8_ imunologi infeksi

30

Upload: vi-vii

Post on 10-Nov-2014

130 views

Category:

Documents


2 download

TRANSCRIPT

Page 1: 8_ IMUNOLOGI INFEKSI
Page 2: 8_ IMUNOLOGI INFEKSI
Page 3: 8_ IMUNOLOGI INFEKSI

3

Macrophage Macrophage (Antigen Presenting Cell)(Antigen Presenting Cell)

Page 4: 8_ IMUNOLOGI INFEKSI

Asbestos fibers engulfed by MacrophageAsbestos fibers engulfed by Macrophage4

Page 5: 8_ IMUNOLOGI INFEKSI

Macrophage reaches out to ensure bacteria with pseudopod

5

Page 6: 8_ IMUNOLOGI INFEKSI

Killer T cell attack cancer cells6

Page 7: 8_ IMUNOLOGI INFEKSI

Killer T cells appear remarkably alive as they attack a cancer cell

7

Page 8: 8_ IMUNOLOGI INFEKSI

MHC pada kromosom ke-6

Lokus A C B D/DR dst

Allel genetik : >20 >12 >20 >6

Penentu

Antigen HLA HLA A1 HLA Cw1 HLA B5 HLA Dw1 HLA A2 HLA Cw2 HLA B8 HLA Dw2

HLA Aw36 HLA Cw3 HLA Bw39 HLA Dw6

Contoh, HLA seseorang : HLA-A1, HLA-A3, HLA-B7, HLA-B8, HLA-Cw1, HLA-Cw2, HLA-Dw2, HLA-Dw3

Page 9: 8_ IMUNOLOGI INFEKSI

NASE & NASAL PHARYNX OROPHARYNXStaphylococci StaphylococciDiphtheroids Streptococcus spNeisseria sp Neisseria spHaemophilus sp Haemophilus sp

MOUTH SKINStaphylococci StaphylococciStreptococci StreptococciActinomyces sp CorynebacteriumHaemophilus sp PropionibacteriumYeasts YeastsEnteric bacteria DiphtheroidsAnaerobic bacteria Enteric bacteria

(rare)Spirochaetes

NORMAL FLORA OF THE SKIN, MOUTH, NOSE AND NASOPHARYNX, AND THE OROPHARYNX

Page 10: 8_ IMUNOLOGI INFEKSI

GASTROINTESTINAL SYSTEM :STOMACH LARGE INTESTINE

Normally sterile Anaerobic bacteria : Gram negative

SMALL INTESTINE Bacteroids sppLactobacilli Fusobacterium spp

Enterococci Gram positiveDiphtheroids Eubacterium sppYeasts (Candida) LactobacilliEnteric bacteria Clostridium sppAnaerobic gram BifidobacteriumNegative bacilli Streptococci

Facultative and aerobic organisms Staphylococci Enterococci Enteric bacteria Proteus spp Pseudomonas spp Yeasts (Candida)

NORMAL FLORA OF THE GASTROINTESTINAL SYSTEM

Page 11: 8_ IMUNOLOGI INFEKSI

NORMAL FLORA OF THE GENITOURINARY TRACT

Page 12: 8_ IMUNOLOGI INFEKSI

Predisposing Factor Effect on Immune system Type of infection

The Compromised host

Drug or X-rays in immunosuppression Allograft recipients (renal. Bone marrow, heart)VirusImmunosuppression e.g. Rubella, herpes, EB virus, hepatitis virus ,HIVTumours

Malnutrition

Smoking, inhalation of dust particles (e.g. Silica, Fungal spores)Chronic endocrine disease (e.g. Diabetes)Primary immune deficiency

Diminished cell- mediated and humoral immunity

Replication of virus in lymphoid cells with resulting impaired function

Replacement of cells of immune systemLymphoid hypoplasiaDecrease in circulating lymphocytesDecreased phagocytic abilityInflammatory lung changes, immune complex deposition to fungal spores

Decreased phagocytic activity

Diminished cell-mediated and/or humoral immunity

Lung infections, bacteraemia, fungal infections, urinary tract infectionsSecondary bacterial infections ( also fungal and protozoal in AIDS)

Bacteraemia, pneumonia, UTIMeasles, tuberculosis, respiratory infections, gastrointestinal infectChronic respiratory infections, allergic responses

Staph, infections Tuberculosis Respiratory infections, bacteraemia

Page 13: 8_ IMUNOLOGI INFEKSI

Bacteria Viruses Fungi

M. tuberculosis Influenza Coccidioides

M. leprae Viral hepatitisCryptococcus

T. pallidum Herpes simplex Histoplasma

Brucella abortus Cytomegalovirus Candida

Salmonella spp. HIV

Measles

Mumps

Rubella

Infectious mononucleosis

Microorganisms affecting cell mediated immune function

Page 14: 8_ IMUNOLOGI INFEKSI

Restoration of normal immmune function is likely to be of more importance in the recovery of the patient than spesific antimicrobial drug treatment.

