Bakteri sebagai agen infeksi

Contamination, infection and disease-

• Contamination-microorganisms are present.

• Infection- multiplication of any parasitic organism within
or upon the host’s body-does not necessarily result in
disease
• Disease- disturbance in the state of health wherein the
body cannot carry out all its normal functions
• Communicable- can be spread from one host to another.
• Contagious diseases- communicable diseases that are
more easily spread than others-such as, influenza,
common cold, rubella.
• Noncommunicable infectious disease- are not readily
spread from one host to another, e.g., tetanus,
botulinum, legionellosis,
 Definisi
 Definisi-definisi
Adherence pelekatan(adhesion, attachment): proses
dimana potongan bakteri melekat pada permukaan sel
inang.

Infeksi adalah multiplikasi agen yang bersifat infeksius

di dalam tubuh.

Multiplikasi bakteri—flora normal pada saluran

gastrointestinal, kulit, umumnya bukan suatu infeksi.

Multiplikasi bakteri patogenik (mis. Salmonella sp.),

dalam tubuh, walaupun tidak menimbulkan
gejala/simptom dianggap infeksi.
Karier: orang atau hewan dengan infeksi tanpa
gejala/simptom yang dapat ditularkan dengan mudah kepada
orang/hewan lain.
Invasi: proses dimana bakteri, parasit hewan, fungi, virus
masuk ke dalam sel inang atau jaringan dan menyebar dalam
tubuh.
Non-patogen: mikroorganisame yang tidak menyebabkan
penyakit (flora normal)
Patogen: mikroorganisame yang dapat menyebabkan
penyakit.
Patogenesitas: kemampuan agen infeksius yang
menyebabkan penyakit.
Toksigenesitas: kemampuan suatu organisme menghasilkan
toksin yang mengkontribusi perkembangan penyakit.
Virulensi: kemampuan secara kuantitatif suatu
agen (mikroorganisme) yang menyebabkan
penyakit. Agen yang virulen menyebabkan
penyakit jika masuk ke dalam inang dalam jumlah
kecil. Virulensi melibatkan invasi dan
toksigenesitas.

Kolonisasi: bila suatu bakteri yang ada terus

menerus di dalam tubuh dan tidak menyebabkan
penyakit.
Contoh: resident microflora
Pathogenecity

Virulensi
bakteri

Jumlah • The "objective" of bacteria is to

bakteri
multiply rather than to cause
disease; it is in the best interest of
the bacteria not to damage or kill
the host.
Sistem imun
hospes • A disease ensues when the
balance between bacterial
pathogenicity and host resistance
is upset
 Pathogenic bacteria can be grouped into three
categories on the basis of their invasive properties for
eukaryotic cells:
 Extracellular
 Obligate Intracellular
 Facultative Intracellular .
• Bacteria cause disease by 2 basic mechanisms
1. Direct damage of host cells
2. Indirectly by stimulating exaggerated host inflamamatory
/ immune respone
 Microbial Mechanisms of
Pathogenicity: How Microorganisms
Cause Disease
Faktor virulensi bakteri

 Virulence factors that promote bacterial colonization

of the host:
Adherence
Capsule
Enzymes  leukocidins; Hemolysins; Coagulase;
Kinases; Hyaluronidase; Collagenase

 Virulence factors that damage the host. toxin

 the cell wall components that bind to host cells causing them to
synthesize and secrete pro-inflammatory cytokines and
chemokines.
 Toxins.
 Induce autoimmune responses.
 Ability to survive inside phagocytic cells
1. Adherence – hampir
semua patogen harus dapat
melekat pada jaringan host

Patogen memiliki
Binding Sites 
adhesins
ligands
Adhesins and ligands umumnya
berada pada pili atau Fimbriae

 Neisseria gonorrhoeae
 ETEC
(Entertoxigenic E. coli)
 Bordetello pertussis
Capsules
 Mencegah fagositosis
 untuk menempel
Streptococcus pneumoniae
Klebsiella pneumoniae
Haemophilus influenzae
Bacillus anthracis
Streptococcus mutans
Yersinia pestis

K. pneumoniae
 Spreading Factors

• "Spreading Factors" are a family of bacterial enzymes that affect

the physical properties of tissue matrices and intercellular spaces,
thereby promoting the spread of the pathogen.
• Hyaluronidase - depolymerize hyaluronic acid, the interstitial
cement substance of connective’ tissue; produced by streptococci,
staphylococci, and clostridia.
• Collagenase - breaks down collagen; produced by Clostridium
histolyticum and Clostridium perfringens.
• Neuraminidase - degrades neuraminic acid (also called sialic acid)
present on epithelial cells of the mucosa; produced by Vibrio
cholerae, Shigella dysenteriae, P.multocida, and M.haemolytica
• Streptokinase and Staphylokinase - convert inactive plasminogen
to plasmin which digests fibrin.
• Edema Factor of B.anthracis - adenylate cyclase activity promote
bacterial invasion.
Leukocidins

