Don't Panic Yet

April 27, 2009 - 7:37 pm
Irradiated by LabRat
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So, mere years after the bird flu that cut a swath of destruction inches wide across North America, the new flu concern is swine flu part two, Mexican boogaloo. Scientists are warning of a pandemic, and an awful lot of folks I know are stocking up on their Purell wipes.

Me, I’m not particularly sweating it right now. I’ll probably get a flu shot when they get the strain sorted out, but then I think flu shots are a good idea anyway. Do I think we’re looking at the potential for an apocalyptic attack on civilization, Spanish Flu the Sequel? Too soon to tell.

First, a little background on influenza, our starring virus. Influenza has the relatively uncommon viral ability to infect several different unrelated species; while influenza is actually quite the slut of an upper respiratory virus and can get at a very wide range of host species with various levels of consequence for the host, the ones we hear the most about are birds and pigs, partly because of the bird’s mobility and partly because both come in domestic forms that have a great deal of interaction with humans. This versatility gives influenza one extra leg up in the evolutionary arms race that is being a pathogen- it mutates with tremendous speed as it picks up new genes and adapts across species. This is why you need a new flu shot every year instead of being good to go with a handful in a lifetime as you are with a human-only species like smallpox. Influenza strains are like popular dance tracks- each new host and generation of host provides its own remix.

This is why influenza is so popular in apocalyptic scenarios; their evolutionary chops make it virtually impossible to produce targeted vaccines and drugs against it, and its versatility in choice of host and method of transmission makes containing it equally impossible once a successful strain gets legs. The way that influenza jumps across multiple species also makes it scarier in one other respect- the normal evolutionary pressures on pathogens are blunted by the way a strain “grown” in one species may do something drastically different in a new one. Normally, an upper-respiratory virus is under pressure to be very successful at infecting, but not to be particularly virulent*; a host that feels well enough to be up and walking around and coming into the office saying “itds justg a liddle code” is a host that’s spreading the virus further and making it more successful. Diseases that depend on on a method of transmission independent of the host’s mobility- like insect-borne diseases and water-borne diseases in regions with poor sanitation- can afford to be more virulent than respiratory viruses. Influenza’s rapid mutation rate and multiple hosts make it a bit of an exception**.

The other reason influenza is so popular as a terrifying pandemic is that we’ve already HAD a terrifying pandemic from one particularly awful strain, the Spanish flu. World War I claimed its bodies, but the flu was responsible for far more of the generational gutting of the period- its death toll was double that of the war. One of the things about the Spanish flu that’s gravely cited in discussions of the epidemic is its odd pattern of fatality- it included a disproportionate number of the young and perfectly healthy. The morbidity and mortality graphs for “normal” flu look like U’s; the very young and the very old, those with undeveloped or compromised immune systems, get sick and die far more often. The 1918 pandemic’s morbidity and mortality graph looked more like a W- there was another big spike in the middle, healthy adults. Right now the hot theory for how this could have happened is the cytokine storm, which boils down to an overreaction by a robust immune system causing more damage than the virus on its own could have. It’s been observed in mouse models infected with the 1918 strain, but is overall not very well understood at all. Aside from the general lack of clarity into what exactly is involved in a “cytokine storm”, there’s plenty of obfuscating factors- the data isn’t great, and there’s also the role that the war itself played in creating massive congregations of young men in poor (immuno-suppressing) conditions and then letting them cough on each other for indefinite periods.

The major problem with projecting a 1918 style pandemic from a modern flu strain is that, in developed countries especially, a number of things have changed since then. In both normal flus and the Spanish flu, the number one killer isn’t/wasn’t influenza itself so much as it was bacterial pneumonias and other opportunists- once the flu set in and started knocking down the immune system and tearing up tissues, secondary infections would set in and finish off the weakened patient. The super-virulent flu of 1918 had its share of acute cases in which (apparently) severe damage to the lungs and intestines rapidly followed infection and death occurred soon after- but these cases were far from the majority. One of the reasons this new “swine flu” is gathering such attention is that this may have happened to some of the Mexico City fatalities- but one of the things missing from the media reports is how very few of the fatalities have been confirmed by culture to BE swine flu, just as the cases in the US have a big question mark attached to them. Unfortunately, our news cycle is a lot faster than our laboratories are. Either way, even if the new flu is every bit as virulent, the developed world isn’t likely to see anything like 1918′s fatality rate- simply because we have medical technologies hospitals of the time lacked, like antibiotics and antiviral agents for more acute cases.

