Download - Imunodefisiensi Fix

8/3/2019 Imunodefisiensi Fix

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IMMUNODEFICIENCY

10703038 10704025 10705001 10705002 10705004 10705028 10705100 10705104 10705120

10705122 10705057 10705019 16207715 10705072 10705026 10705064 10705071 1070504110705008 10705046 10705013 10705113 10705045 10705007 10705053 10705068 1070506910705049 10704062 10704109


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IMMUNODEFICIENCY

Immune disorder

Immune system fails to develop normally orthe immune response is blocked in some way.

Results from:

- embryological developments

problem/ lymphoid organs and

tissues

- infection with virus depress immune function

- treatment/exposure to immunosuppressive agents


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IMMUNODEFICIENCY

Deficiency ofinnate immune mechanism

Complement system deficiencies

Primary immunodeficiencyB-cell deficiency

T-cell deficiency

Combined immunodeficiency

Secondary immunodeficiency

Acquired immunodeficiency syndrome(AIDS)


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IMMUNODEFICIENCY

Primary immunodeficiency

These occurin the human, although somewhat

rarely, as a result of a defect in almost any stage of

differentiation in the whole immune system.

Secondary immunodeficiency

Immunodeficiency may arise as a secondary

consequence of malnutrition, lymphoproliferativedisorders, agents such as X-rays and cytotoxicdrugs, and viral infections.


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PRIMARY IMMUNODEFICIENCYB-cell deficiency

IgA deficiency & Common VariableImmunodeficiency (CVID)

Most common primary immunodeficiencies,represent the extreme ends of a spectrum ofimmunoglobulin deficiencies.

Transient hypo--globulinemia

Immunoglobulin deficiency occurs naturally inhuman infants maternal IgG level . seriousproblem in very premature babies recurrentrespiratory infections, is associated with low IgGlevels which often return somewhat abruptly to

normal by 4 years of age.


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PRIMARY IMMUNODEFICIENCY

T-cell deficiency

No T-cells or poor T-cell function:

- vulnerable to opportunistic infections

- impacts negatively on humoral immunity

- dysfunctional T-cells permit the emergence of

allergies, lymphoid malignancies & autoimmune

syndromes.

Due to: inefficient negative selection in the thymus or

the failure to generate appropriate regulatory cells.


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PRIMARY IMMUNODEFICIENCY

Combined Immunodeficiency

Severe combined immunodeficiency disease (SCID)

involving B-, T- and NK cells.

represents the most severe form of primaryimmunodeficiency defects in cellular and humoralimmunity.

+ severe and recurrent opportunistic infections death.


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SECONDARY IMMUNODEFICIENCY

Immune responsiveness can be depressednonspecifically by many factors.

CMI in particular may be impaired in a state ofmalnutrition. Iron deficiency is particularly important

in this respect, as are zinc and seleniumdeficiencies.

Case

In lepromatous leprosy and malarial infection,

constraint on immune responsiveness imposed bydistortion of the normal lymphoid traffic pathwaysdysfunction of macrophage

Imbalance between Thl and Th2 cells: result ofinfection depress the subset most appropriate for

immune protection.


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RECOGNITION OFIMMUNODEFICIENCY

o Defects in immunoglobulinsquantitative.

2g/L lower limit of normal.

o The humoral immune responsescreening the serum for natural antibodies (Aand B isohemagglutinins, bactericidins against E.coli) attempting to induce active immunizationwith diphtheria, tetanus, pertussis and killedpoliomyelitis-but no live vaccines. CD19, 20 and22 markers enumerate B-cells byimmunofluorescence.


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RECOGNITION OFIMMUNODEFICIENCY

o Patients with T-cell deficiency

hypo- or unreactive in skin tests to such

antigens Active skin sensitization withdinitrochlorobenzene.

o Complement, bactericidal and otherfunctions of polymorphsIn vitro tests.Reduction of nitrobluetetrazolium (NBT) / stimulation of superoxideproduction measure of the oxidative enzymesassociated with active phagocytosis.


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ACQUIRED IMMUNODEFICIENCYSYNDROME

AIDS results from infection by the RNA

retroviruses HN-1 and HN-2.

HIVinfects T-helper cells throughbindingof its envelope gp120 to CD4 and eitherCCR5 or CXCR4 chemokine receptorcofactors. It also infectsmacrophages,microglia, T-cell-stimulating dendritic cells.

chemokines: A family of structurally-related cytokines which selectively induce chemotaxis and activation

of leukocytes. They also play important roles in lymphoid organ development, cell compartmentalizationwithin lymphoid tissues, Th1 /Th2. development, angiogenesis and wound healing.


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Target


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Inti

Gp120

Envelop

HIV


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HIVs Structure

gp120

gp41

Envelop nucleus

p17

p24

p7/p9

RT

Integrase

Protease

RNA HIV

Diploid single

strand

Enzymes


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Siklus Hidup HIV dalam Limfosit-T (CD4)

HIV

RNA

DNA

ds DNA

RT

Integrase

Transkripsi

Proviral DNA

Spliced mRNA

mRNA

Genomic RNA

Polyprotein

Protein

Protease

1

2

3 4

5

6

7

Virion Matang


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AIDS

TheRNAis convertedby thereversetranscriptase to DNA incorporated intothe host's genome dormant until the cell

is activated by stimulators such as TNF.

