181 - Tuberculosis

T cells. This process arrests the local infection for most immunocompetent hosts. At that time, the only sign of the disease may be a positive reaction to the purified protein derivative (PPD) skin test. A delayed hypersensitivity response uses cytotoxic killer CD8 suppressor T cells to kill the other nonactivated macrophages with bacilli. This process creates local tissue destruction and the formation of a caseating granuloma. In immunocompromised patients, this caseous center may expand and then calcify to form a Ghon complex in the lung. If the infection is uncontrolled, primary tuberculous pneumonia may ensue, or infection may spread through blood and lymph, with resulting disseminated TB. Active TB develops months to years later in those patients with decreased capacity for cell-mediated immunity, such as patients with malnutrition, comorbidities, and immunosuppression. Patients with acquired immunodeficiency syndrome are especially prone to develop active disease. As the caseating granuloma liquefies and releases numerous bacilli, a delayed hypersensitivity response is initiated, and local tissue destruction follows. Ultimately, erosion through a bronchial wall creates a cavitary lesion and the development of pneumonia. The high oxygen tension of the cavity lends itself to replication of bacilli and persistent disease.