Tuberculosis and Other Mycobacteria Donald E Gardner PhD Fellow ATS

5 Health Issues

TB is a particularly good illustration of an infectious disease process that involves an ecological lifelong balance between a host and a microbe. TB in humans is predominately an airborne infection of the lungs that is almost always initiated by inhalation. Once the organisms have been inhaled and deposited in the lung, these organisms can be found in the lung's phagocytic cells (alveolar macrophages) that tend to protect them from antibodies and other host immune defenses. Individual susceptibility to TB and the severity of the disease are based on the virulence of the organism, the duration of exposure, concomitant exposure to other toxicants, medication for treatment of other diseases, and the nutritional status of the host. Once the organism has survived the transport through the environment and has infected a susceptible host, the TB infectious process can be divided into two stages that are commonly referred to as primary and secondary infections. During the primary phase, after an incubation period of 4-8 weeks, the infected individual is usually asymptomatic but may produce nonspecific symptoms such as fatigue, weakness, anorexia, and low-grade fever. However, in most cases the host may not even be aware that such a pathogen has invaded the body. Initially, the infecting organisms do not elicit a marked inflammatory reaction because they do not immediately produce any toxins or tissue-destructive enzymes. In most healthy people, the primary infection often subsides spontaneously as a result of the activities of the immune system, especially if the infecting dose is low. Even so, a scar remains on the lungs as evidence of a previous infection. At this stage, approximately 5-10% of the individuals infected with this organism show symptoms and develop active TB within the first year; the remaining infected individuals continue to be at risk with a latent infection. Initially, the macrophages that have become laden with numerous intracellular bacilli may be unable to destroy the invading cells. However, after a few weeks a cellmediated immunity develops. Sensitized lymphocytes attract and activate these macrophages, which greatly enhances the phagocyte's bactericidal capability. As the initial lesion heals, tiny granulomas or tubercles are formed that can harbor the bacilli indefinitely. In the majority of cases, the infection is arrested, and the bacilli remain in a dormant state walled up in these primary lesions (tubercles).

The pathogenesis of this infection cannot be separated from the host's immune response. During the infectious stage, much of the tissue damage is caused by the host's own immune response, rather than by bacterial toxins. Activated macrophages may release various enzymes and cytokines that may ultimately cause damaging inflammation at the site of the infection. TB is a good example of such a host-mediated pathogenesis where the tissue damage is actually caused by toxic factors released from the lymphocytes and macrophages that infiltrate the site of the infection. Often the host response is so intense that the tissue is substantially destroyed, allowing the invading bacteria to proliferate further (6). In most of these infections, the host's cell-mediated immunity generally continues to control the infection. However, within the "healed" lesions, there may still be viable organisms that remain dormant for years, even decades, without producing any further symptoms of the disease.

Most individuals recover from primary TB, but in a small percentage of cases, the primary infection may progress, and further lung destruction can occur. In general, about 10% of the people with latent infections develop active TB sometime in their lives. The risk of reactivating a primary infection is greatest during the first two years after the initial infection. An individual with HIV has a 10-15% risk per year of progression of the infection. This reactivation of the disease is referred to as secondary TB. During this reactivation process, symptoms may include a cough that produces mucopurulent sputum, occasional hemoptysis, and chest pain. During reactivation, the individual pulmonary lesions may merge and enlarge; the resulting necrotic tissue (interior of the tubercle) will become cheese-like (caseous). If the body's defenses arrest the disease at this time, this caseous lesion slowly heals, undergoes fibrosis, or becomes calcified with cavities containing the living bacilli. These cavities show up on X-rays and are referred to as Ghon complexes. Later, this lesion may become more liquid, a process called liquefaction, and will commence to discharge the isolated viable organisms. Within these liquidified cavities, the bacilli can replicate to very high numbers (as many as 109 bacilli in a single lesion). At this stage, the organisms are highly infective and can be expected to serve as a source for the continual spread of the disease.

The organism can exist in these lesions for long periods or can disseminate to almost any organ of the body, including the central nervous system, the genital tract, bone, kidney, or lymph nodes. When the organisms spread to other parts of the body, this condition is known as miliary tuberculosis. The name is derived from the numerous millet seed-like tubercles formed in the infected target tissue. The tubercle bacilli can spread to other organs in three ways: (1) the organism may continue to gradually destroy the infected tissue at the primary site of infection and then proceed to invade other tissues from this initial site; (2) the organism can spread from the initial site of infection along the lymphatic vessels to the lymph nodes that drain the infected area; or (3) the tuberculous lesion may perforate the walls of a blood vessel, releasing millions of bacilli into the blood stream.

Pulmonary disease due to M. avian complex (MAC) typically occurs in white males, 45-65 years old with some preexisting lung disease such as chronic bronchitis, emphysema, a previous TB lesions, bronchiectasis, or pneumoconiosis. Patients with AIDS may have either a focal or disseminated MAC infection. MAC is commonly isolated from sputum or stool cultures from patients with HIV infection. It is thought that MAC is acquired and colonizes in either the gastrointestinal or respiratory tract before dissemination in HIV-infected patients. MAC infectious may also involve the peripheral lymph nodes. Bacteremia occurs in almost all such patients, and the organism can be found in the circulating monocytes (29).

Leprosy is a chronic granulomatous disease. The principal manifestations of the disease includes anesthetic skin lesions and peripheral neuropathy with peripheral nerve thickening. The medical complications of leprosy arise from nerve damage, immune reactions, and infiltration of the organisms to other sites (28).

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