Penyebaran

Hematogen dari fokus primer infeksi

Tertelan basil M.tuberculosis dari
sputum yang terinfeksi
Penyebaran langsung kuman ke GIT
Limfogen
Perkontinuitatum

ESTABLISHMENT

ALVEOLAR MACROPHAGE
INGESTS TB BACILLI

 M. tuberculosis blocks
phagolysosome formation by
inhbiting Ca2+ signals and the
recruitment and assembly of the
proteins that mediate phagosomelysosome fusion

SYMBIOSIS

Tubercle bacilli ingested

By non activated newly recruited
Monocytes.

SYMBIOSIS
Incapable alveolar macrophage bursts.
New monocytes from blood are recruited
to the site mainly by c5a, Monocyte
Chemoattractant protein-1(MCP-1)
TB bacilli multiplies in these non
activated monocytes.
7-21 days (<3weeks) primary TB.
Comes to an end when Th1 cells enters
the site

Secrete IFN

Activates
Macrophag
es

TCELL
Kills the inactivated
macrophages which were
allowing the tb bacilli
growth inside them

EARLY STAGES OF CASEOUS

NECROSIS
Non activated
Macrophages which
allowed the growth of
TB bacilli are killed by
DTH mediated by Tcells
Forming solid caseous
necrosis

EARLY STAGES OF CASEOUS

NECROSIS
TB bacilli remains live
but cannot multiply in
solid caseous
material.
TB bacilli escaping
from the edges of
caseous necrosis are
engulfed by
macrophages and
caseous centre
enlarges.

DTH AND CMI

DTH

CMI AND DTH

ACTIVATED MACROPHAGES
WALLS OFF THE EXPANDING
CAVITY AND PREVENTS
FURTHER INCREASE IN
SIZE IN HOST WITH GOOD
CMI.

POOR CMI

IN HOST WITH POOR CMI

DTH CONTINUES DESTROYS THE
BACILLI
AND LUNG TISSUE TOO.

TB BACILL SPREADS THROUGH

LYMPHATIC AND
HEMATOGENOUS ROUTE TO
OTHER ORGANS.