Page 15: 8_ IMUNOLOGI INFEKSI

Microorganism Effect

Microorganisms that interfere with induction of acquired immunity

Measles, rubella, herpes, Hepatitis virusesLymphadenopathy associated virus of AIDS (HIV)

Malaria paracites

Leprosy bacilli

Trichphyton fungi

Schistosomes

Influenza viruses

Herpes simplex and cytomegalovirus

Infection of cells of immune system and interference with induction of acquired immunity and expression of cell mediated immunity

Depressed lymphocytes responsiveness to mitogens and some antigensAlteration in T:B cell ratio wtih reduction in expression of complement receptors ( ? Bloked by immune complexes)Non-spesific impairment of cell-mediated immune responseRepeated exposure to tricophyton leads to relatively allergy to the fungal antigens and reduced inflamatory responseIncorporate host antigens and prevent recognition of their antigensSuppress mitogenic responses of lymphocytes? Disables macrophages leading to secondary bacterial infectionInduced Fc reseptors in infected cell that bind and thus inactivate antiviral antibody

Page 16: 8_ IMUNOLOGI INFEKSI

IMMUNITY IN INFECTIONTo Understand the detailed cellular events and

differences in responses to infection of individulas it is necessary to take into account more recently acquired knowledge of the role of the major histocompability complex (MHC) in determining the outcome of an immune reponse.

The MHC is a highly polymorphic system of genes that control the expression of the cell surface molecules involved in immunity.

The existence of such a polymorphic system will inevitably result in individulas with different immunological potentials to respond to a given challege.

Page 17: 8_ IMUNOLOGI INFEKSI

Whilst some individulas will be well prepared to resist an infectious agent others will be at risk.

It will come as no surprise to find that certain infective states are linked with the MHC.

For example, the association between viral hepatitis and the HLA-A8 antigen on lymphocytes.

Individuals of blood group O are more susceptible than those of other blood groups to cholera.

In studies of a Children population it was found that people of blood group B had a 50% greater probability than non-B persons of contracting E.coli urinary tract infections.

Page 18: 8_ IMUNOLOGI INFEKSI

Blood group B individuals are more susceptible to gonococccal infections.

Blood group B and AB non-secretors have been found to be three times more susceptible to urinary tract infections.

Page 19: 8_ IMUNOLOGI INFEKSI

BACTERIAL INFECTIONMany microorganisms owe their pathogenic abilities to

the production of exotoxins.

Amongst diseases dependent on this type of mechanism are diphteria, cholera, tetanus, gas gangrene and botulism.

Page 20: 8_ IMUNOLOGI INFEKSI

SCHEME SHOWING THE PROGRESS OF INFECTION AND THE IMMUNOLOGICAL DEFENCE MECHANISMS

MICROORGANISM

INVASION LOCAL PROLIFERATION

Spread via lymphatics Proliferation in local lymph

nodes

Toxin production (Toxigenic bacteria)

Intracellular growth (Chronic bacterial

infection and viruses)

ANTIBACTERIAL IMMUNITY ANTI TOXINS CELL MEDIATED

IMMUNITY

Innate immune mechanisms ( Mechanical barriers anti-bacterial substances phagocytic cells)

Inflammation, Polymorph infiltration Abscess formation

Page 21: 8_ IMUNOLOGI INFEKSI

Bacterial toxins have been largely identified as enzymatic in nature and the antibody in some way is able to interfere with the ability of the enzyme to interact with its substrate.

This idea is supported by the finding that antibody is much more effective against enzymes which have high molecular weight substrates that it is against those with low molecular weight substrate.

Page 22: 8_ IMUNOLOGI INFEKSI

This means that a bacterium coated with antibody and complement will adhere to a phagocytic cell and become susceptible to phagocytosis.

