TUBERCULOUS

LYMPHADENITIS
AND
GRANULATION
TISSUE
GROSS AND MICROSCOPY
Outlines of this competency
• Pathogenesis and pathology of Tuberculous
lymphadenitis
• Features of tuberculous lymphadenitis In gross
and microscopic specimens
 TUBERCULOSIS
• Tuberculosis is a chronic, communicable disease
in which the lungs are the prime target,
although any organ may be infected
• M. tuberculosis is an obligate aerobe, a slender,
beaded, nonmotile, acid-fast bacillus
• They have a waxy cell wall composed of mycolic
acid which makes them acid fast – retain stain
even on treatment with acid and alcohol
 TUBERCULOSIS
Transmission
• Most infections are acquired by person to
person transmission of airborne droplets of
organisms from an active case to susceptible
host
 TUBERCULOSIS
PATHOGENESIS
• M.Tuberculosis enters the macrophages by endocytosis
mediated by several macrophage receptors – mannose
receptors
• bind Lipoarabinomannan, a glycolipid in the bacterial cell wall
• Once inside the macrophage, M.Tuberculosis replicates within
the phagosome by blocking fusion of phagosome & lysosome
• Blocking of phagolysosome formation is by inhibiting ca2+
signals & blocking recruitment & assembly of the proteins
which mediate phagosome-lysosome fusion
TUBERCULOSIS- PATHOGENESIS
 TUBERCULOSIS - PATHOGENESIS
• In the early stage of primary tuberculosis ( 3
weeks ) in the non sensitized individuals the
bacteria proliferates in the macrophages &
air spaces resulting in bacteremia & seeding
of multiple sites.
• During this stage patients are asymptomatic
or have a flu like illness
 TUBERCULOSIS - PATHOGENESIS
TH1 response against M.Tuberculosis
• About 3 weeks after infection TH1 cells are
stimulated by mycobacterial Ag’s drained to the
lymph node, which are presented with class II
Major Histocompatibility proteins by Ag
presenting cells
• Differentiation of TH1 cells depends on the
presence of IL-12 , which is produced by Ag
presenting cells that have encountered the
mycobacteria
 TUBERCULOSIS - PATHOGENESIS
TH1 response against M.Tuberculosis
• Mature TH1 cells both in lymph node & in the lung, produce
IFN – gamma
• Interferon gamma stimulates the formation of the
phagolysosome in infected macrophages, exposing the
bacteria to an acidic environment
• Interferon gamma also stimulates expression of inducible
nitric oxide synthetase, which produces nitric oxide. NO
generates reactive nitrogen intermediates & other free
radicals capable of oxidative destruction of several
mycobacterial constituents from cell wall to DNA
 TUBERCULOSIS - PATHOGENESIS
GRANULOMATOUS RESPONSE
• Activated macrophages, stimulated by IFN-gamma produce TNF,
which recruits monocytes. These monocytes differentiate into the
‘epithelioid histiocytes’ that characterize the granulomatous
response
• The infection progresses due to age or immunosuppression & the
ongoing immune response results in tissue destruction due to
caseation & cavitation
• In some people granulomatous response contains bacteria &
does not cause significant tissue destruction or illness
 TUBERCULOSIS
PRIMARY TUBERCULOSIS
• Primary TB almost always begins in the Lungs
• The inhaled bacilli implant in the distal airspaces
of the lower part of the upper lobe & upper part
of the lower lobe, usually close to the pleura
• As sensitization develops, a 1 – 1.5cm area of
gray-white inflammatory consolidation emerges
known as the Ghon focus
• This combination of parenchymal lung lesion &
nodal involvement is referred to as Ghon
complex
TUBERCULOSIS – GHON COMPLEX
 TUBERCULOSIS
SECONDARY TUBERCULOSIS
• The initial lesion is usually a small focus of consolidation, less
than 2cm in diameter, within 1 to 2cm of the apical pleura
• In favorable cases the initial parenchymal focus undergoes
progressive fibrous encapsulation, leaving only fibrocalcific
scars
• The apical lesion enlarges with expansion of the area of
caseation
• Erosion into a bronchus evacuates the caseous centre, creating
a ragged, irregular cavity lined by caseous material that is
poorly walled by fibrous tissue
• Erosion of blood vessels results in hemoptysis
 TUBERCULOSIS
Miliary pulmonary disease
• This occurs when organisms drain through into the lymphatic
ducts, which empty into the venous return to the right side of
the heart & hence into the pulmonary arteries
• Individual lesions are either microscopic or small, visible foci of
yellow white consolidation scattered through the lung
parenchyma
• The word “miliary” is derived from the resemblance of these
foci to the millet seeds
TUBERCULOSIS
TUBERCULOSIS
TUBERCULOSIS

MATTED LYMPH NODES

TUBERCULOSIS

CASEOUS NECROSIS
 TUBERCULOSIS
GRANULOMA WITH EPITHELIOID CELLS SURROUNDED BY EPITHELIOID CELLS WITH OVAL ELONGATED
LYMPHOCYTES NUCLEI
 TUBERCULOSIS

Central granular caseation surrounded by epithelioid and multinucleate giant cells

(Langhan type)
 TUBERCULOSIS

Sheets of foamy macrophages packed with mycobacteria are seen

(acid-fast stain).
 MILIARY TUBERCULOSIS

LUNG SPLEEN
THANK YOU