I have little doubt that Buttigieg and Klobuchar were promised something for dropping out of the race in such a timely fashion. But my guess is that another reason they dropped out with such alacrity is that neither ever expected to be the Democratic nominee in the first place. They were always positioning themselves to be VP or to get other favors of some sort from the eventual nominee, and their speedy and well-timed withdrawal from the race has only enhanced their positions in that respect.
So far so good for Netanyahu in Israeli election
“So far so good” means exit polls:
Prime Minister Benjamin Netanyahu planned to declare victory in Israel’s election on Monday, a spokesman for his party said, after television exit polls showed him just a seat short of a governing majority in parliament.
A win for Netanyahu, after inconclusive ballots in April and September, would be testimony to the political durability of Israel’s longest-serving leader, who fought the latest campaign under the shadow of a looming corruption trial…
“A giant victory for Israel,” Netanyahu, 70, tweeted after the projections were released.
His main challenger, former armed forces chief Benny Gantz of the centrist Blue and White party, stopped short of conceding defeat in his own posting on Twitter, telling supporters he would “continue to fight for the right path, for you.”
SCOTUS will be hearing another Obamacare challenge
It won’t be happening before the November election, though.
Et tu, Klobuchar?
The rumor is that Amy Klobuchar will be stepping out of the race and throwing her weight (such as it is) behind Biden.
Interesting. Assuming that’s true, the winnowing is happening rather quickly – before Super Tuesday.
But it’s not that dissimilar to what happened to the GOP field in 2016. There was Trump, course, the eventual winner. Cruz, Trump’s final opponent, didn’t drop out till May 3. Rubio left March 15. Kasich stubbornly limped along till May 4. Carson left on March 4. The rest of the field left prior to Super Tuesday. So on Super Tuesday there were five major candidates.
The Democrats seem to be narrowing down to four candidates prior to Super Tuesday: Sanders, Biden, Bloomberg, and Warren. Is Tulsi still around? Was she ever? If she’s still officially in the running, it’s only de jure. De facto she’s really nowhere.
Warren seems to be finished, too, but she’s not admitting it. That would leave the three elderly white guys, two of them Jews (at least nominally) and from New York. But it does seem (at least for the moment) as though the Democratic “establishment” is throwing its considerable weight behind the flawed Biden rather than the flawed Bloomberg. They will not support the flawed Sanders; it he wins the nomination, it will be against their wishes and efforts.
Somewhat like Trump in 2016. I’m not comparing Trump to Bernie except in one way: the attitude of the respective party powers-that-be to their candidacies. Of course, in 2020, the GOP is quite staunchly behind Trump, so that is a big change from 2016.
How about some facts on COVID-19?
I’ve written several posts already, trying to offer the main facts so far as they emerge. But I see so much stuff out there that’s not only obvious fear-mongering, but just plain incorrect.
It’s true that we don’t yet know exactly how this illness works and can come to no firm conclusions. That always takes a while with something that appears novel. But so far there’s been absolutely no indication that this is going to be an illness that’s hugely different and hugely worse than so many that have come down the pike in recent decades. However, you wouldn’t know that from most of the MSM coverage.
If you’re interested in voices that seem more fact-based, you should take a look at this from the New England Journal of Medicine. An excerpt (emphasis mine):
On the basis of a case definition requiring a diagnosis of pneumonia, the currently reported case fatality rate is approximately 2%.4 In another article in the Journal, Guan et al.5 report mortality of 1.4% among 1099 patients with laboratory-confirmed Covid-19; these patients had a wide spectrum of disease severity. If one assumes that the number of asymptomatic or minimally symptomatic cases is several times as high as the number of reported cases, the case fatality rate may be considerably less than 1%. This suggests that the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza (which has a case fatality rate of approximately 0.1%) or a pandemic influenza (similar to those in 1957 and 1968) rather than a disease similar to SARS or MERS, which have had case fatality rates of 9 to 10% and 36%, respectively…
A robust research effort is currently under way to develop a vaccine against Covid-19.10 We anticipate that the first candidates will enter phase 1 trials by early spring. Therapy currently consists of supportive care while a variety of investigational approaches are being explored.11 Among these are the antiviral medication lopinavir–ritonavir, interferon-1?, the RNA polymerase inhibitor remdesivir, chloroquine, and a variety of traditional Chinese medicine products.11 Once available, intravenous hyperimmune globulin from recovered persons and monoclonal antibodies may be attractive candidates to study in early intervention. Critical to moving the field forward, even in the context of an outbreak, is ensuring that investigational products are evaluated in scientifically and ethically sound studies.
