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Mechanism Of Pathogenecity
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Mechanism Of Pathogenecity

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  • 1. Microbial Mechanisms of Pathogenesis
  • 2. Pathogenesis
    • The word comes from the Greek pathos , "disease", and genesis , creation.
    • The term pathogenesis means step by step development of a disease.
    • The chain of events leading to that disease due to a series of changes in the structure and /or function of a cell/tissue/organ.
    • Caused by a microbial, chemical or physical agent.
  • 3. Pathogenicity - Ability to cause disease Virulence - Degree of pathogenicity
    • Many properties that determine a microbe’s pathogenicity or virulence are unclear or unknown
    • But, when a microbe overpowers the hosts defenses, disease results!
  • 4. Portals of Entry
    • 1. Mucus Membranes
    • 2. Skin
    • 3. Parenteral
  • 5. 1. Mucus Membranes
    • A. Respiratory Tract
    • Sticky mucous secretion
    • Muco polysachharides
    • Cough reflex
    • Phagocytic cells
  • 6. Common Diseases contracted via the Respiratory Tract
    • Common cold
    • Flu
    • Tuberculosis
    • Whooping cough
    • Pneumonia
    • Measles
    • Strep Throat
    • Diphtheria
  • 7. Mucus Membranes
    • B. Gastrointestinal Tract
      • Microbes gain entrance thru contaminated food & water or fingers & hands.
      • Most microbes that enter the G.I. Tract are destroyed by HCL & enzymes of stomach or bile & enzymes of small intestine.
  • 8. Common diseases contracted via the G.I. Tract
    • Salmonellosis
      • Salmonella sp.
    • Shigellosis
      • Shigella sp.
    • Cholera
      • Vibrio cholorea
    • Ulcers
      • Helicobacter pylori
    • Botulism
      • Clostridium botulinum
  • 9. Fecal - Oral Diseases
    • These pathogens enter the G.I. Tract at one end and exit at the other end.
    • Spread by contaminated hands & fingers or contaminated food & water
    • Poor personal hygiene.
  • 10. Mucus Membranes of the Genitourinary System Acidic urine Vaginal secretion- Acidic due to fermentation of glycogen by lactobacillus Gonorrhea Neisseria gonorrhoeae Syphilis Treponema pallidum Chlamydia Chlamydia trachomatis HIV Herpes Simplex II
  • 11. Mucus Membranes
    • D. Conjunctiva –
    • Lacrymal secretion
    • Lysozyme
    • Trachoma
      • Chlamydia trachomatis
  • 12. 2. Skin
    • Skin - the largest organ of the body.
    • Sebaceous secretion-containing fatty acids
    • Resident flora
    • When unbroken is an effective barrier for most microorganisms.
    • Some microbes can gain entrance thru openings in the skin: hair follicles and sweat glands
  • 13. 3. Parentarel
    • Microorganisms are deposited into the tissues below the skin or mucus membranes
    • Punctures
    • injections
    • bites
    • scratches
    • surgery
    • splitting of skin due to swelling or dryness
  • 14. Number of Invading Microbes
    • LD 50 - Lethal Dose of a microbes toxin that will kill 50% of experimentally inoculated test animal
    • ID 50 - infectious dose required to cause disease in 50% of inoculated test animals
      • Example: ID 50 for Vibrio cholerea 10 8 cells (100,000,000 cells)
      • ID 50 for Inhalation Anthrax - 5,000 to 10,000 spores
  • 15. How do Bacterial Pathogens penetrate Host Defenses? 1. Adherence - almost all pathogens have a means to attach to host tissue Binding Sites adhesins ligands
  • 16. How Bacterial Pathogens Penetrate Host Defenses
    • 1. Adherence
    • 2. Capsule
    • 3. Enzymes
      • A. leukocidins
      • B. Hemolysins
      • C. Coagulase
      • D. Kinases
      • E. Hyaluronidase
      • F. Collagenase
      • G. Necrotizing Factor
  • 17. Adhesins and ligands are usually on Fimbriae
    • Neisseria gonorrhoeae
    • ETEC (Entertoxigenic E. coli)
    • Bordetella pertussis
  • 18. 2. Capsules
    • Prevent phagocytosis
    • Attachment
    • Streptococcus pneumoniae
    • Klebsiella pneumoniae
    • Haemophilus influenzae
    • Bacillus anthracis
    • Streptococcus mutans
    • Yersinia pestis
    K. pneumoniae
  • 19. 3. Enzymes
    • Many pathogens secrete enzymes that contribute to their pathogenicity
  • 20. A. Leukocidins
