**2. Clinical manifestations**

As the cellular processes occur, tuberculosis may develop differently in each patient, according to the status of the patient's immune system. Stages include latency, primary disease, primary progressive disease, and extrapulmonary disease. Each stage has different clinical manifesta‐ tions [4]. *M. tb* organisms can be enclosed but are difficult to completely eliminate [5]. Persons with latent tuberculosis have no signs or symptoms of the disease, do not feel sick, and are not infectious [5]. However, viable bacilli can persist in the necrotic material for years or even a lifetime [6], and if the immune system later becomes compromised, as it does in many critically ill patients, the disease can be reactivated. Primary pulmonary tuberculosis is often asympto‐ matic. Although it essentially exists subclinically, some self-limiting findings might be noticed. Associated paratracheal lymphadenopathy may occur because the bacilli spread from the lungs through the lymphatic system. Active tuberculosis develops in only 5% to 10% of persons exposed to *M. tb*. Fig. 2 shows typical chest X-ray before (A) and after (B) chemotherapy. Fatigue, malaise, weight loss, low-grade fever, night sweats, cough, sputum, are the main symptoms. The sputum may also be streaked with blood. Hemoptysis can be due to destruc‐ tion of a patent vessel located in the wall of the cavity [7]. Extrapulmonary disease occurs in more than 20% of patients. The most serious location is the central nervous system, where infection may result in meningitis, which could be fatal in most cases. Another fatal form is infection of the blood stream by mycobacteria, this form is called disseminated or military tuberculosis. The most common extrapulmonary tuberculosis is lymphatic tuberculosis. Other possible locations include bones, joints, pleura, and genitourinary system [4].

kills these macrophages, causing enlargement of the caseous center and progression of the disease. If good cell-mediated immunity develops, a mantle of highly activated macrophages surrounds the caseous necrosis. In stage 5, bacilli evade host defenses. When liquefaction of the caseous center occurs, the bacilli multiply extracellularly, frequently attaining very large numbers. The high local concentration of tuberculin-like products derived from these bacilli causes a tissue-damaging delayed-type hypersensitivity response that erodes the bronchial

**Figure 1.** Histologic appearance of tuberculosis A. Staining for acid‐fast bacilli, B. exudative stage, C. productive stage

As the cellular processes occur, tuberculosis may develop differently in each patient, according to the status of the patient's immune system. Stages include latency, primary disease, primary progressive disease, and extrapulmonary disease. Each stage has different clinical manifesta‐ tions [4]. *M. tb* organisms can be enclosed but are difficult to completely eliminate [5]. Persons with latent tuberculosis have no signs or symptoms of the disease, do not feel sick, and are not infectious [5]. However, viable bacilli can persist in the necrotic material for years or even a lifetime [6], and if the immune system later becomes compromised, as it does in many critically ill patients, the disease can be reactivated. Primary pulmonary tuberculosis is often asympto‐ matic. Although it essentially exists subclinically, some self-limiting findings might be noticed. Associated paratracheal lymphadenopathy may occur because the bacilli spread from the lungs through the lymphatic system. Active tuberculosis develops in only 5% to 10% of persons

wall, forming a cavity.

128 Tuberculosis - Current Issues in Diagnosis and Management

A B

C D

**2. Clinical manifestations**

with cavity formation (→), D. proliferative stage with a multinucleated giant cell.

**Figure 2.** Chest X‐ray of pulmonary tuberculosis and cured Tuberculosis A. before chemotherapy with rifampicin, iso‐ niazide, ethambutol and pyrazinamide, B. after chemotherapy. Apical shadow (dotted circle) disappears.
