Re: diseases and immunity

Gerold Firl (
10 Jul 1996 13:10:16 -0700

In article <4s0e88$> Beth Williams) writes:

>Gerold, you're taking a cite from a cite as hard evidence, and you're
>not even sure of the primary data from which the interpretation
>derives? Not very scientific, wouldn't you say?

Oh, I don't know. I'm giving you what data I have. Is it "hard evidence"? I
consider mcneill to be pretty reliable, and it is certainly a well known
fact that unfamiliar diseases will manifest unusual symptoms and virulence.
I'm not sufficiently interested in this topic to go back to the dubos
reference to get more detail, but since you have done actual field work on
TB infection and mortality around the contact period, I expect that you

>The most plausible present-day hypothesis is that Old World *yaws* and
>New World endemic syphillis interacted and formed a new more lethal
>strain of the organism. Hence, we have an example of where the
>pathogen, not the host, mutated (which is not at all uncommon --
>happens every year with the *flu*.)

It happens all the time, with every disease. That is why the immune system
has to have such a huge repertoir of responses; not only does it have to
respond to all the diseases in the current environment, but it must also be
prepared for all the new varieties which will occur. Generation times for a
bacterium are, what, a few hours? Over the course of a human lifetime,
disease organisms go through thousands of generations. Not only that, but
bacteria constantly exchange dna, so advantageous genes spread very quickly
in a bacterial population.

A TB culture will have a continuum of types, ranging from relatively
slow-acting, mild, chronic strains, to raging virulent killers. In an
adapted population, the virulent killers are fringe citizens, heavily
discriminated against by seasoned immune systems. They will constitute a
small percentage of the total. In an unexperienced host population,
however, the virulent strains will be the most successful. They will
rapidly and aggressively expand their market-share, until the epidemic
burns out and the chronic strains take over. This same pattern is found in
many different ecological settings: many weed species are adapted for rapid
exploitation of disturbed soils (milkweed, for example). Lodgepole pines
are adapted for exploitation of fire-cleared forest. Human slash and burn
techniques, whether in amazonia or among balkan gypsy con artists are also

>The problem here is, Gerold, that you have no evidence, and in fact
>there is _negative_ evidence, to support your claims that TB was an
>*epidemic* versus *endemic* disease in either Indian or non-Indian
>populations during the Contact Period.

Among the maori, I believe that TB was the main killer, because smallpox
had a hard time reaching new zealand. In the americas, the only example I
have heard of is the one cited by mcneill. Maybe it's bogus; I guess we'll
need to check dubos to get more information.

>So far, you haven't produced
>any primary documentation that would support such claims, and there is
>ample physical evidence to show that skeletal TB, which you allege to
>show *immunity*, is present in Contact, in most likely, pre-Contact
>populations. Furthermore, one cannot distinguish pre-Contact from
>post-Contact TB, and if there are, as you claim, different *strains*,
>they do not manifest themselves within the human skeleton differently.

Again, I expect that virulent, epidemic TB probably won't produce much in
the way of bone lesions, but we're speculating here without a whole lot of
evidence. Are you planning on looking-up _man adapting_ to get the details
on this case?

>Sit back and think about this one carefully, Gerold. Are you claiming
>that *epidemic* TB behaves like other epidemic diseases, such as
>smallpox and measles, where the victim contracts the disease and either
>dies rapidly, or survives, thus gaining an immunity? Because this is
>the _only_ way that your purported *immunity* could be passed from
>generation to generation, as the dead do not reproduce, and it is
>impossible to pass on immunity _before_ the immunity has been

Here's how it works: start with a population which has never been exposed
to a particular disease - say, an amerindian tribe with smallpox. Each
individual in the tribe will have a different mix of immune factors, giving
variations in their vulnurability to the new disease. Say that 85% die in
the first epidemic. The 15% who survive will now be immune to smallpox, but
even before they generated an immunity they were already unusually
*resistant* to the disease. Why? It's a question of the particular mix of
immune response factors they were born with. This is the form of genetic
variability I mentioned earlier in this thread, and which plays such a
major role in determining human disease resistance.

Immunity is acquired. That is different from the innate resistance which is
built-into our genes.