But that tone is much too sober to serve the twin MSM/left purposes of attracting viewers and hurting Trump economically. However, at least for the moment, something seems to be calming the stock market.
Maybe it’s even the fact that Biden won South Carolina and might have a whisper of a chance of stopping the Bernie runaway locomotive – although I’m not sure why the election of a somewhat-addled mediocrity such as Biden would be soothing. Perhaps the thought is that he will continue business-as-usual and be quite malleable.
The message to take from COVID-19 is that we are too dependent on China. Trump has long been aware of that, although not necessarily because of novel viruses. But let’s just add that to the mix, because novel viruses emerge from China with some regularity. COVID-19 may be the most recent, but it won’t be the last.
For those on this blog of a certain age, you can reminisce (like me) about the Asian flu of 1957 or the Hong Kong flu of 1968:
Asian flu of 1957, also called Asian flu pandemic of 1957, outbreak of influenza that was first identified in February 1957 in East Asia and that subsequently spread to countries worldwide. The 1957 Asian flu was the second major influenza pandemic to occur in the 20th century; it followed the influenza pandemic of 1918–19 (also known as Spanish flu) and preceded the Hong Kong flu pandemic of 1968. The Asian flu outbreak caused an estimated one million to two million deaths worldwide and is generally considered to have been the least severe of the three influenza pandemics of the 20th century.
The 1957 outbreak was caused by a virus known as influenza A subtype H2N2, or Asian flu virus. Research has indicated that this virus was a reassortant (mixed species) strain, originating from strains of avian influenza and human influenza viruses. In the 1960s the human H2N2 strain underwent a series of minor genetic modifications, a process known as antigenic drift. These slight modifications produced periodic epidemics. After 10 years of evolution, the Asian flu virus disappeared, having been replaced through antigenic shift by a new influenza A subtype, H3N2, which gave rise to the Hong Kong flu pandemic.
In the first months of the 1957 Asian flu pandemic, the virus spread throughout China and surrounding regions. By midsummer it had reached the United States, where it appears to have initially infected relatively few people. Several months later, however, numerous cases of infection were reported, especially in young children, the elderly, and pregnant women. This upsurge in cases was the result of a second pandemic wave of illness that struck the Northern Hemisphere in November 1957. At that time the pandemic was also already widespread in the United Kingdom. By December a total of some 3,550 deaths had been reported in England and Wales. The second wave was particularly devastating, and by March 1958 an estimated 69,800 deaths had occurred in the United States.
There certainly was newspaper coverage then, and news filtered down to children – including me. But somehow the country didn’t self-destruct.
Bye Bye…
Buttigieg.
It was going to be hard for white Democrats, both party elites and voters, to mobilize behind a candidate with such weak support among people of color as the center-left alternative to Sanders.
So Buttigieg’s departure may have seemed sudden, but it’s likely that the former mayor was going to struggle on Super Tuesday and possibly run out of campaign funds. So this decision is a face-saving move for him.
That said, I don’t think Buttigieg’s departure is solely due to his struggles. Elite voices in the Democratic Party have been worried that the multiple center-left candidates in the race — Biden, Buttigieg, former New York Mayor Michael Bloomberg, Sen. Amy Klobuchar, etc. — would divide the non-Sanders vote, potentially allowing the Vermont senator to amass a huge lead in delegates on Super Tuesday while his rivals finished below 15 percent in many states. South Carolina is only one state, but Biden’s resounding win there suggests that the former vice-president can combine older, moderate voters, black and white, into a big coalition in a way that Buttigieg probably could not. So my view is that Buttigieg stepped aside in part to help the center-left bloc of the party consolidate around Biden. To some extent, he was being a team player.
