Need truth about Spanish Flu factoid

In a TEDx talk, futurologist Stephen Petranek made this astonishing claim:


Now he was making a point about viruses mutating to increase their lethality, but in the remainder of his talk on that and other subjects he indulges in hyperbole or statements that properly need qualification (e.g., global warming = Earth becoming Venus). So was the second wave of the Spanish Influenza really that lethal, or has Petranek distorted the record?

That can’t be right. The overall case-fatality rate for the Spanish flu is given as about 2.5%. Since most fatalities occurred in the second wave, even though the second wave was more deadly the case-fatality rate couldn’t have been that much higher that the aggregate rate.

Fairly thorough-looking fact check says we can’t really tell all that accurately how many people died in any case (but 100% CFR sounds insane)

Given that FDR had the flu during the second wave (September - November 1918), it seems certain that there was at least one survivor.

As mentioned it was closer to a 2-3% mortality rating. Diseases with a fatality rate of near 100% do exist. But not the spanish flu.

One reason the second wave was so deadly is the war effort resulted in a lot of people mixing and mobilizing together. My understanding is an infectious disease has to pick between infectivity and lethality many times (depending on the vector), at least airborne diseases do, but the war effort allowed the virus to spread to become both lethal and infectious.

My understanding is the 3rd wave had the same lethal strain of the flu as the 2nd wave, but there were fewer deaths since the war was over and there was less interpersonal interaction.

Futurologist? Is that sort of like being a fungineer?

As to the question that seems impossible to me.

Viruses don’t “mutate to increase their lethality”, either. In the first place, mutations are random, and could increase or decrease lethality. In the second place, in so far as mutations have a “direction” at all, it’s that the mutations which help the virus persist, while mutations that hurt it die out (natural selection), and in the real world, that means that pathogens tend to evolve to become less lethal, because a dead host isn’t spreading the virus any more.

“Mutating to increase lethality” only makes sense if you assume that viruses have a goal to kill people, and that they’re actively working towards that goal. But that’s complete nonsense.

+1 Thank you.

Most human diseases originated in animals. They tend to be most lethal when they first enter the human population. The pathogen has not yet had time to adapt to its new host, and may kill it “by accident.” Over time, pathogens tend to become less virulent, because those that kill the host too fast won’t be spread to others.

Ebola outbreaks tend to “burn themselves out” because the disease is so lethal. People die before the can pass it on to too many others. Unfortunately, modern transportation networks have enabled it to spread more widely at times than it normally did.

This conforms with what one of my physician friends who worked through the SARS and MERSA outbreaks said: that virii tend to mutate to forms that are perhaps more contagious, but less lethal. (ETA: Perhaps I should not state it as they tend to mutate that way, but rather its those mutations that tend to survive and spread.) It’s certainly not a universal blueprint for the progress of a virus, but it makes sense for the reasons given in the last sentence quoted.

That’s my understanding as well, but here’s what I can’t understand about it: how does the new mutated virus supplant the old, more lethal, virus?

Meaning, I can understand if a virus that is more lethal and has little chance of becoming widespread for that very reason gets supplanted by a less lethal version of that same virus. Essentially two things are happening which are independent of each other. 1) the older, more lethal virus, dies out, as it would have done in any event, and 2) the newer, less lethal virus, thrives and spreads due to its less lethal nature.

But suppose you have a virus which in its original form has already shown itself to be capable of becoming a worldwide pandemic. OK, so now a new form arises, which is even less lethal and thus even more contagious. So the new form is going to spread even more. But what happens to the older, less lethal version? How does the new version being even more contagious alter the spread of the previously-successful older version? Why wouldn’t both versions continue to thrive at the same time?

Assuming that infection gives a surviving host immunity to both forms, the two forms are in competition for new hosts. Any new uninfected host will be preferentially infected by the less lethal form, making that host unavailable to the more lethal one. It’s natural selection and competition in action.

Firstly, is it correct altogether that it’s not possible to be infected with two forms of the same disease?

But even if it’s so, it’s not like there’s a shortage of hosts (people) to go around. At any point the majority of people are not infected at all and are potential hosts for either version.

It probably is. I’m not sure how that makes a difference.

It doesn’t happen instantaneously, but over time.

A person who’s well enough to walk around will spread the virus to a lot more people than one who’s so sick that he or she can’t walk around. And, of course, a person who’s alive will spread it to a lot more people than one who’s dead. And a person who’s been infected with one strain of a virus will usually have at least partial immunity to all strains. So the less-lethal strains have an evolutionary advantage.

Diseases that spread mostly by direct person-to-person contact are particularly prone to this evolutionary pressure. Diseases that spread in other ways (e.g. through insect vectors) don’t have as much tendency to evolve toward lower lethality. Consider malaria, for example. It depends on mosquitoes for transmission, so whether the host is able to walk around doesn’t affect its rate of transmission much. What it does depend on is a mosquito being infected when it bites a host, and since it takes such a small amount of blood with each meal, it pays for there to be a lot of the infectious agent in the blood. So it’s to the advantage of the malaria parasite to flood the host’s bloodstream with copies of itself, even though that may kill the host.

If it is possible, then the two forms are not in competition with each other. It wouldn’t be analogous to the typical evolutionary situation where the two versions are in direct competition for the same ecological niche.

That doesn’t address the issue.

The bottom line is that you still need for the improved version to deprive the other version of the ability to survive and propagate. In the typical situation, that would indeed happen over time, as the improved version seizes the limited available resources and/or mating opportunities. What I’m questioning is whether this is the case with viruses, at least in the timespan we’re discussing. As long as there are still plenty of ready hosts available, then this dynamic wouldn’t hold.

The most obvious example is AIDS. Anyone who remembers the biggest part of the epidemic in the late 80’s - everyone was dying of the virus, often within a year or two. A significant portion of young adult central Africa was also dying, and so many children were left orphans. Today, many people live decades with the disease. True, some drugs have helped, but the disease itself has become far less lethal because the less lethal version is the one that survives better.

Yes it is. The niche isn’t an individual human, but humans in general. Suppose a host is infected by both forms at the same time. The more contagious/less lethal form is still more likely to be passed on before the less contagious/more lethal form kills you and stops transmission of both forms.

Not all hosts in the population are available at the same time. You have foci or clusters of infection. And for the more contagious/less lethal form, more hosts are available at any one time because it spreads faster and over greater areas. Imagine a herd of gazelles and a cheetah vs a lion. The cheetah has many more individuals in the herd available to it because it can catch them from farther away. The lion can only catch those gazelles that are close to it. (Let’s not nitpick about the habits of actual gazelles and cheetahs. This is just to give the idea.)

Both of these responses seem to be presuming that the less lethal form is separately also more contagious. But that’s not what we’re discussing. The idea here is that the less lethal version is more contagious solely by virtue of being less lethal.

In that case, neither of your responses make sense. If someone is infected with both versions then either version is as likely to infect someone else as long as the person is alive and as unlikely to infect someone else when the person dies, regardless of which version kills them. And your lions vs cheetah analogy also deals with a situation where one version (cheetahs) has an inherent advantage (speed) as regards to catching limited resources (gazelles).

Or is your understanding that the less lethal forms are also separately more contagious, independent of their being less lethal?

It is a reasonable concern that the virus could mutate into a form that’s sufficiently different that it won’t be fought by the same antibodies. But that’s a concern regardless of whether the new form is more or less lethal or contagious. It’d be a problem even if the new form’s statistics were exactly the same as the old’s.