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Tuberculous lymphadenitis

Usually caused by Mycobacterium tuberculi. In immunocompetent patients, atypical mycobacteria such as M. aviumintracellulare (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

Caseous necrosis

Lymphocytes

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.

neovascularisation

macrophages

Plasma cells lymphocytes fibroblasts ulcer neutrophils