There is usually a long asymptomatic phaseafter the early acute viral infection has

been curtailed by a CD8CTL immuneresponse. Virus to the lymphoid follicles destroys the dendritic cell meshwork.


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Long asymptomatic phase


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AIDS

CD4 T-helpers, destroys cell mediateddefenses life threatening infections throughopportunist organisms such as Pneumocystiscariniiand cytomegalovirus.

Infection suppresor factors released by Tsinhibit an immune response before Thstimulating the formation of Tc/plasma cell inadequate number.

Immune system VS virus extremely highrates of viral destruction and CD4 T-cellreplacement.


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AIDS

CD4 T-cell depletion: as a result of directpathogenicity, syncytium formation,susceptibility to apoptosis and possiblyother mechanisms.

AIDS: diagnosed in an individual withopportunistic infections, by low CD4 butnormal CD8 T-cells in blood, poor delayed-type skintests, positive tests for viralantibodies and p24 antigen, lymph nodebiopsy and isolation of live virus ordemonstration ofHNgenome by the PCR.


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AIDS

Highly active antiretroviral drug therapy(HAART), combining inhibitors of reversetranscriptase and protease, can eliminatedetectable virus early in disease, althoughlatent virus remains.

Vaccines are being targeted to Th1responses but it is a very difficult virus to

control.


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HIV/AIDS


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Apa ituHIV/AIDS??


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Inti

Gp120

Envelop

HIVH : HumanI : ImmunodeficiencyV :Virus


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Struktur HIV

gp120

gp41

Envelop Inti

p17

p24

p7/p9

RT

Integrase

Protease

RNA HIV

Diploid single

strand

Enzim-enzim


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Target


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AIDS ?

Acquired

ImmunoDeficiency

Syndrom

Didapat

KekebalanPenurunan

Kumpulan

Gejala


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Siklus Hidup HIV


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Mekanisme CD4

Mekanisme pembunuhan sel T-CD4+ telahditeliti secara in vitro pada kelompokLentivirus.

Langsung (Direct)

Tidak Langsung (Indirect)

Mekanisme Lain


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Replikasi virus HIV


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Di bagian tubuh mana HIVberada?


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cairan sperma

darah

HIV didapatkan di

cairan vagina

air susu ibu


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Bagaimana Cara

Penularannya?


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HolmesGoldwater, Network

Hubungan Seks Transfusi darah

Hubungan perinatal (ibu ke janin)

Penggunaan jarum suntik yang

pernah dipakai orang lain


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Resiko penularan per paparan

Transfusi ~80 %Ibu ke anak 1:4

Seks anal (reseptif) 1:30 -1:125

Penasun bersama 1:150

Tertusuk jarum 1:313(petugas kesehatan)

Seks vaginal (reseptif) 1:700

1:2000Seks vaginal (insertif) 1:1000 -1:3000

Terpercik ke sel lendir


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HIV/AIDS tidak menular

melalui


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KONTAK SOSIAL

HIVTIDAK MENULAR MELALUI


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Ciri-ciri Orang dengan HIV+


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PERKEMBANGAN DARI HIV MENJADI AIDS:

3 - 6 BULAN

PeriodeJendela

3 - 10 TAHUN 1 - 2 TAHUN

Tertular

HIV + AIDS


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Hanya dua cara untuk tahu bilaorang itu HIV positif

Orang itu memberitahukan kepada kita.

Melihat tes HIV

Jumlah CD4 yang rendah dengan jumlah CD8sel T yang normal.

Ditemukan antibodi viral dan antigen P24.


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Statistika tentang AIDS


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Penderita HIV-AIDS berdasarkan GolonganUmur Di Kota Bandung Tahun 2007

Berdasarkan kelompok usia, maka kalangan remaja antara 20-29 tahun

merupakan jumlah terbanyak yaitu 67.06 %

GOLONGAN UMUR

30 - 39 th

20.13%

40 - 49 th

4.97%

15 - 19 th

4.55%0 - 14 th

2.27%

50 th

1.01%

20 - 29 th

67.06%


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Penderita HIV-AIDS berdasarkan Profesidi Kota Bandung Tahun 2007

PEKERJAAN

TIDAKDIKETAHUI

3.71%

SWASTA

19.80%

BURUH

KASAR

0.25%

LAIN-LAIN

0.67%IRT

5.98%

MAHASISWA

20.22%

PEKERJA SEX

9.01%

PNS

2.11%

SUPIR

0.25%

TIDAK

BEKERJA

16.01%

WIRASWASTA

21.99%


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Penderita HIV-AIDS berdasarkan Faktorresiko di Kota Bandung Tahun 2006

FAKTOR RESIKO

HOMOSEKSUAL

6.32%

HETEROSEKSUAL

23.08%

PERINATAL2.02%

TIDAK DIKETAHUI

1.26%

IDU

67.31%


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Bagaimana CaraPengobatannya?


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Highly Active Antiretroviral DrugTherapy (HAART) menggabungkaninhibitor reverse transkriptase dan

protease

Dapat mengeliminasi virus pada

tahap awal penyakit namun viruslaten bertahan


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Terima Kasih !