105-16

6.Chao CYH, Wan MP, Morawska L, et al. Characterization of expiration air jets and droplet size distributions immediately at the mouth opening. J Aerosol Sci 2009 Feb;40(2):122-33

7.Nicas M, Nazaroff WW, Hubbard A. Toward understanding the risk of secondary airborne infection: emission of respirable pathogens. J Occup Environ Hyg 2005 Mar;2(3):143-54

8.Bauchsch DG, Towner JS, Dowell SF, et al. Assessment of the risk of Ebola virus transmission from bodily fluids and fomites. J Infect Dis 2007;196:S142-7

9.Formenty P, Leroy EM, Epelboin A, et al. Detection of Ebola virus in oral fluid specimens during outbreaks of Ebola virus hemorrhagic fever in the Republic of Congo. Clin Infect Dis 2006 Jun;42(11):1521-6

10.Francesconi P, Yoti Z, Declich S, et al. Ebola hemorrhagic fever transmission and risk factors of contacts, Uganda. Emerg Infect Dis 2003 Nov;9(11):1430-7

11.Dowell SF, Mukunu R, Ksiazek TG, et al. Transmission of Ebola hemorrhagic fever: a study of risk factors in family members, Kikwit, Democratic Republic of Congo, 1995. J Infect Dis 1999 Feb;179:S87-91

12.Roels TH, Bloom AS, Buffington J, et al. Ebola hemorrhagic fever, Kikwit, Democratic Republic of the Congo, 1995: risk factors for patients without a reported exposure. J Infect Dis 1999 Feb;179:S92-7

13.Kuhl A, Hoffmann M, Muller MA, et al. Comparative analysis of Ebola virus glycoprotein interactions with human and bat cells. J Infect Dis 2011 Nov;204:S840-9

14.Hunt CL, Lennemann NJ, Maury W. Filovirus entry: a novelty in the viral fusion world. Viruses 2012 Feb;4(2):258-75

15.Bray M, Geisbert TW. Ebola virus: the role of macrophages and dendritic cells in the pathogenesis of Ebola hemorrhagic fever. Int J Biochem Cell Biol 2005 Aug;37(8):1560-6

16.Mohamadzadeh M, Chen L, Schmaljohn AL. How Ebola and Marburg viruses battle the immune system. Nat Rev Immunol 2007 Jul;7(7):556-67

17.Lindsley WG, Blachere FM, Thewlis RE, et al. Measurements of airborne influenza virus in aerosol particles from human coughs. PLoS One 2010 Nov 30;5(11):e15100

18.Caul EO. Small round structured viruses: airborne transmission and hospital control. Lancet 1994 May 21;343(8908):1240-2

19.Chadwick PR, Walker M, Rees AE. Airborne transmission of a small round structured virus. Lancet 1994 Jan 15;343(8890):171

20.Best EL, Snadoe JA, Wilcox MH. Potential for aerosolization of Clostridium difficile after flushing toilets: the role of toilet lids in reducing environmental contamination. J Hosp Infect 2012 Jan;80(1):1-5

21.Gerba CP, Wallis C, Melnick JL. Microbiological hazards of household toilets: droplet production and the fate of residual organisms. Appl Microbiol 1975 Aug;30(2):229-37

22.Barker J, Jones MV. The potential spread of infection caused by aerosol contamination of surfaces after flushing a domestic toilet. J Appl Microbiol 2005;99(2):339-47

23.Piercy TJ, Smither SJ, Steward JA, et al. The survival of filoviruses in liquids, on solid substrates and in a dynamic aerosol. J Appl Microbiol 2010 Nov;109(5):1531-9

24.Jaax N, Jahrling P, Geisbert T, et al. Transmission of Ebola virus (Zaire strain) to uninfected control monkeys in a biocontainment laboratory. Lancet 1995 Dec 23-30;346(8991-2):1669-71

25.Kobinger GP, Leung A, Neufeld J, et al. Replication, pathogenicity, shedding and transmission of Zaire ebolavirus in pigs. J Infect Dis 2011 Jul 15;204(2):200-8

26.Weingartl HM, Embury-Hyatt C, Nfon C, et al. Transmission of Ebola virus from pigs to non-human primates. Sci Rep 2012;2:811

27.Reed DS, Lackemeyer MG, Garza NL, et al. Aerosol exposure to Zaire Ebolavirus in three nonhuman primate species: differences in disease course and clinical pathology. Microb Infect 2011 Oct;13(11):930-6

