Page 171 - Textbook of Pathology, 6th Edition

bronchi to the other parts of the same lung or the opposite ance is typical of tuberculous granulomas with caseation 155
lung. This is called progressive primary tuberculosis. necrosis.
3. At times, bacilli may enter the circulation through erosion Patients with HIV infection previously exposed to
in a blood vessel and spread to various tissues and organs. tuberculous infection have particularly high incidence of
This is called primary miliary tuberculosis and the lesions are reactivation of primary tuberculosis and the pattern of lesions
seen in organs like the liver, spleen, kidney, brain and bone in such cases is similar to that of primary tuberculosis i.e. CHAPTER 6
marrow. with involvement of hilar lymph nodes rather than cavitary
and apical lesions in the lung. In addition, infection with M.
4. In certain circumstances like in lowered resistance and avium-intracellulare occurs more frequently in cases of AIDS.
increased hypersensitivity of the host, the healed lesions of
primary tuberculosis may get reactivated. The bacilli lying FATE OF SECONDARY PULMONARY TUBERCULOSIS.
dormant in acellular caseous material are activated and cause The subapical lesions in lungs can have the following courses:
progressive secondary tuberculosis. It affects children more 1. The lesions may heal with fibrous scarring and
commonly but adults may also develop this kind of calcification.
progression. 2. The lesions may coalesce together to form larger area of
tuberculous pneumonia and produce progressive secondary
B. Secondary Tuberculosis pulmonary tuberculosis with the following pulmonary and
extrapulmonary involvements: Inflammation and Healing
The infection of an individual who has been previously i) Fibrocaseous tuberculosis
infected or sensitised is called secondary, or post-primary or ii) Tuberculous caseous pneumonia
reinfection, or chronic tuberculosis. iii) Miliary tuberculosis.
The infection may be acquired from (Fig. 6.25):
endogenous source such as reactivation of dormant primary I. FIBROCASEOUS TUBERCULOSIS. The original area
complex; or of tuberculous pneumonia undergoes massive central
exogenous source such as fresh dose of reinfection by the caseation necrosis which may:
tubercle bacilli. either break into a bronchus from a cavity (cavitary or open
Secondary tuberculosis occurs most commonly in lungs fibrocaseous tuberculosis); or
in the region of apex. Other sites and tissues which can be remain, as a soft caseous lesion without drainage into a
involved are tonsils, pharynx, larynx, small intestine and bronchus or bronchiole to produce a non-cavitary lesion
skin. Secondary tuberculosis of other organs and tissues is (chronic fibrocaseous tuberculosis).
described in relevant chapters later while that of lungs is The cavity provides favourable environment for
discussed here. proliferation of tubercle bacilli due to high oxygen tension.
The cavity may communicate with bronchial tree and
Secondary Pulmonary Tuberculosis becomes the source of spread of infection (‘open tuberculosis’).
The open case of secondary tuberculosis may implant
The lesions in secondary pulmonary tuberculosis usually tuberculous lesion on the mucosal lining of air passages
begin as 1-2 cm apical area of consolidation of the lung, which producing endobronchial and endotracheal tuberculosis.
may in time develop a small area of central caseation necrosis Ingestion of sputum containing tubercle bacilli from
and peripheral fibrosis. It occurs by haematogenous spread
of infection from primary complex to the apex of the affected endogenous pulmonary lesions may produce laryngeal and
intestinal tuberculosis.
lung where the oxygen tension is high and favourable for
growth of aerobic tubercle bacilli. Microscopically, the appear-
Grossly, tuberculous cavity is spherical with thick fibrous
wall, lined by yellowish, caseous, necrotic material and
the lumen is traversed by thrombosed blood vessels.
Around the wall of cavity are seen foci of consolidation.
The overlying pleura may also be thickened (Fig. 6.26).
Microscopically, the wall of cavity shows eosinophilic,
granular, caseous material which may show foci of
dystrophic calcification. Widespread coalesced
tuberculous granulomas composed of epithelioid cells,
Langhans’ giant cells and peripheral mantle of
lymphocytes and having central caseation necrosis are
seen. The outer wall of cavity shows fibrosis (Fig. 6.27).

Complications of cavitary secondary tuberculosis are as
follows:
a) Aneurysms of patent arteries crossing the cavity
Figure 6.25 Progressive secondary tuberculosis. A, Endogenous producing haemoptysis.
infection from reactivation of dormant primary complex. B, Exogenous
infection from fresh dose of tubercle bacilli. b) Extension to pleura producing bronchopleural fistula.