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Kuliah Blok Infeksi

Proses Peradangan dan Infeksi Lokal

Brian Wasita
•Inflammation
An important physiological reaction which
occurs in response to a wide variety of
injurious agents (e.g. bacterial infection or
physical trauma) ultimately aiming to
perform the dual function of limiting damage
and promoting tissue repair

(Scull et al, 2010)


The outcome of inflammation

(Kumar et at, 2005)


(Lister et at, 2007)
Cardinal sign

1.Rubor (redness)
Due to vessel dilatation and increased blood flow.
2. Calor (heat)
Due to vessel dilatation and increased blood flow.
3.Dolor (pain)
Due to combination of :
•Pressure on nervus ending by swelling
•Direct effect from mediator inflammation released
in inflammation response.
4.Tumor (swelling)
Due to accumulation of exudate
5. Functio laesa (loss of function)

(Kahn MA and Solomon LW, 2007)


Systemic Manifestation of Inflammation

Clinical manifestation
1. Fever (IL-1, IL-6, TNF-α)
2. Chills
3. Malaise
4. Somnolent
5. Anorexia
6. Increased pulse and blood pressure

(Kumar et at, 2005)


Laboratory findings
1.Leukocytosis (IL-1, TNF-α)
2.Leukopenia (ex:thypoid fever, viral
infection)
3.Increased acute phase protein (ex: CRP)

Kumar et at, 2005


Acute Inflammation Chronic Inflammation

Short duration (minutes, Longer duration (weeks,


Duration
several hours, a few days) months)

The presence of
lymphocytes and
Edema macrophages
Main characteristics Emigration of leukocytes Proliferation of blood
(especially neutrophils) vessels
Fibrosis
Tissue necrosis

(Kumar et at, 2005)


Chronic inflammation due
Acute Inflammation due to frostbite to Rheumatoid arthritis

Figures source: Wikipedia


Acute Inflammation
Three major events
1.Changed in vascular caliber that leads in
an increase in blood flow (vascular events)
2.Increased vascular permeability that cause
vascular leakage (vascular events)
3.Leukocyte extravasation and phagocytosis
(cellular events)

(Kumar et at, 2005)


(Kumar et at, 2005)
Changed in vascular caliber and vascular
leakage

(Kumar et at, 2005)


Leukocyte extravasation

Step:
(Kumar et at, 2005)
1.Margination, rolling, and adhesion
2.Diapedesis
3.Migration in interstitial tissue toward chemotactic stimulus
Endothelial/Leukocyte Adhesion Molecules in Leukocyte
extravasation

(Kumar et at, 2005)


Phagositosis

(Kumar et at, 2005)


Chemical mediators of Inflammation

(Kumar et at, 2005)


Arachidonic Acid Pathway

AA is 20-carbon polyunsaturated fatty acid (Kumar et at, 2005)


Source: dietary diet or by conversion from linoleic acid
Release from membrane phospholipids by: mechanical,chemical, physical
stimuli or by other mediatos
(Kumar et at, 2005)
Cytokines in inflammation
Cytokines:
Protein produce by many type of cells (especially activated lymphocytes and
macrophages) that modulate the function of other cell types.

(Kumar et at, 2005)


(Kumar et at, 2005)
Leukocyte induce tissue injury
Leukocyte release product into extracellular sapce which can caused endothelial
injury and tissue damage.
The product released by leukocyte:
lysosomal enzyme, oxygen derived active metabolites, and product of archidonic
acid metabolism (prostaglandins and leukotrienes)

(Kumar et at, 2005)


Treatment of Inflammation
1.Eliminate the source of inflammation
2.Inhibit mediator of inflammation
a.Glucocorticoids (steroid)
•Down regulate specific target gene (COX-2,
gene pro-inflammation(Ristimäki,2004) )
•Up-regulate genes that encode potent anti
inflammatory protein ex: lipocortin 1
b. NSAID
Chronic inflammation
• Prolonged duration of inflammation in which active
inflammation, tissue destruction, and tissue
repairing are proceeding simultaneously
Causes:
1.Persistent infections (tubercle bacilli, treponema
pallidum)
2.Prolonged exposure to potentially toxic agents
(exogenous:silica; endogenous: toxic plasma lipid
components)
3.Autoimmunity:rhematoid arthritis,lupus
erythematosus)
(Kumar et at, 2005)
Histological features

Kumar et at, 2005


1.Infiltration of mononuclear cells (macrophages, lymphocytes, and
plasma cells).
2.Tissue destruction.
3.Connective tissue replacement of damaged tissue, angiogenesis, and
fibrosis.
Cells in chronic inflammation
1. Macrophage (Kupffer cells in liver,
alveolar macrophages in lungs)
2. Lymphocytes (T and B)
3. Mast cells
4. Eosinophils

