Primary Tuberculosis

Primary TB (also called the primary infection stage) follows the patient’s first exposure to the TB pathogen, Mycobacterium tuberculosis. Primary TB begins when the inhaled bacilli implant in the alveoli. As the bacilli multiply over a 3- to 4-week period, the initial response of the lungs is an inflammatory reaction that is similar to any acute pneumonia (see Figure 15-1). In other words, a large influx of polymorphonuclear leukocytes and macrophages moves into the infected area to engulf—but not fully kill—the bacilli. This action also causes the pulmonary capillaries to dilate, the interstitium to fill with fluid, and the alveolar epithelium to swell from the edema fluid. Eventually the alveoli become consolidated (i.e., filled with fluid, polymorphonuclear leukocytes, and macrophages). Clinically, this phase of TB coincides with a positive tuberculin reaction—a positive purified protein derivative (PPD) skin test result (see discussion of diagnosis later in this chapter).

Unlike pneumonia, however, the lung tissue that surrounds the infected area slowly produces a protective cell wall called a tubercle, or granuloma. In essence, the tubercles work to encapsulate—that is, put in a nutshell-like structure—the TB bacilli (see Figure 17-1, A). Although the initial lung lesions may be difficult to identify on a chest radiograph, the lesions may be seen as small, sharply defined opacities. When detected on a chest radiograph, these initial lung lesions are called Ghon nodules. As the disease progresses, the combination of tubercles and the involvement of the lymph nodes in the hilar region is known as the Ghon complex.

Structurally, a tubercle consists of a central core containing TB bacilli. The central core also has enlarged macrophages with an outer wall composed of fibroblasts, lymphocytes, and neutrophils. A tubercle takes about 2 to 10 weeks to form. The function of the tubercle is to contain the TB bacilli, thus preventing the further spread of infectious TB organisms. Unfortunately, the central core of the tubercle has the potential to break down from time to time, especially in a patient with a depressed immune system. When this happens, the center of the tubercle fills with necrotic tissue that resembles dry cottage cheese. During this stage the tubercle is called a caseous lesion or caseous granuloma (see Figure 17-1, B). The patient is potentially contagious at this stage. In most cases, however, the TB bacilli are effectively contained within the tubercles.

Once the bacilli are controlled—either by the patient’s immunologic defense system or by antituberculous drugs—the healing process begins. Tissue fibrosis and calcification of the lung parenchyma slowly replace the tubercle. This tissue fibrosis and calcification cause lung tissue retraction and scarring. In some cases the calcification and fibrosis cause the bronchi to distort and dilate—that is, to develop bronchiectasis.

Finally, when the bacilli are isolated within tubercles and immunity develops, the TB bacilli may remain dormant for months, years, or life. Individuals with dormant TB (also called latent TB) do not feel sick or have any TB-related symptoms. They are still infected with TB but do not have clinically active TB. The only indication of a TB infection is a positive reaction to the tuberculin skin test, or TB blood test, and the finding of possible residual scarring on the chest radiograph. Individuals with dormant (latent) TB are not infectious and cannot spread the TB bacilli to others.

Postprimary Tuberculosis

Postprimary TB (also called reactivation TB, reinfection TB, or secondary TB) is a term used to describe the reactivation of TB months or even years after the initial infection has been controlled. Even though most patients with primary TB recover completely from a clinical standpoint, it is important to note that live tubercle bacilli can remain dormant for decades. A positive tuberculin reaction generally persists even after the primary infection stage has been controlled. At any time, TB may become reactivated, especially in patients with depressed immune systems. Most new TB cases are associated with the following risk factors:

If the TB infection is uncontrolled, cavitation of the caseous granuloma tubercle develops. The patient progressively experiences more severe symptoms, including violent cough episodes, greenish or bloody sputum, low-grade fever, anorexia, weight loss, extreme fatigue, night sweats, and chest pain. It is this gradual wasting of the body that provided the basis for the earlier name for TB—consumption. The patient is highly contagious at this stage. In severe cases a deep tubercle cavity may rupture and allow air and infected material to flow into the pleural space or the tracheobronchial tree. Pleural complications are common in TB (see Figure 17-1, C).

Disseminated Tuberculosis

Disseminated TB (also called extrapulmonary TB, miliary TB, and tuberculosis—disseminated) refers to infection from TB bacilli that escape from a tubercle and travel to sites other throughout the body by means of the bloodstream or lymphatic system. In general, the TB bacilli that gain entrance to the bloodstream usually gather and multiply in portions of the body that have a high tissue oxygen tension. The most common location is the apex of the lungs. Other oxygen-rich areas in the body include the regional lymph nodes, kidneys, long bones, genital tract, brain, and meninges.

Genital TB in males damages the prostate gland, epididymis, seminal vesicle, and testes; and in females, the fallopian tubes, ovaries, and uterus. The spine is a frequent site of TB infection, although the hip, knee, wrist, and elbow can also be involved. Tubercular meningitis is caused by an active brain lesion seeding TB bacilli into the meninges. Over time, the infection may cause mental deterioration, permanent retardation, blindness, and deafness. When a large number of bacilli are freed into the bloodstream, the result can be the presence of numerous small tubercles—about the size of a pinhead—scattered throughout the body. This condition is commonly called miliary TB.

TB is primarily a chronic restrictive pulmonary disorder. The major pathologic or structural changes of the lungs associated with TB (mainly postprimary TB) are as follows: