The Pronk Pops Show 344, October 6, 2014, Story 1: Is The Ebola Dallas Strain (EDS), an airborne, contagious, incurable and lethal virus mutation, now the source of a world-wide pandemic? — The American People Demand To Be Told The Truth — Videos

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The Pronk Pops Show Podcasts

Pronk Pops Show 344: October 6, 2014

Pronk Pops Show 343: October 3, 2014

Pronk Pops Show 342: October 2, 2014

Pronk Pops Show 341: October 1, 2014

Pronk Pops Show 340: September 30, 2014

Pronk Pops Show 339: September 29, 2014

Pronk Pops Show 338: September 26, 2014

Pronk Pops Show 337: September 25, 2014

Pronk Pops Show 336: September 24, 2014

Pronk Pops Show 335: September 23 2014

Pronk Pops Show 334: September 22 2014

Pronk Pops Show 333: September 19 2014

Pronk Pops Show 332: September 18 2014

Pronk Pops Show 331: September 17, 2014

Pronk Pops Show 330: September 16, 2014

Pronk Pops Show 329: September 15, 2014

Pronk Pops Show 328: September 12, 2014

Pronk Pops Show 327: September 11, 2014

Pronk Pops Show 326: September 10, 2014

Pronk Pops Show 325: September 9, 2014

Pronk Pops Show 324: September 8, 2014

Pronk Pops Show 323: September 5, 2014

Pronk Pops Show 322: September 4, 2014

Pronk Pops Show 321: September 3, 2014

Pronk Pops Show 320: August 29, 2014

Pronk Pops Show 319: August 28, 2014

Pronk Pops Show 318: August 27, 2014 

Pronk Pops Show 317: August 22, 2014

Pronk Pops Show 316: August 20, 2014

Pronk Pops Show 315: August 18, 2014

Pronk Pops Show 314: August 15, 2014

Pronk Pops Show 313: August 14, 2014

Pronk Pops Show 312: August 13, 2014

Pronk Pops Show 311: August 11, 2014

Pronk Pops Show 310: August 8, 2014

Pronk Pops Show 309: August 6, 2014

Pronk Pops Show 308: August 4, 2014

Pronk Pops Show 307: August 1, 2014 

Pronk Pops Show 306: July 31, 2014

Pronk Pops Show 305: July 30, 2014

Pronk Pops Show 304: July 29, 2014

Pronk Pops Show 303: July 28, 2014

Pronk Pops Show 302: July 24, 2014

Pronk Pops Show 301: July 23, 2014

Pronk Pops Show 300: July 22, 2014

Pronk Pops Show 299: July 21, 2014

Pronk Pops Show 298: July 18, 2014

Pronk Pops Show 297: July 17, 2014

Pronk Pops Show 296: July 16, 2014

Pronk Pops Show 295: July 15, 2014

Pronk Pops Show 294: July 14, 2014

Pronk Pops Show 293: July 11, 2014

Pronk Pops Show 292: July 9, 2014

Pronk Pops Show 291: July 7, 2014

Pronk Pops Show 290: July 3, 2014

Pronk Pops Show 289: July 2, 2014

Story 1: Is The Ebola Dallas Strain (EDS), an airborne, contagious, incurable and lethal virus mutation, now the source of a world-wide pandemic? — The American People Demand To Be Told The Truth — Videos

The_Hot_Zone_(cover)f and b cover of book1coming-plague-side

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Ebola could be spread through air in tight quarters, some scientists fear

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Pandemic Infectious Diseases: Bacteria Viruses Parasites BBC Horizon Documentary

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Dallas County Judge Clay Jenkins Weighs in on Ebola – Why? October 1, 2014

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Ebola Virus Outbreaks – WARNING

What is a Pandemic?

Hospitals “Full-Up”: The 1918 Influenza Pandemic

We Heard the Bells: The Influenza of 1918 (full documentary)

Spanish Flu: The Forgotten Fallen

The world’s deadliest virus Ebola Plague Fighters Nova Documentary

Ebola – What You’re Not Being Told

Dallas Ebola Victim Acquired His Infection On His Aircraft +50% Probability

Aerosolizing ONE DROP of EBOLA = 1/2 MILLION DEAD

US Army: Ebola like FLU needs Winter Weather to go AIRBORNE

CDC Warns On AIRBORNE EBOLA

Tracking the travel of Ebola patient

How the CDC uses contact tracing to stop Ebola’s spread

‘Contact tracing’: Tracking Ebola in the U.S. | USA NOW

Has The Ebola Pandemic Started?

Ebola in Dallas: Here’s Why This Case is Different

Laurie Garrett: What can we learn from the 1918 flu?

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Author tracks Ebola outbreaks over decades, calls virus “Jack The Ripper”

Ebola Virus Symptoms | Ebola Virus effects on Human Body

What is Ebola? – Truthloader

The Hot Zone by Richard Preston Audiobook 1 of 8

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CDC’s Ebola Containment Failure by Design

CDC Director: Ebola Travel Ban Will Only Make It Worse

Ebola Rolls Out Exactly As Predicted

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Fuel Air Bomb _ Outbreak 1995

Outbreak, biological weapon scene

 

 

CDC: Airborne Ebola possible but unlikely

By Elise Viebeck

The Ebola virus becoming airborne is a possible but unlikely outcome in the current epidemic, Centers for Disease Control and Prevention (CDC) Director Tom Frieden said Tuesday.

The outbreak involves Ebola Zaire, a strain that is passed through bodily fluids, not the air. But some experts have expressed fear about viral mutations due to the unprecedented — and rising — number of Ebola cases.

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Frieden sought to allay those fears during a call with reporters.

“The rate of change [with Ebola] is slower than most viruses, and most viruses don’t change how they spread,” he said. Frieden is unofficially spearheading the U.S. response to Ebola.

“That is not to say it’s impossible that it could change [to become airborne],” he continued. “That would be the worst-case scenario. We would know that by looking at … what is happening in Africa. That is why we have scientists from the CDC on the ground tracking that.”

A change in the way Ebola spreads would make the virus significantly more dangerous. The disease kills roughly half the people it infects, and lacking a vaccine or cure, its traceable chain of transmission through bodily fluids is one reason officials believe they can contain it.

Still, there is almost no precedent for a human virus mutating to become transmissible in a different way, a key piece of evidence in weighing whether that kind of shift is likely for Ebola.

“We have so many problems with Ebola, let’s not make another one that, of course, is theoretically possible but is pretty way down on the list of likely issues,” infectious diseases expert William Schaffner of Vanderbilt University told Scientific American.

Frieden touted new progress against Ebola in West Africa and Dallas, where a Liberian man remains in critical condition, but warned that “globally, this is going to be a long, hard fight.”

The Dallas patient interacted with 10 definite and 38 possible interlocturos who are now being monitored, he said. None have shown symptoms.

http://thehill.com/policy/healthcare/220046-cdc-airborne-ebola-possible-but-unlikely

 

Some Ebola experts worry virus may spread more easily than assumed

Ebola could be spread through air in tight quarters, some scientists fear
Some Ebola experts worry that the virus may spread more easily than thought — through the air in small spaces, for example.
By DAVID WILLMAN contact the reporter NationMedical ResearchAfricaScientific ResearchDiseases and IllnessesEbolaU.S. Centers for Disease Control and Prevention

Ebola researcher says he would not rule out possibility that the virus spreads through air in tight quarters
‘There are too many unknowns here,’ a virologist says of how Ebola may spread
Ebola researcher says he thinks there is a chance asymptomatic people could spread the virus
U.S. officials leading the fight against history’s worst outbreak of Ebola have said they know the ways the virus is spread and how to stop it. They say that unless an air traveler from disease-ravaged West Africa has a fever of at least 101.5 degrees or other symptoms, co-passengers are not at risk.

“At this point there is zero risk of transmission on the flight,” Dr. Thomas Frieden, director of the federal Centers for Disease Control and Prevention, said after a Liberian man who flew through airports in Brussels and Washington was diagnosed with the disease last week in Dallas.

First Ebola infection outside West Africa
Three more people have been hospitalized in Madrid for possible exposure to the Ebola virus after a Spanish nurse tested positive for the virus.
Other public health officials have voiced similar assurances, saying Ebola is spread only through physical contact with a symptomatic individual or their bodily fluids. “Ebola is not transmitted by the air. It is not an airborne infection,” said Dr. Edward Goodman of Texas Health Presbyterian Hospital in Dallas, where the Liberian patient remains in critical condition.

Yet some scientists who have long studied Ebola say such assurances are premature — and they are concerned about what is not known about the strain now on the loose. It is an Ebola outbreak like none seen before, jumping from the bush to urban areas, giving the virus more opportunities to evolve as it passes through multiple human hosts.

Dr. C.J. Peters, who battled a 1989 outbreak of the virus among research monkeys housed in Virginia and who later led the CDC’s most far-reaching study of Ebola’s transmissibility in humans, said he would not rule out the possibility that it spreads through the air in tight quarters.

“We just don’t have the data to exclude it,” said Peters, who continues to research viral diseases at the University of Texas in Galveston.

 

Dr. Philip K. Russell, a virologist who oversaw Ebola research while heading the U.S. Army’s Medical Research and Development Command, and who later led the government’s massive stockpiling of smallpox vaccine after the Sept. 11 terrorist attacks, also said much was still to be learned. “Being dogmatic is, I think, ill-advised, because there are too many unknowns here.”

If Ebola were to mutate on its path from human to human, said Russell and other scientists, its virulence might wane — or it might spread in ways not observed during past outbreaks, which were stopped after transmission among just two to three people, before the virus had a greater chance to evolve. The present outbreak in West Africa has killed approximately 3,400 people, and there is no medical cure for Ebola.

“I see the reasons to dampen down public fears,” Russell said. “But scientifically, we’re in the middle of the first experiment of multiple, serial passages of Ebola virus in man…. God knows what this virus is going to look like. I don’t.”
A resident looks from behind a gate during the Liberian government’s 11-day Ebola quarantine in the West Point district of Monrovia.
Tom Skinner, a spokesman for the CDC in Atlanta, said health officials were basing their response to Ebola on what has been learned from battling the virus since its discovery in central Africa in 1976. The CDC remains confident, he said, that Ebola is transmitted principally by direct physical contact with an ill person or their bodily fluids.

Skinner also said the CDC is conducting ongoing lab analyses to assess whether the present strain of Ebola is mutating in ways that would require the government to change its policies on responding to it. The results so far have not provided cause for concern, he said.

The researchers reached in recent days for this article cited grounds to question U.S. officials’ assumptions in three categories.

 

One issue is whether airport screenings of prospective travelers to the U.S. from West Africa can reliably detect those who might have Ebola. Frieden has said the CDC protocols used at West African airports can be relied on to prevent more infected passengers from coming to the U.S.

“One hundred percent of the individuals getting on planes are screened for fever before they get on the plane,” Frieden said Sept. 30. “And if they have a fever, they are pulled out of the line, assessed for Ebola, and don’t fly unless Ebola is ruled out.”

Individuals who have flown recently from one or more of the affected countries suggested that travelers could easily subvert the screening procedures — and might have incentive to do so: Compared with the depleted medical resources in the West African countries of Liberia, Sierra Leone and Guinea, the prospect of hospital care in the U.S. may offer an Ebola-exposed person the only chance to survive.

