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• Second level
• Third level
• Fourth level
• Fifth level

Granuloma
Dr. Shimaa abdel-Raouf
Pathology Department
Faculty of Medicine
Ain Shams University
 Intended Learning Outcomes (ILOs):
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• By the end of the lecture should be able to:
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• List the causes of Tuberculosis.
• Second level
• Explain its pathogenesis.
• Third level
• Describe
• Fourthitslevel
pathologic morphologic features.
• Fifth level
• Recognize its presenting symptoms and clinical
features.
• Identify its possible complications
• Correlate the clinical features with the pathologic
morphologic features to reach a diagnosis of the
disease
Definition:

• Granuloma is a chronic specific inflammation in which the

inflammatory cells accumulate to form a mass (collection of
modified macrophages called epithelioid cells and rimmed by
lymphoid cells).
Examples of granulomas:
• Bacterial: TB, syphilis, leprosy…
• Fungal: Mycetoma
• Parasitic: Schistosomiasis
• Inorganic dusts: Silicosis
• Foreign bodies: Suture
• Unknown aetiology: Crohn’s disease, Sarcoisosis.
 TUBERCULOSIS
Infectious Granuloma
C.A.: Mycobacterium Tuberculosis (Bacilli)
• Types:
• Human Inhalation.
• Bovine Ingestion of infected milk.
Structure of the bacillus:
Aerobic, non-motile, resists drying, killed by sunlight and acid
and alcohol fast.
• Lipid coat Resists destruction by enzymes.
• Protein part Immunological activity.
• Carbohydrates Small fraction.
• Stained by Ziehl-Neelsen acid fast stain.
 Methods of infection:
• Inhalation.
• Ingestion.
• Direct inoculation.
• Transplacental ( rare).

Predisposing factors:
• Malnutrition, poverty and overcrowding.
• Genetic predisposition: Polymorphism of (NRAMP1) = natural
resistance associated macrophage protein 1 gene.
• Debilitating diseases (Un controlled Diabetes).
• Chronic lung disease.
• Alcoholism.
• Immunocompromised state (AIDS).
Pathogenesis of Tuberculosis:
• Delayed-type hypersensitivity (CD4+ T-cells).
- APCs  IL-12  CD4+ TH0  CD4+ TH1 which:
1. Secretes IFN ::
a. Macrophage activation
. TNF  increase capillar permeability
 more monocytes
. Increase nitric oxide
. Reactive oxygen species
b. Fibroblast proliferation (PDGF and TGF-β )
2. Activates CD8+  direct cell
cytotoxicity (caseation necrosis)
3. Releases mediators of acute inflammation.
• Immunization:
Living attenuated strains of bovine TB (BCG).

• Tuberculin test (Mantoux skin test):

Intradermal injection of PPD develops delayed
hypersensitivity in infected or previously immunized
patients.
Host response:
1) Proliferative reaction:
• Proliferation of the bacilli inside the macrophage kills the
macrophages.
• New macrophages engulf liberated bacilli epithelioid cells.
• Fusion of epithelioid cells Langhans’ giant cells.
• Infilteration of the surrounding tissues by sensitized T-lymphocytes
(helper) Tubercle formation.
-Microscopic picture:
-Rounded or oval
Composed of:
-Caeseous necrosis in center
(structureless eosinophilic material
containing nuclear debris)
-Epitheloid cells (rounded or oval,
pale pink cytoplasm, round or oval
nuclei, ill defined border)
-Few langhan’s giant cells (large,
many nuclei with horse shoe
arrangement.) surrounded by
lymphocytes & some fibroblasts
 Langhan giant
cells

Caseation
necrosis
2) Exudative reaction:
• In serous sacs: Protein-rich fluid with large number of lymphocytes.
• Large dose of bacilli in sensitized person.
• e.g. TB peritonitis, TB pericarditis and TB pleurisy
Fate of TB granuloma:
• Dystrophic calcification (calcified tebis mesenterica)
• Enlargement of the lesion and fibrosis
(fibrocaseous TB)
• Cold abscess in lymph nodes and epididymis
• Sinus
Types of T.B. infection:
Primary T.B.
• First time infection.
• Exogenous
• Common in children.
• Patient is not immune.
• Tonsil, LN, Lung, intesine, skin.
• T.B. lymphangitis with enlarged
lymph nodes (No immunity).
• No caseation.
Secondary T.B.
• Second time infection.
• Exogenous or endogenous.
• Common in adults.
• Patient is immune.
• Any organ.
• Regional lymph nodes are not
severely affected (Immunity).
• Caseation
 Primary
TB MQ

Lymphangitis of
lymphatic vessels

Epithelioid
granuloma

Lymphadeniti
s of draining
LN
Primary complex

TB lesion

Lymph-
angitis Lymphad
enitis
secondary

Th

Th
Tc

Caseation due to delayed

type HS
Primary complexes
• It usually occurs as a primary infection.
• The commonest sites are:
1. 1ry cervical complex: TB of tonsils, TB cervical lymphangitis
and TB cervical lymphadenitis.
2. 1ry pulmonary complex: Primary TB of the lung (Ghon’s
focus), TB hilar lymphangitis and TB hilar lympadenitis.
3. 1ry intestinal complex: Primary TB enteritis, TB
mesenteric lymphangitis, and TB mesenteric
lymphadenitis (tabes mesenterica).

• This is called ‘Primary glandular complex’.

Organs affected in secondary TB:
1. Hollow  ulcer (intestine).
2. Solid  cavity (lung, kidney, Pott’s disease of bone)
Methods of spread of TB infection:
1. Local spread.
2. Lymphatic spread.
3. Blood spread leading to
• Miliary TB, if enormous number of bacilli.
• Isolated organ TB, if small number of bacilli.
4. Spread along natural passages.
General complications Of TB
• 1. Spread:
• a. Local:
• - Subcutaneous tissue/ joints Cold abscess Sinus
• b. Lymphatic: TB focus opens into a lymph vessel TB
lymphangitis/ TB lymphadenitis
• c. Blood: TB focus opens into a pulmonary artery
milliary TB (disseminated TB)
• d. Through natural passages: ex. From ureter to UB and
rest of genitourinary system
• 2. Fibrosis:
• Ex. In peritoneum Intestinal obstruction (adhesions between intestinal
loops)
• In fallopian tube Infertility (tube obliteration by fibrosis)
• 3. Calcification
• 4. Amyloidosis
Thank You
Thank you