Re: diseases and immunity

Philip Deitiker (pdeitik@bcm.tmc.edu)
Fri, 19 Jul 1996 00:24:03 GMT

mbwillia@ix.netcom.com(Mary Beth Williams) wrote:

>In <4sjgiv$fgk@news.sdd.hp.com> geroldf@sdd.hp.com (Gerold Firl)
>writes:

>>Ya know, MB, it amazes me that someone who apparantly resides at the
>>UMass anthropology department, and who has done actual physical anthro
>>fieldwork, could have so little background in biology and evolution.

>Believe me, Gerold, we could compare transcripts and vitas, and I'll
>don't doubt for a second whose had the deeper immersion into biology
>and evolution.

I see the conversation has again devolved into personal attack, and
without inviting me first, my feelings are hurt.

>>Do you have any idea of the mean lifetime of an 18th or 19th century
>>european who was infected with TB? One year? Two? Five? It's in that
>>range.

>Citation please. Actually, are you talking about the *mean lifetime*
>of a person with *lung-fever* or *consumption*? With *lung fever*,
>death usually came within days or weeks. According to Ornter and
>Putschar, if one survived the former, then the disease could remain
>dormant for many years before becoming active (usually due to some
>stress, such as disease or malnutrition... Pregnancy was a major
>trigger.)

Mary, I think you have demostrated,at least about TB to be
well-informed, I think we can take this for granted, now. But as far
as a model for comparing NW and OW immunity, it seems your statements
already indicate that this disease was either as fatal or more fatal
in OWers in the americas as in NW. Not to argue with this but since
the timeframe of mortality was 'on average' longer than most other
epidemic diseases and given the life expectancy of pre-20th century
peoples this was probably not a major cause of depopulation (not that
could be offset by some reproduction). As you also mentioned a
contributing factor for infection was population density and thus is
somewhat limited to the most dense populations, and as we already've
fought out, the denstities were probably such as not to favor TB as
well as other infections in most _areas_ unless extenuating
circumstances become evident.
I think with regard to depopulation the post infection life
expectancy has to be considered as well as the age and the remnant of
average reproductive production remaining at the point of infection,
(i.e. how many offspring one has on average post infection, and how
many potential offspring were forfieted as a result of infection),
since long term depopulation is going to depend more on the failure to
produce filial than on disease specific mortality.

It interesting that in the previous debate I brought up the issue
of stress and malnutirition and you kind of gave the impression that
these factors were 'no lo importante'. While there are a few diseases
in which the contribution of one or more health parameters is of no
influence or ever reverse influence, I think that in most there are
similarities, as I had pointed out.
While you guys can go on discussing a disease of secondary
importance with respect to the selective depopulation of the americas,
I want to correct something said earlier that I think needs
correcting. That is more or less that eurasia was an endless
reservoir of disease (or as stated, if disease X didn't kill disease Y
would have). Although I present the similarities, each disease
existance needs to be treated independently. If smallpox, measles and
a few other diseases by chance did not exist then its unlikely that
endemic peoples would have died until the stresses of american
europeanization began to settle into the continents.
I'm not going to argue the point more than this but one has to
consider both the novelty of each disease X number of diseases and
factor in, in certain circustances contributing factors. There are
numerous instance in related populations in which when one group put a
second group under 'stress' (such as happened in winter battles during
WWII) the stressed group ends up contracting rarely infectious
diseases or dying of diseases that are rarely fatal.

I think you have to get out of your mind the idea that NW disease =>
90%depopulation/100Y. If you look carefully at the entirety of the
americas your going to see that the depopulation/100 Y varied
significantly from place to place. The increase in TB in americans of
eurasian origin is demonstrative of how subtle changes in lifestyle
can increase/decrease susceptibility to disease. Secondarily, as for
TB also, the course of infection of most diseases changes when host
defense mechanisms change and this is often not primarily due to
genetics. If the typical defensive barriers which contain TB to the
lungs break down then its possible for the disease to spread to other
parts of the body, but that in 'normal' health this shouldn't happen.
Of course, if respiratory-TB expands to the point that it compromises
the remainder of the body then TB itself can contribute toward its
spread outside the contained regions; However, the rate of spread in
the lung may be affected by many extraneous factors, and provided an
individual doesn't promote the infection, death is often due to other
causes or as result of TB related death being secondary to another
primary cause.
As an example, I know people which had TB asymptomatically for many
years and were only detected through constuitive physical exams for
unrelated purposes. In addition, TB is fairly common in many parts of
the world and carriers often live into old age with disease, so I have
to wonder, when you find forensic TB evidence how can you ascertain
its impact on the individual.

For example if the infected individual was say 45-80 YO and TB was
highly suspect as the cause of death do you treat this as a single
cause of death or do you demostrate that this persons life was reduced
by X numbers of years as a result of disease. If a person is say 20 to
45 YA and TB may or may not be the principle cause of death how is its
impact assessed, Likewise with the 0 to 20 YO. Again I point to the
issue of longterm depopulation that reproductive success is more
important than survival.

The question that is begged, considering the course of infection for
TB, the infection rate, and other factors, how much did TB really
contribute to diminishing reproductive success, and furthermore how
did it affect the depopulation over longer time frames.

I can give an example in europe concerning the black death. According
to one source 30% of the population died about every 20 years due to
epidemic of the same interval which occured over ~100 year period.
This would have meant that 180% of the population died, except for the
fact that those who survived left more than average number of filial
behind after each epidemic, and there was a bounce in the population.
I think the data you presented that although european population were
hit hard over the long run the populations still kept reasonably
robust (though sub-maximal) numbers.

This type of rebound is expected with all diseases. How does one
account for the apparent lack of rebound in some populations in the
americas and not others?

Philip