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

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Philippines, Viet Nam, China, and India). While the United States continues to bring its TB problem under control, it must be realized that the United States is not an island unto itself, isolated from the rest of the global community. In 1993, the World Health Organization declared TB a global emergency. Approximately 8 million new cases and 2-3 million deaths occur each year around the world from TB. In an effort to reduce TB morbidity and mortality worldwide, we must share our expertise, successes, and failures, if we are to move toward national and global TB elimination. We have the power to relegate this ancient enemy to the confinement of laboratory vials and store it in a deep freeze. As we journey into a new century and a new millennium, we will face new opportunities and challenges and write new chapters in the history of TB. Will we learn from the past? Will we develop and use new technology to the utmost efficiency? Will we utilize our resources prudently, and share information with our neighbors? Will we devote our energies and talents to the elimination of our common enemy? How long will it take us to accomplish our goals? How many more lives will be sacrificed to TB? The answer to those questions rests in each of us who works in TB control. Notable Events in TB Control In 1956, the Minnesota Tuberculosis and Health Association encouraged school children to be Knights of the Double-Barred Cross and to pledge “. . . to do everything . . . to overthrow the enemy, TB.” Are we willing to take the same pledge today? 7 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-yearold 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-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 8 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
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Division of Tuberculosis Control wi
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facilities to provide protection to
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issue recommendations, OSHA has the
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the US with TB. Previously CDC work
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TB Control at the Millennium 80
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TB Control at the Millennium 82
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