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
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
