Classification of Bacteria

Modern Prokaryotic Classification

Eubacteria
Archeabacteria
Cyanobacteria
Thermophiles

Classification of Bacteria

Classification ordering

Nomenclature naming
Often immortalizes the person
who discovered it or its origin
Escherichia coli Theodor
Escherich
coli from colon

Distinguishing identification

Classification of Bacteria

*Kingdom
Phylum
Class
Order
Family
*Genus ( 1st name)
*Species ( 2nd name identifier)

1 Gram Negative Spiral Bacteria

Ramping dan fleksibel,
datang dalam banyak
bentuk yang berbeda
Lebih kaku dari spirochetes
Ex. - Campylobacter jejuni
Gejala - tenesmus: sensasi
keinginan untuk buang air
besar, yang umum dan
sering terjadi, dengan
keluar produksi sejumlah
besar kotoran (sering
sejumlah kecil lendir atau
darah saja berlalu).

2 Gram Negative Spirochetes

patogen
sangat fleksibel
erat melingkar, spiral
melingkar
contoh
sipilis
Treponema pallidum

Gram Negative Spirochetes

Sebagian patogen
sangat fleksibel
Erat melingkar, spiral
melingkar
contoh
Penyakit Lyme
Borrelia burgdorferi
(organisme akan
bersarang di jaringan)

3 Gram Negative Aerobic Rods

Legionella pneumophila
Lower respiratory tract
infection
Needs oxygen

Gram Negative Aerobic Rods

Bordetella pertussis
whooping cough
Needs oxygen

Gram Negative Aerobic Rods

Pseudomonas
aeruginosa (pigmented)
Needs moisture
Common in hospitals
Opportunistic pathogen
causes skin and lung
infection

4 Gram Negative Facultative Rods

Vibrio

V. cholerae
Most well known of group
Very severe dysentery. Can lose
10-15 liters of water/day. Leads
to hypovolemia low water, hardly
any water in body
V. vulnificus
Very pathogenic
Can cause flesh eating disease,
if it gets in a wound
V. parahaemolyticus
Found in shellfish oysters
Halophile loves salt (will find in oceans, estuaries)
Self limiting

Gram Negative Facultative Rods

Enteric
Salmonella
Shigella
E. coli (0157H7)

5 Gram Negative Anaerobic Rods

Fusobacterium

Live in between teeth

and gums
Cause tooth abscesses
and periodontal disease
Teeth have nothing to
anchor bone is
destroyed

6 Gram Negative Cocci or Coccobaccilli (plu

mp rods)

Neisseria gonorrhoeae

Sexually Transmitted
Disease
very antibiotic resistant

Gram Negative Cocci or Coccobaccilli (plump r

ods)

Neisseria meningitidis
very infectious and
communicable.

Gram Negative Cocci or Coccobaccilli (plump r

ods)

Acinetobacter baumanni iv.

lwof
opportunistic, UTI, skin,
and upper respiratory

7 Chlamydia Gram Negative Rods (Transitional)

Very short little rods
Gram negative
Transitional doesnt hold stain
well
Do not have the ability to
synthesize own ATP, therefore
and obligate intracellular parasite
of other animals (humans)
Can go asymptomatic for a long
time
Ex.
C. trachomatis STD, causes
eye infection
C. psittaci parrot (associated
with birds)

8 Rickettsia Gram Negative Rod (Transitional)

Small gram negative rods

Transitional doesnt hold

stain well

Cant synthesize its own

NAD, coenzyme A, therefore
an obligate intracellular
parasite

Causative agent of Rocky

Mountain Spotted Fever

Example
R. Prowazekii

10 Gram Positive Cocci

Staphyloccocus aureus
MRSA
These bacteria can break
down all tissues of body.

Gram Positive Cocci

Streptococcus pyogenes
no antibiotic resistance
right now
These bacteria can break
down all tissues of body.

