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INTRODUCTION AND EPIDEMIOLOGY

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

Tuberculosis infections declined in the United States from 2000 to 2010.3 This reduction is primarily due to efforts targeting high-risk individuals. Improved infection control policies, increased vigilance among physicians, implementation of directly observed therapy, and standardized drug regimens all contributed to the decline of tuberculosis (Table 67-1). Although overall national cases have decreased, the incidence in foreign-born patients remains 12 times that of U.S.-born persons.3 In those 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

Screening and treatment of latent infection in high-risk individuals are key to reducing tuberculosis in the United States.4 However, case detection rates are approximately 64%, with close to 3.3 million people with tuberculosis missed in 2013.5

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

PATHOPHYSIOLOGY

Mycobacterium tuberculosis is a slow-growing aerobic rod that settles in areas of high oxygen content and blood flow. Transmission occurs via aerosolization of bacteria and inhalation of droplet nuclei into the lungs. Persons with active tuberculosis who excrete mycobacteria in saliva or sputum are the most infectious.6 Only 30% of patients become infected after a droplet exposure.7

PRIMARY AND LATENT INFECTION

Once the organisms reach the lungs, host defenses activate. Mycobacteria are highly antigenic, resulting in a rapid immune response. Some organisms survive in the regional lymph nodes, where the host cell-mediated immunity contains the infection. Granulomas, known as tubercles, form from this process, which involves activated macrophages, T lymphocytes, and active bacteria. Tubercles are a sign of primary infection and may progress to caseation necrosis and calcification. These tubercles create a protective area for bacterial growth. In the lung, the Ghon complex (Figure 67-1) is a tubercle, appearing as calcified hilar lymph nodes.

If the tubercle fails to contain the infection, the mycobacteria may spread by hematogenous, lymphatic, or direct mechanical routes. The tendency ...

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