The phagocytic cell in many instances can then digest the microorganism by secreting into the phagocytic vacuole a variety of digestive enzymes carried in the intracellular lysosomes.

The streptococcus carries, as part of its cell wall, a substance known as M protein, which confers the ability to resist digestion by the enzymes.

Page 23: 8_ IMUNOLOGI INFEKSI

Enteric infections such as those due to Salmonella typhi or Vibrio cholerae, antibodies can be secreted into the intestinal lumen and attack the organism before it invades the intestinal mucosa.

The IgA immunoglobulin is selectively produced in intestinal and respiratory mucous membranes.

Page 24: 8_ IMUNOLOGI INFEKSI

T - Lymphosit – macrophage relationships

Natural Killer cell

T LymphositeIL-2 prodn

Macrophage

Altered tissue cell

(virus or Tumor)

Direct cytotoxic effect (NK cell)

Direct cytotoxic effect (Tc cell)

Production of cytotoxic factors

Chemotactic factor

macrofag inhibitory factor

macrofag activation factor

B cells

Kills along with antibody (ADCC)

Direct Effects of Ab

Processed antigen

Presented to T cell

Interleukin 1

Lymphocyte activating factorInterferon Antigen

Activated macrophag kills intracellular microorganisms

Microorganism

Page 25: 8_ IMUNOLOGI INFEKSI

IMMUNE COMPLEXES IN VIRAL INFECTIONSIn infections of humans by hepatitis B virus the surface

antigens are shed into the blood stream and form complexes with antibody.

Persisting levels of hepatitis B antigen can lead to immune complex mediated damage such as polyarteritis nodosa and glomerulonephritis.

In Epstein Barr virus infections viral antigens have been found in immune complexes in the kidneys of patients with Burkitt’s lymphoma.

Deposition of complexes in the choroid plexus has been suggested as underlying behavioural disorder in asymptomatic virus infections.

Page 26: 8_ IMUNOLOGI INFEKSI

The humoral immune response is probably the predominant form of immunity responsible for protection from reinfection by viruses.

For this reason immunisation procedures aim at producing circulating or mucous membrane antibody.

In volunteers infected with influenza virus a correlation was found between cytotoxic T cell activity and diminished shedding of virus.

Page 27: 8_ IMUNOLOGI INFEKSI

Schematic view of virus infection and immune response, indicating some possible consequences

Virus Mucous membrane

Virus in blood stream

Virus infection target cell (viral replication)

Virus specified changes in cell surface

Release of new formed virus

Stimulation of humoral and cell mediated immunity to altered surface antigen

If target cell is component of immune system then alteration in immune reactivity

Stimulation of local IgA

Antiviral IgG immunization on passive administration

Neutralization of virus

Neutralization of virus

PROTECTION

PROTECTION

Neutralization of virusFormation of toxic complexes

PROTECTIONHYPERSENSITIVITY

Removal of virus infected cellsDamage to tissue cells

PROTECTION

HYPERSENSITIVITY

Inhibition of immune responseFailure of self tolerance

PERSISTENCE OF VIRUSLOSS OF IMMUNE SURVEILLANCE

? AUTOIMMUNITY

Page 28: 8_ IMUNOLOGI INFEKSI

SCHEME SHOWING THE ROLE OF Ig E AND EOSINOPHILS IN HELMINTH IMMUNITY

HELMINTH ANTIGENS

T LYMPHOCYTES

LYMPHOKINES

EOSINOPHILSITUATION

Ig E STIMULATION

MAST CELL +Ig E

Ig G, Complement, Leucocytes at site

of infection

EosinophilIg G

Helminth

EOSINOPHIL

Chemotactic factorMediators of infllammtion

Destraction of parasite

Page 29: 8_ IMUNOLOGI INFEKSI

Summary of role of B and T cells in infection

Antigens of microorganism

B cells T cells

Clonal expansion

Antibody producing cells

Antibody in blood lymph, tissue fluids mucous membranes

Clumping OpsonisationLysis of

microorganismInflammation chemotaxis

Memory cells

Lymphoid tissues and

blood

Respond to subsequent exposure

to microorganism

Clonal expansion

Cytotoxic T cell

Production of Immunoregulatory

substance

Memory cells

Macrophague activation and

localization

Chemotactic inflammation

Interferon

NK cell

Page 30: 8_ IMUNOLOGI INFEKSI