Secondary or Reactivated Tuberculosis
Secondary tuberculosis is usually due to the reactivation of old lesions or gradual progression of primary tuberculosis into chronic form. However, recent evidence suggests that reinfection is responsible for some of the secondary tuberculosis. The characteristics of secondary tuberculosis include extensive tissue damages due to immunologic reactions of the host to tubercle bacilli and their products. (see the box below) - Also read the pathology handout of tuberculosis.
Primary vs. Secondary Tuberculosis
As illustrated above, when a host has first contact with tubercle bacilli: (1) An acute exudative lesion develops and rapidly spreads to the lymphatics and regional lymph nodes. The exudative lesion in tissue often heals rapidly. (2) The lymph node undergoes caseation, which usually calcifies. (3) The tuberculin test becomes positive.
If the primary lesion could not contained rapidly, the appearance of hypersensitivity to tuberculin (see below) provokes a dramatic change in the host's response to the organisms. The nonspecific inflammatory response evoked on first exposure to tubercle bacilli becomes granulomatous, evoking the formation of tubercles. The tubercle comprises an organized aggregation of enlarged macrophages that, because they resemble epithelial cells, are referred to as epithelioid cells. A peripheral collar of fibroblasts, macrophages, and lymphocytes surrounds the granuloma. Frequently the central region of epithelioid cells undergoes a characteristic caseous necrosis to produce a "soft" tubercle, the most characteristic hallmark of tuberculosis. When the antigen load at the initial infection site and regional lymph node is large, caseation necrosis may develop and lesions may later calcify. These calcified lesions of the primary site are referred to as the Ghon complex.
After the development of hypersensitivity, the infection becomes quiescent and asymptomatic in the majority of patients (about 90%). In some, however, especially the very young and adults who are immunocompromised or who have other predisposing illnesses, the primary infection may evolve into clinical disease. The progression may be local at the site of the primary lesion, or it may be at one or more distant sites where bacilli have arrived during the early hematogenous spread.
In a small number of persons whose initial tuberculous infection subsidies, secondary disease occurs in spite of acquired cellular immunity. Although the question of whether reinfection tuberculosis results from the breakdown of quiescent foci (endogenous) or from acquisition of new infection from an active case has long been a controversial issue, current opinion favors the endogenous source. In this phase of the disease, lesions are usually localized in the apices of the lungs (remember that tubercle bacilli require oxygen for growth). In about 5% of patients, apical pulmonary tuberculosis manifests itself within 2 years of the primary infection. In others, however, clinical disease may evolve many decades later whenever resistance is lowered. Quiescent foci that harbor viable organisms thus remain a potential hazard throughout a person's lifetime.
Because of the acquired cellular immunity, bacilli are more promptly phagocytized and destroyed by the activated macrophages. As a result, in secondary tuberculosis, lesions remain localized and dissemination of organisms via the lymphatic vessels is usually prevented. Hypersensitivity promotes a more rapid caseation and fibrotic walling-off of the focus. Histologically the reaction is characteristic of tubercle formation, manifested by a local accumulation of lymphocytes and macrophages. T lymphocytes and their chemotactic lymphokines play a major role in the development of tuberculous granuloma. Material in this box is for reference only
These differences between primary infection and post-primary or reactivation are attributed to (1) resistance and (2) hypersensitivity induced by the first infection of the host with tubercle bacilli.