11 Gram positive Endospore Forming Rods

Difficult to get rid of

because of endospores

Example
Clostridium tetani

Gram positive Endospore Forming Rods

Difficult to get rid of

because of endospores

Example
C. perfringens
gangrene

Gram positive Endospore Forming Rods

Difficult to get rid of

because of endospores
Common in hospitals
Example
C. difcile
antibiotic associated
pseudmembraneous
enterocolitis

Clostridium difficile

Gram positive Endospore Forming Rods

Bacillus
B. anthracis anthrax
zoonosis

Gram positive Endospore Forming Rods

Bacillus
B. cereus food
poising
Especially in high carb
foods rice, vermicelli
B. thuringiensis
natures insecticide

12 Coryneforms

Pleomorphic (many shapes)

Example
Corynebacterium diphtheriae

Gram positive and Acid

13Fast
Mycobacteria

Mycobacterium tuberculosis
Respiratory Pathogen
MDR-TB
In the 1950s we sent people
with TB to the sanitariums

Mycobacteria

Gram positive and Acid Fast

M. avium intracellular complex

(MAC)
Really bad bug
Currently no drugs can cure it
Especially bad for people with
AIDS
Can cause atypical TB

Mycobacteria

Gram positive and Acid

Fast
M. leprae
Causative agent of
leprosy
Not very common

Bacterial Pathogenesis

Outline
Bacterial Pathogenesis
Introduction
Host Susceptibility
Pathogenic Mechanisms
Virulence Factors

Introduction of Bacterial Pathogenesis

1.

Infection: growth and multiplication of a microbe in or

on the body with or without the production of disease.

2.

The capacity of a bacterium to cause disease reflects

its relative Pathogenicity.

3.

Virulence is the measure of the pathogenicity of a

microorganism.

4.

Pathogenesis refers both to the mechanism of

infection and to the mechanism by which disease
develops.

Host Susceptibility
1.

Susceptibility to bacterial infections

=> Host Defenses vs Bacterial Virulence

2.

Host Defenses:
- Barriers (skin & mucus) first line
- Innate Immune Responses (complement, macrophages &
cytokines) the early stage
- Adaptive Immune Responses (Ag-specific B & T cells) the
later stage

3.

Host defenses can be comprised by destructing barriers or

defective immune response.
e.x. Cystic Fibrosis => poor ciliary function => NOT clear mucus
efficiently from the respiratory tract => Pseudomonas
aeruginosa => serious respiratory distress.

Strict pathogens
are more virulent and can
cause diseases in a normal
person.
Opportunistic pathogens

are typically members of

normal flora and cause
diseases when they are
introduced into
unprotected sites, usually
occur in people with
underlying conditions.

Entry into the human body

The most frequent portals
of entry- Mucus
- Skin
Routes:
Ingestion, inhalation,
trauma, needles, catheters,
arthropod bite, sexual
transmission
: infection

: shedding

Characteristics of Pathogenic
Bacteria
1. Transmissibility
2. Adherence to host cells
3. Invasion of host cells and tissue
4. Evasion of the host immune system
5. Toxigenicity
A bacterium may cause diseases by
1. Destroying tissue (invasiveness)
2. Producing toxins (toxigenicity)
3. Stimulating overwhelming host immune
responses

Bacterial virulence factors th

at promote colonization

38

Definitions
Pathogenicity = ability to cause disease
Primary pathogens cause disease in healthy
people
Opportunistic pathogens cause disease in p
eople with defect immune defense (immuno de
ficiency)
Normal flora colonize the majority of (all) he
althy people
Virulence describes the aggressiveness (is qu
antitative; more or less virulent)
Virulence factors are bacterial factors that e
nhance the ability to cause disease 39

Why is this knowledge important ?

40

Pathogenic properties
Shedding and spread from original host
Survival during spread
Entry in new host
Survival in the host
Growth, adhesion
Colonisation
Survival of the host response

Damage to the host

41

Damage to the host

Local toxins and enzymes
Peripheral toxins (toxin diseases)
Activation of immune response
Cell invasion
Cross talk

42

WHERE CAN MICROBES INFECT AND

BE SHEDDED?

