Tuberculous lymphadenitis

Usually caused by
Mycobacterium tuberculi.
In immunocompetent patients, atypical
mycobacteria such as M. avium-
intracellulare (MAI) or M. kansasii also
can cause a
necrotizing granulomatous
lymphadenitis.
 Etiopathogenesis
•Primary TB almost always begins in lungs.
Typically the inhaled bacilli implant and develop a 1
to 1.5cm consolidation in lower part of upper lobe
and upper part of lower lobe.
•This is called as ghon’s focus which undergoes
caseous necrosis in the centre.
•The bacilli drain into the regional lymph node
causing their caseation, called as tuberculous
lymphadenitis.
•The combination of lung lesion and nodal
involvement is called as Ghon Complex.
• Lymphadenopathy due to mycobacterium
tuberculosis is a prototypical granulomatous
response which forms caseating tubercles.
• Possible other agents which cause
granulomatous inflam’n include bacteria,
mycobacteria, spirochetes, fungi, parasites, and
viruses.
• Non-infectious specific reaction patterns are
seen in sarcoidosis, collagen vascular disease,
silicosis, and dermatopathic lymphadenopathy.
 GROSS APPEARANCE
• The lymph node is enlarged, matted
rubbery and friable.
• On cut section it looks yellow, cheesy and
opaque.
• Washed out cheesy material can give a
cavitating appearance to the nodes.
 Microscopic appearance
• There are caseous necrotic areas in the centre
made of fragmented dead cells and Tubercle
bacilli.The periphery shows granulomatous
inflam’n, a characteristic f/o chronic inflam’n.
• Granulomas called as “Tubercles” contain
central necrosis, which is surrounded by
epithelioid (epithelium like) cells that are
macrophages transformed to large cells with
pale pink cytoplasm and oval vesicular nuclei
surrounded by a cuff of small lymphocytes and
plasma cells.
• Another component of granulomas are
multi-nucleated giant cells composed of
individual histiocytes that have fused.
They contain 20 or more nuclei arranged
in horse-shoe pattern (Langhans GC)or
haphazardly (foreign body GC).
• Fibroblasts and connective tissue form a
rim at the periphery. Normal nodal
architecture may be seen at the periphery.
Multiple tubercles,

Lymphocytes

Caseous necrosis
 Lymphocytes
Caseous necrosis
Caseous necrosis
Inflammatory granulation
tissue
Inflammatory granulation tissue

• After injury repair can not be established

merely by regeneration of cells but repair
by connective tissue is must. There are
four components of repair by connective
tissue,
– formation of new blood vessels
– migration and proliferation of fibroblasts
– deposition of extra cellular material.
– maturation and organisation of fibrous
tissue.
• Repair begins early in inflammation when
the fibroblast and endothelial cells begin to
proliferate to form a specialised tissue
called as Granulation tissue.
 Gross Appearance
• The granulation tissue has pink soft
granular appearance on surface of wound.
• The margins appear sloping and bluish
white.
 Microscopic Appearance-1

• Surface of wound contains mixture of blood fibrin

and inflammatory exudates.
• Beneath this lies the granulation tissue which is
characterised by:
– Formation of new blood vessels (angiogenesis).
– Proliferation of fibroblasts.
– These new blood vessels are leaky allowing passage of
RBC and proteins into extravascular space thus
causing oedema.
– Inflammatory cells like neutrophils(initially),later
replaced by lymphocytes and macrophages may be
seen in the exudate.
 Microscopic Appearance-2
• The epithelium grows from the edges of
wound in spurs.
• Granulation tissue matures from below
upwards and late stages show dense
collagen, scanty vascularity and few
inflammatory cells.
 macrophages Plasma cells lymphocytes fibroblasts
neovascularisation ulcer neutrophils