U.S. To Increase Airport Screening For Ebola
The deteriorating conditions in Africa make it more likely additional cases of Ebola will appear in the United States and officials are pushing for increased screenings at airports.
A person could pass body temperature checks performed at the airports by taking ibuprofen or any common analgesic. And prospective passengers have much to fear from identifying themselves as sick, said Kim Beer, a resident of Freetown, the capital of Sierra Leone, who is working to get medical supplies into the country to cope with Ebola.

“It is highly unlikely that someone would acknowledge having a fever, or simply feeling unwell,” Beer said via email. “Not only will they probably not get on the flight — they may even be taken to/required to go to a ‘holding facility’ where they would have to stay for days until it is confirmed that it is not caused by Ebola. That is just about the last place one would want to go.”

Liberian officials said last week that the patient hospitalized in Dallas, Thomas Eric Duncan, did not report to airport screeners that he had had previous contact with an Ebola-stricken woman. It is not known whether Duncan knew she suffered from Ebola; her family told neighbors it was malaria.
The potential disincentive for passengers to reveal their own symptoms was echoed by Sheka Forna, a dual citizen of Sierra Leone and Britain who manages a communications firm in Freetown. Forna said he considered it “very possible” that people with fever would medicate themselves to appear asymptomatic.

It would be perilous to admit even nonspecific symptoms at the airport, Forna said in a telephone interview. “You’d be confined to wards with people with full-blown disease.”

On Monday, the White House announced that a review was underway of existing airport procedures. Frieden and President Obama’s assistant for homeland security and counter-terrorism, Lisa Monaco, said Friday that closing the U.S. to passengers from the Ebola-affected countries would risk obstructing relief efforts.

CDC officials also say that asymptomatic patients cannot spread Ebola. This assumption is crucial for assessing how many people are at risk of getting the disease. Yet diagnosing a symptom can depend on subjective understandings of what constitutes a symptom, and some may not be easily recognizable. Is a person mildly fatigued because of short sleep the night before a flight — or because of the early onset of disease?
Moreover, said some public health specialists, there is no proof that a person infected — but who lacks symptoms — could not spread the virus to others.

“It’s really unclear,” said Michael Osterholm, a public health scientist at the University of Minnesota who recently served on the U.S. government’s National Science Advisory Board for Biosecurity. “None of us know.”

Russell, who oversaw the Army’s research on Ebola, said he found the epidemiological data unconvincing.
“The definition of ‘symptomatic’ is a little difficult to deal with,” he said. “It may be generally true that patients aren’t excreting very much virus until they become ill, but to say that we know the course of [the virus’ entry into the bloodstream] and the course of when a virus appears in the various secretions, I think, is premature.”

The CDC’s Skinner said that while officials remained confident that Ebola can be spread only by the overtly sick, the ongoing studies would assess whether mutations that might occur could increase the potential for asymptomatic patients to spread it.

Finally, some also question the official assertion that Ebola cannot be transmitted through the air. In late 1989, virus researcher Charles L. Bailey supervised the government’s response to an outbreak of Ebola among several dozen rhesus monkeys housed for research in Reston, Va., a suburb of Washington.

What Bailey learned from the episode informs his suspicion that the current strain of Ebola afflicting humans might be spread through tiny liquid droplets propelled into the air by coughing or sneezing.

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“We know for a fact that the virus occurs in sputum and no one has ever done a study [disproving that] coughing or sneezing is a viable means of transmitting,” he said. Unqualified assurances that Ebola is not spread through the air, Bailey said, are “misleading.”

Peters, whose CDC team studied cases from 27 households that emerged during a 1995 Ebola outbreak in Democratic Republic of Congo, said that while most could be attributed to contact with infected late-stage patients or their bodily fluids, “some” infections may have occurred via “aerosol transmission.”

Ailing in Monrovia, Liberia
Relatives pray over a weak Siata Johnson, 23, outside the Ebola treatment center at a hospital on the outskirts of Monrovia, Liberia. (John Moore / Getty Images)
Skinner of the CDC, who cited the Peters-led study as the most extensive of Ebola’s transmissibility, said that while the evidence “is really overwhelming” that people are most at risk when they touch either those who are sick or such a person’s vomit, blood or diarrhea, “we can never say never” about spread through close-range coughing or sneezing.

“I’m not going to sit here and say that if a person who is highly viremic … were to sneeze or cough right in the face of somebody who wasn’t protected, that we wouldn’t have a transmission,” Skinner said.

Peters, Russell and Bailey, who in 1989 was deputy commander for research of the Army’s Medical Research Institute of Infectious Diseases, in Frederick, Md., said the primates in Reston had appeared to spread Ebola to other monkeys through their breath.

 

The Ebola strain found in the monkeys did not infect their human handlers. Bailey, who now directs a biocontainment lab at George Mason University in Virginia, said he was seeking to research the genetic differences between the Ebola found in the Reston monkeys and the strain currently circulating in West Africa.

Though he acknowledged that the means of disease transmission among the animals would not guarantee the same result among humans, Bailey said the outcome may hold lessons for the present Ebola epidemic.

“Those monkeys were dying in a pattern that was certainly suggestive of coughing and sneezing — some sort of aerosol movement,” Bailey said. “They were dying and spreading it so quickly from cage to cage. We finally came to the conclusion that the best action was to euthanize them all.”

http://www.latimes.com/nation/la-na-ebola-questions-20141007-story.html#page=2

No gloves, no masks: Dallas officials send a message of calm amid Ebola fears

By Abby Phillip

Dallas County Judge Clay Jenkins pulled into the Ivy Apartments community late in the evening Friday wearing suit pants and a lavender dress shirt.

There were hazardous materials trucks all around, as cleaning crews had arrived to remove materials that might have been touched by Thomas Duncan, a Liberian man who is hospitalized in Texas with Ebola. The hazmat workers were covered from head to toe in bright yellow body suits, green gloves and breathing masks.

Jenkins walked into the apartment in building No. 6 to greet Louise Troh, her family and others who live with her and had been court-ordered to stay in their home because they were considered high risk after coming into contact with Duncan.

It was time to move, and Troh, her 13-year old son, a relative of Duncan’s and another man — all of whom lived in the apartment — got into the judge’s car for the 45-minute drive to their new, temporary home, in an undisclosed part of Dallas.

Jenkins, the judge, never covered up.

“I’m a married man with a little girl,” Jenkins told reporters later that night. “I’m wearing the same shirt I was when I was in the car with that family.

“I was in their house next to those materials, meeting with them, listening to them, and assuring them last night and again of course today. If there were any risk, I would not expose myself or my family to that risk.”

He added: “There is zero risk.”

In the face of widespread fear — and in some cases misinformation — about Ebola following the first diagnosis of the virus in the United States, Dallas officials have taken a notable visual approach to make the point that, at least right now, the city is safe.
The Ebola outbreak in West Africa has reached the United States, as officials confirm one case in Dallas. Here’s how U.S. health officials plan to stop the virus. (Gillian Brockell and Jorge Ribas/The Washington Post)
On a daily basis, workers monitoring the temperatures and health of as many as nine individuals who they believe might have had direct contact with Duncan have entered those people’s homes with no gloves, no masks and no personal protective equipment whatsoever.

And city officials including Jenkins, Dallas Mayor Mike Rawlings and Dallas County Health and Human Services Director Zachary Thompson have interacted with the family no differently that they might have if the four people who are in a state of semi-isolation had been suspected of having come into contact with somebody sick with the flu.
“Based on our assessment, they were asymptomatic; therefore, I didn’t feel they posed any threat to me,” Thompson said in an interview with The Washington Post on Monday. “There is a standard procedure for when they should be using the PPE’s (personal protective equipment). In this case we knew our nurses, our staff, had assessed that they were asymptomatic.”

So far, none of the people who have potentially had contact with Duncan are showing any symptoms, Thompson said.

Yet concern and stigma are widespread in Dallas.

Photographs from Liberia, Sierra Leone and Guinea — where the epidemic is spiraling out of control — frequently show fully masked health workers carrying infected people to hospitals or burial sites. Those images have become closely associated with the virus and the outbreak in the public’s mind.

And for one day, similar images briefly appeared in Dallas as cleaning crews removed materials from Troh’s apartment that might have come into contact with the virus.
A hazmat team arrives on Oct. 3 to clean a unit at the Dallas apartment complex where the confirmed Ebola patient was staying. (Joe Raedle/Getty Images)
The decision for the crew to wear personal protective equipment was made by the company, the “Cleaning Guys,” according to Dallas officials.

“We train for this type of thing,” company executive Brad Smith told ABC News. “Obviously, we haven’t trained for Ebola because there hasn’t been a situation in Texas until now.”

The Ebola virus is not very hearty outside of the human body.

Still, touching and destroying potentially infected materials is far different from speaking to or being in the same room with people who might have been exposed to the virus.

And public health expert Gavin Macgregor-Skinner, who worked in Nigeria to end that country’s outbreak, said that treating people with a sense of humanity and not feeding hysteria is critical to managing the Dallas Ebola case and others that might occur around the world.

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“Even in West Africa when we do contact tracing, we don’t put on personal protective equipment,” said Macgregor-Skinner, an assistant professor in the Department of Public Health Sciences at the Penn State Milton S. Hershey Medical Center. “We have the six-feet rule: We stay about six feet away from people and I can interview them and I can make them feel like people.

“If they have no symptoms, we need to make them feel normal, like they’re part of the community, like they are still loved.”

Dallas officials have also urged residents to go about their normal activities and attend community gatherings and fairs without fear.

“The broader perspective is that we had done immediate disease tracking and contact tracing and the family had been identified who had had close contact and they had not shown any symptoms,” said Thompson. “Other than that one case, basically, his virus has been contained.”

http://www.washingtonpost.com/news/to-your-health/wp/2014/10/06/no-gloves-no-masks-dallas-officials-send-a-message-of-calm-amid-ebola-fears/

 

‘In 1976 I discovered Ebola – now I fear an unimaginable tragedy’

Peter Piot was a researcher at a lab in Antwerp when a pilot brought him a blood sample from a Belgian nun who had fallen mysteriously ill in Zaire
Peter Piot
Professor Peter Piot, the Director of the London School of Hygiene and Tropical Medicine: ‘Around June it became clear to me there was something different about this outbreak. I began to get really worried’ Photograph: Leon Neal/AFP

Professor Piot, as a young scientist in Antwerp, you were part of the team that discovered the Ebola virus in 1976. How did it happen?

I still remember exactly. One day in September, a pilot from Sabena Airlines brought us a shiny blue Thermos and a letter from a doctor in Kinshasa in what was then Zaire. In the Thermos, he wrote, there was a blood sample from a Belgian nun who had recently fallen ill from a mysterious sickness in Yambuku, a remote village in the northern part of the country. He asked us to test the sample for yellow fever.

These days, Ebola may only be researched in high-security laboratories. How did you protect yourself back then?

We had no idea how dangerous the virus was. And there were no high-security labs in Belgium. We just wore our white lab coats and protective gloves. When we opened the Thermos, the ice inside had largely melted and one of the vials had broken. Blood and glass shards were floating in the ice water. We fished the other, intact, test tube out of the slop and began examining the blood for pathogens, using the methods that were standard at the time.

But the yellow fever virus apparently had nothing to do with the nun’s illness.

No. And the tests for Lassa fever and typhoid were also negative. What, then, could it be? Our hopes were dependent on being able to isolate the virus from the sample. To do so, we injected it into mice and other lab animals. At first nothing happened for several days. We thought that perhaps the pathogen had been damaged from insufficient refrigeration in the Thermos. But then one animal after the next began to die. We began to realise that the sample contained something quite deadly.