That’s from FiveThirtyEight. Selfless Pete, falling on his sword for the good of the moderates in the Party (which he’s really not). Others have a slightly different take.
Like this guy:
Pete Buttigieg is OUT. All of his SuperTuesday votes will go to Sleepy Joe Biden. Great timing. This is the REAL beginning of the Dems taking Bernie out of play – NO NOMINATION, AGAIN!
— Donald J. Trump (@realDonaldTrump) March 1, 2020
Clever. Trump is insinuating what a lot of people are thinking, which is that some person or people either twisted Buttigieg’s arm or made it worth his while, or both, to drop out in order to hurt Sanders and help Biden. And Trump is also doing a fair amount of concern-trolling of the Bernie Bros, reminding them of the way they believe they got screwed by the Party in 2016. The hope on Trump’s part is that if Biden gets the nomination, Bernie’s supporters stay home.
Perhaps that’s true. But perhaps it’s as I wrote on February 12:
In 2016 I thought if only either Cruz or Rubio (or other contenders) would drop out, all the others’ votes would go to the last Trump-opponent standing, and that person would win. But as time went on, I didn’t see that happening. I saw Trump getting a significant percentage of the votes of each person as that person exited. I began to realize that Trump could get the whole thing.
And I think something similar has a good chance of happening with Bernie. Will it? I certainly don’t know, but I see it as a strong possibility.
Time will tell.
Biden up, Steyer out
The Democratic primary voters of South Carolina have spoken and Biden has won a resounding victory there.
I can’t quite imagine voting for someone as addled as Joe. But then again, consider the alternatives. Bernie Sanders came in a distant second, and Steyer is taking his marbles and going home.
Fifty-five percent of South Carolina voters in this primary were black. That’s a very different demographic than in the previous primary states.
Now, on to Super Tuesday. Here are the forecasts from FiveThirtyEight, with a chart. Sanders is heavily favored, with strong showings predicted for Biden and – of all people – Bloomberg (587 for Sanders, 305 for Biden, and 211 for Bloomberg, with the rest left behind in a cloud of dust).
But that FiveThirtyEight article was written on February 26, before tonight. Will Biden get that old-fashioned Joementum?
Ulanova vs. all the other Juliets
Galina Ulanova was one of the most famous Russian dancers of the Soviet era. I saw her in person when I was very very young and she was close to 50 and nearing the end of her dancing days.
She was best in “real” roles where she played girls or women rather than sprites or fantasies. By the time the film I’m going to be highlighting here was made in 1954 she was 44 years old, no spring chicken in ballet terms, and the closeups aren’t kind (she was never a great beauty anyway). Films aren’t a good way to see ballet, but they’re all we have of Ulanova at this point.
Her proportions were not those of today’s ballerinas, nor of course was her technique or style, which some think is overdramatic. I don’t agree with that. She is always, always, always, expressing a character, never just doing steps and carefully showing off like so many of today’s dancers. Their emotional restraint and physical prowess were not her interests. She doth teach the torches to burn bright, even at the age of 44 without the forgiving distance a stage and theater provides.
The video I’m talking about is unfortunately unable to be embedded here; it must be watched at YouTube. So please go here and view minutes 21:24-23:00. This is a short variation where Juliet is introduced at the ball.
The second scene is from around 30:09 to 33:05 at the same video. It begins with a lift to which you should pay particular attention (you’ll see it again later, when she is an 86-year old teacher, in the next-to-last video I will post -and that one can be embedded, unlike this one). She originated the role of Juliet in this production. The male dancer, her Romeo, is a handsome guy but also far from a teenager or being able to pass as one. He’s not much of a dancer, either, although in those days standards for male dancers were very very different than now, and significantly lower. But he’s very much in the style of the time: strong and masculine. And boy, can he lift! The two of them make those lifts look like the easiest and most natural things in the world. They are most assuredly not (again, I refer to 30:09 to 33:05):
And here Ulanova is at 86, still showing em how it’s done:
No one today is even remotely like her. But then maybe no one was like her, even then.
