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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
TB Control in New York City: A Recent History
Not by DOT Alone
Baltimore at the New Millennium
From Crickets to Condoms and Beyond
The Denver TB Program: Opportunity, Creativity, Persistence, and Luck
National Jewish: The 100-Year War Against TB
Earthquakes, Population Growth, and TB in Los Angeles County
TB in Alaska
CDC and the American Lung Association/ American Thoracic Society: an Enduring Public/Private Partnership
The Unusual Suspects
The Model TB Prevention and Control Centers: History and Purpose
My Perspective on TB Control over the Past Two to Three Decades
History of the IUATLD
Thoughts about the Future of TB Control in the United States
Where We've Been and Where We're Going: Perspectives from CDC
Early History of the CDC TB Division, 1944-1985
CDC Funding for TB Prevention and Control
Managed Care and TB Control - A New Era
Early Research Activities of the TB Control Division
The First TB Drug Clinical Trials
Current TB Drug Trials: The Tuberculosis Trials Consortium (TBTC)
TB Communications and Education
TB Control in the Information Age
Field Services Activities
TB's Public Health Heroes
Infection Control Issues
A Decade of Notable TB Outbreaks: A Selected Review
International Activities
The Role of CDC's Division of Quarantine in the Fight Against TB in the U.S.
The STOP TB Initiative, A Global Partnership
Seize the Moment - Personal Reflections
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This is an archived document. The links are no longer being updated.

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 highly infectious.

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.


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