But you continued?

Other samples from the nun, who had since died, arrived from Kinshasa. When we were just about able to begin examining the virus under an electron microscope, the World Health Organisation instructed us to send all of our samples to a high-security lab in England. But my boss at the time wanted to bring our work to conclusion no matter what. He grabbed a vial containing virus material to examine it, but his hand was shaking and he dropped it on a colleague’s foot. The vial shattered. My only thought was: “Oh, shit!” We immediately disinfected everything, and luckily our colleague was wearing thick leather shoes. Nothing happened to any of us.

In the end, you were finally able to create an image of the virus using the electron microscope.

Yes, and our first thought was: “What the hell is that?” The virus that we had spent so much time searching for was very big, very long and worm-like. It had no similarities with yellow fever. Rather, it looked like the extremely dangerous Marburg virus which, like ebola, causes a haemorrhagic fever. In the 1960s the virus killed several laboratory workers in Marburg, Germany.

Were you afraid at that point?

I knew almost nothing about the Marburg virus at the time. When I tell my students about it today, they think I must come from the stone age. But I actually had to go the library and look it up in an atlas of virology. It was the American Centres for Disease Control which determined a short time later that it wasn’t the Marburg virus, but a related, unknown virus. We had also learned in the meantime that hundreds of people had already succumbed to the virus in Yambuku and the area around it.

A few days later, you became one of the first scientists to fly to Zaire.

Yes. The nun who had died and her fellow sisters were all from Belgium. In Yambuku, which had been part of the Belgian Congo, they operated a small mission hospital. When the Belgian government decided to send someone, I volunteered immediately. I was 27 and felt a bit like my childhood hero, Tintin. And, I have to admit, I was intoxicated by the chance to track down something totally new.

Suspected Ebola patient in MonroviaA girl is led to an ambulance after showing signs of Ebola infection in the village of Freeman Reserve, 30 miles north of the Liberian capital, Monrovia. Photograph: Jerome Delay/APWas there any room for fear, or at least worry?

Of course it was clear to us that we were dealing with one of the deadliest infectious diseases the world had ever seen – and we had no idea that it was transmitted via bodily fluids! It could also have been mosquitoes. We wore protective suits and latex gloves and I even borrowed a pair of motorcycle goggles to cover my eyes. But in the jungle heat it was impossible to use the gas masks that we bought in Kinshasa. Even so, the Ebola patients I treated were probably just as shocked by my appearance as they were about their intense suffering. I took blood from around 10 of these patients. I was most worried about accidentally poking myself with the needle and infecting myself that way.

But you apparently managed to avoid becoming infected.

Well, at some point I did actually develop a high fever, a headache and diarrhoea …

… similar to Ebola symptoms?

Exactly. I immediately thought: “Damn, this is it!” But then I tried to keep my cool. I knew the symptoms I had could be from something completely different and harmless. And it really would have been stupid to spend two weeks in the horrible isolation tent that had been set up for us scientists for the worst case. So I just stayed alone in my room and waited. Of course, I didn’t get a wink of sleep, but luckily I began feeling better by the next day. It was just a gastrointestinal infection. Actually, that is the best thing that can happen in your life: you look death in the eye but survive. It changed my whole approach, my whole outlook on life at the time.

You were also the one who gave the virus its name. Why Ebola?

On that day our team sat together late into the night – we had also had a couple of drinks – discussing the question. We definitely didn’t want to name the new pathogen “Yambuku virus”, because that would have stigmatised the place forever. There was a map hanging on the wall and our American team leader suggested looking for the nearest river and giving the virus its name. It was the Ebola river. So by around three or four in the morning we had found a name. But the map was small and inexact. We only learned later that the nearest river was actually a different one. But Ebola is a nice name, isn’t it?

In the end, you discovered that the Belgian nuns had unwittingly spread the virus. How did that happen?

In their hospital they regularly gave pregnant women vitamin injections using unsterilised needles. By doing so, they infected many young women in Yambuku with the virus. We told the nuns about the terrible mistake they had made, but looking back I would say that we were much too careful in our choice of words. Clinics that failed to observe this and other rules of hygiene functioned as catalysts in all additional Ebola outbreaks. They drastically sped up the spread of the virus or made the spread possible in the first place. Even in the current Ebola outbreak in westAfrica, hospitals unfortunately played this ignominious role in the beginning.

After Yambuku, you spent the next 30 years of your professional life devoted to combating Aids. But now Ebola has caught up to you again. American scientists fear that hundreds of thousands of people could ultimately become infected. Was such an epidemic to be expected?

No, not at all. On the contrary, I always thought that Ebola, in comparison to Aids or malaria, didn’t present much of a problem because the outbreaks were always brief and local. Around June it became clear to me that there was something fundamentally different about this outbreak. At about the same time, the aid organisation Médecins Sans Frontières sounded the alarm. We Flemish tend to be rather unemotional, but it was at that point that I began to get really worried.

Why did WHO react so late?

On the one hand, it was because their African regional office isn’t staffed with the most capable people but with political appointees. And the headquarters in Geneva suffered large budget cuts that had been agreed to by member states. The department for haemorrhagic fever and the one responsible for the management of epidemic emergencies were hit hard. But since August WHO has regained a leadership role.

There is actually a well-established procedure for curtailing Ebola outbreaks: isolating those infected and closely monitoring those who had contact with them. How could a catastrophe such as the one we are now seeing even happen?

I think it is what people call a perfect storm: when every individual circumstance is a bit worse than normal and they then combine to create a disaster. And with this epidemic there were many factors that were disadvantageous from the very beginning. Some of the countries involved were just emerging from terrible civil wars, many of their doctors had fled and their healthcare systems had collapsed. In all of Liberia, for example, there were only 51 doctors in 2010, and many of them have since died of Ebola.

The fact that the outbreak began in the densely populated border region between Guinea, Sierra Leone and Liberia …

… also contributed to the catastrophe. Because the people there are extremely mobile, it was much more difficult than usual to track down those who had had contact with the infected people. Because the dead in this region are traditionally buried in the towns and villages they were born in, there were highly contagious Ebola corpses travelling back and forth across the borders in pickups and taxis. The result was that the epidemic kept flaring up in different places.

For the first time in its history, the virus also reached metropolises such as Monrovia and Freetown. Is that the worst thing that can happen?

In large cities – particularly in chaotic slums – it is virtually impossible to find those who had contact with patients, no matter how great the effort. That is why I am so worried about Nigeria as well. The country is home to mega-cities like Lagos and Port Harcourt, and if the Ebola virus lodges there and begins to spread, it would be an unimaginable catastrophe.

Have we completely lost control of the epidemic?

I have always been an optimist and I think that we now have no other choice than to try everything, really everything. It’s good that the United States and some other countries are finally beginning to help. But Germany or even Belgium, for example, must do a lot more. And it should be clear to all of us: This isn’t just an epidemic any more. This is a humanitarian catastrophe. We don’t just need care personnel, but also logistics experts, trucks, jeeps and foodstuffs. Such an epidemic can destabilise entire regions. I can only hope that we will be able to get it under control. I really never thought that it could get this bad.

What can really be done in a situation when anyone can become infected on the streets and, like in Monrovia, even the taxis are contaminated?

We urgently need to come up with new strategies. Currently, helpers are no longer able to care for all the patients in treatment centres. So caregivers need to teach family members who are providing care to patients how to protect themselves from infection to the extent possible. This on-site educational work is currently the greatest challenge. Sierra Leone experimented with a three-day curfew in an attempt to at least flatten out the infection curve a bit. At first I thought: “That is totally crazy.” But now I wonder, “why not?” At least, as long as these measures aren’t imposed with military power.

A three-day curfew sounds a bit desperate.

Yes, it is rather medieval. But what can you do? Even in 2014, we hardly have any way to combat this virus.

Do you think we might be facing the beginnings of a pandemic?

There will certainly be Ebola patients from Africa who come to us in the hopes of receiving treatment. And they might even infect a few people here who may then die. But an outbreak in Europe or North America would quickly be brought under control. I am more worried about the many people from India who work in trade or industry in west Africa. It would only take one of them to become infected, travel to India to visit relatives during the virus’s incubation period, and then, once he becomes sick, go to a public hospital there. Doctors and nurses in India, too, often don’t wear protective gloves. They would immediately become infected and spread the virus.

The virus is continually changing its genetic makeup. The more people who become infected, the greater the chance becomes that it will mutate …

… which might speed its spread. Yes, that really is the apocalyptic scenario. Humans are actually just an accidental host for the virus, and not a good one. From the perspective of a virus, it isn’t desirable for its host, within which the pathogen hopes to multiply, to die so quickly. It would be much better for the virus to allow us to stay alive longer.

Could the virus suddenly change itself such that it could be spread through the air?

Like measles, you mean? Luckily that is extremely unlikely. But a mutation that would allow Ebola patients to live a couple of weeks longer is certainly possible and would be advantageous for the virus. But that would allow Ebola patients to infect many, many more people than is currently the case.

But that is just speculation, isn’t it?

Certainly. But it is just one of many possible ways the virus could change to spread itself more easily. And it is clear that the virus is mutating.

You and two colleagues wrote a piece for the Wall Street Journalsupporting the testing of experimental drugs. Do you think that could be the solution?

Patients could probably be treated most quickly with blood serum from Ebola survivors, even if that would likely be extremely difficult given the chaotic local conditions. We need to find out now if these methods, or if experimental drugs like ZMapp, really help. But we should definitely not rely entirely on new treatments. For most people, they will come too late in this epidemic. But if they help, they should be made available for the next outbreak.

Testing of two vaccines is also beginning. It will take a while, of course, but could it be that only a vaccine can stop the epidemic?

I hope that’s not the case. But who knows? Maybe.

In Zaire during that first outbreak, a hospital with poor hygiene was responsible for spreading the illness. Today almost the same thing is happening. Was Louis Pasteur right when he said: “It is the microbes who will have the last word”?

