Professional Documents
Culture Documents
Depart. of Microbiology,
Medical Faculty, Hasanuddin University.
2007
Pathogens :
- in medicine: the pathogen is any microorganisms capable
of causing diseases
Pathogen opportunistic
The non-pathogen bacteria pathogen on susceptible host
Pathogenesis = pathogeny:
the organization & development of the infection
Carrier state
-Transient NF:
acquired from the environment
establish themselves briefly
excluded by:
competition
hosts innate or immune defense mechanisms.
for the
two organisms involved.
parasite.
in dental carries.
Exclusionary effect
- Lactobacilus vaginal flora protect host
against transmitted N. gonorrhea
- Exclusionary effect makes entrance of
pathogens more difficult
Progression
Resolution
Transmission
Skin & Mucous
Site of Microbial Contamination
or
Exogenously
Human to human:
direct contact
- Non-direct contact
- Blood-borne
- Vertical
-
Nonhuman to human
Human to human:
-Direct contact
: Gonorrhea
- Non-direct contact : Dysentry
- Blood-borne
: Syphilis
- Vertical (mother to her baby):
Transplacental
At time of birth
Breast milk
: Triponema pallidum
Cytomegalovirus
: Chlamydia trachomatis
Neisseria gonorrhoe
: Staphyloococcus aureus
Nonhuman to human
Soil source
: Tetanus
: Cat-scratch fever
Pili = fimbriae
Bacteria :
adhesin
Host epithel:
receptor
Non- fibrillae
- Pilli or fibrillae
- Afibrial adhesins
* Lectin (carbohydrate-binding-protein)
* Lipoteichoic acid
* Fibronectin-binding-protein
* M-protein
* Outer membrane protein
* Polysaccharide capsule
1. Contamination
2. Attachment to host cells
3. Invasion
Multiply
Colonization
Carrier state
(pathogen)
Getting into
cells multiplication
Mechanisms
Survival the phagocyte &
Complement attack
Inhibition of chemotaxis
Killing by phagocyte before
ingestion
Avoiding ingestion (Phagocytose)
Examples
C5a peptidase by Str. pyogenes
-toxin and leukocidin by Staph.
aureus
Bacterial capsule (Streptococcus
pneumoniae.)
LPS O Ag in Gr-neg rods
Coating with IgA Antibodies
(Neisseria meningitidis)
M. protein (Streptococcus
pyogenes)
Mechanisms
Examples
Inhibition of phagosome fusion
(Chlamydia trachomatis)
Escape phagolysosome
(Listeria monocytogenes)
Resistance to lysosomal product
(Salmonella typhimurium)
Inhibition of early host gene
expression (M. tuberculose)
Antigenic variation
Tolerance
Immunosuppression
-Destroying lymphocytes
- Proteolysis of antibodies
Presence in inaccessible sites
Prenatal infections
Depletion of CD4+ T cells by HIV
IgA protease by H. influenzae
Latent infection in dorsal root
ganglia (Herpes simplex virus)
Metabolite excretion
Tissue Damage
Primary lesion
Production of toxins
Examples
See next table
Cytomegalovirus
Respiratory syncytial
virus
Rabies
Herpes viruses
Human papilloma-viruses
type 16
Examples
Cytotoxic hypersensitivity
Tuberculosis granuloma
NO.
V. FACTORS
USED FOR
1.
2.
Protein pilli
Attachment
Polysaccharide/Polypeptide Avoiding ingestion
capsule
3.
4.
Protein M
Outer membrane protein
Attachment
Attachment
5.
6.
Toxin
Hyaluronidase
7.
8.
IgA protease
DNAse
9.
Coagulase
Avoiding ingestion
Comparison of Properties
Sources
Secreted from
cell
Yes
No
Chemistry
Polypeptide
Lipopolysaccharide
Location of gene
Plasmid or bacteriophage
Bacterial chromosome
Toxicity
High
Low
Clinical Effect
Various effects
Fever shock
Mode of action
Various mode
Antigenicity
Poorly antigenic
Vaccine
Toxoids
No toxoid or vaccines
avaiable
Heat stability
Typical diseases
Tetanus, botulisms,
Meningococcemia, sepsis
Sources
Toxin
Endotoxin
(LPS, lipid
A)
Gr- Bacteria
Endotoxin
Macrophage,
Neutrophils,
lymphocytes,
Plasma
components
Septic shock
Membrane
disrupting
toxins
Staph. aureus
-toxin
Many cells
types
Tissue necrosis
L.monocytoges
Listeriolysin
Many cells
types
Many cells
types
Gas gangrene
Cl. tetani
Tetanospasmin
Synaptic
transmission
Spastic paralysis
C. diphtheriae
Diphtheria
toxin
Many cells
types
Paralysis
Intestinal
cells
Profuse watery
diarrhea
Str. pyogenes
T. cells,
macrophage
Fever, eruption,
toxic-shock like
A-B type
toxins
Superantigen
Streptococcal
pyogenic
Target
Effects
1. Encounter entry
2. Attachment to host cells
3. Invasion
4. Multiplication
5. Dissemination
Directly
Indirectly
-hematogenously
--lymphatogenously
3. Antibiotics therapy
Symptomatic
Asymptomatic disease
= sub-clinic diseases
Depend on:
1. The organisms ability to breach host barrier & to
evade destruction by innate local and tissue host defences.
ROUTE
DISEASE-PRODUCING DOSE
Rhinovirus
Pharynx
200
Salmonella typhi
Oral
105
Shigella spp.
Oral
10 - 1000
Vibrio cholerae
Oral
108
Mycobacterium
tuberculosis
Inhalation
1 - 10
1. Normal Flora
2. Transmission of Bacteria
3. Pathogen:
- Posses virulence factors
- Opportunistic pathogen:
NF or colonization of pathogens on carrier
Environment bacteria
FURTHER READING
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integrated curricula with self-assessment, Churchill-Livingstone,
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