CDC History of Tuberculosis Control - Medical and Public Health ...

and all patients were x-rayed annually to
screen for TB. It seemed pretty evident that
his TB was due to reactivation of some of
those old scars.
So, I sought the help of my four older siblings
(including Eugene, who is 10 years my senior
and at the time was Chairman of Medicine at
Duke). We were able to piece together a likely
scenario. Dad’s father had died of “consumption”
in 1890 when Dad was a healthy 15-yearold.
In 1902 he had some illness of which we
had no details except that a doctor had suggested
that Dad sleep out-of-doors as much as
possible. Later, as a traveling salesman over
four southern states, he would sleep in a tent
at the edge of whatever town he happened to
be in at dusk. Eugene traveled with him some
summers and attests to this story.
I can recall that Dad commonly “hawked and
spit” a greenish-yellow sputum. Gene recalled
that he required frequent massage of a “boggy”
prostate gland and that he had a number of
episodes of painless hematuria, all of which
suggested chronic renal TB. Finally, in 1941 a
sister returned home with a pre-school son
who at age 6 developed an illness with a
cough, positive tuberculin skin test (TST), and
abnormal CXR. He was confined to bed for 6
months. At the time Dad was not suspected as
the source. Two of my siblings and I had
positive tuberculin tests. Mother remained
well but I have no information on her TST.
With this scenario suggesting a long and
largely healthy life with TB, I began to question
the dogma of adult TB being due to an
exogenous reinfection. Fortunately, the
Sanatorium had vast numbers of old CXRs,
some back to glass plates. With these I was
able to find old scars in a fairly large percentage
of our active cases of TB and published
two papers on the natural history of TB in
man (Am Rev Respir Dis, 1967, and New Engl J
Med, 1967).
TB Control at the Millennium
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At about the same time we showed that
primary TB in adults can produce the full
spectrum of pulmonary lesions seen in cases of
reactivated TB (Ann Intern Med, 1968).
It was not until the 1970s as TB Controller for
Arkansas that I really began to understand TB.
In 1976 we encountered an outbreak of TB in
our state prison with evidence that it had been
going on for at least 5 years. Ten active cases
among 1,500 inmates gave an incidence of 667/
100,000 vs 21 in the state at large that year.
We found about 100 TST converters, evenly
split between black inmates and white inmates
(JAMA, 1978). At the time I did not realize
that there were about 1,000 white and only
500 black inmates. So, I missed the difference
in their infectibility. I held a monthly Chest
Clinic at the prison for 8 years to screen new
inmates for TB and to see that TST reactors
got INH therapy.
My next shock came in 1978 when we found
an outbreak at a nursing home. I was not
surprised at finding a case of TB in a nursing
home, because most of the population would
be TST positive from living through the 1920s
and 1930s when TB was so common.
Hermione Swindol, PHN, argued that it
would spread and she proved to be right.
What I did not know then was that healthy
elderly people often outlive their TB germs
and the TST reverts to negative. Only 15%-
20% of new admissions were TST positive,
leaving 80%-85% susceptible to a new infection.
We found 60 converters, 10 of whom
had active TB (Ann Intern Med, 1981).
Because of these findings we got the 225
nursing homes in Arkansas to do two-step
TSTs on all new admissions not known already
to be positive. Twice a year they report
TSTs of their new admissions and update the
data on other residents. At first I kept the
records in a Radio Shack TRS80 Model 1
computer. I now have demographic, skin test,
and TB data on 115,000 nursing home residents
from 1984 through 1998 (Int J Tuberc