Clinical Manifestations of Tuberculosis

Easy fatigability
Anorexia or loss of appetite
Weight loss and body wasting
Persistent, long term low- grade fever
Chills and night sweats
Persistent, progressive cough which may be non-productive at first but may produce
purulent sputum in the long term (2 weeks or more)
Non-resolving bronchopneumonia
Dull or pleuritic chest pains
Dyspnea
Hemoptysis
Anemia in some
Schematic Diagram for Tuberculosis
Predisposing Factors:

Precipitating Factors:

Age: Children below 14 y. o.

& Adults more than 65 y. o.

Immunocompromised person

Native Americans, Eskimos,

Asians and Blacks

Economically- disadvantaged
or homeless/ poor housing

Malnourished individuals

Living in overcrowded areas

Alcohol abuse/ dependent
Poor hygiene
Lack of access to health care

Inhalation of droplet infected with Mycobacterium

Tuberculosis

It is trapped first in the upper airways, where the

primary defenses is activated referring to the mucussecreting goblet cell and the cilia.

When the initial prevention of infection is not

successful, the bacteria reaches and deposits itself in
the lung periphery usually in the lower part of the
upper lobe or the upper part of the lower lobe;
specifically in the alveoli.

The bacteria is quickly surrounded by

polymorphonuclear leukocytes and engulfed by the
alveolar macrophages

Some mycobacterial organisms are carried off by the

lymphatics to the hilar lymp nodes

It is now called as the Ghon Complex, but it rarely

results in the spread to other body organs.

As macrophages (epithelial cells) engulf the

bacteria, these cells join and form into giant cells
that encircle the foreign cell.

As a result of hypersensitivity to the organism,

inside the giant cells caseous necrosis occurs
(granular chessy appearance)

There is then the proliferation of T- lymphocytes in

the surrounding of the central core of the caseous
necrosis causing some lesions.

Fibrosis and calcification happens as the lesion ages

resulting to granuloma formation called as tubercle.

Collagenous scar tissue encapsulates the tubercle to

separate the organisms from the body.

As the process progress the bacteria may or may not

be killed and it continue to grow and multiply
resulting to a cell mediated immunity (which can be
detected through PPD)

Pulmonary Tuberculosis

Progression of
infection may
lead to latent
stage to active
stage
depending on
both the
virulence of
the bacteria
and the
microbicidal
ability of the
alveolar
macrophages

For poorly immunocompromised clients, the necrotic

tissue liquefies and the fibrous walls losses its
structural integrity

The semiliquid necrotic material is drained into the

bronchous or in the nearby blood vessel, leaving an airfilled cavity at the original site.

If drained in the
bronchous as purulent
discharge, it could infect
other people through
droplet transmission.

If drained into a vessel, it

could enter the blood
stream or in the lymphatic
system; where new
caseous granulomas may
form.

EXTRAPULMONARY
TUBERCULOSIS