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Chapter 15

Chapter 15. Microbial Mechanisms of Pathogenicity. How Microbes Enter a Host. 15-1 Identify the principal portals of entry. 15-2 Define ID 50 and LD 50 . 15-3 Using examples, explain how microbes adhere to host cells. . Mechanisms of Pathogenicity.

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Chapter 15

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  1. Chapter 15 Microbial Mechanisms of Pathogenicity

  2. How Microbes Enter a Host • 15-1 Identify the principal portals of entry. • 15-2 Define ID50 and LD50. • 15-3 Using examples, explain how microbes adhere to host cells.

  3. Mechanisms of Pathogenicity • Pathogenicity: the ability to cause disease • Virulence: the extent of pathogenicity

  4. Portals of Entry • Mucous membranes • Skin • Parenteral route • Preferred portal of entry

  5. Numbers of Invading Microbes • ID50: infectious dose for 50% of the test population • LD50: lethal dose (of a toxin) for 50% of the test population

  6. Bacillus anthracis

  7. Toxins

  8. Adherence • Adhesins/ligands bind to receptors on host cells • Glycocalyx: Streptococcus mutans • Fimbriae: Escherichia coli • M protein: Streptococcus pyogenes • Form biofilms

  9. Figure 15.1a Adherence. Adhesin (ligand) Pathogen Host cell surface Receptor Surface molecules on a pathogen, called adhesins or ligands, bind specifically to complementary surface receptors on cells of certain host tissues.

  10. Figure 15.1b-c Adherence. E. coli bacteria (yellow-green) on human urinary bladder cells Bacteria (purple) adhering to human skin

  11. List three portals of entry, and describe how microorganisms gain access through each. 15-1 • The LD50 of botulinum toxin is 0.03 ng/kg; the LD50 of Salmonella toxin is 12 mg/kg. Which is the more potent toxin? 15-2 • How would a drug that binds mannose on human cells affect a pathogenic bacterium? 15-3

  12. How Pathogens Penetrate Host Defenses • 15-4Explain how capsules and cell wall components contribute to pathogenicity. • 15-5 Compare the effects of coagulases, kinases, hyaluronidase, and collagenase. • 15-6 Define and give an example of antigenic variation. • 15-7 Describe how bacteria use the host cell’s cytoskeleton to enter the cell.

  13. Capsules • Prevent phagocytosis • Streptococcus pneumoniae • Haemophilus influenzae • Bacillus anthracis

  14. Cell Wall Components • M protein resists phagocytosis • Streptococcus pyogenes • Opa protein inhibits T helper cells • Neisseria gonorrhoeae • Mycolic acid (waxy lipid)resists digestion • Mycobacterium tuberculosis

  15. Enzymes • Coagulase: coagulates fibrinogen • Kinases: digest fibrin clots • Hyaluronidase: hydrolyzes hyaluronic acid • Collagenase: hydrolyzes collagen • IgA proteases: destroy IgA antibodies

  16. Chapter 15, unnumbered figure A, p. 434. Blocked coronary artery

  17. Chapter 15, unnumbered figure B, p. 434. Necrotizing fasciitis

  18. Chapter 15, unnumbered figure C, p. 434. Mechanism of streptokinase Streptokinase Blood clot Plasminogen Plasmin Fibrin breakdown

  19. Figure 15.2 Salmonella entering intestinal epithelial cells as a result of ruffling. Ruffling of host cell plasma membrane Salmonella typhimurium

  20. Antigenic Variation ANIMATION Virulence Factors: Hiding from Host Defenses

  21. Figure 22.16 How trypanosomes evade the immune system. Clone A Clone B Clone C Relative number of trypanosomes 1 2 4 0 3 Weeks after infection

  22. Penetration into the Host Cell Cytoskeleton • Invasins • Salmonella alters host actin to enter a host cell • Use actin to move from one cell to the next • Listeria

  23. Figure 21.12 Cold sores, or fever blisters, caused by herpes simplex virus.

  24. What function do capsules and M proteins have in common? 15-4 • Would you expect a bacterium to make coagulase and kinase simultaneously? 15-5 • Many vaccines provide years of protection against a disease. Why doesn’t the influenza vaccine offer more than a few months of protection? 15-6 • How does E. coli cause membrane ruffling? 15-7

  25. How Pathogens Damage Host Cells • 15-8Describe the function of siderophores. • 15-9 Provide an example of direct damage, and compare this to toxin production. • 15-10 Contrast the nature and effects of exotoxins and endotoxins.

  26. How Pathogens Damage Host Cells • 15-11 Outline the mechanisms of action of A-B toxins, membrane-disrupting toxins, and superantigens. Classify diphtheria toxin, erythrogenic toxin, botulinum toxin, tetanus toxin, Vibrio enterotoxin, and staphylococcal enterotoxin. • 15-12 Identify the importance of the LAL assay. • 15-13 Using examples, describe the roles of plasmids and lysogeny in pathogenicity.