The thing about the word “pandemic” is that while it technically means just the same thing it always did- a global epidemic- the differences in fatality rate are now tremendously more local than they were even as late as the beginning of the twentieth century. This is why, when we hear about some scary new flu, SARS, or other virus du jour, the fatalities seem to kick hell out of the less developed world and then virtually halt by the time they hit first-world nations; not only is the medical treatment available of a much higher quality for victims, but the level of sanitation and rapid identification of victims tends to put a huge damper on the spread of infection. This is why ordinary flu is regarded in the US as interchangeable with “a sucky week off from work”, whereas if you live in rural Madagascar it’s a serious risk of death. To put it in some perspective, bear in mind that right now the worldwide death toll for all influenzas hovers around the hundreds of thousands… whereas deaths from simple diarrheal diseases, particularly for children, are in the millions.

So, could the swine flu be as virulent as the 1918 flu? It’s a possibility. There’s not near enough known about it yet to tell, though it’s good that people are getting serious early about trying to contain it. Should you listen to the media? Take with several large grains of salt- reporters tend to be no better educated on the subject than “the flu was a horrible pandemic once!”. Should you worry about the flu-caused collapse of civilization? Really, I wouldn’t.

*Virulence: the technical term for just how severely a disease kicks the shit out of its host. A disease like herpes has very low virulence, whereas one like ebola has extremely high virulence. Infectivity- how good it is at breaching immune defenses and setting up shop- is an independent trait.

**This may well be one reason the 1918 pandemic lasted less than a year- terrifying as it was, it was also not very fit by virus standards.

No Responses to “Don't Panic Yet”

  1. Cybrludite Says:

    “This may well be one reason the 1918 pandemic lasted less than a year- terrifying as it was, it was also not very fit by virus standards.”

    A lady-friend of mine describes Y. Pestis as being a poorly designed bacteria because of its historical tendency to its kill hosts before they could stagger to the next village. A longer incubation period and/or a reduced lethality rate would make it a much better bug from a Darwinian standpoint.

  2. perlhaqr Says:

    “And knowing is half the battle!”

    Thanks for the rundown.

  3. Kristopher Says:

    I still have my face colander ready.

    People are getting rich in Mexico City right now, selling cheap face masks … and a soccer game was televised yesterday, with an attendance of one, as the cameras zoomed on some poor dude on the roof sweeping.

  4. pdb Says:

    So on the subject of Purell wipes, are we doing ourselves any favors by using those? Or are we selectively breeding a hardier strain?

  5. J.R. Shirley Says:

    Excellent essay, as usual.

    Cybrludite, there is quite a bit of evidence suggesting that the historical black death was not Yersinia pestis. Y. pestis kills much more slowly (onset of symptoms in 2 to 6 days), kills a much lower percentage of infected hosts, and does not cause immunity to future Y. pestis infestation by a host. Further, Y. pestis symptoms do not match many described symptoms of black death victims.

    Whatever caused the historical pandemics, it doesn’t actually seem to have been Y. pestis. I personally think it was some adaptation of Staphylococcus aureus, which can cause every symptom believably described by primary sources.


  6. Don Gwinn Says:

    The 6th graders are in panic mode (which for them is about 10% actual fear, 90% excuse to be louder and wackier than usual.)

    Apparently, the Swine Flu is “only 3 hours away” and that kid? Who missed Monday and Tuesday? I heard that Jenny heard that he totally has Swine Flu, but he came to school today ’cause he doesn’t want anybody to know.

  7. Blackwing1 Says:

    It’s interesting to note that a “human-only species like smallpox” is still similar enough to cowpox (present in both cows and humans) that innoculation with cowpox can prevent smallpox infection in humans. This, despite the fact that no known animal species other than humans can be infected with smallpox.

  8. BobG Says:

    Years ago I had a conversation with an ears, nose, and throat specialist who had been practicing medicine during the 1918 epidemic; he said most of the casualties he saw were caused by pneumonia, which attacked the people while they were weakened.

  9. Sigivald Says:

    I suspect (but have no hard data for the hypothesis) that another factor is modern nutrition and general health.

    Apart from being relatively fat (which is bad for your heart, but not terrible for the immune system), I’m pretty sure first-worlders today are generally healthier than they were in 1918, if only from better diet and having vitamin supplements.

    In 1918, unless you were astoundingly wealthy, you ate local food, in season, and preserved meats and staple grains, after all – no fresh fruit and vegetables year round, vitamin supplements in all sorts of things, and all the other factors that let even almost the laziest of us eat a comparatively healthy diet.

    (Yeah, we eat a lot of fat, and not everyone eats a lot of vegetables. I’d still bet it was better than the average diet in 1918, even outside of war-induced privation.)

