Published ahead of print on August 9, 2007, doi:10.1164/rccm.200603-440OC Am. J. Respir. Crit. Care Med., Volume 176, Number 9, November 2007, 936-944 A more recent version of this article appeared on November 1, 2007
Submitted on March 29, 2006 Quantitative Impact of Human Immunodeficiency Virus Infection on Tuberculosis DynamicsKathryn DeRiemer1*,1 School of Medicine, University of California, Davis, Davis, CA, USA, 2 Tuberculosis Section, San Francisco Department of Public Health, San Francisco, CA, USA; Francis J. Curry National Tuberculosis Center, San Francisco, CA, USA, 3 Francis J. Curry National Tuberculosis Center, San Francisco, CA, USA; Division of Pulmonary and Critical Care Medicine, Department of Medicine, San Francisco General Hospital and University of California, San Francisco, San Francisco, CA, USA, 4 Division of Pulmonary and Critical Care Medicine, Department of Medicine, San Francisco General Hospital and University of California, San Francisco, San Francisco, CA, USA; Division of Mycobacterial and Respiratory Infections, National Jewish Medical and Research Center, Denver, CO, USA * To whom correspondence should be addressed. E-mail: kderiemer{at}ucdavis.edu.
Rationale: Human immunodeficiency virus (HIV) infection has a major but unquantified impact on the risk of tuberculosis. Objective: To quantify the impact of HIV infection on the number of tuberculosis cases in San Francisco. Methods: We studied all patients reported with tuberculosis in San Francisco from 1991 to 2002. The initial isolates of Mycobacterium tuberculosis were genotyped using IS6110 restriction fragment length polymorphism genotyping as the primary method, and clustered cases (identical genotype patterns) were identified. Measurements and Main Results: We determined the case number, case rate, and the fraction of tuberculosis attributable to HIV infection. Of 2,991 reported tuberculosis cases, 2,193 (73.3%) had a genotype pattern of M. tuberculosis available. Genotypic clusters with at least one HIV-positive person were larger, lasted longer, and had a shorter time between successive cases relative to clusters with only HIV-uninfected persons (p < 0.00005, p = 0.0009, p =0.018, respectively). Overall, 13.7% of the tuberculosis cases were attributable to HIV infection and an estimated 405 excess tuberculosis cases occurred. Conclusions: During a period encompassing the resurgence and decline of tuberculosis in San Francisco, a substantial number of the tuberculosis cases was attributable to HIV infection. Coinfection with HIV amplified the local tuberculosis epidemic. Key words: Tuberculosis, HIV infection, transmission, genotyping
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