Of course, we are a long way away from declaring victory over bacteria and viruses. HIV is still here; in London alone, five gay men become infected daily. An increasing number of bacteria are becoming resistant to antibiotics. And I can still see the Ebola patients in Yambuku, how they died in their shacks and we couldn’t do anything except let them die. In principle, it’s still the same today. That is very depressing. But it also provides me with a strong motivation to do something. I love life. That is why I am doing everything I can to convince the powerful in this world to finally send sufficient help to west Africa. Now!

http://www.theguardian.com/world/2014/oct/04/ebola-zaire-peter-piot-outbreak

Ebola virus disease

From Wikipedia, the free encyclopedia
“Ebola” redirects here. For other uses, see Ebola (disambiguation).
Ebola virus disease
Classification and external resources
7042 lores-Ebola-Zaire-CDC Photo.jpg

A 1976 photograph of two nurses standing in front of Mayinga N., a person with Ebola virus disease; she died only a few days later due to severe internal hemorrhaging.
ICD10 A98.4
ICD9 065.8
DiseasesDB 18043
MedlinePlus 001339
eMedicine med/626
MeSH D019142

Ebola virus disease (EVD), Ebola hemorrhagic fever (EHF), or simply Ebola is a disease of humans and other primates caused by an ebolavirus. Symptoms start two days to three weeks after contracting the virus, with afever, sore throat, muscle pain, and headaches. Typically, vomiting, diarrhea, and rash follow, along with decreased function of the liver and kidneys. Around this time, affected people may begin to bleed both within the bodyand externally.[1]

The virus may be acquired upon contact with blood or bodily fluids of an infected human or other animal.[1] Spreading through the air has not been documented in the natural environment.[2] Fruit bats are believed to be a carrier and may spread the virus without being affected. Once human infection occurs, the disease may spread between people, as well. Male survivors may be able to transmit the disease via semen for nearly two months. To make the diagnosis, typically other diseases with similar symptoms such as malaria, cholera and other viral hemorrhagic fevers are first excluded. To confirm the diagnosis, blood samples are tested for viral antibodies, viralRNA, or the virus itself.[1]

Outbreak control require community engagement, case management, surveillance and contact tracing, a good laboratory service, and safe burials.[1] Prevention includes decreasing the spread of disease from infected animals to humans. This may be done by checking such animals for infection and killing and properly disposing of the bodies if the disease is discovered. Properly cooking meat and wearing protective clothing when handling meat may also be helpful, as are wearing protective clothing and washing hands when around a person with the disease. Samples of bodily fluids and tissues from people with the disease should be handled with special caution.[1]

No specific treatment for the disease is yet available.[1] Efforts to help those who are infected are supportive and include giving either oral rehydration therapy (slightly sweet and salty water to drink) or intravenous fluids.[1] This supportive care improves outcomes.[1] The disease has a high risk of death, killing between 50% and 90% of those infected with the virus.[1][3] EVD was first identified in an area of Sudan that is now part of South Sudan, as well as in Zaire (now the Democratic Republic of the Congo). The disease typically occurs in outbreaks in tropical regions of sub-Saharan Africa.[1] From 1976 (when it was first identified) through 2013, the World Health Organization reported a total of 1,716 cases.[1][4] The largest outbreak to date is the ongoing 2014 West African Ebola outbreak, which is affecting Guinea, Sierra Leone, Liberia, and Nigeria.[5][6] As of 28 September 2014, 7,157 suspected cases resulting in the deaths of 3,330 have been reported.[7] Efforts are under way to develop a vaccine; however, none yet exists.[1]

Signs and symptoms

Signs and symptoms of Ebola.[8]

Signs and symptoms of Ebola usually begin suddenly with an influenza-like stage characterized by fatigue, fever, headaches, joint, muscle, and abdominal pain.[9][10] Vomiting, diarrhea, and loss of appetite are also common.[10]Less common symptoms include the following: sore throat, chest pain, hiccups, shortness of breath, and trouble swallowing.[10] The average time between contracting the infection and the start of symptoms (incubation period) is 8 to 10 days, but it can vary between 2 and 21 days.[10][11] Skin manifestations may include a maculopapular rash (in about 50% of cases).[12] Early symptoms of EVD may be similar to those of malaria, dengue fever, or other tropical fevers, before the disease progresses to the bleeding phase.[9]

In 40–50% of cases, bleeding from puncture sites and mucous membranes (e.g., gastrointestinal tract, nose, vagina, and gums) has been reported.[13] In the bleeding phase, which typically begins five to seven days after first symptoms,[14] internal and subcutaneous bleeding may present itself in the form of reddened eyes and bloody vomit.[9] Bleeding into the skin may create petechiae, purpura, ecchymoses, and hematomas (especially around needle injection sites). Sufferers may cough up blood, vomit it, or excrete it in their stool.

Heavy bleeding is rare and is usually confined to the gastrointestinal tract.[12][15] In general, the development of bleeding symptoms often indicates a worse prognosis and this blood loss can result in death.[9] All people infected show some signs of circulatory system involvement, including impaired blood clotting.[12] If the infected person does not recover, death due to multiple organ dysfunction syndrome occurs within 7 to 16 days (usually between days 8 and 9) after first symptoms.[14]

Causes

Life cycles of the Ebolavirus

EVD is caused by four of five viruses classified in the genus Ebolavirus, family Filoviridae, order Mononegavirales. The four disease-causing viruses are Bundibugyo virus (BDBV), Sudan virus (SUDV), Taï Forest virus (TAFV), and one called, simply, Ebola virus (EBOV, formerly Zaire Ebola virus)). Ebola virus is the sole member of the Zaire ebolavirus species and the most dangerous of the known Ebola disease-causing viruses, as well as being responsible for the largest number of outbreaks.[16] The fifth virus, Reston virus (RESTV), is not thought to be disease-causing in humans. These five viruses are closely related to the Marburg viruses.

Transmission

Human-to-human transmission can occur via direct contact with blood or bodily fluids from an infected person (including embalming of an infected dead person) or by contact with objects contaminated by the virus, particularly needles and syringes.[17] Other body fluids with ebola virus include saliva, mucus, vomit, feces, sweat, tears, breast milk, urine, and semen. Entry points include the nose, mouth, eyes, or open wounds, cuts and abrasions.[18] The potential for widespread EVD infections is considered low as the disease is only spread by direct contact with the secretions from someone who is showing signs of infection.[17] The symptoms limit a person’s ability to spread the disease as they are often too sick to travel.[19] Because dead bodies are still infectious, traditional burial rituals may spread the disease. Nearly two thirds of the cases of Ebola in Guinea during the 2014 outbreak are believed to be due to burial practices.[20][21] Semen may be infectious in survivors for up to 7 weeks.[1] It is not entirely clear how an outbreak is initially started.[22] The initial infection is believed to occur after ebola virus is transmitted to a human by contact with an infected animal’s body fluids.

One of the primary reasons for spread is that the health systems in the part of Africa where the disease occurs function poorly.[23] Medical workers who do not wear appropriate protective clothing may contract the disease.[24] Hospital-acquired transmission has occurred in African countries due to the reuse of needles and lack of universal precautions.[25][26] Some healthcare centers caring for people with the disease do not have running water.[27]

Airborne transmission has not been documented during EVD outbreaks.[2] They are, however, infectious as breathable 0.8– to 1.2-μm laboratory-generated droplets.[28] The virus has been shown to travel, without contact, from pigs to primates, although the same study failed to demonstrate similar transmission between non-human primates.[29]

Bats drop partially eaten fruits and pulp, then land mammals such as gorillas and duikers feed on these fallen fruits. This chain of events forms a possible indirect means of transmission from the natural host to animal populations, which has led to research towards viral shedding in the saliva of bats. Fruit production, animal behavior, and other factors vary at different times and places that may trigger outbreaks among animal populations.[30]

Reservoir

Bushmeat being prepared for cooking in Ghana, 2013. Human consumption of equatorial animals in Africa in the form of bushmeat has been linked to the transmission of diseases to people, including Ebola.[31]

Bats are considered the most likely natural reservoir of the EBOV. Plants, arthropods, and birds were also considered.[1][32] Bats were known to reside in the cotton factory in which the first cases for the 1976 and 1979 outbreaks were observed, and they have also been implicated in Marburg virus infections in 1975 and 1980.[33] Of 24 plant species and 19 vertebrate species experimentally inoculated with EBOV, only bats became infected.[34] The absence of clinical signs in these bats is characteristic of a reservoir species. In a 2002–2003 survey of 1,030 animals including 679 bats from Gabon and the Republic of the Congo, 13 fruit bats were found to contain EBOV RNA fragments.[35] As of 2005, three types of fruit bats (Hypsignathus monstrosus, Epomops franqueti, and Myonycteris torquata) have been identified as being in contact with EBOV. They are now suspected to represent the EBOV reservoir hosts.[36][37] Antibodies against Zaire and Reston viruses have been found in fruit bats in Bangladesh, thus identifying potential virus hosts and signs of the filoviruses in Asia.[38]

Between 1976 and 1998, in 30,000 mammals, birds, reptiles, amphibians and arthropods sampled from outbreak regions, no ebolavirus was detected apart from some genetic traces found in six rodents (Mus setulosus andPraomys) and one shrew (Sylvisorex ollula) collected from the Central African Republic.[33][39] Traces of EBOV were detected in the carcasses of gorillas and chimpanzees during outbreaks in 2001 and 2003, which later became the source of human infections. However, the high lethality from infection in these species makes them unlikely as a natural reservoir.[33]

Transmission between natural reservoir and humans is rare, and outbreaks are usually traceable to a single case where an individual has handled the carcass of gorilla, chimpanzee or duiker.[40] Fruit bats are also eaten by people in parts of West Africa where they are smoked, grilled or made into a spicy soup.[37][41]

Virology

Genome

Electron micrograph of an Ebola virus virion

Like all mononegaviruses, ebolavirions contain linear nonsegmented, single-strand, non-infectious RNA genomes of negative polarity that possesses inverse-complementary 3′ and 5′ termini, do not possess a 5′ cap, are notpolyadenylated, and are not covalently linked to a protein.[42] Ebolavirus genomes are approximately 19 kilobase pairs long and contain seven genes in the order 3′-UTRNPVP35VP40GPVP30VP24L5′-UTR.[43] The genomes of the five different ebolaviruses (BDBV, EBOV, RESTV, SUDV, and TAFV) differ in sequence and the number and location of gene overlaps.

Structure

Like all filoviruses, ebolavirions are filamentous particles that may appear in the shape of a shepherd’s crook or in the shape of a “U” or a “6”, and they may be coiled, toroid, or branched.[43] In general, ebolavirions are 80 nm in width, but vary somewhat in length. In general, the median particle length of ebolaviruses ranges from 974 to 1,086 nm (in contrast to marburgvirions, whose median particle length was measured at 795–828 nm), but particles as long as 14,000 nm have been detected in tissue culture.[44]

Replication

The ebolavirus life cycle begins with virion attachment to specific cell-surface receptors, followed by fusion of the virion envelope with cellular membranes and the concomitant release of the virus nucleocapsid into the cytosol. The viral RNA polymerase, encoded by the L gene, partially uncoats the nucleocapsid and transcribes the genes into positive-strand mRNAs, which are then translated into structural and nonstructural proteins. Ebolavirus RNA polymerase (L) binds to a single promoter located at the 3′ end of the genome. Transcription either terminates after a gene or continues to the next gene downstream. This means that genes close to the 3′ end of the genome are transcribed in the greatest abundance, whereas those toward the 5′ end are least likely to be transcribed. The gene order is, therefore, a simple but effective form of transcriptional regulation. The most abundant protein produced is the nucleoprotein, whose concentration in the cell determines when L switches from gene transcription to genome replication. Replication results in full-length, positive-strand antigenomes that are, in turn, transcribed into negative-strand virus progeny genome copy. Newly synthesized structural proteins and genomes self-assemble and accumulate near the inside of the cell membrane. Virions bud off from the cell, gaining their envelopes from the cellular membrane they bud from. The mature progeny particles then infect other cells to repeat the cycle. The Ebola virus genetics are difficult to study due to its virulent nature.[45]

Pathophysiology

Pathogenesis schematic

Endothelial cells, macrophages, monocytes, and liver cells are the main targets of infection. After infection, a secreted glycoprotein (sGP) known as the Ebola virus glycoprotein (GP) is synthesized. Ebola replication overwhelms protein synthesis of infected cells and host immune defenses. The GP forms a trimeric complex, which binds the virus to the endothelial cells lining the interior surface of blood vessels. The sGP forms a dimeric protein that interferes with the signaling of neutrophils, a type of white blood cell, which allows the virus to evade the immune system by inhibiting early steps of neutrophil activation. These white blood cells also serve as carriers to transport the virus throughout the entire body to places such as the lymph nodes, liver, lungs, and spleen.[46]

The presence of viral particles and cell damage resulting from budding causes the release of chemical signals (to be specific, TNF-α, IL-6, IL-8, etc.), which are the signaling molecules for fever and inflammation. The cytopathic effect, from infection in the endothelial cells, results in a loss of vascular integrity. This loss in vascular integrity is furthered with synthesis of GP, which reduces specific integrins responsible for cell adhesion to the inter-cellular structure, and damage to the liver, which leads to improper clotting.[47]

Diagnosis

The travel and work history along with exposure to wildlife are important to consider when the diagnosis of EVD is suspected. The diagnosis is confirmed by isolating the virus, detecting its RNA or proteins, or detecting antibodiesagainst the virus in a person’s blood. Isolating the virus by cell culture, detecting the viral RNA by polymerase chain reaction (PCR) and detecting proteins by enzyme-linked immunosorbent assay (ELISA) works best early and in those who have died from the disease. Detecting antibodies against the virus works best late in the disease and in those who recover.[48]

During an outbreak, virus isolation is often not feasible. The most common diagnostic methods are therefore real-time PCR and ELISA detection of proteins, which can be performed in field or mobile hospitals.[49] Filovirions can be seen and identified in cell culture by electron microscopy due to their unique filamentous shapes, but electron microscopy cannot tell the difference between the various filoviruses despite there being some length differences.[44]

Phylogenetic tree comparing the Ebolavirus and Marburgvirus. Numbers indicate percent confidence of branches.

