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

NATURAL RESISTENCE ANATOMIC BARRIER PHAGOCYTOSIS COMPLEMENT NUTRTIONAL HORMONAL GENETIC HOST DEFENCE LOCAL SYSTEMIC NONSPECIFC HUMORAL CELLULAR

BAKTERI,VIRUS, PARASITES

INFECTION UNCOMMON

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

mikroba
stimulasi

epithel
Sitokin ,TNF

makrophag

HOST DEFENSES AGAINTS ATTACHEMENT TO EPITHELIAL CELL

NORMAL MICROBIAL FLORA LOCAL FACTOR : FIBRONECTIN,GLYCOPROTEINS AND Ph ANTIBODY ON MUCOSAL SURFACE IgA LACTOFERIN

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) Function laesa

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