    • Attack certain types of WBC’s
    • 1. Kills WBC’s which prevents phagocytosis
    • 2. Releases & ruptures lysosomes
      • lysosomes - contain powerful hydrolytic enzymes which then cause more tissue damage
  • 21. B. Hemolysins - cause the lysis of RBC’s Streptococci
  • 22. 1. Alpha Hemolytic Streptococci - secrete hemolysins that cause the incomplete lysis or RBC’s
  • 23. 2. Beta Hemolytic Streptococci - Secrete hemolysins that cause the complete lysis of RBC’s
  • 24. C. Coagulase - cause blood to coagulate
    • Blood clots protect bacteria from phagocytosis from WBC’s and other host defenses
    • Staphylococci - are often coagulase positive
      • boils
      • abscesses
  • 25. D. Kinases - enzymes that dissolve blood clots
    • 1. Streptokinase - Streptococci
    • 2. Staphylokinase - Staphylococci
    • Helps to spread bacteria - Bacteremia
    • Streptokinase - used to dissolve blood clots in the Heart (Heart Attacks due to obstructed coronary blood vessels)
  • 26. E. Hyaluronidase
    • Breaks down Hyaluronic acid (found in connective tissues)
    • “Spreading Factor”
    • Mixed with a drug to help spread the drug through a body tissue
  • 27. F. Collagenase
    • Breaks down collagen (found in many connective tissues)
    • Clostridium perfringens - Gas Gangrene
      • uses this to spread thru muscle tissue
  • 28. G. Necrotizing Factor - Causes death (necrosis) to tissue cells “ Flesh Eating Bacteria”
  • 29. Bacterial Toxins
    • Poisonous substances produced by microorganisms
    • Toxins - primary factor - pathogenicity
    • 220 known bacterial toxins
      • 40% cause disease by damaging the Eukaryotic cell membrane
    • Toxemia
      • Toxins in the bloodstream
  • 30. Types of Toxins
    • 1. Exotoxins
      • Exotoxins are generated by the bacteria and actively secreted
      • Secreted outside the bacterial cell
    • 2. Endotoxins
      • Part of the outer cell wall of Gram (-) bacteria
      • The body's response to endotoxin can involve severe inflammation.
  • 31. Exotoxins
    • Mostly seen in Gram (+) Bacteria
    • Heat labile, can be inactivated by heating at 60-80 ۠ C.
    • Excreted [ secreted] from the microbial cells into the surrounding ie culture media or circulatory system
    • Don’t require bacterial death or cell lysis for their release.
  • 32. Types of Exotoxins
    • 1. Cytotoxins
      • Kill cells- shigella, vibrio
    • 2. Neurotoxins
      • Interfere with normal nerve impulses
      • Clostridium botulinum
      • Clostridium tetani
    • 3. Enterotoxins
      • Effect cells lining the G.I. Tract
      • E. coli
      • Salmonella
  • 33. Response to Toxins
    • If exposed to exotoxins: antibodies against the toxin ( antitoxins )
    • Exotoxins inactivated ( heat, formalin or phenol) no longer cause disease, but stimulate the production of antitoxin
      • altered exotoxins - Toxoids
    • Toxoids - injected to stimulate the production of antitoxins and provide immunity
  • 34. Endotoxins
    • Part of the Gram (-) Bacterial cell wall.
    • Biological activity or toxicity of endotoxin is largely due to lipid A.
    • Relatively heat stable can withstand heat over 60 ۠ C for many hours.
    • Released upon cell lysis or death.
    • Less potent than exotoxins, active in large doses only.
    • Pyrogenic often produce fever in hosts.
    • Salmonella, Shigella, Escherichia, Neisseria.
  • 35. Bacteriocin
    • Bacteriocins were first discovered by A. Gratia in 1925.
    • He called his first discovery a colicine because it killed E. coli.
    • Bacteriocins are proteinaceous toxins produced by bacteria to inhibit the growth of similar or closely related bacterial strain(s).
    • They are typically considered to be narrow spectrum antibiotics, though this has been debated.
  • 36.
    • Classification:
    • Class I: Small peptide inhibitors .
    • Class II: Small heat-stable proteins .
    • Class III: Large, heat-labile protein bacteriocins
  • 37.
    • Medical significance
    • Bacteriocins are of interest in medicine because they are made by non-pathogenic bacteria that normally colonize the human body.
    • Loss of these harmless bacteria following antibiotic use may allow opportunistic pathogenic bacteria to invade the human body.