Classification

The genera Ebolavirus and Marburgvirus were originally classified as the species of the now-obsolete Filovirus genus. In March 1998, the Vertebrate Virus Subcommittee proposed in the International Committee on Taxonomy of Viruses (ICTV) to change the Filovirus genus to the Filoviridae family with two specific genera: Ebola-like viruses andMarburg-like viruses. This proposal was implemented in Washington, DC, on April 2001 and in Paris on July 2002. In 2000, another proposal was made in Washington, D.C., to change the “-like viruses” to “-virus” resulting in today’s Ebolavirus and Marburgvirus.[50]

Rates of genetic change are 100 times slower than influenza A in humans, but on the same magnitude as those of hepatitis B. Extrapolating backwards using these rates indicates that Ebolavirus and Marburgvirus diverged several thousand years ago.[51] However, paleoviruses (genomic fossils) of filoviruses (Filoviridae) found in mammals indicate that the family itself is at least tens of millions of years old.[52] Fossilized viruses that are closely related to ebolaviruses have been found in the genome of the Chinese hamster.[53]

Differential diagnosis

The symptoms of EVD are similar to those of Marburg virus disease.[54] It can also easily be confused with many other diseases common in Equatorial Africa such as other viral hemorrhagic fevers, falciparum malaria, typhoid fever, shigellosis, rickettsial diseases such astyphus, cholera, gram-negative septicemia, borreliosis such as relapsing fever or EHEC enteritis. Other infectious diseases that should be included in the differential diagnosis include the following: leptospirosis, scrub typhus, plague, Q fever, candidiasis, histoplasmosis,trypanosomiasis, visceral leishmaniasis, hemorrhagic smallpox, measles, and fulminant viral hepatitis.[55] Non-infectious diseases that can be confused with EVD are acute promyelocytic leukemia, hemolytic uremic syndrome, snake envenomation, clotting factordeficiencies/platelet disorders, thrombotic thrombocytopenic purpura, hereditary hemorrhagic telangiectasia, Kawasaki disease, and even warfarin poisoning.[56][57][58][59]

Prevention

A researcher working with the Ebola virus while wearing a BSL-4 positive pressure suit to avoid infection

Infection control and containment

The risk of transmission is increased among those caring for people infected. Recommended measures when caring for those who are infected include isolating them, sterilizing equipment and surfaces, and wearing protective clothing including masks, gloves, gowns, and goggles.[22] If a person with Ebola dies, direct contact with the body of the deceased patient should be avoided.[22]

In order to reduce the spread, the World Health Organization recommends raising community awareness of the risk factors for Ebola infection and the protective measures individuals can take.[60] These include avoiding contact with infected people and regular hand washing using soap and water.[61] Traditional burial rituals, especially those requiring washing or embalming of bodies, should be discouraged or modified.[62][63] Social anthropologists may help find alternatives to traditional rules for burials.[64] Airline crews are instructed to isolate anyone who has symptoms resembling Ebola virus.[65]

The Ebola virus can be eliminated with heat (heating for 30 to 60 minutes at 60 °C or boiling for 5 minutes). On surfaces, some lipid solvents such as some alcohol-based products, detergents, sodium hypochlorite (bleach) or calcium hypochlorite (bleaching powder), and other suitable disinfectants at appropriate concentrations can be used as disinfectants.[66][67]

In laboratories where diagnostic testing is carried out, biosafety level 4-equivalent containment is required, since Ebola viruses are World Health Organization Risk Group 4 pathogens. Laboratory researchers must be properly trained in BSL-4 practices and wear proper personal protective equipment.

Quarantine

Quarantine, also known as enforced isolation, is usually effective in decreasing spread.[68][69] Governments often quarantine areas where the disease is occurring or individuals who may be infected.[70] In the United States, the law allows quarantine of those infected with Ebola.[71] During the 2014 outbreak, Liberia closed schools.[72]

Contact tracing

Contact tracing is regarded as important to contain an outbreak. It involves finding everyone who had close contact with infected individuals and watching for signs of illness for 21 days. If any of these contacts comes down with the disease, they should be isolated, tested, and treated. Then repeat the process by tracing the contacts’ contacts.[73][74]

Treatment

Standard support

A hospital isolation ward in Gulu, Uganda, during the October 2000 outbreak

No ebolavirus-specific treatment is currently approved.[75] However, survival is improved by early supportive care with rehydration and symptomatic treatment.[1] Treatment is primarily supportive in nature.[76] These measures may include management of pain, nausea, fever and anxiety, as well as rehydration via the oral or by intravenous route.[76] Blood products such as packed red blood cells, platelets or fresh frozen plasma may also be used.[76] Other regulators of coagulation have also been tried including heparin in an effort to prevent disseminated intravascular coagulation and clotting factors to decrease bleeding.[76] Antimalarial medications and antibiotics are often used before the diagnosis is confirmed,[76] though there is no evidence to suggest such treatment is in any way helpful.

Intensive care

Intensive care is often used in the developed world.[77] This may include maintaining blood volume and electrolytes (salts) balance as well as treating any bacterial infections that may develop.[77] Dialysis may be needed for kidney failure while extracorporeal membrane oxygenation may be used for lung dysfunction.[77]

Prognosis

The disease has a high mortality rate: often between 25 percent and 90 percent.[1][3] As of September 2014, information from WHO across all occurrences to date puts the overall fatality rate at 50%.[1] There are indications based on variations in death rate between countries that early and effective treatment of symptoms (e.g., supportive care to prevent dehydration) may reduce the fatality rate significantly.[78] If an infected person survives, recovery may be quick and complete. Prolonged cases are often complicated by the occurrence of long-term problems, such as inflammation of the testicles, joint pains, muscle pains, skin peeling, or hair loss. Eye symptoms, such as light sensitivity, excess tearing, iritis, iridocyclitis, choroiditis, and blindness have also been described. EBOV and SUDV may be able to persist in the semen of some survivors for up to seven weeks, which could give rise to infections and disease via sexual intercourse.[1]

Epidemiology

For more about specific outbreaks and their descriptions, see List of Ebola outbreaks.

CDC worker incinerates medical waste from Ebola patients in Zaire in 1976

The disease typically occurs in outbreaks in tropical regions of Sub-Saharan Africa.[1] From 1976 (when it was first identified) through 2013, the World Health Organization reported 1,716 confirmed cases.[1][4] The largest outbreak to date is the ongoing 2014 West Africa Ebola virus outbreak, which is affecting Guinea, Sierra Leone, Liberia and Nigeria.[5][6] As of 13 August, 2,127 cases have been identified, with 1,145 deaths.[5]

1976

The first identified case of Ebola was on 26 August 1976, in Yambuku, a small rural village in Mongala District in northern Democratic Republic of the Congo (then known as Zaire).[79] The first victim, and the index case for the disease, was village school headmaster Mabalo Lokela, who had toured an area near the Central African Republic border along the Ebola river between 12–22 August. On 8 September he died of what would become known as the Ebola virus species of the ebolavirus.[80] Subsequently a number of other cases were reported, almost all centered on the Yambuku mission hospital or having close contact with another case.[80] 318 cases and 280 deaths (a 88% fatality rate) occurred in the DRC.[81] The Ebola outbreak was contained with the help of the World Health Organization and transport from the Congolese air force, by quarantining villagers, sterilizing medical equipment, and providing protective clothing. The virus responsible for the initial outbreak, first thought to be Marburg virus, was later identified as a new type of virus related to Marburg, and named after the nearby Ebola river. Another ebolavirus, the Sudan virus species, was also identified that same year when an outbreak occurred in Sudan, affecting 284 people and killing 151.[82]

1995 to 2013

The second major outbreak occurred in 1995 in the Democratic Republic of Congo, affecting 315 and killing 254. The next major outbreak occurred in Uganda in 2000, affecting 425 and killing 224; in this case the Sudan virus was found to be the ebolavirus species responsible for the outbreak.[83] In 2003 there was an outbreak in the Republic of Congo that affected 143 and killed 128, a death rate of 90%, the highest to date.[84]

In August 2007, 103 people were infected by a suspected hemorrhagic fever outbreak in the village of Kampungu, Democratic Republic of the Congo. The outbreak started after the funerals of two village chiefs, and 217 people in four villages fell ill.[83][85][86] The 2007 outbreak eventually affected 264 individuals and resulted in the deaths of 187.[1]

On 30 November 2007, the Uganda Ministry of Health confirmed an outbreak of Ebola in the Bundibugyo District in Western Uganda. After confirmation of samples tested by the United States National Reference Laboratories and the Centers for Disease Control, the World Health Organization confirmed the presence of a new species of Ebolavirus, which was tentatively named Bundibugyo.[87] The WHO reported 149 cases of this new strain and 37 of those led to deaths.[1]

The WHO confirmed two small outbreaks in Uganda in 2012. The first outbreak affected 7 people and resulted in the death of 4 and the second affected 24, resulting in the death of 17. The Sudan variant was responsible for both outbreaks.[1]

On 17 August 2012, the Ministry of Health of the Democratic Republic of the Congo reported an outbreak of the Ebola-Bundibugyo variant[88] in the eastern region.[89][90] Other than its discovery in 2007, this was the only time that this variant has been identified as the ebolavirus responsible for an outbreak. The WHO revealed that the virus had sickened 57 people and claimed 29 lives. The probable cause of the outbreak was tainted bush meat hunted by local villagers around the towns of Isiro and Viadana.[1][91]

2014 outbreak

Increase over time in the cases and deaths during the 2014 outbreak

In March 2014, the World Health Organization (WHO) reported a major Ebola outbreak in Guinea, a western African nation.[92] Researchers traced the outbreak to a two-year old child who died on 28 December 2013.[93][94] The disease then rapidly spread to the neighboring countries of Liberia and Sierra Leone. It is the largest Ebola outbreak ever documented, and the first recorded in the region.[92]

On 8 August 2014, the WHO declared the epidemic to be an international public health emergency. Urging the world to offer aid to the affected regions, the Director-General said, “Countries affected to date simply do not have the capacity to manage an outbreak of this size and complexity on their own. I urge the international community to provide this support on the most urgent basis possible.”[95] By mid-August 2014, Doctors Without Borders reported the situation in Liberia’s capital Monrovia as “catastrophic” and “deteriorating daily”. They reported that fears of Ebola among staff members and patients had shut down much of the city’s health system, leaving many people without treatment for other conditions.[96] By late August 2014, the disease had spread to Nigeria, and one case was reported in Senegal.[97][98] [99][100] On 30 September 2014, the first confirmed case of Ebola was diagnosed in the United States at Texas Health Presbyterian Hospital in Dallas, Texas.[101]

Aside from the human cost, the outbreak has severely eroded the economies of the affected countries. A Financial Times report suggested the economic impact of the outbreak could kill more people than the virus itself. As of 23 September, in the three hardest hit countries, Liberia, Sierra Leone, and Guinea, there were only 893 treatment beds available while the current need was 2122. In a 26 September statement, the WHO said, “The Ebola epidemic ravaging parts of West Africa is the most severe acute public health emergency seen in modern times. Never before in recorded history has a biosafety level four pathogen infected so many people so quickly, over such a broad geographical area, for so long.”[102]

By 29 September 2014, 7,192 suspected cases and 3,286 deaths had been reported, however the World Health Organization has said that these numbers may be vastly underestimated.[103] The WHO reports that more than 216 healthcare workers are among the dead, partly due to the lack of equipment and long hours.[104][105]

History

For more about the outbreak in Virginia, US, see Reston virus.

