Graph I made of deaths from Ebola in West Africa as reported by WHO. Days are numbered from start of 2014 on “X” axis and cumulative deaths on “Y” axis. Grid lines are every 21 days and every 200 deaths. Red line is a best fit to the curve. Last date is Oct. 15th.
Well, at least we know it’ll eventually come to an end when the virus encounters its equivalent of “sooner or later you run out of other people’s money.”
It looks like the number of deaths will almost double by this time next month. Is the growth curve purely exponential or is there a logistic component?
The death figures are the official ones reported by the governments involved. They are likely an under-count. Among the other errors is that the decision as to whether someone has died of Ebola or something else is in the hands of local political figures. They have pressure on them from above to have the numbers improve and pressure from families to not have a relative be classed as Ebola which then means no traditional funeral just a bagging and cremation.
It seems to not quite double every 3 weeks. Also the total infection numbers, which are much more guesswork like, in each report, are twice the total deaths.
The curve that is here would fit with a weekly deaths of 10,000 by the end of the year but I expect it will slow though if it spreads outside these three countries in large numbers then it could get even worse.
– O’bumblefuck…There is nothing he can’t find to lie about.
– If it turns out that Jug ears intentionally lied and we see an expansion of the Ebola problem with more cases his days may finally be numbered even less than remains of his term in office.
The graph is not exactly accurate as it makes the assumption that incident cases are occurring at the same rate everywhere, (which is not the case), and the number of cases in the graph include both the incident (new) and prevalent (existing) cases.
I recommend the WHO SITREPS to get perspective on what is really going on. If you look at today’s, for example, the number of incident cases in Liberia and Monrovia are decreasing over time, in Guinea and its capital province of Conarky, the number of cases has bobbled up and down, and only in Sierra Leone has there been a steady increase lately.
Of further interest is that Liberia accounts for 55% of all cases and their case fatality rate is 58%, in Sierra Leone,
Damnit -hit send too early.
In Sierra Leone, with 26% of the cases, their case fatality rate is only 33%.
It is also important to note that with a population at risk of around 30 million, 8973 cases isn’t exactly a lot, particularly given that the population density in the capitals (e.g., Conarky) is about the same as Miami.
So – the graph is interesting, but not really representative of what is actually happening – if Guinea continues its basically flatline, and Liberia its decline, the graph is OBE.
As a point of order, the first case reported was in January (or December, depending on source), not March.
We have Top Men on this. And maybe some Top Transgendered/Questioning. Don’t worry about a thing. We have this completely under control. Or we will as soon as the new mood lighting is installed.
What, haters? Back that xenophobia up!
Good analysis, EA. The graph is far too idealized and tends to the speculative.
Perhaps predictive, if Ebola is successfully weaponized and/or becomes as transmissible as a common rhinovirus. Probably quite a few radically-inclined misanthropes seeking to fund that research right this minute.
(Oh, unrelated, has anyone seen AlGore lately ?)
The first to die will be the weaponizers.
And I think as it spreads through the population at large it will mutate into something less horrible. Having that many interactions with (what to the virus is) alien DNA can only push its effects back toward the mean.
That’s why rhino and influenza are so hard to control — being so contagious they mutate quickly. Only its relatively slow spread has prevented ebola from going soft since it was identified.
– Jug ears is now considering a travel ban, which he says he is not philosophically opposed to. He has to assure everyone of that because in most cases he’s against anything normal people would consider common sense. He also says he is considering a Ebola czar, this a few hours after his payed WH liar said no czar was being considered.
– I think the chaos inside this administration is the first epidemic we need to deal with.
I did not say the first case was in March. The first data point used was 50 cases and was in March. The numbers are from the “sitreps” and are cumulative.
From WHO.
– Gore popped his head up a few days ago to chime in on the Climate change bullshit.
Link for above.
I’m waiting for a jihadi to infect himself with Ebola, wait for the fever, and blow his ass up in some location with a fair density of unbelievers.
A speedy Ebola tester government official from a 3rd world state.
I’m not sure I understand why that would be so.
If this supposition is correct, that would hearten me with respect to antibiotic resistance which is increasing at an alarming rate.
don’t worry. remember top men/chauffeurs are on the job.
> Tommy Vietor said:
“Only in America can people who don’t believe in evolution or global warming browbeat actual professionals leading the CDC.”<
link
“Dude!.”
“President Obama Authorizes National Guard Reserve Activation For West African Ebola Deployments…”
The Obama Administration: Less competent than Nigeria. At this point I’m not even sure they could pull off even a simple email scam if the fate of the entire US depended on it.
“I did not say the first case was in March.”
Yeah, I know, but nigh everyone else keeps repeating that tidbit as TRVTH.
“In Guinea, Liberia, and Sierra Leone, new cases continue to explode in areas that looked like they were coming under control.”