43

Possibleoutcomesof
exposuretomicro
organisms
Exposure

Organismsbecome
partofnormal
flora
Carrierstate
(nosymptoms
butorganisms
areshed)

Colonization

Organismseliminated
byhostdefenses

Pathogenicity

Infectiousdisease

44

Definitions
Host:
an organism that shelters and supports the growth of a pathogen
Virulence:
the degree of pathogenicity
Toxigenicity:
the ability of a microorganism to produce a toxin that contributes to the
development of disease
Spreading Factors:
is a descriptive term for a family of bacterial enzymes that affect the physical
properties of tissue matrices and intercellular spaces, thereby promoting the
spread of the pathogen

Definitions
Disease (dis-ease):
is an abnormal state in which part or all of the body is not properly adjusted or
is incapable of performing normal functions
is an impairment of health or a condition of abnormal functioning
Disturbed homeostasis
Infection:
is the invasion and growth of pathogens in the body with or without disease
Infectious disease:
a clinically manifesting disease of humans or animals resulting from an
infection
Pathogens:
microorganisms capable of causing disease
Pathogenicity:
ability of an infectious agent (pathogen) to cause disease by overcoming the
defenses of a host

Pathogenesis of Bacterial Infection

Includes initiation of the infectious process and the mechanisms that lead to the
development of signs and symptoms of the disease
Characteristics of bacteria that are pathogens include transmissibility, adherence
to host cells and tissues, toxigenicity and the ability to evade the hosts defenses

Challenges that pathogens face in order to survive

1.

Maintain a reservoir in which it can survive before and after infection

2.

Leave its reservoir and enter the body of a human host (transmission- revise
how diseases can be transmitted)

3.

Adhere (attach)firmly to the hosts body and thereby colonize it

4.

Invade the body in order to enter cells or deeper tissues

5.

Evade the hosts elaborate defenses

6.

Multiply within the body, perhaps producing toxic products or stimulating

host reactions that cause disease

7.

Leave the body and return to the reservoir and/or enter a new host

Prokaryotic and Eukaryotic

Interactions

EukaryoticCell

Intracellular

ProkaryoticCell

Pilioradhesins

Controlofvirulencefactors:
(Pilin,capsule,invasins,toxinsetc)

Receptor

COLONIZATIO
N

VirulentBacteria

Adherenceblockers

INVASION

Virulence factors that promote c

olonization and survival of infect
ing bacteria
Pili, function : adherence to mucosal sur
face
Nonfimbrial adhesins, F : tight binding t
o host cells
Bacterial triggering of actin rearrangem
ent in host cell, F : forced phagocytosis
of bacteria by normally nonphagocytic h
ost cells; movement of bacteria within h
ost cells or from one host cell to anothe
r
50

Movement of bacterium
from cell to cell

51

 Binding to and entry of M cell, F: M cell

used as natural port of entry into underl
ying tissue
Motility and chemotaxis, F : reaching m
ucosal surfaces (especially areas with fa
st flow)
sIgA proteases, F : prevent trapping of
bacteria in mucin)
Siderophores, surface protein that bind
transferrin, lactoferin, feritin, or hemin,
F: Iron acquisition
52

Need for iron to survive

 Capsule, F : prevent phagocytic uptake;

reduce complement activation
Altered LPS O antigen, F : MAC not form
ed; serum resistance
C5a peptidase, F : interferes with signali
ng function of complement
Toxic protein, F : kil phagocytes, reduce
strength of oxidative burst
Variation in surface antigens, F : evade
antibody response

54

PATHOLOGICALEFFECTSOFINFECTION
cell

Microorganism

cytolysis

bacteria
toxins
endotoxin

clotting

exotoxin

PMN
enzymes

MF

TNF,IL1

IFN
antibody
complement
complexes

T
Tcell

IL16

mastcell
IgE
antibody

tissue
damage

cytotoxicity
56

Invasion of cells

57

TOOLS TO EVADE THE IMMUNE

SYSTEM
Capsuletoresistphagocytosis
Antiopsonizingcellsurfaceproteins
Abilitytosurviveinneutrophilsandmacrophages
Antigenicvariation
Surfacemasking
Abilitytoresistlysisbycomplementsystem
IgAprotease
Leucocidins
Biofilmformation

