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

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

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

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

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,

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

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)

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

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

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

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

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

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,

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