Posted on 08/05/2014 5:50:07 AM PDT by 2ndDivisionVet
(VIDEO-AT-LINK)
CNN’s Dr. Sanjay Gupta spoke about six patients in New York City that were tested for Ebola and one who had recently traveled to Africa that is undergoing tests for the Ebola virus on Monday’s broadcast of “Wolf.” Gupta said, “I would guess by tomorrow sometime we'll have a better idea” what malady the individual has.
He also pointed out that even though the patient isn’t in isolation, “This isn't the kind of thing that they worry about spreading to other patients in the hospital, spreading to people who are walking around the hospital. This is not an airborne virus. This is something that spreads only when somebody is very sick and they start to actually shed the virus in their bodily fluids. So, it's somebody who comes in contact with those bodily fluids who is not protected. While we don't know the particular story with this patient, we don't know if in fact he has the Ebola infection, in terms of concern for the hospital population at large or the population around the hospital, it's still very minimal.”(continued)
(Excerpt) Read more at breitbart.com ...
It’s hard to say to what extent she was presenting. That all five picked it up sets off alarm bells, for sure. That’s pretty efficient.
I would be delighted to be wrong.
What is irrefutable is that this is NOT Zaire. The incubation period alone is all the evidence one requires to establish that as a fact. This is a mutated strain of Ebola. Reston provided evidence that Ebola could mutate such that aerosolization of the virus could transmit the disease. In fact, Reston was so efficient that it migrated through the air ducts and killed all the monkeys from a Friday evening to a Monday morning. They all died within a weekend. It was Sunday night that the CDC carted off the dead monkeys and shut down the facility, and Preston marveled at the CDC’s dumb luck in all of that.
“Ebola Zaire is the only strain that has been known to go airborne and that was ONE test and has not been independently verified.
Now for your regularly scheduled panic...”
Not to question either the implied premise of the above, but are you aware of any published tests of airborne transmission of any other strain?
Sources, please.
Thank you.
Dont you mean Captain Trips?
I pray you are wrong. I suspect you may not be.
Zaire is the causative agent, but it appears that this is a new strain and it has evolved in parallel.
In March 2014, the World Health Organization was notified of an outbreak of a communicable disease characterized by fever, severe diarrhea, vomiting, and a high fatality rate in Guinea. Virologic investigation identified Zaire ebolavirus (EBOV) as the causative agent. Full-length genome sequencing and phylogenetic analysis showed that EBOV from Guinea forms a separate clade in relationship to the known EBOV strains from the Democratic Republic of Congo and Gabon. Epidemiologic investigation linked the laboratory-confirmed cases with the presumed first fatality of the outbreak in December 2013. This study demonstrates the emergence of a new EBOV strain in Guinea.
...
Phylogenetic analysis of the full-length sequences established a separate clade for the Guinean EBOV strain in sister relationship with other known EBOV strains. This suggests that the EBOV strain from Guinea has evolved in parallel with the strains from the Democratic Republic of Congo and Gabon from a recent ancestor and has not been introduced from the latter countries into Guinea.
http://www.nejm.org/doi/full/10.1056/NEJMoa1404505?query=featured_home&&&;
LOL, I do.
Meant to ping you to 84.
The problem with the analysis is how they are mixing the terminology. Using the terms ‘causative agent’ and ‘sister’ in the same analysis is very confusing.
The peg on which to hang ones hat here is that the Guinea strain is new. New species, same genus. If Guinea is a sister to Gabon and Congo, then its saying that Zaire was the parent to all three (same genus), but the sisters all went off to have their own families (new species).
Congo and Gabon bore Dad’s traits - fast incubation, fast infection, quick (relatively) death, fast burnout.
Not Guinea. This sister ‘evolved’ (crappy term to use in talking about what really is mutation) into having unfortunate characteristics:
1. It infects people (not all Ebola does).
2. It takes a while to incubate.
3. It is not confirmed as to when a patient can communicate the disease.
4. It is not confirmed as to how it is communicated.
5. It is not confirmed as to how long the virus can remain viably active on a surface or in the presence of sunlight (UV).
What would be a big break is if we found out that being infected with some other virus could make you immune to Ebola Guinea. Being sick with cowpox made you immune to smallpox, for example.
This is why all the ‘family tree’ stuff matters. I don’t buy that Zaire is the ‘causative agent’. I buy that Ebola Guinea mutated off of Zaire in parallel to Gabon and Congo, who also mutated off of Zaire, and that Guinea, unfortunately (yes, its probability we are playing with here) has all of these unfortunate properties.
