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Mekanisme Infeksi

(Keperawatan)
Oleh : Joni Haryanto

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Joni Haryanto, S.Kp., MSi., Dr. Kep
Lecturer Nursing Faculty. UA Surabaya
Chairman of the Commission for Health Research Ethics
Chairman of Legal & Politics Division of Nursing Organization in
East Java
Member of Elderly Regional Commission Prov. East Java
Member of Community Nursing Collegium Indonesia
Member of the Gerontological Advance Practice Nurse
Association (GAPNA)
Practitioner of Nursing Complementary & Alternative
Chief of Diploma Program of Nursing

E-mail: joni.h.unair@gmail.com
WA: +6289630281001
HP: +6281357431666

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Pendahuluan

• Infeksi merupakan proses invasi dan


multiplikasi berbagai mikroorganisme
ke dalam tubuh (seperti bakteri,
virus, jamur, dan parasit), yang saat
dalam keadaan normal,
mikroorganisme tersebut tidak
terdapat di dalam tubuh

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Humoral Immunity

• Active humoral immunity:


– B-cells encounter & respond to antigen
to produce an antibody

• Passive humoral immunity:


– Introduced “non-native” antibody

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Active Humoral Immunity
• Naturally acquired: natural exposure to
antigen (i.e. infection)
• Artificially acquired: vaccines;
dead/attenuated or fragmented pathogen
injected to elicit an immune response
– Bestow immunity without disease; primary
response
– Booster shots (secondary response); intensify
response
– Shortcomings – adverse reactions & the
immunity is less durable (poor memory) & has
less cell mediated component
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Passive Humoral Immunity
• Natural: maternal antibody crosses the
placental barrier conferring temporary
immunity to the baby (degrades after a
few months)

• Artificial: antibodies harvested from an


outside source given by injection protect
from immediate threat but no memory is
formed (antitoxins, antivenins , gamma
globulin, etc.)

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Respon Imun Humoral
• Bersifat tdk lgs dan dilaksanakan oleh imunoglobulin spesifik
(antibodi) yang dihasilkan sel B aktif (sel plasma) & dibantu
o/sistem komplemen
– IgG (gama) plg banyak di tubuh, mampu menembus
plasenta melindungi tbh dr bakteri
– IgM plg besar bertanggung jawab dalam respon imun
primer
– IgA tdpt dlm sekresi tbh; kolostrum, air mata, air liur,
sekresi sal nafas, GIT, sal kemih. Fgs utama
mempertahankan permukaan mukosa thd virus dan
bakteri
– IgE melekat ke sel mast dan basofil, terlibat dalam reaksi
hipersensitifitas tipe I
– IgD tdpt dlm jml kcl di serum, kemungkinan mempengaruhi
defisiensi limfosit B kendati peranannya blm jelas

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• IgG merupakan komponen utama didalam Ig serum
dengan kadar di dalam darah sekitar 75 % dari semua
immunoglobulin. IgG dapat menembus plasenta dan
masuk ke fetus dan berperan dalam imunitas bayi
sampai berusia 6-9 bulan. IgG dan komplemen
bekerja saling membantu di dalam sebagai opsonin
pada pemusnahan antigen. IgG juga berperan di
dalam imunitas sellular.

• IgA ditemukan dalam jumlah yang sedikit didalam


darah. IgA di dalam serum dapat Amengagglutinasi
kuman. Mengganggu motilitasnya
hingga memudahkan fagositosis oleh sel PMN.

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• IgM merupakan antibody dalam respon imun primer
terhadap kebanyakan antigen. IgM dapat mencegah
gerakan mikroorganisme patogen, memudahkan
fagositosis dan merupakan aglutinator poten protein.

• IgD ditemukan dengan kadar yang sangat rendah


didalam sirkulasi. IgD merupakan 1% dari total
immunoglobulin dan ditemuksan banyak pada sel
membran sel B bersama IgM dan berfungsi sebagai
reseptor pada aktivasi sel B.

• IgE ditemukan dalam serum dengan kadar yang


rendah di dalam serum dan meningkat pada penyakit
alergi, infeksi cacing.

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Fungsi Imunoglobulin
• Menyebabkan sitotoksisitas
• Memungkinkan imunisasi pasif
• Meningkatkan opsonisasi (pengendapan
komplemen pd suatu antigen shg kontak
lekat dg sel fagositik mjd lbh stabil)
• Mengaktifkan komplemen
• Dapat menyebabkan anafilaksis

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Fungsi utama Komplemen
1.Menyebabkan lisis sel
komplemen berinteraksi satu sama lain
membentuk membrane attack complex
(MAC) di permukaan sel sasaran =>
memasukkan molekul pembuat pori di
membaran sel imunogen => membran
rusak => air dan elektrolit masuk sel =>
sel pecah dan mati

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Fungsi utama Komplemen
2.Pembentukan berbagai mediator
imun, berperan dalam proses
peradangan
3.Opsonisasi ; sel fagositik akan lbh
mampu menelan apabila bahan
imunogen dilapisi komplemen.
=> ex; histamin, bradikinin