  10. Hypnagogue Says:

    Purell wipes do not result in “breeding a hardier strain” of a virus. Viruses aren’t hardy at all, and can be destroyed with ordinary soap and water, or even light. They can only be transmitted by the most outrageous exchanges of warm, fresh bodily fluids — but that’s enough apparently. Humans are disgusting creatures.

    Bacteria are another topic altogether.

  11. bullbore Says:

    Viruses can be very hearty. Sure HIV is weak but hepatoviruses can survive bleach, Gamma irradiation, and dessication for up to 60 days.

  12. LabRat Says:

    PDB- Purell wipes and their cousins are good ideas if there’s a strain of nasty going around and you’re wiping down unknown/likely to be infective surfaces, like the handles of grocery carts or bathroom doorknobs- but I wouldn’t make a habit of them. Your very best bet is regular soap and water; soap strips off the layer of oil on your hands that the vast majority of bugs are living in. It’s a mechanical solution rather than a chemical one, and thus less likely to create resistance.

    John- Bear in mind that Y. pestis today is not Y. pestis of hundreds of years ago; it very likely HAS evolved to be, as Cybrludite essentially said, a better bug. Syphilis is an excellent example of a pathogenic bacteria has changed massively over time- from the time it hit the shores of Europe, it changed from a viciously virulent bug that could kill within a few months to one that had a lifespan covering decades of the host’s life before entering a fatal stage. It took it less than a century to adapt into an efficient human STD. We do know that the original black death was carried by rodent hosts- one reason the disease faded out (mostly) was that the black rat was displaced by the aggressively invasive Norwegian rat, which isn’t favored by the plague-carrying fleas. More obnoxious rat- but not plague-bearers. S. aureus doesn’t go through an insect host, BUT it IS an awfully opportunistic infection when other things have gone pear-shaped.

    Blackwing- yup, but you’ll note smallpox vaccine is derived from smallpox rather than cowpox nowadays- more effective. A huge number of human pathogens are either relatives of or direct crossovers from our domestic animals… measles, for example, is a cousin of canine distemper. And some people still don’t believe in evolution…

    Sigivald- there’s little doubt you’re right about that.

    Hypnagogue- it really depends on the virus, like bullbore said. Some are outrageously hardy- parvovirus, for example, can survive on the ground through freezes and drought for a year. Upper respiratory viruses need to be much hardier than STDs if they’re to be transmitted at all.

  13. Kresh Says:

    The panic makes me wonder what the media isn’t reporting. Not the “Black Helicopter” stuff, but what other gaffe has the current administration/ governmental wanna-be-overlords done this week that they don’t want us to notice.

    Cue “Twilight Zone” music…

  14. Dixie Says:

    “influenza is actually quite the slut of an upper respiratory virus” I LOL’d. Great post.

  15. J.R. Shirley Says:

    “John- Bear in mind that Y. pestis today is not Y. pestis of hundreds of years ago; it very likely HAS evolved to be, as Cybrludite essentially said, a better bug.”

    I understand your point, LabRat- but part of that evolution would surely not be reduced speed of transmission! In India, Y. pestis didn’t/doesn’t have nearly the pervasiveness of the historical black death, and was spread much slower.

  16. LabRat Says:

    True, but Y. pestis is also an import from Asia to begin with- one of the reasons it was so devastating to Europe was that it was a novel pathogen. Think smallpox and native Americans.

  17. J.R.Shirley Says:

    Well, you know Y. pestis is here in these United States, and considering the brief span it’s been present, must surely still count as “novel”. Do you know how slowly it is moving, even with abundant potential hosts? By your own reasoning (which I typically admire greatly, mind you), shouldn’t Y. pestis be rampant in the U.S. population instead of the 10-15 known cases a year in humans?


  18. LabRat Says:

    Why? It’s a new age- simple Tetracycline kills Y. pestis quite, quite dead, which is a powerful evolutionary pressure toward lesser virulence. The bug that gets noticed, dies. Cholera is still endemic in the U.S., but this doesn’t tend to be known except by microbiologists- the Vibrio cholerae strain that’s native to the southern US nowadays is so nonvirulent it’s asymptomatic.

    Far more important than that, however, is the fact that while potential hosts might be abundant, good hosts aren’t- that bug prefers the flea that prefers black rats, which have been basically shoved out of temperate climes by Norwegian rats. When shipping still carried black rats in from the tropics, the U.S. had plague outbreaks- balmy San Francisco being the most vulnerable.

    The next best thing seems to be prairie dogs and some southwestern rodents, which is why our own home state still gets plague cases from time to time. Most vulnerable are the wildlife biologists that interact with wildlife corpses- fleas that like prairie dogs and wood mice don’t tend to care enough for the taste of human blood to go out of their way, it seems.