Here’s a sampler of some excellent dancers of today – or of a little while ago (it’s not Ulanova who is number 2; that’s a mislabeling). They are so careful, so unspontaneous, and for the most part the tempos are slow and ponderous. I have to say, though, that the last dancer in the group, Ferri, is someone I saw in person, and this video doesn’t capture how wonderful she actually was in person. Very different from Ulanova, but still great:
On coronavirus (COVID-19) so far: Part II
[NOTE: Part I can be found here.]
While musing about COVID-19, I wondered whether the virus really is novel. Perhaps it’s been around for a while and just wasn’t causing all that many deaths and therefore wasn’t even noticed until the spike occurred in China. Now that the virus has been recognized and is being tested for, perhaps we’re finding it all over the place (in small quantities so far) because it’s long been all over place and not caused all that much damage.
This seemed an odd thought. But it turns out it’s not so odd after all:
…”[H]as this virus ever entered the population undetected and been spreading?” asks Andrew Pekosz, a biologist at the Johns Hopkins Bloomberg School of Public Health. If in previous instances it induced only mild disease, “it may not have registered a large enough number of cases to get on the public health radar screen.”
Ebola and HIV both turned out to have existed for many years before scientists recognized the diseases those viruses cause. Scientists discovered that by running antibody tests on blood that had been stored long ago.
An antibody test is sorely needed, in order to tease out an answer to that question. It would also help us to learn whether there are a great many mild or even symptomless cases that have gone unrecognized, which would change our perception of the lethality of the virus.
There are two main issues with COVID-19, and we don’t know all that much about either yet: contagiousness and lethality. But the situation of the Diamond Princess cruise passengers offers an opportunity to learn about both under a sort of worst case scenario, which is confinement of healthy with ill passengers in a closed system, and an especially susceptible population because of a high percentage of people of advanced age. So let’s take a look.
The first thing you’ll notice is that the headline blares that the ship started with 10 passengers testing positive for the virus and ended with 700 testing positive within the two weeks of the quarantine. That’s quite a leap. The total number of people on the ship was 3,711. So the final number testing positive represented about 19% of the whole, or a little less than a fifth. Of that number – in the month since the first person from the ship was diagnosed – 6 have died, which is .16% of the whole, and .86% of those who tested positive. Both figures are under 1%. That only represents a months’ time, of course, two weeks of which involved quarantine on the ship. But it’s a fairly low figure, especially considering the advanced ages of so many of the passengers. Time will tell whether there will be any more deaths of people who were on that ship.
A large part of the linked article is about the terrible conditions of confinement and fear on the cruise, and how certain things probably fostered the spread of the disease. It’s missing a clear timeline of when people were tested and whether some of the rise in cases over time represented the fact that only certain people were tested at first (perhaps only the symptomatic?). It’s really unclear from the article, and perhaps the health officials on the ship were the ones who were unclear in communicating exactly how the testing went.
This part is especially interesting:
More than half of the infected people (322) showed no symptoms at all, which suggests that some coronavirus carriers in China could be going undetected.
That’s a fact that indicates less mortality – and even less morbidity – than has commonly been reported.
This article also describes the people who died. The first two were 87 and 84, both with underlying pre–existing health issues. The next two were also people in their 80s, and it’s unclear what their previous health status had been. The fifth person was in her 70s, and the sixth was of as-yet unreported age. This is further indication that advanced age is a big factor, just as it is in pneumonia deaths and deaths from most varieties of flu (although not the 1918 flu, where the majority of deaths were of younger adults ).
One question as yet unanswered is, if you eliminate the asymptomatic passengers, what percentage of the others testing positive had only mild symptoms. But we don’t know; at least I haven’t seen this reported, even though it would be important information. This article, based not on the ship data but on Chinese health officials’ reports, says that 80.9% of cases in China have been mild. However, that probably misses almost all the cases that are asymptomatic, and so it doesn’t tell us much about that phenomenon. Of the 19% of confirmed cases in China that have been considered serious, 2.3% were critical, and all the deaths were in that group.