Two interesting questions occur to me:
1. Can an animal, like a monkey, contract Guinea? If so, and the animal is able to survive it, can we learn something from it?
2. What your supplied analysis confirms is that Zaire is precisely what this new bug IS NOT. As such, can you be infected with a related virus that is less problematic and become immune to Guinea?
Presuming (the word they used) that Guinea mutated from Zaire may allow it to determine what changed genetically to make this species of Ebola so much more dangerous than Zaire.
Zaire is bad. The worst. But it killed quickly, so you could ‘starve’ it off - quit supplying it with fresh human hosts to transmit the disease. (Reston was the worst, worse than Zaire, but only infected monkeys)
This one is so much more insidious.
Bottom line: Zaire may or may not be the father. Gabon and Congo are apparently sister species, but Guinea’s properties indicate they bear many of Zaire’s properties, but empirically not all of them. In the mean time, between catching it and dying from it, you are vectoring it for some unknown period of time in an unknown way (fluids, aerosol, parasites). I love how people in the press make a distinction between ‘body fluids’ - human waste, sputum, blood, puss, semen, etc. Then they talk about ‘aerosol’ like the fluids in your breath aren’t really body fluids, even though the fluids present in your breath only just recently resulted from the interaction between the air in your lungs and the blood that arrived in the lungs for the oxygenization.
So far, nobody in the press is talking about this virus in a way that any medical person would break down its characteristics comprehensively to other medical people or policy makers. It feels like the press is doing as much speculating as any of us are. That leads the pundits to ASSUME things about Guinea that are not in evidence, like Guinea transmits like Zaire. The anecdotal reports seem to contradict that assertion.
It leaves us all to speculate even more, which accelerates the ‘panic’ problem. Zaire doesn’t incubate like Guinea, and if that’s true, than how else is Guinea unlike Zaire?
See the issue? Against the backdrop of the clown car we call the 44th Presidential Administration of the USA, you then reasonably assume they are lying their asses off.
Not what you want when Drudge has a new headline twice a day talking about all these people presenting classic symptomology, but somehow they are all testing negative.
When push comes to shove, they won’t have the moral authority to get people to do the right thing, even when they are right about what they are asking people to do.
It’s called sweat.
Close contact is sufficient.
You’re causing me some concern. I wasn’t really concerned about Ebola Guinea spreading in the U.S. because of our advanced medical facilities/treatments and the substantially different societal/sociological concerns. Now I’m a little concerned. So, two questions.
1. How realistic is a Contagion-like event (the movie) with Ebola Guinea, in your opinion?
2. Did Gabon and Congo burn out because they were so virulent that they killed their hosts before they could spread the virus any further or because the rural environments prevented the rapid spread we’re seeing in urban West Africa?
Doctors in W.A. say it’s spinning out of control. If that is because it’s a deadlier strain, it’s worrisome. If that is because the epidemic is not being handled “properly,” it’s less worrisome to me.
I have quite enough infectious diseases (from illegals) to worry about here in Texas, but most of them have a cure.
There’s is only this as others have referred to it, it’s a flawed experiment.
http://healthmap.org/site/diseasedaily/article/pigs-monkeys-ebola-goes-airborne-112112
Wherein lies the failure of this experiment?
IIRC, it was a simple experiment.
Infected and subject animals in cages separated by several feet, but in the same room, and the uninfected subject animals contracted Ebola.
“You would need to find the number of deaths corresponding to the subset of cases that were laboratory confirmed, which would be much smaller.”
Those lab results were obtained by African, who also took the specimens, “isolated” aid specimens, etc.
Sorry, but this is Africa we are discussing, and the reason the phrase “Africa wins again.” became so widely known and accepted is that the people are Africans, virtually all tribal primitives.
Bkmk
The answer is: it depends.
I haven’t seen any updated mortality figures in about five days. I anticipate the death toll to be at 1300 soon. If it is already 1300, then the death rate is doubling every four to six days now. This will accelerate if it is truly out of control. The curve was already exponential, but if the trend continues and the death rate starts doubling every couple of days then you have a real problem.
Nobody has talked about the R0 factor yet. This is also called ‘R naught’. R naught is the ‘basic reproductive number’, and used in epidemiology to figure out what level of response you need to start lining up in order to deal with what you are up against. It is a variable used in a complex differential equation called a Jacobian, that is used to model this sort of stuff.
And you thought you’d never use Calculus!
