Re: diseases and immunity

Gerold Firl (
15 Jul 1996 21:04:55 GMT

In article <>, Fred G. Athearn <> writes:

|> >>>>> "Gerold" == Gerold Firl <> writes:

|> If we assume for the sake of argument that TB had the
|> spectacular sort of virulence you suggest in early Indian
|> populations there remains the problem of transmission. How is a
|> disease that kill within weeks transmitted? Clearly not in the
|> way TB seems to be today.

I'm not sure how TB is transmitted, though I've always assumed that it
was by inhalation of the bacilli within a drop of sputum (ever heard
someone with TB cough? Nasty.)

Here's a simple model of the population dynamics of a pathogen upon
reaching a virgin-soil host population: instead of taking several
years to die, these new hosts die in several days or weeks. They are
also totally open to infection, with no appreciable immune reaction.
This results in a new selection pressure on the pathogen: it needs to
jump to a new host quickly, and it doesn't need to be very picky about
what part of the body is colonized.

The pathogen thus evolves to become highly contagious, which, in
practical terms, means being able to survive temperature fluctuations
and dessication. Using TB as an example, it also will change so-as to
no longer restrict itself to the lungs. (Bacteria have a varied
repertoir of cell-membrane proteins which attach to different host
tissues; lungs, intestines, blood cells, nerves, cartilage, etc) In an
immunilogically experienced population, TB resides in the lungs; in an
inexperienced host, that restriction is no longer necessary.

As soon as TB invaded amerindian populations, the new environment led
to an evolutionary shift. Highly contagious strains were favored,
since the less-contagious ones died along with their hosts, while more
transmittable strains had already infected a few other people before
their host died.

|> If syphilis (as Gerold suggests) killed within days of exposure
|> when it first came to the old world that would have place very
|> big limits on its ability to propagate itself as a sexually
|> transmitted disease.

True. I've looked for references on early virulence of syphilis in
europe, but I haven't been able to find them. Of course, the people
who succumbed in a matter of days would be at the extreme end of the
vulnurability spectrum; others would take longer (that genetic
variability thing again.)

|> In that context genes from a local endemic disease which slowed
|> down the progress of the infection by marking it for immune
|> system attack could be considered "advantageous".

Absolutely. It's important to understand the balancing act between
host and pathogen, resistance and virulence. The pathogen "wants" to
find an optimum level, eventually tending towards a low level endemic
infection. This is accomplished by natural selection of host and

|> Gerold> ...In an unexperienced host population,
|> Gerold> however, the virulent strains will be the most
|> Gerold> successful. They will rapidly and aggressively expand
|> Gerold> their market-share, until the epidemic burns out and
|> Gerold> the chronic strains take over.
|> It is incorrect to jump from the idea of virulents to the idea of
|> raging and expanding epidemic.

Why? The lack of indian immune defense accounts for the high kill
ratios, and their rapid demise accounts for the selection pressure for
extreme contagiousness.

|> The fact remains that any theory of a blitz krieg attack on the
|> American Indian population by one very virulent disease needs to
|> explain how transmission could take place between groups that
|> were quite spread out.

A big factor there is the way people will flee from an epidemic.
Crosby describes how refugees from disease spread it far and wide,
probably accounting for the devastation of the mound builders, far
ahead of any colonization.

Note also that syphilis reached china about a decade *before*
europeans arrived; I think it was around 1515 or so. Germs travel

|> This is not just a problem of history. There is an arithmetic to
|> epidemics that has to be taken into account. It seems that to
|> make your theory work you would need to come up with a different
|> transmission method for TB within the target population.--

I've suggested one way that a disease can suddenly become much more
contagious: simply improve robustitude in the face of environmental
fluctuations such as temperature and humidity. (It is well known that
such parameters are stored on auxiliary genetic packets within the
bacillus which are constantly being exchanged, leading to a very rapid
diffusion of advantageous characteristics) If such a change involves a
thicker cell membrane, or one which is more excitory to the immune
response, that won't be a disadvantage in an inexperienced host.

Disclaimer claims dat de claims claimed in dis are de claims of meself,
me, and me alone, so sue us god. I won't tell Bill & Dave if you won't.
=-=-=-=-=-=-=-=-=-=-=-=-=-=---- Gerold Firl @ ..hplabs!hp-sdd!geroldf