Microbial Mechanisms of Pathogenicity Copyright 2006 Pearson Education
Microbial Mechanisms of Pathogenicity Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Microbial Mechanisms of Pathogenicity Microbial pathogenesis is the process by which microorganisms cause disease. Microbial pathogenesis begins with exposure and adherence of microorganisms to host cells (Fig), followed by invasion, infection, and ultimately, disease. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Infection is the growth of microorganisms that are not normally present within the host. A host is an organism that harbors a pathogen, another organism that lives on or in the host and causes disease. Disease is tissue damage or injury that impairs host function. Unique properties of each pathogen contribute to its pathogenicity, the ability of a microorganism to cause disease. Pathogenicity differs considerably among pathogens, as does the resistance or susceptibility of the host to the pathogen. An opportunistic pathogen causes disease only in the absence of normal host resistance. For example, even normal microflora can cause infections and disease if host resistance is compromised, as may happen in diseases such as cancer and acquired immunodeficiency syndrome (AIDS). Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
OVERVIEW Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
OVERVIEW Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Portals of Entry or How Microbes Enter a Host § Mucous membranes § Skin § Parenteral route Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Portals of Entry or How Microbes Enter a Host Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Portals of Entry or How Microbes Enter a Host Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Numbers of Invading Microbes § ID 50: Infectious dose for 50% of the test population. § LD 50: Lethal dose (of a toxin) for 50% of the test population. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Bacillus Anthracis Portal of Entry ID 50 Skin 10 -50 endospores Inhalation 10, 000 -20, 000 endospores Ingestion 250, 000 -1, 000 endospores Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Adherence § Adhesions/ligands bind to receptors on host cells § Glycocalyx: Streptococcus mutans § Fimbriae: Escherichia coli § M protein: Streptococcus pyogenes § Opa protein: Neisseria gonorrhoeae § Tapered end: Treponema pallidum Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Adherence Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
How Bacterial Pathogens Penetrate Host Defenses Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
How Bacterial Pathogens Penetrate Host Defenses § Capsule § Cell Wall Components – M protein, Opa, mycolic acid Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Chemicals that Promote Bacterial Invasions § Coagulase: Coagulate blood § Kinases: Digest fibrin clots § Hyaluronidase: Hydrolyses hyaluronic acid § Collagenase: Hydrolyzes collagen § Ig. A proteases: Destroy Ig. A antibodies § Siderophores: Take iron from host iron-binding proteins § Antigenic variation: Alter surface proteins § Invasins – cause ruffling of membrane and enhance penetration Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Penetration into the Host Cell Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Figure 15. 2
HOST CELL DAMAGE Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
ROBBING THE HOST CELL OF NUTRIENTS Takes it from: Hemoglobin, lactoferrin, Transferrin, and Ferritin Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Siderophore with Iron
DIRECT DAMAGE OCCURS AS BACTERIAL CELLS MULTIPLY AND RUPTURE INFECTED CELLS. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Toxins § Toxin: Substances that contribute 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. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
DISEASES Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Table 15. 4
Endotoxins Source: Relation to microbe: Gram – Present in LPS of outer membrane Chemistry: Lipid Fever? Yes Neutralized by antitoxin? No LD 50: Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Relatively large Figure 15. 4 b
Exotoxin Source: Relation to microbe: Chemistry: Mostly Gram + By-products of growing cell Protein Fever? No Neutralized by antitoxin? Yes LD 50: Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Small Figure 15. 4 a
Exotoxins § A-B toxins Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Figure 15. 5
Exotoxins § Membrane-disrupting toxins § Lyse host’s cells by § Making protein channels in the plasma membrane (e. g. , leukocidins, hemolysins). § Disrupting phospholipid bilayer. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Exotoxins § Superantigens § Cause an intense immune response due to release of cytokines from host cells. § Fever, nausea, vomiting, diarrhea, shock, and death. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Exotoxins § Specific for a structure or function in host cell Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Figure 15. 4 a
Exotoxins Exotoxin Lysogenic conversion 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 + Superantigen. + Corynebacterium diphtheriae Staphylococcus aureus Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Endotoxins Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Figure 15. 6
Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Cytopathic Effects of Viruses Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Table 15. 4
Pathogenic Properties of Fungi § Fungal waste products may cause symptoms. § Chronic infections provoke an allergic response. § Tichothecene toxins inhibit protein synthesis. § Fusarium § Proteases § Candida, Trichophyton § Capsule prevents phagocytosis. § Cryptococcus § Ergot toxin § Claviceps Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Pathogenic Properties of Fungi § Aflatoxin § Aspergillus § Mycotoxins § Neurotoxins: Phalloidin, amanitin § Amanita Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Pathogenic Properties of Protozoa § Presence of protozoa. § Protozoan waste products may cause symptoms. § Avoid host defenses by § Growing in phagocytes § Antigenic variation Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Pathogenic Properties of Helminths § Use host tissue. § Presence of parasite interferes with host function. § Parasite's metabolic waste can cause symptoms. Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
Pathogenic Properties of Algae § Paralytic shellfish poisoning § Dinoflagellates § Domoic acid intoxication § Diatoms Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Figure 27. 15
Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings Figure 15. 9 (5 of 5)
Portals of Exit § Respiratory tract § Coughing and sneezing § Gastrointestinal tract § Feces and saliva § Genitourinary tract § Urine and vaginal secretions § Skin § Blood § Biting arthropods and needles or syringes Copyright © 2006 Pearson Education, Inc. , publishing as Benjamin Cummings
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