Cases of ebola fever in Africa from 1979 to 2008.

The first recorded outbreak of EBD occurred in Southern Sudan in June 1976. A second outbreak soon followed in the Democratic Republic of the Congo (then Zaire).[106] Virus isolated from both outbreaks was named “Ebola virus” by Belgian researchers[107] after the Ebola River, located near the Zaire outbreak.[108] Although it was assumed that the two outbreaks were connected, scientists later realized that they were caused by distinct species of filoviruses, Sudan virus and Ebola virus.[106]

In late 1989, Hazelton Research Products’ Reston Quarantine Unit in Reston, Virginia suffered a mysterious outbreak of fatal illness (initially diagnosed as Simian hemorrhagic fever virus (SHFV)) among a shipment of crab-eating macaque monkeys imported from the Philippines. Hazelton’s veterinary pathologist sent tissue samples from dead animals to the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) at Fort Detrick, Maryland, where a laboratory test known as an ELISA assay showed antibodies to Ebola virus.[109] An electron microscopist from USAMRIID discoveredfiloviruses similar in appearance to Ebola in the tissue samples sent from Hazelton Research Products’ Reston Quarantine Unit.[110]

Shortly afterward, a US Army team headquartered at USAMRIID went into action to euthanize the monkeys which had not yet died, bringing those monkeys and those which had already died of the disease toFt. Detrick for study by the Army’s veterinary pathologists and virologists, and eventual disposal under safe conditions.[109]

Blood samples were taken from 178 animal handlers during the incident.[111] Of those, six animal handlers eventually seroconverted, including one who had cut himself with a bloody scalpel.[46][112] When the handlers did not become ill, the CDC concluded that the virus had a very low pathogenicity to humans.[112]

The Philippines and the United States had no previous cases of Ebola infection, and upon further isolation, researchers concluded it was another strain of Ebola, or a new filovirus of Asian origin, which they named Reston ebolavirus (REBOV) after the location of the incident.[109]

Society and culture

Ebolavirus is classified as a biosafety level 4 agent, as well as a Category A bioterrorism agent by the Centers for Disease Control and Prevention. It has the potential to be weaponized for use in biological warfare,[113][114] and was investigated by the Biopreparat for such use, but might be difficult to prepare as a weapon of mass destruction because the virus becomes ineffective quickly in open air.[115]

Literature

Richard Preston‘s 1995 best-selling book, The Hot Zone, dramatized the Ebola outbreak in Reston, Virginia.[116]

William Close‘s 1995 Ebola: A Documentary Novel of Its First Explosion and 2002 Ebola: Through the Eyes of the People focused on individuals’ reactions to the 1976 Ebola outbreak in Zaire.[117]

Tom Clancy‘s 1996 novel, Executive Orders, involves a Middle Eastern terrorist attack on the United States using an airborne form of a deadly Ebola virus strain named “Ebola Mayinga” (see Mayinga N’Seka).[118]

Other animals

Wild animals

It is widely believed that outbreaks of EVD among human populations result from handling infected wild animal carcasses. Some research suggests that an outbreak in the wild animals used for consumption, bushmeat, may result in a corresponding human outbreak. Since 2003, such outbreaks have been monitored through surveillance of animal populations with the aim of predicting and preventing Ebola outbreaks in humans.[119]

Recovered carcasses from gorillas contain multiple Ebola virus strains, which suggest multiple introductions of the virus. Bodies decompose quickly and carcasses are not infectious after three to four days. Contact between gorilla groups is rare, suggesting transmission among gorilla groups is unlikely, and that outbreaks result from transmission between viral reservoir and animal populations.[120]

Ebola has a high mortality among primates.[121] Frequent outbreaks of Ebola may have resulted in the deaths of 5,000 gorillas.[122] Outbreaks of Ebola may have been responsible for an 88% decline in tracking indices of observed chimpanzee populations in 420 square kilometer Lossi Sanctuary between 2002 and 2003.[120] Transmission among chimpanzees through meat consumption constitutes a significant risk factor, while contact between individuals, such as touching dead bodies and grooming, is not.[123]

Domesticated animals

Reston ebolavirus (REBOV) can be transmitted to pigs.[124] This virus was discovered during an outbreak of what at the time was thought to be simian hemorrhagic fever virus (SHFV) in crab-eating macaques in Reston, Virginia (hence the name Reston elabavirus) in 1989. Since the initial outbreak it has since been found in nonhuman primates in Pennsylvania, Texas, and Italy. In each case, the affected animals had been imported from a facility in the Philippines,[70] where the virus had infected pigs.[125] Despite its status as a Level‑4organism and its apparent pathogenicity in monkeys, REBOV has not caused disease in exposed human laboratory workers.[126] In 2012 it was demonstrated that the virus can travel without contact from pigs to nonhuman primates, although the same study failed to achieve transmission in that manner between primates.[124] According to the WHO, routine cleaning and disinfection of pig (or monkey) farms with sodium hypochlorite or other detergents should be effective in inactivating the Reston ebolavirus. If an outbreak is suspected, the area must be immediately quarantined.[82]

While pigs that have been infected with REBOV tend to show symptoms of the disease, it has been shown that dogs may become infected with EBOV and remain asymptomatic. Dogs in some parts of Africa scavenge for their food and it is known that they sometimes eat infected animals and the corpses of humans. Although they remain asymptomatic, a 2005 survey of dogs during an EBOV outbreak found that over 31.8% showed a seroprevalence for EBOV closest to an outbreak versus 9% a farther distance away.[127]

Research

A number of experimental treatments are being studied.[128] In the United States, the Food and Drug Administration (FDA)’s animal efficacy rule is being used to demonstrate reasonable safety to obtain permission to treat people who are infected with Ebola. It is being used as the normal path for testing drugs is not possible for diseases caused by dangerous pathogens or toxins. Experimental drugs are made available for use with the approval of regulatory agencies under named patient programs, known in the US as “expanded access”.[129] On 12 August 2014 the WHO released a statement that the use of not yet proven treatments is ethical in certain situations in an effort to treat or prevent the disease.[130]

Medications

Researchers looking at slides of cultures of cells that make monoclonal antibodies. These are grown in a lab and the researchers are analyzing the products to select the most promising of them.

As of August 14, 2014, the United States Food and Drug Administration (FDA) has not approved any drugs to treat or prevent Ebola and advises people to watch out for fraudulent products.[131] The unavailability of experimental treatments in the most affected regions during the 2014 outbreak spurred controversy, with some calling for experimental drugs to be made more widely available in Africa on a humanitarian basis, and others warning that making unproven experimental drugs widely available would be unethical, especially in light of past experimentation conducted in developing countries by Western drug companies.[132][133]

The FDA has allowed three drugs: ZMapp, an RNA interference drug called TKM-Ebola, and brincidofovir to be used in people infected with Ebola under these programs during the 2014 outbreak.[134][135] BioCryst’s BCX4430 small molecule is undergoing further animal testing as a possible therapy in humans.[136] Another drug favipiravir has been used with apparent success in a patient medically evacuated to France.[137]

ZMapp is a monoclonal antibody vaccine. The limited supply of the drug has been used to treat a small number of individuals infected with the Ebola virus. Although some of these have recovered the outcome is not consideredstatistically significant.[138] ZMapp has proved effective in a trial involving Rhesus macaque monkeys.[139]

Antivirals

A number of antiviral medications are being studied. Favipiravir, an anti-viral drug approved in Japan for stockpiling against influenza pandemics, appears to be useful in a mouse model of Ebola.[9][140] On 4 October 2014, it was reported that a French nun who contracted Ebola while volunteering in Liberia was cured with Favipiravir treatment.[141] BCX4430 is a broad-spectrum antiviral drug developed by BioCryst Pharmaceuticals and currently being researched as a potential treatment for Ebola by USAMRIID.[142] The drug has been approved to progress to Phase 1 trials, expected late in 2014.[143] Brincidofovir, another broad-spectrum antiviral drug, has been granted an emergency FDA approval as an investigational new drug for the treatment of Ebola, after it was found to be effective against Ebolavirus in in vitro tests.[144] It has subsequently been used to treat the first patient diagnosed with Ebola in the USA, after he had recently returned from Liberia.[145] The antiviral drug lamivudine, which is usually used to treat HIV / AIDS, was reported in September 2014 to have been used successfully to treat 13 out of 15 Ebola-infected patients by a doctor in Liberia, as part of a combination therapy also involving intravenous fluids and antibiotics to combat opportunistic bacterial infection of Ebola-compromised internal organs.[146] Western virologists have however expressed caution about the results, due to the small number of patients treated and confounding factors present. Researchers at the NIH stated that lamivudine had so far failed to demonstrate anti-Ebola activity in preliminary in vitro tests, but that they would continue to test it under different conditions and would progress it to trials if even slight evidence for efficacy is found.[147]

Antisense technology

Other promising treatments rely on antisense technology. Both small interfering RNAs (siRNAs) and phosphorodiamidate morpholino oligomers (PMOs) targeting the Zaire Ebola virus (ZEBOV) RNA polymerase L protein could prevent disease in nonhuman primates.[148][149] TKM-Ebola is a small-interfering RNA compound, currently being tested in a Phase I clinical trial in humans.[134][150] Sarepta Therapeutics has completed a Phase I clinical trial with its Morpholino oligo targeting Ebola.[151]

Other

Two selective estrogen receptor modulators used to treat infertility and breast cancer (clomiphene and toremifene) have been found to inhibit the progress of Ebola virus in infected mice. Ninety percent of the mice treated with clomiphene and fifty percent of those treated with toremifene survived the tests.[152]

A 2014 study found that three ion channel blockers used in the treatment of heart arrhythmias, amiodarone, dronedarone and verapamil, block the entry of Ebolavirus into cells in vitro.[153] Given their oral availability and history of human use, these drugs would be candidates for treating Ebola virus infection in remote geographical locations, either on their own or together with other antiviral drugs.