  27. Figure 15.3 Structure of enterobactin, one type of bacterial siderophore.

  28. Direct Damage • Disrupt host cell function • Produce waste products • Toxins ANIMATION Virulence Factors: Penetrating Host Tissues ANIMATION Virulence Factors: Enteric Pathogens

  29. Of what value are siderophores? 15-8 • How does toxigenicity differ from direct damage? 15-9

  30. The Production of Toxins • Toxin: substance that contributes to pathogenicity • Toxigenicity: ability to produce a toxin • Toxemia: presence of toxin in the host’s blood • Toxoid: inactivated toxin used in a vaccine • Antitoxin: antibodies against a specific toxin

  31. Figure 15.4 Mechanisms of Exotoxins and Endotoxins. exotoxins endotoxins Exotoxins are proteins produced inside pathogenic bacteria, most commonly gram-positive bacteria, as part of their growth and metabolism. The exotoxins are then secreted into the surrounding medium during log phase. Endotoxins are the lipid portions of lipopolysaccharides (LPS) that are part of the outer membrane of the cell wall of gram-negative bacteria (lipid A; see Figure 4.13c). The endotoxins are liberated when the bacteria die and the cell wall breaks apart. Cell wall Exotoxin: toxic substances released outside the cell Salmonella typhimurium, an example of a gram-negative bacterium that produces endotoxins Clostridium botulinum, an example of a gram-positive bacterium that produces exotoxins Endotoxins: toxins composed of lipids that are part of the cell membrane

  32. Exotoxins • Specific for a structure or function in host cell ANIMATION Virulence Factors: Exotoxins

  33. Figure 15.5 The action of an A-B exotoxin. DNA Exotoxin mRNA 1 Bacterium produces and releases exotoxin. A (active) A Exotoxin polypeptides B (binding) B Bacterium A Receptor B Plasma membrane 2 B (binding) component of exotoxin attaches to host cell receptor. Nucleus Cytoplasm Host cell 3 A-B exotoxin enters host cell by receptor-mediated endocytosis. A B 4 A-B exotoxin enclosed in pinched-off portion of plasma membrane during pinocytosis. A B B 5 A-B components of exotoxin separate. The A component alters cell function by inhibiting protein synthesis. The B component is released from the host cell. A B B A Protein

  34. Membrane-Disrupting Toxins • Lyse host’s cells by • Making protein channels in the plasma membrane • Leukocidins • Hemolysins • Streptolysins • Disrupting phospholipid bilayer

  35. Superantigens • Cause an intense immune response due to release of cytokines from host cells • Symptoms: fever, nausea, vomiting, diarrhea, shock, and death

  36. Exotoxin

  37. Exotoxins and Lysogenic Conversion

  38. Endotoxins

  39. Figure 15.6 Endotoxins and the pyrogenic response. Endotoxin Macrophage Hypothalamus of brain Endotoxin Cytokines Nucleus Prostaglandin Fever Blood vessel Pituitary gland Vacuole Bacterium 1 2 3 4 The bacterium is degraded in a vacuole, releasing endotoxins that induce the macrophage to produce cytokines IL-1 and TNF-. The cytokines induce the hypothalamus to produce prostaglandins, which reset the body’s “thermostat” to a higher temperature, producing fever. A macrophage ingests a gram-negative bacterium. The cytokines are released into the bloodstream by the macrophages, through which they travel to the hypothalamus of the brain.

  40. LAL Assay • Limulus amebocyte lysate assay • Amebocyte lysis produces a clot • Endotoxin causes lysis ANIMATION Virulence Factors: Endotoxins

  41. Differentiate an exotoxin from an endotoxin. 15-10 • Food poisoning can be divided into two categories: food infection and food intoxication. On the basis of toxin production by bacteria, explain the difference between these two categories. 15-11

  42. Washwater containing Pseudomonas was sterilized and used to wash cardiac catheters. Three patients developed fever, chills, and hypotension following cardiac catheterization. The water and catheters were sterile. Why did the patients show these reactions? How should the water have been tested? 15-12 • How can lysogeny turn the normally harmless E. coli into a pathogen? 15-13

  43. Pathogenic Properties • 15-14 List nine cytopathic effects of viral infections. • 15-15 Discuss the causes of symptoms in fungal, protozoan, helminthic, and algal diseases. • 15-16 Differentiate portal of entry and portal of exit.

  44. Figure 15.7 Some cytopathic effects of viruses. Inclusion body Cytoplasmic mass Nuclei

  45. Figure 15.8 Transformed cells in culture.

  46. Pathogenic Properties of Fungi • Fungal waste products may cause symptoms • Chronic infections provoke an allergic response • Trichothecene toxins inhibit protein synthesis • Fusarium • Proteases • Candida, Trichophyton • Capsule prevents phagocytosis • Cryptococcus

  47. Pathogenic Properties of Fungi • Ergottoxin • Claviceps • Aflatoxin • Aspergillus • Mycotoxins • Neurotoxins: phalloidin, amanitin • Amanita

  48. Pathogenic Properties of Protozoa • Presence of protozoa • Protozoan waste products may cause symptoms • Avoid host defenses by • Growing in phagocytes • Antigenic variation

  49. Pathogenic Properties of Helminths • Use host tissue • Presence of parasite interferes with host function • Parasite’s metabolic waste can cause symptoms

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