• 1. merusak lekosit sehingga mencegah fagositosis

• 2. releases & ruptures lysosomes
• lysosomes - contain powerful hydrolytic enzymes which then cause more
tissue damage
 B. Hemolysins – melisis eritrosit

Streptococci
Alpha Hemolytic Beta Hemolytic
Streptococci Streptococci
- secrete hemolysins that - secrete hemolysins that cause
the complete lysis of RBC’s
cause the incomplete lysis or
RBC’s
 TOKSIN

• Exotoxin
• Endotoxin
Perbedaan relatif eksotoksin & endotoksin
-Sekret sel hidup, konsentrasi -Bagian integral dinding sel bakteri
tinggi pada medum cair gram -, dilepas seluruhnya pada
bakteri yang mati
-Dihasilkan oleh bakteri gram + & - -Dihasilkan oleh bakteri gram –

-Polipeptida, BM 104 – 9.105 -Lipopolisakarida kompleks,

-Labil, rusak pada suhu 60°C -Stabil

-Antigeniknya tinggi, menstimulasi -Immunogenik lemah
pembentukan antibodi
-Toksisitas tinggi, fatal bagi hewan -Toksisitas sedang
dalam jumlah besar
-Biasanya berikatan dengan -Tidak ada resetor spesifik
reseptor spesifik di dalam sel
-Tidak menunjukkan gejala demam -Menunjukkan gejala demam, IL-1

-Diubah menjadi antigenik, toksoid

dengan formalin, asam, panas
 Toxins
• Poisonous substances produced by microorganisms
• toxins - primary factor - pathogenicity
• 220 known bacterial toxins
• 40% cause disease by damaging the Eukaryotic cell membrane
• Toxemia
• Toxins yang masuk dan berada dalam darah
 Response to Toxins

• Jika terekspos eksotoksin : tubuh akan

mengeluarkan antibodi untuk melawan toksin
tersebut (antitoxins)
• Eksotoksin inaktif ( heat, formalin or phenol) 
tidak lagi menyebabkan penyakit, tetapi masih
dapat menstimulasi produksi antitoksin
• altered exotoxins - Toxoids
• Toxoids - diinjeksikan untuk menstimulasi produksi
antitoksin dan menimbulkan imunitas
Harmful effect of glycopeptides and techoid
acid released during gram-positive infections
• LPS of Gram-negative bacteria,
and teichoic acids and
glycopeptides of Gram-positive
bacteria induces cytokine
production and secretion
 Harmful Effects of LPS-Endotoxin
a. fever production
b. inflammation
c. tissue destruction
d. respiratory distress
e. capillary damage (leading to petechial rash , capillary leakage, and
hypovolemia)
f. intravascular coagulation
g. hypotension
h. decreased cardiac output
i. irreversible shock
j. wasting of the body
k. diarrhea (from endotoxin in intestines)
l. allow bacteria to cross the blood-brain barrier
Types of Exotoxins
• On the basis of mode of action:
• super antigens, e.g. Toxic shock syndrome toxin-1 produced by some strains
of Staphylococcus aureus
• toxins that act on the extracellular matrix of connective tissue, e.g.
Clostridium perfringens collagenase
• A-B Toxin ( Active-Binding Toxin)
• exotoxins that damage host cell membranes, e.g. botulinum toxin

On the basis of site of action:

• cytotoxins, e.g.diphtheria toxin and erythrogenic toxins
• neurotoxins, e.g.botulinum toxin and tetanus toxin.
• enterotoxins, e.g. cholera toxin and staphylococcal enterotoxin
• Toxin bind directly to the MHC-II
molecules on
• cross linking causes stimulation of up
to 1 in 5 T-cells in the body (normal
antigens cause stimulation of 1 in
10,000).
• results in the secretion of excessive
amounts of interleukin-2 (IL-2)  high
levels of IL-2 in the blood lead to
symptoms such as fever, nausea,
vomiting, diarrhea, and malaise.
• stimulation of IL-2 secretion can also
lead to production of other cytokines
such as TNF-alpha, IL-1, IL-8, and PAF,
which can lead to SIRS (Systemic
Inflammatory Response Syndrome)
• e.g., Toxic shock syndrome toxin-1
(TSST-1), produced by some strains of
Staphylococcus aureus
A-B toxins
• Examples
• Diphtheria toxin: ADP-ribosylation of host EF-2; host cells are
killed due to the blocking of translation of mRNA into
polypeptides.
• Cholera toxin: ADP-ribosylation of a cAMP regulatory
protein, which causes loss of ion regulation, water loss,
diarrhea.
• Shiga toxin: cleaves host rRNA, which blocks translation and
kills the host cell.
• Clostridium botulinum: large subunit targets neurons, small
subunit cleave snare proteins inhibiting neurotransmitter
release from neurons-causes paralysis
Ability to survive inside phagocytic cells

• Mycobacterium tuberculose
• Legionella pneumophila
Incubation period is
the interval between
exposure and illness Infectious Disease
onset.

Depending on various factors an individual Convalescence is a time of

may still be infectious during either recuperation and recovery
incubation or convalescence. from illness.