Melatonin has also been suggested as a potential treatment for Ebola based on promising in vitro results.[154]

Blood products

The WHO has stated that transfusion of whole blood or purified serum from Ebola survivors is the therapy with the greatest potential to be implemented immediately, although there is little information as to its efficacy.[155] At the end of September, WHO issued an interim guideline for this therapy.[156] The blood serum from those who have survived an infection is currently being studied to see if it is an effective treatment.[157] During a meeting arranged by WHO this research was deemed to be a top priority.[157] Seven of eight people with Ebola survived after receiving a transfusion of blood donated by individuals who had previously survived the infection in an 1999 outbreak in the Democratic Republic of the Congo.[76][158] This treatment, however, was started late in the disease meaning they may have already been recovering on their own and the rest of their care was better than usual.[76] Thus this potential treatment remains controversial.[77] Intravenous antibodies appear to be protective in non-human primates who have been exposed to large doses of Ebola.[159]The World Health Organisation has approved the use of convalescent serum and whole blood products to treat people with Ebola.[160]

Vaccine

As of September 2014, no vaccine was approved for clinical use in humans.[131][157] It was hoped that one would be initially available by November 2014.[157] The most promising candidates are DNA vaccines[161] or vaccines derived from adenoviruses,[162] vesicular stomatitis Indiana virus (VSIV)[163][164][165] or filovirus-like particles (VLPs)[166] because these candidates could protect nonhuman primates from ebolavirus-induced disease. DNA vaccines, adenovirus-based vaccines, and VSIV-based vaccines have entered clinical trials.[167][168][169][170]

Vaccines have protected nonhuman primates. Immunization takes six months, which impedes the counter-epidemic use of the vaccines. Searching for a quicker onset of effectiveness, in 2003, a vaccine using an adenoviral (ADV) vector carrying the Ebola spike protein was tested on crab-eating macaques. Twenty-eight days later, they were challenged with the virus and remained resistant.[162] A vaccine based on attenuated recombinant vesicular stomatitis virus (VSV) vector carrying either the Ebola glycoprotein or the Marburg glycoprotein in 2005 protected nonhuman primates,[171] opening clinical trials in humans.[167] The study by October completed the first human trial, over three months giving three vaccinations safely inducing an immune response. Individuals for a year were followed, and, in 2006, a study testing a faster-acting, single-shot vaccine began; this new study was completed in 2008.[168] Trying the vaccine on a strain of Ebola that more resembles one that infects humans is the next step.[172] On 6 December 2011, the development of a successfulvaccine against Ebola for mice was reported. Unlike the predecessors, it can be freeze-dried and thus stored for long periods in wait for an outbreak.[173] An experimental vaccine made by researchers at Canada’s national laboratory in Winnipeg was used, in 2009, to pre-emptively treat a German scientist who might have been infected during a lab accident.[174] However, actual EBOV infection was never demonstrated beyond doubt.[175] Experimentally, recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of EBOV or SUDV has been used successfully in nonhuman primate models as post-exposure prophylaxis.[176][177] The CDC’s recommendations are currently under review.[citation needed]

Simultaneous phase 1 trials of an experimental vaccine known as the NIAID/GSK vaccine commenced in September 2014.[178] GlaxoSmithKline and the NIH jointly developed the vaccine,[178] based on a modified chimpanzee adenovirus, and contains parts of the Zaireand Sudan ebola strains.[178] If this phase is completed successfully, the vaccine will be fast tracked for use in West Africa. In preparation for this, GSK is preparing a stockpile of 10,000 doses.[179][180]

See also

References

Notes

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  152. Jump up^ Johansen LM, Brannan JM, Delos SE, Shoemaker CJ, Stossel A, Lear C, Hoffstrom BG, Dewald LE, Schornberg KL, Scully C, Lehár J, Hensley LE, White JM, Olinger GG (2013). “FDA-approved selective estrogen receptor modulators inhibit Ebola virus infection”. Sci Transl Med 5 (190): 190ra79.doi:10.1126/scitranslmed.3005471. PMC 3955358.PMID 23785035. Lay summaryHealthline Networks, Inc.
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Bibliography

External links

http://en.wikipedia.org/wiki/Ebola_virus_disease

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The Pronk Pops Show 342, October 2, 2014, Story 1: Obama Spreading Communicable Diseases Across United States With Illegal Aliens in Schools and Communities– TB, Virus, Ebola — What’s Next? — Pandemic! — Videos

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The Pronk Pops Show Podcasts

Pronk Pops Show 342: October 2, 2014

Pronk Pops Show 341: October 1, 2014

Pronk Pops Show 340: September 30, 2014

Pronk Pops Show 339: September 29, 2014

Pronk Pops Show 338: September 26, 2014

Pronk Pops Show 337: September 25, 2014

Pronk Pops Show 336: September 24, 2014

Pronk Pops Show 335: September 23 2014

Pronk Pops Show 334: September 22 2014

Pronk Pops Show 333: September 19 2014

Pronk Pops Show 332: September 18 2014

Pronk Pops Show 331: September 17, 2014

Pronk Pops Show 330: September 16, 2014

Pronk Pops Show 329: September 15, 2014

Pronk Pops Show 328: September 12, 2014

Pronk Pops Show 327: September 11, 2014

Pronk Pops Show 326: September 10, 2014

Pronk Pops Show 325: September 9, 2014

Pronk Pops Show 324: September 8, 2014

Pronk Pops Show 323: September 5, 2014

Pronk Pops Show 322: September 4, 2014

Pronk Pops Show 321: September 3, 2014

Pronk Pops Show 320: August 29, 2014

Pronk Pops Show 319: August 28, 2014

Pronk Pops Show 318: August 27, 2014 

Pronk Pops Show 317: August 22, 2014

Pronk Pops Show 316: August 20, 2014

Pronk Pops Show 315: August 18, 2014

Pronk Pops Show 314: August 15, 2014

Pronk Pops Show 313: August 14, 2014

Pronk Pops Show 312: August 13, 2014

Pronk Pops Show 311: August 11, 2014

Pronk Pops Show 310: August 8, 2014

Pronk Pops Show 309: August 6, 2014

Pronk Pops Show 308: August 4, 2014

Pronk Pops Show 307: August 1, 2014 

Pronk Pops Show 306: July 31, 2014

Pronk Pops Show 305: July 30, 2014

Pronk Pops Show 304: July 29, 2014

Pronk Pops Show 303: July 28, 2014

Pronk Pops Show 302: July 24, 2014

Pronk Pops Show 301: July 23, 2014

Pronk Pops Show 300: July 22, 2014

Pronk Pops Show 299: July 21, 2014

Pronk Pops Show 298: July 18, 2014

Pronk Pops Show 297: July 17, 2014

Pronk Pops Show 296: July 16, 2014

Pronk Pops Show 295: July 15, 2014

Pronk Pops Show 294: July 14, 2014

Pronk Pops Show 293: July 11, 2014

Pronk Pops Show 292: July 9, 2014

Pronk Pops Show 291: July 7, 2014

Pronk Pops Show 290: July 3, 2014

Pronk Pops Show 289: July 2, 2014

 

Story 1: Obama Spreading Communicable Diseases Across United States With Illegal Aliens in Schools and Communities– TB, Virus, Ebola — What’s Next? — Pandemic! — Videosgraphic_InfectiousCommunication Diseases - Daysebola-symptoms1Ebola-outbreak-graphicWhat-are-the-symptoms-of-Ebolaillness-flu3EbolaSymptoms3ebola-united-states-dallas-texas-meme-3

symptoms of tbtuberculosis-of-the-lungsCOMMUNICABLEfunny-pictures-barack-obama-talking-about-illegal-aliens-are-now-called-undocumented-democratsobama_bull

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Latest influx of illegal aliens brings disease

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Experts: Ebola Could Go Airborne, Kill Millions

Medical Experts Warns Ebola Virus May already be Airborne

We Heard the Bells: The Influenza of 1918 (full documentary)

In 1918-1919, the worst flu in recorded history killed an estimated 50 million people worldwide. The U.S. death toll was 675,000 – five times the number of U.S. soldiers killed in World War I. Where did the 1918 flu come from? Why was it so lethal? What did we learn?

Killer Flu Documentary

The Genesis of the 1918 Spanish Influenza Pandemic

US Army: Ebola like FLU needs Winter Weather to go AIRBORNE

Aerosolizing ONE DROP of EBOLA = 1/2 MILLION DEAD

 

COMMENTARY: Health workers need optimal respiratory protection for Ebola

Courtesy of 3M Company
A powered air-purifying respirator (PAPR).

Editor’s Note: Today’s commentary was submitted to CIDRAP by the authors, who 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 fluids2,3 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.17The 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 al24 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 pigs25 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 [Abstract]
  2. CDC. Ebola hemorrhagic fever: transmission. 2014 Aug 13 [Full text]
  3. ECDC. Outbreak of Ebola virus disease in West Africa: third update, 1 August 2014. Stockholm: ECDC 2014 Aug 1 [Full text]
  4. Martin-Moreno JM, Llinas G, Hernandez JM. Is respiratory protection appropriate in the Ebola response? Lancet 2014 Sep 6;384(9946):856 [Full text]
  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 [Abstract]
  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 [Abstract]
  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 [Abstract]
  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 [Full text]
  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 [Full text]
  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 [Full text]
  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 [Full text]
  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 [Full text]
  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 [Full text]
  14. Hunt CL, Lennemann NJ, Maury W. Filovirus entry: a novelty in the viral fusion world. Viruses 2012 Feb;4(2):258-75 [Full text]
  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 [Full text]
  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 [Abstract]
  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 [Full text]
  18. Caul EO. Small round structured viruses: airborne transmission and hospital control. Lancet 1994 May 21;343(8908):1240-2 [Full text]
  19. Chadwick PR, Walker M, Rees AE. Airborne transmission of a small round structured virus. Lancet 1994 Jan 15;343(8890):171 [Full text]
  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 [Full text]
  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 [Full text]
  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 [Full text]
  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 [Full text]
  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 [Abstract]
  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 [Full text]
  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 [Full text]
  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 [Abstract]
  28. Roy CJ, Milton DK. Airborne transmission of communicable infection—the elusive pathway. N Engl J Med 2004 Apr;350(17):1710-2 [Preview]
  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

 

 

 

Ebola Patient in Dallas Lied on Screening Form, Liberian Airport Official Says

U.S. Patient Aided Ebola Victim in LiberiaOCT. 1, 2014

 

A Hospital From Hell, in a City Swamped by EbolaOCT. 1, 2014

graphic

What Are the Chances Ebola Will Spread in the United States?JULY 31, 2014

Mr. Duncan, who was a family friend and also a tenant in a house owned by the Williams family, rode in the taxi in the front passenger seat while Ms. Williams, her father and her brother, Sonny Boy, shared the back seat, her parents said. Mr. Duncan then helped carry Ms. Williams, who was no longer able to walk, back to the family home that evening, neighbors said.

Photo

The family of Marthalene Williams said Thomas Eric Duncan helped carry her to and from a hospital in the capital, Monrovia, last month. Marthalene died the next day. Liberian health officials said Wednesday that Mr. Duncan was the man who flew to Dallas and was later found to have the Ebola virus. CreditDaniel Berehulak for The New York Times

“He was holding her by the legs, the pa was holding her arms and Sonny Boy was holding her back,” said Arren Seyou, 31, who witnessed the scene and occupies the room next to Mr. Duncan’s.

