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TB Notes 1, 2000
Where We've Been and Where We're Going: Perspectives
from CDC's Partners in TB Control
Changes I've Seen in TB, 1949 - 1999
by William W. Stead, MD, MACP
Former Director, TB Program
Arkansas Department of Health
Professor of Medicine Emeritus, UAMS
When I took a junior staff position with the TB Service at the
Minneapolis Veterans Hospital in July 1949, under Drs. J.A. Myers
and W.B. Tucker, I had no interest in TB. In my spare time I worked
with Drs. Richard Ebert and Don Fry in the physiology of emphysema.
The TB dogma at the time was that primary TB occurred in childhood
and almost never became serious except in infants. TB in adults
was the challenge and was said to be caused by catching a new infection
on "previously sensitized tissues."
I lived with this paradigm until 1953 when I was recalled by the
army as the Assistant Chief of the TB Service at the Fitzsimons
Army Hospital in Denver. We had an 80-bed ward full of young men
returning from Korea with what was then called "idiopathic
pleural effusion." Because of the occasional need to explore
one of these, we learned that such effusions were due to soiling
of the pleura by a small subpleural lesion of primary TB in the
lower half of one lung (Am Rev Tuberc Pulm Dis, 1955).
My real immersion in TB came in 1960 at Marquette University as
Chief of the Pulmonary Disease Section of the Milwaukee County Hospital/Muirdale
TB Sanatorium. This was 3 years after the death of my 83-year-old
father, whose autopsy showed cavitary TB in the right upper lobe
and active renal involvement. I felt pretty sure he had not been
reinfected, because there were old scars on the screening chest
x-ray (CXR) done on admission to the extended care facility 3 years
earlier 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-year-old. 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).
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 Lung Dis, 1998). Only 5%-10%
of admissions to our nursing homes are TST positive now.
Perhaps the principal discovery that has come from these data is
that there is a significant difference in innate resistance to TB
infection between whites and blacks. In addition, study of our TB
case data base from 1976-1997 shows that blacks with active TB are
50% more likely than whites to be sputum-smear positive and thus
Image 1: Photograph of clinician giving medication. It is important
for persons at high risk for TB to take a full course of treatment.
I am now preparing a paper to show the important public health
implications of such a difference in TB risk. While health departments
routinely try to identify all close contacts with infectious cases
of TB, a particularly great effort should be made among the African
American and Native American contacts because of their greater risk
both of infection and of becoming infectious. It is important for
such reactors to take the full course of chemoprophylaxis to prevent
development of TB and further spread. This applies especially to
exposures in close living quarters, i.e., dormitories, nursing homes,
shelters, and prisons.
It has been an interesting half century. The best part was the
quarter century in public health in Arkansas from 1973-1998.