58

Immune Evasion by Bacteria: Av

oidance of Complement, Antibod
y and T Cell Responses

Immune Evasion by Bacteria

Out run the immune syst
em
Avoid/inactivate comple
ment
Avoid/inactivate antibody
Avoid/inactivate phagocy
tic cells
Avoid/inactivate cytokine
s

Evasion: Replication

Bacteria replicate rapidly

Rapid increase in numbers before
immunity kicks in
Large number induces systemic s
pread
Large number overwhelms immune respons
e
Leads to systemic collapse (LPS, shock)

Immune Evasion by Bacteria

Out run the immune syste
m
Bacterial surface structures
Defenses against complem
ent
Defenses against antibody
Defenses against phagocyti
c cells
Defenses against cytokines

Evasion: Surface structures

Capsules
LPS-Outer membr
ane
Peptidoglycan

Evasion: Capsules

(slime layer; glycocalyx)

Gram-negative or -posi
tive
Composition
Homo- or Heteropoly
saccharide
Polypeptide (polyglut
amic acid) (Bacillus anthracis)

Capsules vary in thickness and can easily be 2 times the volume

of the organism. In a capsule stain, the background is stained
grayish blue and the cells are stained red. The capsule is
unstained and appears as a halo around the cell. Judy Bowen
Buckman Laboratories International, Inc.
Memphis, Tennessee, USA and The MicrobeLibrary

Evasion: Capsules
(slime layer; glycocalyx)

Immunogenicity
Not highly immunogenic
Capsules of bacteria contain eukaryotic molecules
Sialic acid (E. coli K1)
Hyaluronic acid (Streptococcus pyogenes)
Surface charge
Prevents antibody or complement deposition (S. pneumonia
e)
Protects against defensins (cationic proteins) (Bacillus anthr
acis)
Barrier function
Hide bacterial components
Peptidoglycan, LPS -outer membrane proteins
Prevents complement insertion (H. influenzae, E. coli, N. me
ningitidis)
Thickness of slime layer and biofilm formation

Evasion: LPS

Immunogenicity
Carbohydrate moieties (O serotypes)
Lipid A highly conserved among bacteria, but some b
acteria (Salmonella) have enzymes to modify lipid A
Surface charge
Modifications of O-polysaccharide prevent opsonizatio
n
Lysozyme (natural opsonin) neutralizes charge
Modifications of lipid A decrease membrane negative
charge
Barrier functions
Density of carbohydrates prevents insertion of comple
ment

Evasion: Outer membrane

Immunogenicity
Structural components: porin proteins, pili, flagella
Hide bacterial components
peptidoglycan, periplasmic proteins
Permeability barrier
Barrier to lysozyme
Barrier to hydrophobic compounds of GI tract (bile s
alts)

Evasion: Peptidoglycan

Highly immunogenic
PAMP (pathogen-associated molecular pattern)
Intracellular PRP
Nod1: recognizes Gram-negative peptidoglycan
Nod2: recognizes Gram-positive peptidoglycan
Recognition leads to NFB activation and infla
mmation
Surface-located and -secreted peptidoglycan hydrolases
cleave peptidoglycan to promote inflammatory response
and recruitment/uptake by macrophages (Listeria)

Immune evasion by bacteria

Surface structures
Disabling comple
ment
Disabling antibody
Antigenic variabilit
y
Evading phagocyt
osis
Odds and Ends

Evasion: Complement

Thick capsule coat Neisseria meningitidis Strept

ococci, Staphylococci
Bacteria coated with sialic acid Neisseria gonorr
hoeae
Sialic acid keeps C3b from binding to host cel
ls
Density and length of LPS O-antigen Salmonella
typhimurium, E. coli prevent complement activi
ty

Immune evasion by bacteria

Surface structures
Disabling comple
ment
Disabling antibody
Antigenic variabilit
y
Evading phagocyt
osis