28.Roy CJ, Milton DK. Airborne transmission of communicable infection—the elusive pathway. N Engl J Med 2004 Apr;350(17):1710-2

29.Canadian Standards Association. Selection, use and care of respirators. CAN/CSA Z94.4-11

30.Wolz A. Face to face with Ebola—an emergency care center in Sierra Leone. (Perspective) N Engl J Med 2014 Aug 27

http://www.cidrap.umn.edu/news-perspective/2014/09/commentary-health-workers-need-optimal-respiratory-protection-ebola

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

Introducing the first bank of feces

BY Erika Engelhaupt

A new nonprofit called OpenBiome is hoping to do for fecal transplants what blood banks have done for transfusions. It’s a kind of Brown Cross.

And it’s an idea whose time has come. Recent trials testing transplants of fecal microbes from the healthy to the sick have been so promising that people are attempting dangerous do-it-yourself fecal transplants by enema, for lack of access to authorized medical procedures.

Graduate students Carolyn Edelstein and Mark B. Smith got the idea for OpenBiome after a friend had trouble getting a fecal transplant to treat an infection with Clostridium difficile. The bacterium causes dangerous, even fatal, diarrhea and in an increasing number of cases is resistant to antibiotics.

People tend to get C. difficile infections after antibiotics or chemotherapy has knocked out helpful bacteria, allowing what is normally a background player to take over. Transplants of fecal bacteria from healthy donors can help reset the microbiome, the mix of bacteria in the body, and crowd out C. difficile. A 2011 review of 317 patients treated for C. difficile found that fecal transplants cleared up infections in 92 percent of patients. And more recent research showed that taking a round of pills containing bacteria isolated from fecal matter (without the feces itself) resolved C. difficile infections in all of 32 patients treated.

There’s also interest in transplanting healthy fecal microbiomes into people with inflammatory bowel disease or even obesity. In one recent test, mice implanted with fecal microbes from thin humans stayed thin, while mice given bacteria from obese people gained weight.

But the transplants are hard to get. As Edelstein and Smith’s friend learned, the U.S. Food and Drug Administration requires lots of paperwork for the experimental therapy, and donor feces has to be screened for a host of potential pathogens.

That’s where OpenBiome steps in. The nonprofit offers hospitals fecal samples for $250 that have been prescreened to ensure they are free of pathogens and parasites. Since October, they’ve sent more than 100 samples to a dozen hospitals and clinics, according to an interview with Smith in the Chronicle of Higher Education. Edelstein, who’s studying public affairs at Princeton, and Smith, who’s studying microbiology at MIT, recruited friends and donors and negotiated permissions with the FDA to set up the organization, which houses its samples at MIT. OpenBiome is also offering to collaborate with researchers for long-term follow-up on patients’ microbiomes.

Because FDA considers feces to be a drug in the context of transplants, OpenBiome is providing stool only for treatment of C. difficile. People hoping to shift their microbiomes for other purposes are still out of luck. Until more testing and approval comes through, that leaves open the risk that some people may resort to home transplants.

Let me be very clear about this: Whipping up an enema of your friend’s stool is a terrible idea.There are excellent reasons why people normally avoid poop: It can carry pathogens and parasites that cause serious disease. Even a donor who appears perfectly healthy might be carrying around bacteria or viruses that his or her immune system or particular microbiome mix is able to deal with. Your mileage may vary.

Your genetics, your immune system, your diet and environment — all these things create the ecology of your insides, making it hard to predict what your outcome might be. What’s more, you may need to make other medically supervised changes along with the transplant. Research on microbiome links to obesity, for instance, suggests that a new “skinny” microbiome has to be accompanied by a switch to a diet lower in fat and calories, or else the new microbes will just be outcompeted.

These dangers and complicating factors are why a supply of prescreened stool is so important. The procedures need to be done under medical supervision, and when done right the results look really promising. The recently tested pill approach avoids some of the yuck factor of fecal transplants, but most transplants are done via an enema, colonoscopy or nose tube to the gut.

If you get transplant material from OpenBiome, you’ll have to submit to one of the usual transplant methods rather than a pill, but you can rest assured you’re getting high-quality stuff. Not only are the samples screened, the donors are among the best and brightest: a few young researchers and scientists from Harvard and MIT.

Introducing the first bank of feces

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