An R0 < 1 meant that an infection (like, and especially like, Ebola Zaire) would burn out in the ‘long run’. An R0 > 1 means that the likelihood of the infection spreading through a population is probable. The higher the R naught, the higher the probability, and the faster the infection rate. R naught is NOT a probability, it’s a ratio related to number of cases and number of deaths.
For diseases that don’t include a ‘intermediate vector’, which would be a mosquito (for malaria, for example), the R naught is not as useful an indicator of how fast a disease will spread, nor can it be used to determine how many healthy people in a given uninfected population need to be vaccinated in order to stop the spread of the disease.
If there are no intermediate vectors, then the proportion of uninfected people you need to vaccinate to stop the contagion is roughly equal to (1-1/R0).
It would be logical that somebody has tried to nail down the R naught at this point. That will allow you to run a projection, which would look like a curve plotted with time on the X axis and cases on the Y.
You take that plot, you print it out, and then you start gathering your reports, and you plot your numbers over a period of a few days. If your points line up with the curve, you’ve confirmed your R0.
If there’s an intermediary vector, then R0 is going to be a bigger number depending on what species is propagating the pathogen. If the intermediary vector is the primary vector of the disease, your R0 will be lower. If the intermediary is only a secondary vector, meaning both humans and the species in question can spread the bug, then you have to worry about what the intermediary is.
If it is a common mosquito, you should worry a lot. If it is a rare mosquito, or something that crawls or doesn’t reproduce efficiently, then you have less to worry about.
So, to take your question, and replace it with the exact right, no bullshyte question a knowledgeable reporter might ask, the right question to ask is:
“Doctor, what is the R0 of Ebola Guinea, and if you haven’t established R0 yet, what is the current estimate being used in the models you are using for policy making purposes at this point?”
Any value of R0 higher than 1 is bad news. The higher R0 is, the closer the scenarios get to a ‘Contagion’ scenario. A value of 2 or higher and it will mean a change in our way of living until a vaccine is identified.
The good news here is that there’s some sort of serum being used. Interestingly, the method of testing isn’t unlike what would happen in the movie.
This is why I asked the question I did in the last post. Can you infect a monkey with it, and will they develop the same symptoms. If you can’t, then you have to test it on human beings, because you don’t have any other choice.
Maybe they did, and maybe they didn’t. You can use rats, but rats aren’t as close genetically as chimps are. In the end, there is very, very little to lose in human testing on something like this, outside of mutation.
The worst case scenario is that Guinea mutates into something like Reston, but lethal to people. Nothing says a pathogen like this can’t take that kind of turn. What is MORE LIKELY to happen if there is a mutation, is that the mutation may change the properties of the disease such that it may no longer kill people.
That’s the nature of mutations - it is worse than roulette. You get a bug that can do this, its like hitting Satan’s jackpot - everybody loses - but the chances of Satan pulling the lever and getting all million wheels to come up ‘6’s’ again and give you an even more lethal version the Spanish Flu, for example, is incredibly remote.
It’s more likely a mutation screws up the virus’ ability to do damage than it is increase its ability to do so.
I met a historian once out of UC Davis who provided me with compelling evidence that the what killed people in Europe in the 1500’s was actually a strain of Ebola, and not a flu. People died quick, hemorrhaged a lot, and it killed a lot of people, but eventually burned itself out.
He went back to the diaries of the medical folks of the day and correlated the symptoms. Sure sounded more like Ebola than something else.
R naught is the right question to ask at this point. Whatever R naught FEMA and the UN is using will tell you everything you need to know.
I have a question, since you obviously have clues.
What do you think happened in mid/late May that took an outbreak that seemed to have been fairly well controlled and turned the curve exponential? It seems to have happened around the same time in all the affected regions.
I suspect mosquitos (rainy season there begins late April, give time for hatchout of first and second bout of skeeters + time for symptoms to appear) but would genuinely appreciate another less inflammatory opinion :)
As others said above it was not a truly controlled experiment and there has been no independent verification that I’m aware of.
It sat in wait in the Congola,
It killed a bunch of African peopola,
Got a ride to the US freeola,
Decided to mutate into one bad asshola,
Now we wait for the SH*T TO HIT THE FANOLOA.
I don’t have enough information to comment, but I since the outbreak left its cage in recent days, I’ve suspected that they are being disingenuous about the vectors - both the number and the character of the vectors.
One report said one could become infected by as little as 1 to 10 virus in any given human. Compare that to, say sperm and impregnation. You send millions down the pipe and many times nothing happens.
