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P. 174
7 Infections 159
Pneumonia-like consolidation of middle and lower lobes,
hilar lymphadenopathy and pleural effusion (cavitation is rare)
Lymphatic or haematogenous dissemination
Tuberculous meningitis and miliary tuberculosis
FLOWCHART 7.2. Progressive primary tuberculosis.
Secondary Tuberculosis
• Secondary tuberculosis occurs due to reinfection or reactivation of a silent primary focus
in a previously sensitized individual.
• Mostly involves apex of one or both lungs (Simon focus). Due to pre-existing hyper-
sensitivity, the bacilli induce a rather prominent and rapid response which walls off the
infective focus.
• Localized, apical, secondary pulmonary tuberculosis may heal with fibrosis either spon-
taneously or after therapy (usual outcome in an immunocompetent host), or the disease
may progress and extend along several different pathways (in the elderly or the immu-
nocompromised).
• Secondary tuberculosis is typically characterized by less nodal involvement and more
cavitation (cavitary tuberculosis). The apical lesion enlarges and drainage of caseous
necrosis into a bronchus creates a cavitary lesion.
• Cavitation can lead to rupture of vessels within it, thus presenting with haemoptysis.
• Also, cavitation aids in spread of disease by haematogenous, lymphatic or contiguous
routes and can have one of the following outcomes:
• Irregular cavities, now free of caseation necrosis, may remain as such or collapse due
to surrounding fibrosis.
• Involvement of pleura can result in pleural effusion or tuberculous empyema.
• Bacilli may spread to upper respiratory tract via lymphatics or during expectoration
of infected material, producing endobronchial and endotracheal tuberculosis.
• Laryngeal and intestinal tuberculosis may follow endotracheal tuberculosis. Tuber-
culous enteritis spreads via intestinal lymphatics to cause transverse (circumferen-
tial) ulceration, which may eventually heal by fibrosis to cause stricture formation.
• Miliary tuberculosis (Fig. 7.2) is characterized by distinct, yellow-white, firm
1–2 mm (millet like) areas of consolidation that usually do not have grossly visible
necrosis or cavitation, but microscopically show typical caseation. It occurs due to
lymphatic and haematogenous dissemination from the primary site. Organisms can
FIGURE 7.2. X-ray lung (PA view) showing millet like areas of consolidation.
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