Evasion: Disabling of Antibody

Bacterial products destroy antibody
IgA proteases (Neisseria spp.); elsatase of Pseu
domonas aeruginosa)
Cleave at hinge region: Detaches Fc portion
Soluble bacterial products absorb antibodies
Release of capsular polysaccharides absorb circu
lating anti-polysaccharide antibodies before ant
ibodies can react with capsule of intact bacteriu
m
Protein A (S. aureus) as part of cell surface or r
eleased in soluble form
Binds Fc region of IgG
Bacterial autolysis: releasing antigenic surface c
omponents in a soluble form

Immune evasion by bacteria

Surface structures
Disabling antibod
y
Antigenic variabili
ty
Evading phagocyt
osis

Evasion: Antigenic variability

Strain variation
Colonization
Antigenic variation
Antigenic mimicry

Antigenic variability: Strain Vari

ation
Antigenicity differs amo
ng strains of related bac
teria
Polysaccharide/protei
n variation
Serotypes
LPS (O) antigens
Flagellar (H) antigens

Antigenic variability: Colonizatio

n
Morphological changes in bacteria
Sometimes referred to as phase variation
Surface components change during infe
ction
Pili used during colonization not present
after adherence to host cell (Pseudomon
as aeruginosa)
Changes in mucopolysaccharide product
ion after colonization (Pseudomonas aer
uginosa)
Biofilm formation

Antigenic variability: Antigenic V

ariation
Bacterial periodically change protei
n structure
Genomic rearrangement
Site-specific inversions; gene conv
ersions; reading frame shifts; rearr
angements of DNA

Previous antibodies have no targ

et
Pili alleles (Neisseria gonorrhoeae)

Bacterial Evasion of Antibody

Surface structures
Evading antibody
Antigenic masking
Evading phagocyto
sis

Survival in phagocytes

79

Mechanis
ms for dis
ease

Virulence Factors That D

amage the Host

Exotoxin
Characteristics and Nomenclatur
Exotoxin : toxic bacterial protein
Many bacterial exotoxin are excreted into the me
dium the medium by growing bacteria
Produced by a variety of bacteria, -/+ gram bacter
ia
In some species, most strains of the species prod
uce the same exotoxin
Exotoxin very considerably in their activities and t
he host cell types they attack

Some toxins are named to indicate the type of ho

st cells they attack
Exotoxin that attack a variety of different cell type
s are called cytotoxin
Whereas exotoxin that attack specific cell type ca
n be designated by the cell type or organ affected
, such as neurotoxin, leukotoxin, hepatotoxin,
and cardiotoxin
Exotoxin can also be named for the species that p
roduces them or for the disease with which they
are associated.

Examples are Cholera toxin, produced by Vibrio

cholerae, the cause of cholera, Shiga toxin, prod
uced by Shigella sp, a cause of bacterial dysenter
y; diphtheria toxin, produced by Clostridium tet
ani, the cause of tetanus
toxin can also be named on the basis of their acti
vities, for example, adenylate cyclase ( a toxin pr
oduced by Bordetella pertusiss) and lechitinase (
a toxin produced by Clostridium perfrigens)

- Some toxin have more than one name. For examp

le, Shiga-like toxin of E. coli (so-called because it h
as the same mechanism as Shiga toxin) has also b
een called Verotoxin because it is toxic for a cell l
ine called Vero.

Exotoxin structure and function

Exotoxin can be divided into three types
1. A-B toxin, which gets its name from the fact that
the portion of the toxin B that binds a host cell r
eceptor is separate from the portin A that media
te the enzymatic activity responsible for toxicity.
2. Hemolysin and phospholipase
3. Superantigen, also lacks an A-B type structure an
d acts by stimulating T cells to release cytokine.

A-B toxin

The simplest kind of A-B toxin is synthesized as a

single polypeptide
Which has one binding and one enzymatic portio
n.
A portion of most A-B exotoxin catalyze the same
type of reaction. They remove the ADP-ribosyl gro
up from NAD and attach it covalently to some hos
t cell protein.

The A portion of diphtheria toxin ADP-ribosylate e

longation factor-2, a protein that plays an essenti
al role in host cell protein synthesis.
Thus the effect of diphteria toxin is to kill the host
cell by stoppping protein synthesis.

