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A Molecular Epidemiologic Analysis of Tuberculosis Trends in San Francisco, 1991–1997

Robert M. Jasmer, MD; Judith A. Hahn, MA; Peter M. Small, MD; Charles L. Daley, MD; Marcel A. Behr, MD, MSc; Andrew R. Moss, PhD; Jennifer M. Creasman, MSPH; Gisela F. Schecter, MD, MPH; E. Antonio Paz, MD; and Philip C. Hopewell, MD
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From San Francisco General Hospital Medical Center, the University of California, San Francisco, Francis J. Curry National Tuberculosis Center, and Department of Public Health, San Francisco, California; and Stanford University School of Medicine, Stanford, California.

Ann Intern Med. 1999;130(12):971-978. doi:10.7326/0003-4819-130-12-199906150-00004
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Background: To decrease tuberculosis case rates and cases due to recent infection (clustered cases) in San Francisco, California, tuberculosis control measures were intensified beginning in 1991 by focusing on prevention of Mycobacterium tuberculosis transmission and on the use of preventive therapy.

Objective: To describe trends in rates of tuberculosis cases and clustered cases in San Francisco from 1991 through 1997.

Design: Population-based study.

Setting: San Francisco, California.

Patients: Persons with tuberculosis diagnosed between 1 January 1991 and 31 December 1997.

Measurements: DNA fingerprinting was performed. During sequential 1-year intervals, changes in annual case rates per 100 000 persons for all cases, clustered cases (cases with M. tuberculosis isolates having identical fingerprint patterns), and cases in specific subgroups with high rates of clustering (persons born in the United States and HIV-infected persons) were examined.

Results: Annual tuberculosis case rates peaked at 51.2 cases per 100 000 persons in 1992 and decreased significantly thereafter to 29.8 cases per 100 000 persons in 1997 (P < 0.001). The rate of clustered cases decreased significantly over time in the entire study sample (from 10.4 cases per 100 000 persons in 1991 to 3.8 cases per 100 000 persons in 1997 [P < 0.001]), in persons born in the United States (P < 0.001), and in HIV-infected persons (P = 0.003).

Conclusions: The rates of tuberculosis cases and clustered tuberculosis cases decreased both overall and among persons in high-risk groups. This occurred in a period during which tuberculosis control measures were intensified.




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Figure 1.
KaplanMeier estimates of the probability of a DNA fingerprint match in tuberculosis cases in San Francisco.solid linedashed lines

- The curve represents estimates ( ) and 95% CIs ( ) from a Kaplan-Meier analysis of the time between diagnosis dates of tuberculosis cases with matched DNA fingerprints; analysis is based on all fingerprinted cases identified from 1 January 1991 through 31 December 1997. Cases with no matching fingerprints were censored at the end of the study period (31 December 1997). For all clustered isolates, approximately 70% of those with matching fingerprint patterns were identified within 1 year.

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Figure 2.
The rate of clustered (striped bars) and nonclustered (white bars) cases of tuberculosis overall and in various subgroups in San Francisco from 1 July 1991 through 31 December 1997, assessed at 1-year intervals. A.PPB.PPC.PD.PPE.PP

Population as a whole. The rate of clustered ( < 0.001) and nonclustered ( = 0.01) cases decreased significantly over time. Persons born in the United States. The rate of clustered ( < 0.001) and nonclustered ( = 0.002) cases decreased significantly over time. Persons born outside of the United States. The rate of clustered and nonclustered cases did not change significantly over time ( > 0.2 for both comparisons). Persons infected with HIV. The rate of clustered ( = 0.003) and nonclustered ( = 0.004) cases decreased significantly over time. Persons negative for HIV or persons with unknown HIV status. The rate of clustered ( < 0.001) cases decreased significantly over time, whereas the rate of nonclustered ( > 0.2) cases did not change.

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