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BACTERIAL
MECHANISMS
OF PATHOGENICITY
VETERINARY MEDICINE
BRAWIJAYA UNIVERSITY

2. PATHOGENICITY1
VIRULENCE2

3. disease
Metabolite production/ toxigenicity
Damage the host tissue
Penetrate / no penetration
Evade host defenses
Adhere to host tissue
HOW MICROORGANISMS ENTER A HOST
Transmissibility
Evade the host
Immune system

4. Transmission
Direct: sexual contact, contact with patient
lesion
Indirect:
By vector (mechanic & biologic)
Via contaminated materials: air, water,
food, equipment, etc

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6. Mucous Membranes
-Respiratory tract: inhaled
into the nose or mouth
influenza, pneumonia, tuber-
culosis, etc
-Gastrointestinal tract
Most microbe HCl & enzymes
in the stomach or small intestine
or by bile
Pathogens are eliminated from
the host with feces
Transmitted via food, water,
contaminated finger
Poliomyelitis, hepatitis A & E,
shigellosis, amoebic dysentery,
salmonellosis, etc
-Genitourinary tract
Most as sexually transmitted
disease (STD)
herpes, warts, etc
-Conjunctiva
Most by contaminated fingers
Secreted via discharge
conjunctivitis
PORTALS
OF ENTRY
Skin
-The largest organs of the
body
- Is a important defense
mechanism against
pathogens
-Unbroken skin impene-
trable by the most m.o
-Enter by opening skin
(hair follicles, sweat
gland ducts), injury
The parenteral route
-If the pathogen directly into
the tissues beneath the skin
or mucous membrane when
the barriers are penetrated
or injured
-Via punctures, injection,
bites, cuts, wounds, surgery
& splitting due to swelling or
drying
-Hepatitis virus, gangrene,
tetanus, rabies, etc.
HOW MICROORGANISMS ENTER A HOST

7. THE PREFERRED PORTAL OF ENTRY
Entered the body cause disease????
The occurrence of disease depends on several factors
 Many pathogen have a preferred portal of entry
 Number the organism
 The presence of normal flora
 Host condition (immune system)

8. Enzymes
Tissue-degrading Enzymes
 lecithinase, collagenase degrade the
major protein of fibrous connective tissue
invasion
 coagulase work conjunction with serum factor
fibrin wall around the bacteria lesions
persist in the tissue & protect them from
phagocytosis, antibody & drugs
 Hyaluronidase hydrolyze hyaluronic acid
ground substance of connective tissue
 Streptokinase (fibrinolysin) dissolve
coagulated plasma, fibrin clots

9.  Cytolysin hemolysins/streptolysins,
leucosidins
 IgA1 Proteases
 Produce some bacteria causing disease
 Split IgA1 at specific proline-threonine or
proline-serine bonds in hinge region IgA1
(antibody) inactivation

10. Antiphagocytic factors
Some pathogens evade phagocytosis or leukocytes
microbicidal
 Staphylococcus aureus , has surface protein A
binds to Fc of IgG
 Streptococcus pneumoniae
polysaccharide capsule
 Streptococcus pyogenes (group A) protein M
 Mostly show much antigenic heterogeneity
 > 90 capsular polysaccharides
 > 80 protein types

11. Intracellular Pathogenicity
Some m. o. live and grow in the hostile
environment , in polymorphonuclear cells,
macrophages, or monocytes
 Prevent phagolysosomes fusion and live in
cytocol of the phagocyte cells
 Or may be resistant to lysosomal enzymes &
survive in phagolysosome
Resistant to phagocyte killing mechanism
Difficult reached by antibody and by drugs

12. Antigenic Heterogeneity
The surface structure of bacteria have
considerable antigenic heterogeneity
Antigenic drift
Antigenic shift
Antigenic changes

13. Iron requirement
Iron is essential nutrient for the infectious process
Iron has a wide oxidation-reduction potential
important for variety of metabolic function
The host’s iron metabolism denies pathogenic
bacteria an adequate source of iron for growth
Bacteria have developed several methods to
obtain sufficient iron for essential metabolism
 Siderofor catechol (phenolate): enterobactin
hydroxamate
The availability of iron affects the virulence of
pathogens

14. The role of biofilm
Exopolysaccharides produces by the bacteria
Mucilagenous layer
 Adhere to hard surface
 Bind between bacteria
Produces by one species bacteria or more than
one species
Difficult reached by immune system
Difficult reached by some antimicrobial drugs

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