Study of respiratory symptoms among sputum positive

I I
Interpersonal spread of tuberculosis may be enhanced in areas of
overcrowding, poor air circulation, or recirculated, unfiltered air. Rates of
tuberculosis infection in exposed contacts of individuals with active
tuberculosis may also be dependent on the duration of exposure (Onorato
and Ridzon 1995). In a study of a student with laryngeal tuberculosis,
infection was noted as little as 5 hours ofexposure (Braden, 1995).
Pathogenesis of pulmonary tuberculosis
The development of pulmonary tuberculosis from its onset to its
various clinical manifestations is dependent upon a series ofinteractions or
"battles" between the host and the bacillary invader (Lurie, 1964 and
Dannenberg 1993).
An inhaled unit of one to three bacilli is ingested by an alveolar
macrophage. Either the bacillus is destroyed before any lesion is produced
or it multiplies within the alveolar macrophage, which dies and reduces the
amplified infection agent. Many of the bacilli are then ingested by and
grow within monocyte\macrophage that have emigrated from the blood
stream. The cells accumulate at the site, fanning a microscopic lesion.
When the host becomes tuberculin positive a caseous center develops in
this lesion. A lesion with a small caseous center (up to 2mm in diameter)
may enlarge or may heal (or stabilize) before it is detectable by
radiography (Dannenberg and Tomashefski. 1998).
A larger caseous lesion may also heal or stabilize, or it may enlarge,
shedding bacilli into the blood and lymph. Alternatively, a caseous lesion
may liquefy and form a cavity (from which the bacilli enter the bronchial
tree). In the liquefied caseum, the bacilli will grow extracellularly (for the
first time), and from the cavity they spread to other parts ofthe lung and to
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