One puzzling difficulty I have always had with the WHO is their hype not matching their data.
from the crusader front news:
Casting Crowns – Thrive
>One puzzling difficulty I have always had with the WHO is their hype not matching their data.<
be nice don't argue about bad data:)
vienna 1683 news
Until The Whole World Hears
I have a problem with this type of graph. The Y axis is a cumulative value. What would be more informative is a graph of the first derivative, which would be the infection rate. Now, if that second graph is rising, then it would mean the problem is getting worse, and if the second graph is falling it means things are under control. But a cumulative graph like the one presented above will always rise, or at best level off. People are far more used to seeing things like inflation rate or unemployment rate graphs, and will look at the cumulative graph as if it is a graph of infection rate.
What’s not on the table ? And, why isn’t this working now?
And if you think ZEBOV isn’t sneeze-transmissive, I’ve got some dead macaques to show you..
That’s dated 2011, and proof positive that our Government Lies.
Cranky, I was talking about viruses, which are essentially scraps of DNA. They infect by interacting with the DNA of their hosts to reproduce themselves.
Bacteria are complete, single-celled organisms. Whole different kettle of fish.
“I was talking about viruses, which are essentially scraps of DNA.”
DNA or RNA, the filoviri (Ebola, Marburg) are RNA viri, as are dengue, hep C, polio, and a pile of others.
Regardless, your point is correct and speaks to the concept of efficient and inefficient viri. An efficient virus is, like rhinoviri or the various flu viri, easy to transmit (e.g., one sneeze in a crowded room), are highly infective but of low virulence so that they make the host miserable for a bit, but doesn’t bump them off or debilitate them so severely that theycannot go on to infect more people. An inefficent virus, such as ebola, is the opposite. Regarding serr8d’s study, there is no evidence of human true aerosol transmission of ebola either observationally, or epidemiologically. Were it transmissible via true aerosol, the attack rate should be much higher (like flu), unless, however, it is just not very infective via an aerosol route. Having blood coughed in one’s face is another story.
From my reading, allegedly one can be infected lethally by exposure to a single ebola virus, so aerosol transmission shouldn’t make a difference there. There must be something about the virus that prevents a viable specimen from being included in an aerosol droplet, or remaining in it during transit.
Or it’s contained in fluids that change so much once in aerosol form that any contained ebola virus is dismembered.
“Whole different kettle of fish.”
I had a pet shrimp named Scraps.
She could swim like the dickens, but she still got et by a *pwloop*
“…allegedly one can be infected lethally by exposure to a single ebola virus…”
It would be interesting to see the source as it would be a swag at best as it is easy to find reference to the TCID50, but not what number of viral particles that represents, though in one pig study one million TCID50 of ebola Reston failed to produce clinical illness, though another with the same dose of Zaire did produce illness – still, if one were enough, why mess around with one million (or whatever the number really is).
I’ll have to break down and look in some books to see if I can find a better answer, but one particle – in someone severely immunocompromised, maybe, and infected in the strictest sense of the word, OK, but I seriously doubt lethally given an aggregate case fatality rate since 1976 of about 50%.
Regardless, here is a nifty, but not definitive, paper on transmission risk assessment full of nifty info.
There are still unknowns. Meanwhile, since this mess started in January, a half million or so Africans have died from malaria which used to be prevalent in this continent clear up into Canada.
Nothing about Africa’s health situation surprises me since I read about the notion that deflowering a virgin could cure AIDS.
Okay, I understand the difference between bacteria and viruses. Viruses hijack the cells they infect to produce copies of themselves.
Still, I don’t see why widespread exposure of the virus to humans would cause it to be less lethal. I would think that more opportunities for mutation would result in both more lethal and less lethal strains, both at either end of the natural distribution.
On speculation cranky-d (strictly on speculation), we might think that reproductive success is a high criterion in the drift of evolutionary change, as well as in the stability of the organism, if we can call sugar-coated bags of genetic material “organisms”. So if a mutation which tends not to kill the parasite’s host and yet does result in great numbers of reproduced copies being passed along (infecting) to the more victims, so resulting in a kind of reproductive “swamping” of the older “victim-killing” varietals of the bug. The more efficient bug wins. The walking wounded look to be a better means of infection than the dead and mouldering, sorta deal, I think. None of that is to say any such mutation is necessary, but just an example of the kind of mechanism we might expect to cause such a change.
I was just going on the observed fact that the more contagious a virus is, the less lethal it usually tends to be.
That strikes me as more than just a random interesting factoid. There would have to be some reason for it, and what sdferr offers sounds like a good one.
Arguing against that picture though, virus seems to be in many respects very fragile as compared with other more complex organisms, if only because the whole viral genome is so small. I take influenza for an example of this: the stuff is constantly in flux it seems, mixed and re-mixed in duck and pig reservoirs and so on. The killer 1918 flu-bug was largely gone by 1921 or so, replaced by a newer form, and only rediscovered in the frozen corpses of buried victims a few years ago. So in respect of “stability”, it looks in general as though there may be no expectation of such a thing in virus.
Also, survivors of a less lethal strain, once they’ve regained their health and assuming they’re not left permanently immunocompromised, stand a better chance of surviving the killer strain if they are exposed to it.
1918 may be the high-water mark within recorded history for a lethal flu strain. Influenza as a franchise owes its continued existence to the fact it is so mutable because survivors gain immunity to whatever strain they’ve previously had.