If only a sample of 1 to 10 individual virii is all it takes to catch the bug, and I say IF, because we don’t know that’s true at this point; you can easily see how that many virii can live on the end of the mouth of a mosquito. To know for sure, you’d have to catch a mosquito that had been dining on a patient and test your theory.
But there are all kinds of issues with secondary vectors. Locally, a mosquito can help you wipe out a great deal of people very quickly - even the ones who are being good and isolating themselves and their families within their homes. A mosquito gets in, bites you in your sleep and you wake up 3 weeks later symptomatic and think it was an evil form of magic.
We haven’t seen any anecdotes that would indicate that’s happening. When you read stories where old shut-ins are dying alone in their homes of the bug, then you start worrying about that. When malaria was off the chain, you had that sort of thing happen - shut ins getting the bug and you wonder how the heck it was happening. Well, during the summer, it comes in through the window.
With plague, it was the fleas. Fleas are perfect as a vector, because they are hardy, efficient at reproduction, and they travel well.
Again, if it only takes 1 to 10 virii, then a flea would be a nightmare intermediate vector.
From what I’m reading, I don’t think that’s what’s happening.
However, now you hear reports of bodies dumped out on the streets. Sorry, but if that’s happening then numbers like 729 dead are likely out the window, and because the bodies are being fed upon efficiently by all the usual suspects that do nature’s clean up job on things that die, you might just find that an intermediate vector will pop up and drop the accelerator on this bug.
Based on what I’ve read, what fits best is the following:
1. Aerosol is a vector.
2. Patients become contagious somewhere in the timeline between infection and first presentation of symptoms.
Based on the incubation period, I tend to believe the reports that it only takes 1 to 10 virii. The answer is math.
The virus has to attach to a viable human cell, inject its RNA into the nucleus, and convert that cell into a manufacturer of more virii. The new virii infect other cells, and they become manufacturers, and on, and on.
You start with just one cell, it takes time to build the numbers required to start bringing the immune system down to the point where you start presenting.
With Zaire, the incubation process was so rapid you started presenting almost right away.
Not so with this one. It builds up, and there is likely a some point prior to the presentation of symptoms that you become contagious. That explains, for me, the five people who died in the communal cab. If the infected person has so much as a runny nose or a dust-induced cough, there is no way they would have let her ride. None.
Africans have cell phones. Word spreads faster now that it did in the 60’s when some of these contagions would hit countries down there. Everybody is going to be looking for symptomatic people and turning them out.
If I had to GUESS why it left the chain, I’d say it was because the Generals started fighting the last war - it looked like Ebola, tested out Ebola, and since Ebola is spread through blood and fluids, we will rig for Ebola.
Problem is that while it IS Ebola, it’s a little different this time, and different enough that they were too slow on the containment end. Add to that carelessness and fatigue, and you end up with a whole bunch of infected health care workers. In other Ebola outbreaks, they didn’t have the infection rate among docs and nurses that this one appears to have.
British Airways closed down ‘infected’ countries today. That list will grow before Friday gets here, because now it is apparently in Nigeria, and maybe Gabon.
I would expect South Africa to seal its borders in the next couple of weeks or so. They are far enough away that sealing now may keep it out of there. They’ll screen and actively test freight traffic into it, but civilian travel into SA from infected countries could well close soon.
Sorry about the non-answer answer, but there isn’t enough information for even an analysis of what probably happened. All we have is anecdotal information about patterns of infection.
There has been ZERO about intermediate vectors in the press - not even speculation.
Thank you so much for a very informed reply.
I agree re: aerosol transmission. If it requires only 1 virii to infect then someone coughing can easily infect a whole room.
Sealed hospital rooms would be detrimental in this case vs. camp tents in the bush. And would explain why this particular outbreak in urban/suburban areas ramped up so quickly.
If it’s spread before people become noticeably symptomatic that would explain why the villagers think the healthcare workers bring it with them. Given so many healthcare workers have become ill, they MAY be bringing it with them.
I will pray that mosquitos aren’t a vector. if they are, Africa will depopulate drastically.
To comment on your earlier post, it would appear from the graph that R0 is much greater than one at this point? But who really knows how many dead bodies there are. It’s Africa. And people are in a panic.
Would you think the difference between the mortality of this outbreak vs the past ones may be that so many people have become infected so quickly that they simply haven’t had time to die and become mortality datapoints just yet?
Bush meat is off the table???
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