FC: Eric Lerner on SARS and evidence for secondary infection

[Declan McCullagh <declan () well com>]

----- Forwarded message from Eric Lerner <elerner () igc org> -----

From: Eric Lerner <elerner () igc org>
Subject: SARS: statistical evidence for secondary infection
To: politech
Date: Tue, 06 May 2003 22:53:26 -0400
X-Mailer: Mozilla 4.78 [en] (Win98; U)

I would like to call attention to evidence that, it seems to me, points
strongly to the existence of a secondary infectious agent  being
responsible for the deaths from SARS. I am researching  a feature
article on the search for the cause of SARS and did a statistical
analysis of SARS cases and deaths. As I am also a research physicist, I
am experienced in analyzing time  series data. The point I raise may be
obvious, but I have not seen it mentioned in the press or on the web, so
I pass it along in the chance that it has been overlooked.

I was struck by the fact that both the number of SARS cases and the
number of SARS deaths lie extremely close to a simple exponential growth
rate curve. But the exponential rate of growth of the deaths is VERY
different than that for the cases. Using WHO data for the last month,
the rate of growth of the caseload is 40% per 10 days, while the rate of
growth of the number of deaths is 78% per ten days.  The death curve
lies remarkably close to an exponential curve, with most points within
5% of the curve.  Extrapolating the curve backwards, the Feb. 11 report
by the Chinese authorities of 5 deaths on that date also lies on the
curve.

In addition to the very different growth rates, the case curve and the
death curve do not intersect the axis at the same date, indicating
different index cases.  For the case load, the first case, extrapolating
backwards, would be Aug.1 ,2002, but for the deaths, the first case
would be Jan. 1, 2003 (assuming the first death to come 14 days after
that case started.)

If the data for China alone is used, the deviations are greater, as
there is an admitted understatement of cases and deaths in the period
before April 20, but the general pattern is very similar. Using the Feb.
11 estimate of 300 cases and 5 deaths, the growth rate of cases in China
is 38% per 10 days and of deaths 58% per ten days. (The rate of increase
of death is identical if only the last month of data is used.) The index
case from the case curve would be Aug. 10, 2002 and from the death curve
Jan.5, 2003.

This data is very consistent with an initial, non-fatal infection
starting in August, and a secondary infection by a different organism,
with high mortality rate, starting in January.  By comparing weekly
number of deaths with weekly cases two weeks earlier, it appears that
such a secondary infection has a mortality rate of at least 25% and
spreads much more rapidly that the SARS infection itself, perhaps by a
different method.  The widely noted increase in the mortality rate of
SARS would then be seen to be a consequence of the spread of the
secondary infection, with more and more of total SARS patients now
having the deadly secondary infection.  This would also explain why
patients are showing up in India and Canada with SARS coronavirus
infection, but no symptoms--they have not been infected by the secondary
infection organism.

The data seems to indicate a secondly infection, which requires the SARS
infection first, not  a mutation of the SARS virus.  Since the secondary
infection, or whatever causes the deaths, is spreading far more rapidly
than the basic SARS infection, if it was an independent cause of the
sysmtpoms, the case load would also begin to increase more rapidly. In
Hong Kong, this certainly does not seem to be the case, as death as a
percentage of two-week-old cases are still rising rapidly, while the
overall level of SARS cases declines.

But this behavior would be very consistent with a secondary infection
which can only spread among those who already have the initial SARS
virus.

I admit that the Canadian results, which show the SARS virus positive
tests declining with time could indicate the more pessimistic
alternative, that the secondary infection can spread on its own, without
prior infection by the SARS coronavirus. However, in Hong Kong they
appear to be getting positive coronavirus tests from all SARS patients.


If this hypothesis is valid, there should be an infectious agent that
shows up only in SARS dead and in those who become very sick and need
ventilators(who presumably would die without treatment).  Also, it
implies that death rates will rise in mainland China until they reach
the levels of Hong Kong, which is nearly 25%.

Eric Lerner
Lawrenceville Plasma Physics
elerner () igc org




----- End forwarded message -----



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