Tuberculosis

The Etiology of Tuberculosis

The development of TB follows various stages based upon the progression of various defense mechanisms initiated by the human immune response system. Initially, toxic chemicals released by the TB bacteria induce the human body to produce characteristic swellings or lesions at sites where the bacteria become clustered in the infected tissue. During the later stages, the immune system attempts to prevent the spread of TB to other parts of the body by enveloping the lesions in a thick fibrous coating of collagen, while bacteria that do escape the encapsulation are destroyed by immune response agents known as macrophages. The encapsulation eventually forms a hard grain called a granuloma that appears as a small dot on a chest X-ray. The resultant walled-off bacterial clusters can lie dormant in this latent phase for many years. At this stage, the individual is otherwise healthy and noninfectious and is classified as a nonactive case. In roughly 5 to 10 percent [Page 472]of the latent cases, the disease may become activated if the individual's immune system becomes weakened or damaged later in time. During this active stage, the bacteria may overcome the body's defense mechanisms and proliferate in the lungs, where they can be spread more easily to others through respiratory secretions, or be discharged into the circulatory and lymph system, where they can spread to other parts of the body. In terms of developing and implementing effective public health responses to TB, it is important to distinguish between cases that are the result of recent transmission (i.e., secondary cases) and those resulting from reactivation of old infections, especially since the original site of infection may be very distant from where the latent case currently resides, as well as very distant in the past.

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