This is how the death rates for COVID-19 so far (mostly in China) compare to previous novel illnesses that have gotten a lot of publicity:
Overall, however, the COVID-19 fatality rate is far lower than that of past coronavirus epidemics. Based on the ratio of deaths to confirmed cases so far, it appears to be about 2%. Severe acute respiratory syndrome (SARS), by contrast, killed 9.6% of those infected, and Middle East respiratory syndrome (MERS) killed 34.4% of cases.
But on the other hand, those illnesses were seemingly less contagious and therefore more easily contained
The following is encouraging, and it makes sense to me:
Fauci and other experts, however, think the existing fatality rate will drop as more mild cases are counted.
And this article points out something that might be obvious but that’s still important to note: novel threats, even if they’re less dangerous than pre-existing threats, can cause more fear. People are used to the familiar.
As I mentioned in Part I, COVID-19 has been hyped by the press and the Democrats, the better to get clicks and/or sell papers, and to criticize and blame Trump. But there’s another factor, which is the increase in our economic dependence on products and shipments from China. That’s real, and any disruption in the supply chain from China could be very problematic. Ironically for the left, another thing Trump’s been doing for quite a while is trying to lessen our trade connection to China. But don’t sit on a hot stove waiting for the left to praise him for it.
Bernie ♥ his myth of Denmark
Paul Mirengoff of Powerline points out the ways in which Bernie Sanders’ vision of turning the US into Denmark is a dream based on a myth of what Denmark actually is, and what other Scandinavian countries he admires actually are. In his post, he quotes this op-ed by Fareed Zakaria that appeared in the WaPo:
Take billionaires. Sanders has been clear on the topic: “Billionaires should not exist.” But Sweden and Norway both have more billionaires per capita than the United States — Sweden almost twice as many. Not only that, these billionaires are able to pass on their wealth to their children tax-free. Inheritance taxes in Sweden and Norway are zero, and in Denmark 15 percent. The United States, by contrast, has the fourth-highest estate taxes in the industrialized world at 40 percent.
Zakaria also notes that Sweden, another country much admired by Sanders, had to abandon the sort of economic policies Sanders likes in order to keep itself from going under:
In Sweden, government spending as a percentage of gross domestic product doubled from 1960 to 1980, going from approximately 30 percent to 60 percent. But as Swedish commentator Johan Norberg points out, this experiment in Sanders-style democratic socialism tanked the Swedish economy. Between 1970 and 1995, he notes, Sweden did not create a single net new job in the private sector. In 1991, a free-market prime minister, Carl Bildt, initiated a series of reforms to kick-start the economy. By the mid-2000s, Sweden had cut the size of its government by a third and emerged from its long economic slump.
Mirengoff concludes:
Sanders favors policies much more along the lines of those that failed Scandinavia in the 1960s and 1970s. Or perhaps a mixture of those policies and the ones that are failing in Venezuela today.
You could try running those facts by any Sanders supporters you know. But I wonder whether it would matter to them. I think Sanders’ popularity is a combination of many things, but one of them is that his promises sound well-intentioned and idealistic to his followers, many of whom may not actually expect him to achieve his goals. It’s a sort of virtue-signaling gone wild.
Does Bernie himself even believe that he could accomplish what he promises? I doubt it. But he sounds sincere – at least to his followers. As either Jean Giraudoux or George Burns (quite a combo!) said: “The key to success is sincerity. If you can fake that you’ve got it made.”
Is Sanders faking? I don’t know. But it actually would be better if he were faking, because if he believes his own blather – and somehow manages to convince enough people to get elected – we’d be in even more trouble than if he were just saying it in order to get votes.
What do I think? I think he’s sincerely sincere.
And because in my youth an enormous number of Broadway show tunes became embedded in my head, right after I wrote that last line I thought of this apropos number from “Bye Bye Birdie.” I saw the show in its original run on Broadway at exactly the right age to love it. I had no interest in the movie that came out a few years later, but here it is because the clip features the song I’m talking about. Incidentally – and I only learned this from the YouTube comments – the building in this scene is the same set later used for “Back to the Future”:
New plan: Part II of “On coronavirus (COVID-19) so far” coming tomorrow
I thought I’d get Part II of my coronavirus update published today. But in the meantime, I decided to write just a little teeny tiny post on the question of the 1918 flu epidemic and aspirin.
