IMMUNITY & INFECTION

Randanan Bandaso
Bagian Patologi FK Unhas
INFECTION
IMMUNITY
INSEPERABLE
I
N
F
L
A
M
M
A
T
I
O
N
H0W ANIMAL
BECOMES IMMUNE
NATURAL AND ARTIFICIAL
IMMUNOLOGY
BAKTERI,VIRUS, PARASITES
INFECTION UNCOMMON
NATURAL RESISTENCE
ANATOMIC BARRIER
PHAGOCYTOSIS
COMPLEMENT

NUTRTIONAL
HORMONAL
GENETIC

HOST DEFENCE
LOCAL
SYSTEMIC
NONSPECIFC
HUMORAL
CELLULAR
MAN
OBSERVED
RECOVERY FROM INFECTION
IMMUN
JENNER : VACCINATION OF SMALL FOX
SUCCESFULL APLICATION OF OBSERVATION
NONSPESIFIC IMMUNITY
BODY SURFACE
DISCHARGE MICROORGANISM FROM
THE BODY
LOCAL PRODUCTION OF CHEMICAL
ANTIMICROBES
BACTERIAL INTERFERENCE
LACTOBACILLUS
BODY SURFACE
MICROORGANISME TO PRODUCE
INFECTION SLIP TO BARRIER
SURFACE DEFENCES
THIKNESS OF EPITHELIAL IS DIFFER
NONSFECIFIC
DISCHARGE
OF MICROORGANISME
FROM THE BODY
MUCOCILIARY ESCALATOR OF THE RESPIRATORY
TRACT OROPHARYNX COUGHED OR
SWALLOWED
DESQUAMATION OF EPITHELIAL CELL REMOVED
LARGE AMOUNT OF BACTERIAL
DEFECATION ELIMINATE 10.000 000 000 000 /DAY
URINATION ELIMINATE BACTERIAL COLONIZING
IN URETHRAL EPITHELIUM RETENTION OF URINE
ENHANCE THE RISK OF INFECTION
SALIVATION, LACRIMATION, SNEEZING
DISPLACE POTENTIALLY INFECTIVE
MICROORGANISME
RESPONS IMUN NON SPESIFIK
PALING LUAR
KULIT
SUHU TINGGI
PERGANTIAN KULIT.
LEMAK KULIT
FLORA NORMAL
KULIT
MUKOSA
PERGANTIAN
MUKOSA
ASAM LAMBUNG
SALIVA
PERISTALTIK USUS
BATUK
FLORA
NORMALORAL,GIGI,
VAGINA, KOLON
RESPON IMUN NON SPESIFIK
LAPIS KEDUA
MONOSIT
MAKROFAG
GRANULOSIT
NEUTROFIL
EOSINOFI
BASOFIL
DIBAWAH KULIT
DIBAWAH
MUKOSA
epithel
mikroba
makrophag
stimulasi
Sitokin ,TNF
NORMAL MICROBIAL FLORA
LOCAL FACTOR :
FIBRONECTIN,GLYCOPROTEINS
AND Ph
ANTIBODY ON MUCOSAL SURFACE
IgA
LACTOFERIN
HOST DEFENSES AGAINTS
ATTACHEMENT TO EPITHELIAL CELL
CELLULAR SYSTEM OF
SYSTEMIC IMMUNITY
PROFESIONAL PHAGOCYTIC
PMN
MACROPHAGE
NONPROFESIONAL PHAGOCYTIC
ENDOTHELIAL, EPITHELIAL, FIBROBLAST
SIGNIFICANCE OF EPITHELIAL
CELL PROLIFERATION
MICROBIAL ATTACHEMENT IS NOT NECESSARY
FOLLOWED BY CELL PENETRATION
M.PNEUMONIAE, C.DIPHTERIAE,
B.PERTUSSIS,V.CHOLERA SURFACE
SHIGELLA PENETRATE EPITHELIAL CELL
SALLMONELA PROCEED TO SYSTEMIC
INFECTION
INTRAEPITHELIAL PATHOGENS PROTECTECTED
FROM ANTIBODY, ANTIBIOTIC, AND INGESTION
AND KILLING BY PMN
SYSTEMIC IMMUNITY TO
INFECTION
HUMORAL SYSTEM
CELL MEDIATED IMMUNITY
IMFLAMATION
RESPONSE OF TISSUE TO DAMAGING
AGENT
ACUTE IMFLAMMATION
INITIAL RESPONSE OF TISSUE
CHRONIC IMFLAMTION
DAMAGING AGENT PERSISTS
INFLAMATION
BLOOD SUPPLY INCREASED
GLUCOSA
OKSIGEN
INCREASED IN CAPILLARY
PERMIABILITY
MIGRATION OF NEUTROPHYL,
MACROPHAGES, LYMPHOCYTE
CLINICAL EFFECTS OF ACUTE
INFLAMMATION
RUBOR (REDNESS)
CALOR (HEAT)
DOLOR (PAIN)
TUMOR (SWELLING)
STEPS OF CHANGES
SMALL VESSEL DILATED AND
INCREASED BLOOD FLOW
ENDOTHELIAL CELL SWELL AND
RETRACTLEAKING
EXUDATION
PMN MARGINATION EMIGRATION
LATER MONOCYTE, LYMPHOCYTE
ALSO MIGRATE
CONTROL OF INFLAMATION
CYTOKINES
PRODUCTS OF PLASMA ENZYMES
VASOACTIVE MEDIATOR
MAST CELLS
BASOPHILS
PLATELETS
MEDIATOR OF INFLAMATION
HISTAMINE MAST CELLS + BASOPPHYL
VASCULAR PERMIABILITY, SMOOTH MUSCLE
CONTRACTION
SEROTONIN PLATLETS VASC PERMIABILITY,
SMOOTH MUSCLE CONTRACTION
IL8 LYMPHOCYTES MONOCYTE
LOCALIZATION
C3A COMPLEMENT C3 MAST CELL
DEGRANULATION + SMOOTH MUSCLE
CONTRACTION.
BRADYKININ KININ SYSTEM VASODILATATION
Mediator in inflammation
Vasodilatation : Histamine,Prostaglandins, nitric oxide.
Increased Permiability :
Histamine,C3a,C5a,bradykinin,Leukotrienes,PAF, Nitric
Oxyde
Neutrophil Adhesion : IL-1,TNF,PAF,C5a
Neutrophil chemotaxis : C5a, bacterial components
Fever: IL1,TNF,Prostaglandins
Pain : Prostaglandins, bradykinin
Tissue Necrosis: Neutrophil, lysosomal granules,free
radical generated by PMN
CELLULAR MEDIATOR
STORED : HISTAMIN
ACTIVE SYNTHESIS:
PROSTAGLANDINS,
LEUKOTRIENES,PLATELET
ACTIVATING FACTOR, CYTOKINES,
NITRIC OXIDE
PLASMA DERIVE:
BRADYKININ, HAGEMAN FACTOR,
PLASMAIN, C3a, C3b and C5a
The End