But, because they’re still around to suffer a new strain, the flu remains a more successful virus than one that kills 50% of its victims on the first try.
If ebola became as contagious as flu, it would become subject to the same evolutionary pressure that turned the flu into what it is: something everybody gets, every few years.
. . . stand a better chance of surviving the killer strain if they are exposed to it.
That’s appears to be a sound proposition McG, in the sense that the sugar-coating of the “bag” is the means of our immune-system attack on the virus. I don’t believe the bag would play the first role in the destruction of the victim’s own intra-cellular apparatus but merely plays its role in attachment to the victim’s external cellular membrane, and perhaps some role in the injection of the viral genetic material into the cell. So barring mutation in that viral surface, preservation of that envelope would seem to augur against the older killer form’s escape from our immune defenses, and thus that mechanism would contribute to the swamping phenomenon.
Too, I guess, perhaps it’s worth mentioning that sexual reproduction itself may have arisen precisely as a means to avoid too much “stability” in the complex organisms because of the constant assault upon them by parasitic organisms, and the immune system uses of some mutative variability in the population. We could point to people who were naturally bequeathed some immunity to the Black Death, for instance, as an example of this sort of variation in effect.
DHS Started Expediting Visa Extensions from Ebola Countries in August
“1918 may be the high-water mark within recorded history for a lethal flu strain.”
The important thing to note is that the lethality of the the 1918-19 flu was not the virus in of itself, but due to the secondary effects (e.g., pneumonia) for which there was no cure and despite which having today, is still the reason for the 30-40,000 American deaths that will occur with this year’s batch.
“Still, I don’t see why widespread exposure of the virus to humans would cause it to be less lethal.”
Koch’s Triad – stuff that kills the host is a reproductive (and evolutionary) dead end, even if there are asymptomatic animal reservoirs. The same is true for bacteria and parasites, consider Entamoeba gingivalis which most of have in our mouths and actually help prevent cavities, vs. Entamoeba histolytica which, when in the gut, can bump you off from dysentery. Speaking of the gut we die without good bacteria, but too much C. difficile and you might join the choir invisible.
BuzzFeed Accidently Gives MSM Game Away
Sound arguments, gentlemen. I agree with your conclusions.
If I may interject my inexpert commentary: while I don’t dispute the notion of at least some degree of inherited immunity as mentioned by sdferr above, I’d remind everyone that we regularly inoculate infants today against diseases to which their parents have already developed a resistance. I also recall reading somewhere* that successive rounds of the plague would hit the infant generational cohort the hardest, not only because of its members’ undeveloped natural immunity, but also because of their lack of acquired immunity.
*yeah, I know, not a very authoritative citation.
Given their relative life cycles, evolutionary pressure is more immediately effective on the virus side than the host side — and unless I’m mistaken that’s the aspect we were discussing.
I think it is a question of semantics regarding “bequeathed”.
“We could point to people who were naturally bequeathed some immunity to the Black Death, for instance, as an example of this sort of variation in effect.”
I took this to mean that some individuals simply had been born with natural immunity, which is certainly correct for nigh any communicable disease, not that they had necessecarily been passed said immunity through their parents which might be correct, but would be unknown in any event, hence a need to immunize children (or adults at risk).
Regarding inherited immunity, at least at a macro evolutionary level, there is certainly evidence given species specificity of some diseases, e.g., birds will not get human P. falciparium malaria (or any of the other 3 types), but can get P. relictum avian malaria, whereas humans will not.
Researchers say the chief trait accompanying Neanderthal DNA in those modern humans that have it, is some immunities not found in those who don’t. I believe sickle-cell, which seems to attack those of African descent almost exclusively, was named as one example.
Granted, the genetic code would not be changed by an individual’s exposure to disease (or are there some diseases which act as DNA mutagens?), but might it be possible for the embryonic environment to cultivate some level of disease resistance within the fetus if the mother had developed an immunity? Surely, there is some material exchange between mother and fetus — isn’t there?
Once again, I would like to emphasize that I am inquiring from a position of ignorance. Is there a doctor in the house? — or, as Barack would say, “is there a lawyer in the house?”
“Surely, there is some material exchange between mother and fetus — isn’t there?”
There is immunoglobulin transfer from the mother to the fetus by around week 6 which likely aids in prevention of congenital infections, there is no DNA swapping other than conception.
Many diseases, particularly viral, act as mutagens to the host cells, but the result is generally cancer, e.g., EBV and T-cell lymphoma, HPV and cervical cancer, and a possible link between viri and some breast cancers.
As well as the bacterium H. Pylori, implicated in some stomach cancers. I think that’s how my grandfather developed his fatal cancer.
Good comment thread.
“As well as the bacterium H. Pylori…”
True, but the difference is that with viri, the viral genome is incorporated into a host chromosome which leads to a plethora of ultimately oncogenic cellular changes, whereas the H. pylori activate intracellular pathways which lead to various inflammatory processes, which lead to the oncogenic transformation.
Hmm. Okay. I hadn’t known how it worked. Thanks.
I really do like learning stuff.
Also, I second bh.
I third, BH.