Sonny Boy, 21, also started getting sick about a week ago, his family said, around the same time that Mr. Duncan first started showing symptoms.

In a sign of how furiously the disease can spread, an ambulance had come to their house on Wednesday to pick up Sonny Boy. Another ambulance picked up a woman and her daughter from the same area, and a team of body collectors came to retrieve the body of yet another woman — all four appeared to have been infected in a chain reaction started by Marthalene Williams.

A few minutes after the ambulance left, the parents got a call telling them that Sonny Boy had died on the way to the hospital.

Photo

Marie Wread, a friend of a neighbor of Marthalene Williams, became ill and was carried away by health workers in Monrovia on Wednesday. CreditDaniel Berehulak for The New York Times

Mr. Duncan had lived in the neighborhood, called 72nd SKD Boulevard, for the past two years, living by himself in a small room that he rented from the Williams couple. He had told that them and his neighbors that his son lived in the United States, played baseball, and was trying to get him to come to America.

For the past year, Mr. Duncan had worked as a driver at Safeway Cargo, the Liberian customs clearance agent for FedEx, said Henry Brunson, the company’s manager.

In an office with a large FedEx sign outside the building in downtown Monrovia, Mr. Brunson said that Mr. Duncan quit abruptly on Sept. 4, giving no reason. But Mr. Brunson said he knew that Mr. Duncan had family members in the United States as well.

“His sister came from the United States and he asked for a day off so that he could go meet her at the Mamba Point Hotel,” Mr. Brunson said, mentioning a hotel popular among foreigners. “He quit a few weeks after that.”

Officials on Tuesday said they were confident that standard procedures for controlling an infection can contain Ebola in the United States. The C.D.C. is sending experts to Texas to trace anyone who may have come in contact with the patient while he was sick with symptoms.

Doctors across the country are being reminded to ask for the travel history of anybody who comes in with a fever. Patients who have been to West Africa are being screened and tested if there seems to be a chance they have been exposed.

It helps that Ebola does not spread nearly as easily as Hollywood movies about contagious diseases might suggest. In 2008, a patient who had contracted Marburg – a virus much like Ebola – in Uganda was treated at a hospital in the United States and could have exposed more than 200 people to the disease before anyone would have known what she had. Yet no one became sick.

When did the man infected with Ebola arrive in the U.S.?
A man who traveled to Dallas from Liberia has been found to have Ebola, the Centers for Disease Control and Prevention reported on Tuesday. He was screened for fever before boarding the plane — a standard airport procedure in Liberia — and showed no symptoms at that time.

Sunday

Monday

Tuesday

Wednesday

Thursday

Friday

Saturday

Sept. 19

20

After being

checked for

symptoms,

man boards

flight from

Liberia.

Man arrives in

Dallas to visit

family.

21

22

23

24

25

26

27

Man begins

to develop

symptoms.

Man seeks

care at Dallas

hospital but

is sent home.

28

29

30

Man is admitted to Dallas hospital and is placed in isolation.

C.D.C. confirms that man’s blood is positive for

Ebola.

How many people have been infected?
More than 7,000 people in Guinea, Liberia, Nigeria, Senegal and Sierra Leone have contracted Ebola since March, according to the World Health Organization, making this the biggest outbreak on record.More than 3,300 people have died. In the first case diagnosed in the United States, a man who traveled from Liberia to Dallas tested positive for the virus on Sept. 30.
Guinea8001,6002,4003,2004,000MAR 21OCT 1710deaths1,157casesLiberia8001,6002,4003,2004,000MAR 21OCT 11,998deaths3,696casesSierra Leone8001,6002,4003,2004,000MAR 21OCT 1622deaths2,304casesNigeria8001,6002,4003,2004,000MAR 215deaths11cases
Where is the outbreak?
The disease continues to spread in Guinea, Liberia and Sierra Leone. The C.D.C. said Tuesday that Nigeria appears to have contained its outbreak.

EBOLA CASES

SENEGAL

MALI

1

15

150

250

500 or more

GUINEA-

BISSAU

GUINEA

Atlantic Ocean

Guéckédou

SIERRA

LEONE

IVORY COAST

Kenema

WEST AFRICA

Monrovia

150 Miles

NIGERIA

LIBERIA

DETAIL

Source: USAID

Note: Areas affected as of Sept. 29

How big can the outbreak become?
The Centers for Disease Control and Prevention said on Sept. 23 that in a worst-case scenario, cases could reach 1.4 million in four months. The centers’ model is based on data from August and includes cases in Liberia and Sierra Leone, but not Guinea (where counts have been unreliable).Estimates are in line with those made by other groups like the World Health Organization, though the C.D.C. has projected further into the future and offered ranges that account for underreporting of cases.

1,400,000

Cumulative cases in Liberia and Sierra Leone

 

Best-case scenario

Worst-case scenario

1,200,000

11,000-27,000 cases through Jan. 20

537,000-1.4 million cases through Jan. 20

Assumes 70 percent of patients are treated in settings that confine the illness and that the dead are buried safely. About 18 percent of patients in Liberia and 40 percent in Sierra Leone are being treated in appropriate settings.

If the disease continues spreading without effective intervention. Dr. Thomas R. Frieden, the C.D.C. director, said, “My gut feeling is, the actions we’re taking now are going to make that worst-case scenario not come to pass. But it’s important to understand that it could happen.”

1,000,000

800,000

600,000

Range

400,000

200,000

0

Oct.

Nov.

Dec.

Jan.

Oct.

Nov.

Dec.

Jan.

Sept.

Sept.

2014

2015

2014

2015

Source: Centers for Disease Control and Prevention

What is the United States doing to help?
President Obama announced Sept. 16 an expansion of military and medical resources to combat the outbreak. He said that the United States would help Liberia in the construction of as many as 17 Ebola treatment centers in the region, with about 1,700 beds, and will also open a joint command operation to coordinate the international effort to combat the disease. The American response will include the deployment of some 3,000 American military personnel, including doctors, to Liberia and Senegal.
How does this compare to past outbreaks?
It is the deadliest, eclipsing an outbreak in 1976, the year the virus was discovered.

Ebola cases and deaths by year, and countries affected

Cases

Deaths

1976

1995

2000

2007

2014

2nd-worst year

5th

3rd

4th

1st

Sudan, Democratic Republic of Congo

Democratic Republic of Congo

Uganda

Uganda, Democratic Republic of Congo

Guinea, Liberia, Nigeria, Senegal and Sierra Leone

602 cases

431 deaths

315 cases

254 deaths

425 cases

224 deaths

413 cases

224 deaths

6,553 cases

3,083 deaths

as of Sept. 26

Source: World Health Organization

Officials have emphasized that people are only infectious if they have symptoms of Ebola. There is no risk of transmission from people who have been exposed to the virus but are not yet showing symptoms. You are not likely to catch Ebola just by being in proximity to someone who has the virus. It is not spread through the air like the flu or respiratory viruses such as SARS.Instead, Ebola spreads through direct contact with bodily fluids. If an infected person’s blood or vomit gets in another person’s eyes, nose or mouth, the infection may be transmitted. In the current outbreak, most new cases are occurring among people who have been taking care of sick relatives or who have prepared an infected body for burial.Health care workers are at high risk, especially if they have not been properly equipped with protective gear or correctly trained to use and decontaminate it.The virus can survive on surfaces, so any object contaminated with bodily fluids, like a latex glove or a hypodermic needle, may spread the disease.
Why is Ebola so difficult to contain?
The epidemic is growing faster than efforts to keep up with it, and it will take months before governments and health workers in the region can get the upper hand, according to Doctors Without Borders.In some parts of West Africa, there is a belief that simply saying “Ebola” aloud makes the disease appear. Such beliefs have created major obstacles for physicians trying to combat the outbreak. Some people have even blamed physicians for the spread of the virus, opting to turn to witch doctors for treatment instead. Their skepticism is not without a grain of truth: In past outbreaks, hospital staff members who did not take thorough precautions became unwitting travel agents for the virus.

Ahmed Jallanzo/European Pressphoto Agency

Liberian health workers on the way to bury a woman who died of the Ebola virus.

How does the disease progress?
Symptoms usually begin about eight to 10 days after exposure to the virus, but can appear as late as 21 days after exposure, according to the C.D.C. At first, it seems much like the flu: a headache, fever and aches and pains. Sometimes there is also a rash. Diarrhea and vomiting follow.Then, in about half of the cases, Ebola takes a severe turn, causing victims to hemorrhage. They may vomit blood or pass it in urine, or bleed under the skin or from their eyes or mouths. But bleeding is not usually what kills patients. Rather, blood vessels deep in the body begin leaking fluid, causing blood pressure to plummet so low that the heart, kidneys, liver and other organs begin to fail.
How is the disease treated?
There is no vaccine or definitive cure for Ebola, and in past outbreaks the virus has been fatal in 60 percent to 90 percent of cases. The United States government plans to fast-track development of a vaccine shown to protect macaque monkeys, but there is no guarantee it will be effective in humans. The question of who should have access to the scarce supplies of an experimental medicine has become a hotly debated ethical question. Beyond this, all physicians can do is try to nurse people through the illness, using fluids and medicines to maintain blood pressure, and treat other infections that often strike their weakened bodies. A small percentage of people appear to have an immunity to the Ebola virus.
Where does the disease come from?
Ebola was discovered in 1976, and it was once thought to originate in gorillas, because human outbreaks began after people ate gorilla meat. But scientists have since ruled out that theory, partly because apes that become infected are even more likely to die than humans.Scientists now believe that bats are the natural reservoir for the virus, and that apes and humans catch it from eating food that bats have drooled or defecated on, or by coming in contact with surfaces covered in infected bat droppings and then touching their eyes or mouths.The current outbreak seems to have started in a village near Guéckédou, Guinea, where bat hunting is common, according to Doctors Without Borders.
How does Ebola compare with other infectious diseases in the news?
The biggest headlines have tended to involve outbreaks of deadly viruses that medical workers have few, if any, tools to combat. The four most prominent are compared below. No cure is known for any of them, nor has any vaccine yet been approved for human use.
Ebola Marburg MERS SARS
Emerged / identified 1976; latest outbreak in 2014 1967; latest major outbreak in 2005 2012-2013 2002-2003
Locus Originally, Congo Basin and central Africa; latest strain, West Africa Originally, central Europe; latest major outbreak, Angola Arabian peninsula Southern China
Suspected source Fruit bats, by way of monkeys and other animals Fruit bats, sometimes by way of monkeys Bats, by way of camels Bats, by way of civets
Type of virus Filovirus Filovirus Coronavirus Coronavirus
Type of illness Hemorrhagic fever Hemorrhagic fever Respiratory syndrome Respiratory syndrome
Fatality rate in outbreaks 50% to 90% 24% to 88% About 30% About 10%
Known cases 4,000+ 570+ 830+ 8,200+
Known deaths 2700+ 470+ 290+ 775+
Person-to-person transmission Readily by close contact or fluids; not by aerosol Readily by close contact or fluids; not by aerosol Not very readily; mechanism unclear Very readily by aerosol, fluids or close contact
Note: On Sept. 30, officials with the federal Centers for Disease Control and Prevention said Mr. Duncan first went to the hospital on Sept. 26. On Oct. 1, the Texas Health Presbyterian Hospital issued a statement that he first arrived there after 10 p.m. on Sept. 25.

 

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