Membrane-disrupting toxin
The first is a protein that insert into the host cell
membrane and form channel (pore) , thus allowi
ng cytoplasmic contents to leak out and water ent
er, which causes the cell to swell and rupture
- A receptor for pore-forming toxin is usually chole
sterol not carbohydrate moiety

The second : phosphoplipase=hemolysins

Phospholipase remove the charge head group fr
om the lipid portion of phospholipid. The charge
head group stabilize phospholipid bilayer structu
re of the host cell plasma membrane, and cell lys
is result.

Superantigen
A pprotein that exerts its effect by forming a bridge
between MHC class II of Macrophage or APC and
receptor T cell that interact with the class II MHC.
Normally APCs process protein antigen by cleavin
g them into peptide and displaying one of the res
ulting peptides in a complex with MHC class II on
the APC surface.
Only a few helper T cells will have receptor that r
ecognize this particular MHC-peptide complex, so
only a few T cell will be stimulated.

Stimulation of T cell causes them to produce prot

ein cytokine such as IL-2 that stimulate T cell prol
iferation and T cell inetraction with B cell leading
to antibody production by B cells.
Superantigen are not processed by proteolytic dig
estion inside APCs but binds diretly to MHC class
II on the APC surface. Because superantigen do t
his rather indiscriminately, many APCs will have s
uperantigen molecules bound to their surfaces.

APC stimulating 1 in 10000 cell (in normal respon

to the antigen)
As many as 1 in 5 cell can be stimulated by the b
ridging action of superantigen (this is way, they ar
e call superantigen).
Superatigen action causess excessively high levels
of IL-2 to be released. Normally Il-2 act locally, bu
t production of abnormally high levels can lead to
circulation of IL-2 in bloodstream, giving rise to v
ariety of simptoms, nausea, vomiting, malaise an
d fever and respon inflammatory.

superantigen

Exotoxin Derivative as vaccine

Old vaccine- toxoid
Today - the fact that action of A-B toxin is depend
ent of the binding of the B region to host cell rece
ptor molecule suggest that antibodies against th
e B portion of an A-B toxin is non-toxic, it should
be a good vaccine.

Hydrolytic enzyme
Such as hyaluronidase and protease degrade e
xtracellular matrix component and thus disrupt h
ost tissue culture
These enzyme provide bacteria with sources of ca
rbon and energy by breaking host polimers into u
seable low-molecular-weight sugars and amino a
cid

Bacterial Product that Product an Aut

oimmune Response

Such an attack on self is called an autoimmune re

sponse

Pathological Mechanisms of Bacterial

Infections
1.

Bacteria-mediated
Pathogenesis

2.

Host-mediated
Pathogenesis

3.

Bacterial virulence
factors

=> bacterial factors

causing diseases

Adopted from Samuel Baron Medical Microbiology

Bacterial Virulence Mechanisms

Bacterial virulence factors

Adhesins
Pili (fimbriae)
Nonfimbrial adhesins
Invasion of host cells
Tissue damage
Tissue-degrading enzymes
Immunopathogenesis
Toxins
Exotoxins (cytolytic enzymes
and A-B toxins); enterotoxins;
superantigens;
endotoxin and other cell wall
components

Antiphagocytic factors
Intracellular survival
Antigenic heterogeneity
Antigenic variation
Phase variation

Iron acquisition
Siderophores
Receptors for
iron-containing molecules
Resistance to antibiotics

Adhesion

Back

Adherence of bacterium to epithelial or endothelial

cells allow them to colonize the tissue.
Common adhesins: pili (fimbriae), slime, lipoteichoic
acid, surface proteins or lectins.
Biofilm, formed on a surface by the bacteria that are
bound together within a sticky web of polysaccharide,
is a special bacterial adaptation that facilitates
colonization on the surgical appliances (e.g., artificial
valves or indwelling catheters) and dental plaque. It
can protect the bacteria from host defenses and
antibiotics.