Well, a lot of research and 1525 words later, I’ve decided to hang up my coronavirus-research hat for the day.
That sort of thing happens a lot. I expect a post will be short and easy, like that aspirin one, and it turns out to be anything but.
Aspirin and the 1918 flu death rate
Recently there’s been some talk (including in the comments on this blog) of a theory that high doses of aspirin played a key role in exacerbating the number of deaths in the 1918 flu pandemic:
The high case-fatality rate—especially among young adults—during the 1918–1919 influenza pandemic is incompletely understood. Although late deaths showed bacterial pneumonia, early deaths exhibited extremely “wet,” sometimes hemorrhagic lungs. The hypothesis presented herein is that aspirin contributed to the incidence and severity of viral pathology, bacterial infection, and death, because physicians of the day were unaware that the regimens (8.0–31.2 g per day) produce levels associated with hyperventilation and pulmonary edema in 33% and 3% of recipients, respectively. Recently, pulmonary edema was found at autopsy in 46% of 26 salicylate-intoxicated adults. Experimentally, salicylates increase lung fluid and protein levels and impair mucociliary clearance. In 1918, the US Surgeon General, the US Navy, and the Journal of the American Medical Association recommended use of aspirin just before the October death spike. If these recommendations were followed, and if pulmonary edema occurred in 3% of persons, a significant proportion of the deaths may be attributable to aspirin.
I don’t see that it’s especially relevant these days, because no one is recommending doses anywhere near that, and aspirin isn’t as widely used in general even in low doses (except for those who have had cardiovascular problems, who take aspirin in tiny doses to prevent the occurrence of a subsequent event). But putting that aside, I don’t think aspirin was a big deal in the death rate even in 1918, although it might have had some role.
Here’s why I say that:
The international characteristics of the pandemic make the salicylate hypothesis difficult to sustain as the primary explanation for the unusual virulence of the 1918–1919 influenza pandemic. Worldwide, an estimate of the mortality of the 1918–1919 pandemic is 50 million deaths, with a range of up to 100 million deaths. Taking the 50 million figure, this was about 2.5% of the world population. By contrast, in the United States, mortality was on the order of 0.5%. Clearly, the rest of the world was struck more severely, on average, than the United States.
India serves as a useful vignette. Mortality in India was staggering, with estimates of 18.5 million persons dead and higher. Indeed, the Indian peasant population was so severely affected that economics Nobel laureate Theodore W. Schultz used the pandemic as a natural experiment in per capita agricultural output. Given the huge number of deaths in India and the burden among subsistence agricultural workers, it is extremely implausible that salicylates played an exacerbating role in anything other than a trivial percentage of Indian mortality.
Thus, Starko’s intriguing hypothesis fails the test of dose-response. That is to say, in countries such as the United States, where salicylates were more available, mortality was much lower compared with regions where salicylates were less readily available. These observations are at the ecological level, and such comparisons are notoriously susceptible to confounding. However, if the salicylate hypothesis applies universally, then the ecological confounding would have to operate such that the salicylate-influenza connection is stronger in countries with less access to aspirin, which seems a priori unlikely. Indeed, the overwhelming majority of the millions of Indian peasants who were killed by the flu certainly had no access to salicylates whatsoever. If the salicylate hypothesis only works in the United States and in similar settings, then we question its validity given the worldwide scope of severe mortality in 1918–1919.
To summarize: the US had a much lower mortality rate for flu cases in 1918 than a lot of other areas. Of course, as the author of the above quote acknowledges, there may have been (and probably were) many factors that went into that lower mortality. But if in countries where aspirin use was basically nil, the mortality rates were much higher, then it does cut into the likelihood that aspirin was a big factor here, although it doesn’t eliminate it.
