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Tuberculosis remains an important worldwide infection, with more than one third of the overall population harboring the bacterium. It is the second leading cause of death among infectious diseases and a major cause of death among those with human immunodeficiency disease (HIV), especially in countries with limited resources.1,2 Despite therapeutic progress over the past 20 years, drug resistance and HIV coinfection continue to challenge the global control of tuberculosis.2

Tuberculosis has been on the decline in the United States, with an average 3.8% decrease each year from 2000 to 2010.3 This reduction is primarily due to tuberculosis control programs targeting high-risk individuals. In addition, improved infection control policies, increased vigilance among physicians, implementation of directly observed therapy, and standardized drug regimens all contributed to the decline of tuberculosis rates. Although overall national cases have decreased, the incidence in foreign-born patients remains 12 times that of U.S.-born persons.3 In foreign-born patients, clinical tuberculosis is usually from reactivation of latent disease. Overall, reactivation of latent tuberculosis is responsible for 70% of active tuberculosis cases.4

Continued improvement in tuberculosis control and prevention requires recognition and treatment of high-risk populations (Table 67-1). Screening and treatment of latent infection in high-risk individuals are key to reducing tuberculosis in the United States.4

TABLE 67-1Patients with a High Prevalence of Tuberculosis (Highest to Lowest Risk)


Mycobacterium tuberculosis is a slow-growing aerobic rod that has a multilayered cell wall containing lipids that account for its acid-fast staining property. Because the organism is an obligate aerobe, it settles in areas of high oxygen content and blood flow. Transmission from person to person occurs through inhalation of droplet nuclei into the lungs. Persons with active tuberculosis who excrete mycobacteria in saliva or sputum are the most infectious.5 Only 30% of patients actually become infected after a droplet exposure.6


Once the organisms reach the lungs, host defenses are activated. Some organisms survive and are transported to the regional lymph nodes, where the host cell-mediated immunity is activated to contain the infection. Granulomas, known as tubercles, form as a result of this process, which involves activated macrophages and T lymphocytes in addition to active bacteria in most cases. Tubercles are a sign of primary infection and may progress to caseation necrosis and calcification. In the lung, the Ghon complex (Figure 67-1) is a manifestation, appearing as calcified hilar lymph nodes.


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