The bacteria may invade via the M cells

M (Microfold) cells

Back

Endotoxin (LPS)-mediated toxicity

Lipid A of
lipopolysaccharide is
responsible for
endotoxin activity
Pathogenesis of
sepsis (septicemia)

Endotoxin-mediated toxicity
Fever,
leukopenia followed by leukocytosis,
activation of complement, thrombocytopenia,
disseminated intravasacular coagulation,
decreased peripheral circulation and perfusion to
major organs (multiple organ system failure),
Shock and death.
Peptidoglycan, teichoic and lipoteichoic acids of grampositive bacteria stimulate pyrogenic acute phase
responses and produce endotoxin-like toxicity
Back

Superantigen-mediated toxicity

1. Bind to TCR and activate T

cells w/o Ag
2. Autoimmune-like responses
3. S. aureus =>Toxic shock
syndrome toxin
S. pyogenes=> Erythrogenic
toxin A orC

Back

Superantigen (sags) adalah kelas antigen yang menyebabkan aktivasi non-spesifik Tsel yang menghasilkan poliklonal aktivasi sel T dan pelepasan sitokin besar. Sags
diproduksi oleh beberapa virus dan bakteri patogen yang paling mungkin sebagai
mekanisme pertahanan terhadap sistem kekebalan tubuh. [1] Dibandingkan dengan
respon sel-T antigen-induced normal di mana 0,0001-0,001% dari T-sel tubuh
diaktifkan, sags ini mampu mengaktifkan hingga 25% dari T-sel tubuh. [rujukan?]
Selain itu, Anti-CD3 dan Anti-CD28 Antibodi (CD28-SuperMAB) juga terbukti
superantigens sangat ampuh (dan dapat mengaktifkan hingga 100% dari sel T).
Banyaknya T-sel diaktifkan menghasilkan respon imun besar yang tidak spesifik
untuk setiap epitop tertentu pada SAg sehingga merusak salah satu kekuatan
fundamental dari sistem kekebalan tubuh adaptif, yaitu, kemampuan untuk
menargetkan antigen dengan spesifisitas yang tinggi. Lebih penting lagi, sejumlah
besar sel-T diaktifkan mengeluarkan sejumlah besar sitokin, yang paling penting
adalah Interferon gamma. Ini jumlah kelebihan IFN-gamma pada gilirannya
mengaktifkan makrofag. Makrofag yang diaktifkan, pada gilirannya, lebihmemproduksi sitokin proinflamasi seperti IL-1, IL-6 dan TNF-alpha. TNF-alpha
sangat penting sebagai bagian dari respon inflamasi tubuh. Dalam keadaan normal itu
dirilis secara lokal di tingkat rendah dan membantu kekebalan tubuh patogen sistem
kekalahan. Namun, ketika itu secara sistemik dirilis dalam darah dan kadar yang
tinggi (karena aktivasi sel-T massa yang dihasilkan dari SAg mengikat), dapat
menyebabkan gejala yang parah dan mengancam jiwa, termasuk syok dan kegagalan
organ multiple.

The A-B toxins

A chain has the inhibitory activity against some vital function
B chain binds to a receptor and promotes entry of the A chain
Mode of action
Inhibition of
protein synthesis
Hypersecretion
Inhibition of
neurotransmitter
release
In many cases
the toxin gene is
encoded on a
plasmid or a
lysogenic phage

Back

Regulation of bacterial virulence factors

Environmental factors often control the expression of
the virulence genes.
Common factors: temperature, iron availability,
osmolarity, growth phase, pH, specific ions, specific
nutrient factors, bacterial cell-density, interaction with
host cells.

SUMMARY
1. Host Defenses:
- Barriers (skin & mucus) first line
- Innate Immune Responses (complement, macrophages &
cytokines) the early stage
- Adaptive Immune Responses (Ag-specific B & T cells) the
later stage
2. Susceptibility to bacterial infections depends on the balance
between host defenses and bacterial virulence.
3. Pathogenic mechanisms of bacterial infections include

Bacteria-mediated Pathogenesis

Host-mediated Pathogenesis

Thank you!