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Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
Mechanism Of Pathogenecity
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Mechanism Of Pathogenecity

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

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