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Adaptive, Humoral Immunity
• Antigen = any substance that can mobilize the immune
system & provoke an immune response*
*Humoral and/or cell mediated

• Complete antigens (proteins, nucleic acids, lipids,


polysaccharides):
• Immunogenicity: the ability to stimulate specific
lymphocytes & specific antibodies
• Reactivity: the ability to react with activated lymphocytes &
antibodies

• Hapten (an incomplete antigen): a smaller molecule


that is not immunogenic until attached to proteins

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Adaptive, Humoral Immunity
• Antigenic determinants: sites on an antigenic molecule that are
immunogenic
– Epitope

• Major Histocompatibility Complex (MHC): cell surface


glycoproteins associated with self recognition
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Antibodies
• A.K.A Immunoglobulin's & gamma globulins
• Structure
– variable
– hypervariable
– constant

Antibody Classes:
IgM, IgG, IgA, IgD,
IgE (Ig =
immunoglobulin)

Figure 21.13a
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Antibodies
• Constant (C) region defines antibody class
• Determines chemical & cellular interactions
• Determines how class functions to eliminate antigens

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Antibody Classes

• IgG: the most abundant circulating Ig. The dominant


circulating Ig of the primary & the secondary response.
Crosses the placenta. Complement binding
(Monomer).

• IgA: the Ig of secretions. Helps prevent antigen


penetration of membranes (Dimer).

• IgD: the Ig of B-cell activation. Found on B-cell


surface (Monomer).

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Antibody Classes
• IgM: occurs as a monomer & a pentamer

– Occurs on the B-cell surface (Monomer).

– The Ig of early primary plasma cell response,


circulating antibody; a potent agglutinator.
Complement binding (Pentamer).

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Antibody Classes
• IgE: the Ig associated with allergies.
– Stem binds to mast cells & basophiles.
– Receptor binding results in histamine release &
inflammation.
– Found mostly in mucosa of respiratory & GI tract
(Monomer).

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Antibody Targets & Functions
• Immune complex formation = antigen-antibody binding.

• All the following events are initiated by antigen-antibody


binding.
• Complement fixation:
• Neutralization:
• Agglutination:
• Precipitation:
• Inflammation & phagocytosis prompted by debris
 Monoclonal antibodies: antibodies produced by
descendants of a single cell
 Pure antibody preparations that are specific for a single
antigenic determinant
 Research / diagnostic / therapeutic use
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Antibody Targets & Functions

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Respon Imun Seluler

• Respon imun yang dilaksanakan


oleh limfosit T
• Peran sel T ;
– Fungsi pengendali; sel T penolong /CD4
(cluster of deferentiation 4)
– Fungsi pelaksana; sel T sitotoksik
(pemusnah) / CD8 => mampu
mematikan sel terinfeksi virus, sel
tumor

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Fungsi Sel CD4

• Pengendali ; mengaitkan sist monosit-


makrofag ke sist limfoid
• Berinteraksi dg sel penyaji antigen untuk
mengendalikan ig
• Menghasilkan sitokin yang memungkin
tumbuhnya sel CD4 dan CD8
• Berkembang menjadi sel pengingat

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Tipe Imunitas
• Imunitas alami
– Aktif=> didapat stlh sembuh dari peny
(ex; cacar air)
– Pasif => antibodi yang sdh jadi
diperoleh bayi mll plasenta atau
kolostrum
• Imunitas buatan
– Aktif => pembentukan stlh vaksinasi
– Pasif => imunitas yang sdh jadi (ex;
antitoksin tetanus)

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Regulasi Sistem Imun
• Regulasi sistem imun atau imunoregulasi
adalah pengendalian respon dan interaksi
imun spesifik antara limfosit B dan T serta
makrofag.
• Pada dasarnya keutuhan tubuh
dipertahankan oleh dua sistem
pertahanan yaitu sistem pertahan tubuh
non spesifik (natural) dan spesifik
(adaptive).

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Immune System

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Fig 21.1
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Innate Immune System
• Innate: structural defenses; responds to nonspecific
foreign substances
– First line: external surface epithelium & membranes
– Second line: inflammatory processes – antimicrobial proteins,
phagocytes, etc.

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Adaptive Immune System
• Adaptive: responds to specific foreign substances

Innate & adaptive mechanisms work together


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Jaringan idiopatik

• Jaringan dalam biologi adalah sekumpulan sel yang


memiliki bentuk dan fungsi yang sama. Jaringan-
jaringan yang berbeda dapat bekerja sama untuk
suatu fungsi fisiologi yang sama membentuk organ.
Jaringan dipelajari dalam cabang biologi yang
dinamakan histologi,

Idiopatik berarti penyebabnya tidak diketahui.

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Fibrosis Pulmoner Idiopatik

• Pembentukan jaringan parut,


penebalan dan peradangan pada
jaringan paru yang penyebabnya
tidak diketahui.