One would also have to know how often aspirin actually was used in the US in people who had the 1918 flu. The article speaks of certain spikes in deaths that occurred in waves. But those spikes and waves in which the death tolls were different at different times, even in the same country, are common around the world in flu epidemics. And what’s more, they also occurred in 1918 in other countries where aspirin usage doesn’t seem to have been practiced, much less megadoses of aspirin. It is often part of the natural history of such a disease for its lethality to wax and wane in waves, so attributing that waxing and waning in the US to aspirin usage seems quite iffy to me – especially since we don’t have a good sense of the ways in which aspirin usage waxed and waned in 1918.
And by the way, those mortality figures in the first paragraph of the first quote – 2.5% around the world and .5% in the US – illustrate something I wrote at length about yesterday, which is the confusion that sometimes arises in the reader because mortality percentages can be given in two different ways. To repeat: the figure can represent an illness’ mortality rate as a percentage of the entire population (in a city, a country, or the world). Or, the figure can represent an illness’ mortality rate among those infected (for infectious diseases, of course) or who suffer from it (for a non-infectious disease such as cancer). Quite obviously, the percentages of deaths in the afflicted are significantly higher than in the population as a while. The figures given in the excerpt here are for the percentage of the entire population – that is, 2.5% of the population of the entire world died, and .5% of the population of the US died.
And although the flu was especially bad in India, that country was not even the worst in terms of death rates:
Though other countries lost a higher fraction of their populations—Western Samoa (now Samoa) lost 22 percent, for example, compared to 6 percent in India—because of the larger size of the Indian population, that 6 percent translated into a staggering slew of death. Between 1918 and 1920, an estimated 18 million Indians lost their lives to influenza or its complications, making India the focal point of the disaster in terms of mortality. Asia as a whole experienced some of the highest flu-related death rates in those years, but the story of how the disease ravaged the continent is relatively unknown. The 1918 flu pandemic has been called the “forgotten” pandemic, and ironically the continent that seems to have forgotten it most thoroughly is the one that bore the brunt of it.
And here’s some information about the way that characteristic “wave” pattern I wrote about yesterday operated in 1918, as well as the contagiousness/lethality balance I also mentioned in that earlier post (emphasis mine):
Hunger weakens the immune system, and hunger was rife in many regions of the world in 1918, partly due to disrupted supply lines. Other infectious diseases, such as tuberculosis and typhus, had made inroads into human populations, capitalising on the disruption wrought by war and rendering their victims more vulnerable than usual to a new respiratory infection. Large numbers of people, both troops and refugees, were on the move, providing the ideal vehicle for disseminating that infection. Meanwhile, the very lack of mobility of one group may have helped brew a particularly lethal germ that year, or at least kept it lethal for longer. Once the virus reached the Western Front—the 16-kilometre-wide system of trenches that gashed France from the Belgian to the Swiss border—it encountered large numbers of young men who, packed into those trenches, did not go anywhere for weeks or months. Paul Ewald, an evolutionary biologist at the University of Louisville in Kentucky, has argued that under such exceptional conditions, the evolutionary pressure on the virus to moderate its virulence may have been relieved. It became the mobile one in the host-virus relationship, and it raced through the trenches, killing as it went.
Flu pandemics have a characteristic structure, engulfing the world in waves. The first wave, sometimes called the herald wave, is often quite mild, resembling a seasonal flu. This tends to be followed by a more deadly second wave, and in some cases, subsequent waves of varying severity. The flu pandemic of 1918, though unusually virulent, was no different in this respect. There was a mild herald wave in the northern-hemisphere spring of 1918, a much more lethal second wave in the latter part of that year, and a final recrudescence in the early months of 1919, which was intermediate in severity between the other two. The pattern was repeated in the southern hemisphere, but it was staggered in time with respect to the north, meaning that the waves tended to strike later there. The pandemic is conventionally considered to have been over by March 1920, although earlier this year, the epidemiologist Dennis Shanks and his colleagues at the University of Queensland in Brisbane reported that it dragged on in the Pacific islands for another year, with cases still being reported in New Caledonia in July 1921.
It’s rather complicated, and we’re still learning about it. But if aspirin played much of a role, I think it was a tiny one.