Kumar et at, 2005


Morphologic variation in acute and chronic
inflammation

1. Serous inflammation
2. Fibrinous inflammation
3. Supurative inflammation
4. Ulcers

(Kumar et at, 2005)


Chronic inflammation

• Inflammation of prolonged duration (weeks or


months) in which active inflammation, tissue
destruction, and attempts at repair are proceeding
simultaneously

(Kumar et at, 2005)


Characteristic

1. Mononuclear infiltration
2. Tissue destruction
3. Connective tissue replacement

(Kumar et at, 2005)


Specific pattern of chronic inflammation

Granulomatous inflammation
Predominant cell type is an activated macrophage with a modified epithelial-like
appearance.
(ex: tuberculosis, sarcoidosis, leprosy, syphilis)

Granuloma:
A focal area of granulomatous inflammation, consists of a microscopic aggregation
of macrophages that are transformed into eptithelium-like cells surrounded by a colar
of mononuclear leukocytes principally lymphocytes and occasionally plasma cells.

Kumar et at, 2005


(Kumar et at, 2005)
Tuberculous granuloma
Local infection
An infection that is limited to a small area (a certain
site or focus) of the body.

Example: pneumonia, urinary tract or bladder


infections, appendicitis, and skin infections.

Skin abscess Acute appendicitis


Inflammatory response for infection
1.Suppurative (Polymorphonuclear) Inflammation

The reaction to acute tissue damage

Characteristic Increased vascular permeability


Leukocytic infiltration, predominantly of
neutrophils
Pus formation
Infectious agent extracellular Gram-positive cocci and Gram-
negative rods.

(Kumar et al, 2005)


2.Mononuclear and granulomatous inflammation

Characteristic Mononuclear
Diffuse infiltrate of predominantly mononuclear cells
Plasma cells : primary syphilis
Lymphocytes : HBV, viral infection

Granulomatous:
Giant celss: TBC
Infectious agent Viruses, intracellular bacteria, spirochetes, intracellular
parasites or helminths.

(Kumar et al, 2005)


3. Cytopathic-cytoproliferative Inflammation
Virus-mediated damage to individual host cells in the
absence of host inflammatory response

Characteristic Depent on the type of virus


Inclusion bodies : CMV or adenovirus
Polykaryons: measles virus or herpes virus
Blisters : herpes virus
Unusual individual and aggregate morphologic lession
(veneral warts) : HPV
Infectious agent Virus : CMV, measles virus, herpes viruses, HPV, poxviruses

(Kumar et al, 2005)


4. Necrotizing Inflammation

Characteristic Rapid and severe tissue damage with only few/no


involvement of inflammatory cells.

Infectious agent Clostridium perfringens, Entamoeba hystolitica, herpes virus,


HBV

(Department of Pathology University of Pittsburgh School of Medicine)


(Kumar et al, 2005)
5. Chronic inflammation and scarring
Final common pathway of many infection

Characteristic Rarely appear in pure form, they frequently overlap


In cutaneous leishmaniasis:
Central part: ulcerated area filled with neutrophils
Peripheral area: a mixed infiltrate of lymphocytes
and mononuclear cells
Infectious agent Schistosoma, Leishmania, CMV

(Kumar et al, 2005)


References
1.Department of Pathology University of Pittsburgh School of Medicine
http://path.upmc.edu/cases/index.html
2.Kahn MA and Solomon LW: Basic Human Pathology Lecture 5: Acute Inflammation/
Wound Healing & Repair I,University of Tufts ; 2007
3.Kumar V, Abbas AK,Vausto N, editors. Robbins and Cotran PATHOLOGIC BASIS OF
DISEASE.7thed. Philadelphia: Elseiver Saunders; 2005.
4.Lister MF, Sharkey J , Sawatzky DA , Hodgkiss JP, Davidson DJ, Rossi AG and
Finlayson K. The role of the purinergic P2X7 receptor in inflammation. J Inflamm (Lond)
2007, March 16; 4:5
5.Ristimäki A. Cyclooxygenase 2: from inflammation to carcinogenesis. Novartis Found
Symp. 2004;256:215-21; discussion 221-6, 259-69.
6.Scull CM, Hays WD, Fischer TH. Macrophage pro-inflammatory cytokine secretion is
enhanced following interaction with autologous platelets. J Inflamm (Lond). 2010 Nov
11;7:53.