Professional Documents
Culture Documents
of infection
Microbe
No infection
Entry of agents
pathogenic action
Portals of Entry
Skin
Mucous membrane
Respiratory, gastrointestinal, urinary,
reproductive tracts
Conjunctiva, the thin membrane covering
the surface of the eyeball and the
underside of each eyelid
Placenta
(Parenteral route)
Is not a portal entry, but instead a means
by which the portals of entry can be
circumvented
Colonization
To colonize a site populated by normal flora,
the new arrival must compete successfully
with:
established organisms for space and
nutrients (siderophores)
overcome their toxic product
counter the bodys defenses aimed at
protecting the surfaces (IgA proteases)
Adhesion / Attachment
The process by which microorganisms
attach themselves to cells
Adhesion factors:
Specialized structures
Adhesion disk (protozoa), suckers, hooks
(helminthes)
Ligands: Surface lipoprotein and
glycoprotein (bacteria, viruses)
Adhesin (bacteria): found on fimbrae,
flagella, glycocalyses
Attachment protein (viruses)
Adherence mechanism
factors support the adherence mechanism
Virulence
Degree of pathogenicity
Virulence factors
A variety of traits that interact with a host and enable
the pathogen to enter a host, adhere to host cells,
gain access to nutrients, and escape detection or
removal by the immune system
Virulence Factors
Extracellular Enzymes (Hyaluronidase and
collagenase, Coagulase, Kinase)
Toxin (Exotoxin, endotoxin)
Antiphagocytic factor (capsule, antiphagocytic
chemical)
Invasion factor
Siderophore
Lipopolysacharides
Virulence Factors
Extracellular Enzymes
Hyaluronidase and
collagenase degrade specific
molecules to enable bacteria
to invade deeper tissue
Coagulase --- coagulate blood
protein --- form clot --
providing a hiding place for
bacteria within a clot
Kinase such as
staphylokinase and
streptokinase digest blood
clots
Virulence Factors
Toxins
Exotoxin
Cytotoxins: kills host cells in
general or affect their function
Neurotoxins: specifically
interfere with nerve cell function
Enterotoxins: affects cell lining
the gastrointestinal tract
Endotoxin
Lipid A, lipid portion of the
membranes lypopolysaccharide
Toxin Nomenclatur : has no systematic basis
Lyses cells
Capsules
Composed of chemicals that are normally
found in the body (including
polysaccharides) do not stimulate a
hosts immune response
Protect the bacteria from the host
inflammatory response (complement
activation and phagocyte mediated killing)
Capsules prevent formation of C3
convertase
Antiphagocytic chemicals
Prevent the fusion of lysosomes with
phagocytic vesicles, which allows the
bacteria to survive inside of phagocytes
S.pyogenes produces a protein on its cells
wall and fimbrae (M protein), that resist
phagocytosis and thus increases virulence
Virulence Factors
Invasion factors
Severity of disease
Cytopathic ability of virus
Immune status
Competence of immune system
Prior immunity to the virus
Immunopathology
Virus inoculum size
Length of time before resolution of infection
General health of the person
Nutrition
Other diseases influencing immune status
Host genetic makeup
Age
Tahap-tahap dalam patogenesis infeksi
virus
1. Masuknya virus dan replikasi primer
2. Tropisma dan penyebaran virus dalam tubuh
3. Kerusakan sel/ jaringan dan manifestasi
klinis
4. Pemulihan dari infeksi dan tipe infeksi
5. Penyebaran virus ke luar tubuh/ lingkungan
Virus spread in human body
Tahap-tahap dalam patogenesis infeksi
virus
1. Masuknya virus dan replikasi primer
- Jalan masuk
- replikasi primer pada tempat masuk
- masa inkubasi
2. Tropisma dan penyebaran virus dalam tubuh
- Mekanisme penyebaran dalam tubuh
bervariasi: aliran darah, limfatik, saraf
perifer, antar sel
- spesifik jaringan/ sel
- Faktor-faktor sel/ jaringan dan faktor-
faktor virus yang mempengaruhi tropisma
- reseptor spesifik
- ekspresi gen virus
- enzim yg diperlukan untuk replikasi virus
Tropisma
Receptor & co-receptor Hemaglutinin dan neuraminidase of
Of HIV influenza virus
Binding of a virus to its receptor on the host cell
surface result in penetration of the cell or the delivery
of virus nucleic acid to the cytoplasm of the cell
Cytopathic viruses
Ultimately kill the host cell, the result is often local necrosis
Can trigger apoptosis or programmed cell death
Noncytopathic viruses
Do not immediately produce cell death and result in latent or
persistent infections
Productive: virus produce persistent infection with the release of
only a few new viral particles at a time
Non-productive: viruses do not actively make virus at detectable
levels for a period of time (latent infection)
3. Kerusakan sel/ jaringan dan manifestasi klinis
- Iceberg concept of infection : tipe
respons sel/ pejamu terhadap infeksi
- Lokal, sistemik
- Jaringan tertentu lebih tahan thd
kerusakan dibandingkan lainnya (misal
jar.usus vs otak)
- Mekanisme pertahanan tubuh dan proses
imunopatologis
Syncytia in paramyxovirus infection
Neoplasia:
The phenomenon of uncontrolled cell division
Cell undergoing neoplasia are said to be neoplastic, and
a mass of neoplastic cells is a tumor
Tumor: benign and malignant
Protooncogenes: genes
that play a role in cell
division
VIRUS KANKER
Virus RNA
Virus Hepatitis C Karsinoma hepatoseluler
HTLV-1 ATL
Virus DNA
Virus hepatitis B Karsinoma hepatoseluler
Virus papilloma manusia Papilloma dan karsinoma
Herpes virus 8 Sarkoma Kaposi
Virus Epstein Barr Limfoma Burkitt,
ca nasofaring
Oncogenic viruses :
- Establish persistent infection
- Stimulate uncontrolled cell growth transformation and
immortalization
Usually the first step but not sufficient to cause oncogenesis / tumor
formation
Immortalization accumulation of mutations/
chromosomal rearrngement tumor
Immortalization more susceptible to co-factors tumor
Adenovirus E1A,
SV40-LT, HPV16&18 E7
-- bind to Rb-related proteins