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TRANSCRIPT
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
PowerPoint® Lecture Slide Presentation prepared by Christine L. Case
Microbiology
B.E Pruitt & Jane J. Stein
AN INTRODUCTIONEIGHTH EDITION
TORTORA • FUNKE • CASE
Chapter 15Microbial Mechanisms of Pathogenicity
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Microbial Mechanisms of Pathogenicity
• Pathogenicity The ability to cause disease
• Virulence The extent of pathogenicity
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• Mucous membranes – resp. tract, GI tract, conjunctiva, urogenital
• Skin – damaged skin, hair follicles, sebaceous gland/sweat gland ducts
• Parenteral route – direct deposition into tissues – punctures, bites, lacerations, injections, splitting
Portals of Entry
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• ID50: Infectious dose for 50% of the test population
• Number of particles required to cause disease
• LD50: Lethal dose (of a toxin) for 50% of the test population
• Potency of a toxin
Numbers of Invading Microbes
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Bacillus anthracis
Portal of entry ID50
Skin 10-50 endospores
Inhalation 10,000-20,000 endospores
Ingestion 250,000-1,000,000 endospores
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• Adhesions/ligands bind to receptors on host cells
• Glycocalyx Streptococcus mutans• Glucosyltransferase converts glucose to dextran (sticky) to form glycocalyx
• Fimbriae Escherichia coli• Adhesins specific for cells in GI tract
• M protein Streptococcus pyogenes• Cell wall component
• Opa protein Neisseria gonorrhoeae• Outer membrane protein, in addition to fimbriae
• Tapered end Treponema pallidum
Adherence
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• Coagulase S. aureus Coagulate blood
• Kinases S. pyogenes, S. aureus Digest fibrin clots• Hyaluronidase Streptococci, Clostridia Hydrolyses hyaluronic
acid (cell junction carbohydrates)
• Collagenase Clostridia Hydrolyzes collagen
• IgA proteases Nieisseria Destroy IgA antibodies
• Siderophores Take iron from host iron-binding proteins
• Antigenic variation Alter surface proteins to evade immune response
Enzymes
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Penetration into the Host Cell
Figure 15.2
Invasins –
rearrange actin fibersassociated with host cell membraneSalmonella, E. coli
Causes membrane ‘ruffling” – result of cytoskeletal disruption
Microbe sinks into ruffle and is Ingested by cell.
Actin can be used as propulsion once inside host cell (shigella spp)
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Toxins
• Toxin Substances that contribute to pathogenicity
• Toxigenicity Ability to produce a toxin
• Toxemia Presence of toxin the host's blood
• Toxoid Inactivated toxin used in a vaccine
• Antitoxin Antibodies against a specific toxin
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Exotoxin – many are enzyme-like
Source Mostly Gram +
Metabolic product By-products of growing cell
Chemistry Protein
Fever? No (mostly…except type 1)
Neutralized by antitoxin Yes (good antigen)
LD50Small
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• A-B toxins or type III toxins
Exotoxins
Figure 15.5
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• Membrane-disrupting toxins or type II toxins
• (example – Staph. aureus, Streptococci spp.)
• Lyse host’s cells by:
• Making protein channels in the plasma membrane (e.g., leukocidins, hemolysins)
• Disrupting phospholipid bilayer
• Also allow escape from phagosomes into cytoplasm
Exotoxins
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• Superantigens or type I toxins
• Cause an intense immune response due to release of cytokines from T-lymphocytes
• Fever, nausea, vomiting, diarrhea, shock, death
Exotoxins
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Exotoxins
Exotoxin Lysogenic conversion
• Corynebacterium diphtheriae A-B toxin. Inhibits protein synthesis. +
• Streptococcus pyogenes Membrane-disrupting. Erythrogenic. +
• Clostridium botulinum A-B toxin. Neurotoxin +
• C. tetani A-B toxin. Neurotoxin
• Vibrio cholerae A-B toxin. Enterotoxin +
• Staphylococcus aureus Superantigen. Enterotoxin.
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Exotoxins
Figure 15.4a
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Endotoxin
Figure 15.4b
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Endotoxins
Figure 15.6
(A cytokine)
TNF – tumor necrosis factor – another cytokine secreted by phagocytes– damages capillaries
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Endotoxins
Source Gram–
Metabolic product Present in LPS of outer membrane
Chemistry Lipid-polysaccharide
Fever? Yes
Neutralized by antitoxin No (poor antigen)
LD50 Relatively large
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Test for endotoxin presence
Endotoxins are heat resistant, may persist on surfaces.
LAL- Limulus Amoebocyte Lysate – presence of minute amounts of endotoxin lyses amoebocytes which release lysate
Lysate then causes coagulation of the media
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Cytopathic Effects of Viruses
Table 15.4
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• Fungal waste products may cause symptoms
• Chronic infections provoke an allergic response
• Tichothecene toxins inhibit protein synthesis• (headaches, chills, nausea, vomiting, visual disturbances)
• Fusarium, Stachybotris (common molds)
• Proteases – modify host cell membranes• Candida, Trichophyton (cutaneous mycoses)
• Capsule prevents phagocytosis• Cryptococcus – (meningitis)
• Ergot toxin – LSD is a derivative
• Claviceps purpurea - grain
Pathogenic Properties of Fungi
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• Aflatoxin - carcinogenic
• Aspergillus
• Mycotoxins
• Neurotoxins: Phalloidin, amanitin
• Amanita – “Death cap mushroom”
Pathogenic Properties of Fungi
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• Presence of protozoa and protozoan waste products may cause symptoms
• Plasmodium (malaria)- Invasion and lysis
• Toxoplasma – are phagositized and survive in phagosome of macropahge
• Avoid host defenses by
• Growing in phagocytes
• Antigenic variation
Pathogenic Properties of Protozoa
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• Use host tissue for nutrients/incubation
• Presence of parasite interferes with host function
• Parasite's metabolic waste can cause symptoms
• Wuchereria bancrofti roundworm - elephantiasis
• Tapeworms, flukes
Pathogenic Properties of Helminths
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• Neurotoxins produced by dinoflagellates
• Saxitoxin
• Paralytic shellfish poisoning
Pathogenic Properties of Algae
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• Respiratory tract
• Coughing, sneezing
• Gastrointestinal tract
• Feces, saliva
• Genitourinary tract
• Urine, vaginal secretions
• Skin
• Blood
• Biting arthropods, needles/syringes
Portals of Exit
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Mechanisms of Pathogenicity
Figure 15.9