• Fibrosis paru dapat disebabkan oleh


berbagai penyakit, terutama yang
berkaitan dengan kelainan sistem
kekebalan

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Innate, Internal Defenses:
Inflammation
Tissue response to injury
Triggered by injury – trauma, heat, chemical
irritation, infection, etc.
Beneficial effects
Prevents spread of injury
Disposes of cellular debris & pathogens
Promotes repair

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Innate, Internal
Defenses: Inflammation
• Cardinal signs of inflammation
– Redness
– Heat
– Swelling
– Pain
– (Functional impairment rigor)

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Innate, Internal
Defenses: Inflammation
• Inflammatory response: signs are
associated with vasodilation &
increased vascular permeability.
– Dilation: redness, heat
– Permeability: edema, (increased
pressure) pain
– Pain also associated with bacterial
toxins & some mediators (kinins, PGs)

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Innate, Internal Defenses:
Inflammatory Response
• Mechanisms causing vasodilation &
vascular permeability
– Injured cells release inflammatory
mediators
• Histamines
• Kinins
• Prostaglandins
• Complement
• Cytokines (also activated by receptors on
macrophages in response to microbial
glycocalyx)

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Innate, Internal Defenses:
Inflammatory Response
• Edema
– Dilutes harmful substances
– Provides nutrients (& O2) for repair
– Enhances entry of clotting protein

• Epithelial breaches also stimulate b-


defensin release from epithelial cells

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Figure 21.3

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Innate, Internal Defenses:
Inflammatory Response
• Phagocyte mobilization: infiltration of damaged
area by neutrophils & macrophages

 Leukocytosis: leukocytosis inducing factors released by


injured cells promote rapid release of WBCs from
marrow
 Margination: increased vascular permeability causes
decreased fluid in vessels; blood flow slows &
neutrophils are able to move to vessel margins. Here
endothelial markers (CAMs) allow neutrophils to cling
to vessel walls (pavementing).
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Innate, Internal Defenses:
Inflammatory Response
• Diapedesis: neutrophils migrate through
capillary walls
• Chemotaxis – inflammatory chemicals
attract neutrophils to move up the
chemical concentration gradient
(neutrophils respond first)
• As the process continues, monocytes
diapedes into the area & become
macrophages. With chronic inflammation,
macrophages predominate

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Inflammatory Response: Phagocytic
Mobilization

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Innate, Internal Defenses: Inflammatory
Response
• Macrophages clean up cellular debris & pathogens
• If pathogens were associated with the injury,
activation of the complement cascade occurs &
elements of adaptive immunity join the process
Viral replication – (viruses lack metabolic processes)
Viruses release nucleic acid (RNA or DNA) into
cytoplasm.
The information on the nucleic acid is incorporated into
the cell’s DNA. Normal cellular mechanisms then
produce viral structural components.
Multiple new viral particles are produced & released from
the cell (sometimes killing the cell)
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Reaksi hipersensitivitas

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Reaksi hipersensitivitas
TIPE 1
• Diperantarai Ig E
• Ig E mengikat antigen ( Allergen )
• Ig E melekat pada receptornya pada
basofil- mast cell dan menyebabkan
lepasnya mediator inflamasi
• Mediator inflamasi akan menyebabkan
tubuh mengalami perubahan

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Penyakit pada HS tipe 1

• Sistemik anafilaksis
• Asthma
• Eczema
• Allergy makanan
• Urticaria

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Reaksi hipersensitivitas
TIPE 2
• Di perantarai oleh Ig G dan Komplemen
• Antigen pada permukaan sel akan
merangsamg melekatnya IgG
• Berikutnya IgG akan merangsang
melekatnya komplemen
• IgG dan komplemen akan melekat pada
Limfosit T sitotoksik yang berakibat
kerusakan pada sel tersebut

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Penyakit pada HS Tipe 2

• Reaksi Tranfusi
• Eritroblastosis Foetalis
• Anemia hemolitik autoimun

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Penyakit pada HS tipe 3

• Reaksi Arthus
• Serum sickness
• Glomerulonephritis
• Rheumatoid arthritis
• Sistemik Lupus Erithromatosus

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Reaksi hipersensitivitas TIPE 4

• Diperantarai oleh sel


• Antigen akan mengaktivasi sel T
melepaskan mediator, Mediator akan
merangsang aktivasi Makrofag atau
Limfosit T sitotoksik
• Makrofag atau T sitotoksik akan
merusak sel atau jaringan

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Penyakit pada HS tipe 4

• Dermatitis kontak
• Lesi Granuloma
• Graft Rejection

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Penyakit Autoimun
• Antibodi atau sel T melawan self antigen
• Interaksi antibodi atausel T terhadap
jaringan berpengaruh pada proses
penyakit
• Terjadi disfungsi imun
• Penyakit bisa tertranfer melalui AB atau sel
T

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Penyakit Autoimun
Sistemik
Organ spesifik
• Rheumatoid
arthritis
• Grave disease
• Scleroderma
• DM tipe 1
sistemik
• Myasthenia gravis
• SLE

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Penutup

Terimakasih atas perhatian


semuanya

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