1. BACTERIAL PATHOGENESIS
Initiation of infectious process & mech that lead to the development of S & S of disease
ADHERENCE –
INFECTION –multiplication of an infectious agent in the body
INVASION –process by which bacteria enter & spread in the body
PATHOGEN –a microorg capable of causing disease

2. BACTERIAL PATHOGENESIS
OPPORTUNISTIC PATHOGEN –A microorg capable of causing disease only when host,s resistance is impaired
PATHOGENICITY –the ability of an infectious agent to cause disease
TOXIGENICITY –the ability of an microorg to produce a toxin that contribute to development of disease
VIRULENCE –the quantitative ability of an agent to cause disease

3. BACT PATHOGENESIS -STAGES
1 -entery in to host with evasion of host primary defenses
2 -adhesion of microorg to host cells
3 -propagation of org
4 - damage to host cells by toxins or inflammatory response
Evasion of host secondary defenses

4. BACT PATH -DETERMINANTS
TRASMISSION –
ROUTES – inhalation, ingestion, inoculation

5. BACT PATH –PORTAL OF ENTERY
RESP TRACT –S. pneumonia, N. meningitidis, H. influenzae, M. tuberculosis, influenza virus,
GIT –Shigella spp, Salmonella spp, V. cholerae, HAV, HEV, poliovirus
SKIN –C. tetani, Rabies virus, plasmodium spp,
GENITAL TRACT –N. gonorrhoeae,
T. pallidum, C. trachomatis, Candida albicans, HSV,

6. MODES OF TRANSMISSION HUMAN TO HUMAN – Direct contact –gonorrhea
No direct contact- dysentery
Nonhuman to human –
Soil –tetanus
Water –legionnaire,s disease
Animal source-
Directly –cat scratch disease
Via insect vector –Lyme disease

7. BACT PATHOGENESIS ADHERENCE TO HOST CELLS –
Fimbrial (Pili) –N. gonorrhea, E. coli
Afimbrial –cell surface adhesion molecule -Glycocalyx – Staph epidermidis, S.viridans - endothlium of heart valves
Extracellular polysccharides of Streptococcus mutans ( enamel surface)

8. BACT PATHOGENESIS INVASION- depend on bacterial enzymes
Collagenase & hyaluronidase ( cellulitis by S. pyogenes)
Coagulase –S. aureus
Ig A protease –N. gonorrhea, H. influenza. S. pneumonia
Leukocidins

9. BACT PATHOGENESIS Antiphagocytic factors –
Capsule –S. pneumonia, N. meningitidis,
Cell wall protein of Gram +ve cocci
M protein of S. pyogenes
Protein A of S. aureus
Invasion is followed by inflammation –pyogenic or granulomatous depending on org

10. BACT PATH PROPERTY EXOTOXIN ENDOTOXIN source Gram +ve & -ve bacteria
Cell wall of Gram –ve bacteria
composition
polypeptide
LPS
secreted
yes No
Location of genes
Plasmid or bacteriophage
Bact chromosomes
toxicity
high
Low
Mode of action
variable
TNF, IL-1

11. PROPERTY
EXOTOXIN
ENDOTOXIN
clinical effects
variable
Fever, shock
Antigenicity
strong
poor
Vaccines
toxoids no
Heat stability
Destroyed at 600C except staph enterotoxin, E. coli(ST)
Stable at 100 0C for one hr
diseases
Diphtheria, tetanus
sepsis

12. MODE OF ACTION ENDOTOXIN
IL-1(fever)
TNF(fever,hypotension
NO(hypotension)

13. Effects of IL -1
In vivo –hypotension, fever, edema, leukocytosis, wasting,
In vitro –direct cytotoxicity, cell-mediated cytotoxicity, vascular adhesion,
Effects of IL –2 –
Hypotension, fever, edema,

14. BACT EXOTOXINS MECH of ACTION EXOTOXINS ADP- ribosylation
Diphtheria toxin, cholera toxin, E. coli LT toxin, pertussis toxin
protease
Tetanus toxin, botulinum toxin
Superantigen
TSST,stph enterotoxin, erythrogenic toxin
lecithinase
C. perfringens