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Module 9 Pathogenicity

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Module 9 Pathogenicity Module 9 Pathogenicity © 2013 Pearson Education, Inc. Chapter 15 Microbial Mechanisms of Pathogenicity © 2013 Pearson Education, Inc. LecturesLectures prepared prepared by byChristine Helmut L. Kae Case Microbial Mechanisms of Pathogenicity § Pathogenicity: the ability of a pathogen to cause a disease by overcoming the defenses of the host § Virulence: the degree or extent of pathogenicity § A pathogenic organism is able to cause a disease § A pathogen that is highly virulent causes damaging disease © 2013 Pearson Education, Inc. Portals of Entry § Portals of entry: avenues that pathogens can use to gain entry into the human body § Mucous membranes § Skin § Parenteral route © 2013 Pearson Education, Inc. Mucous membranes § Respiratory tract, gastrointestinal (GI) tract, genitourinary (GU) tract, conjunctiva § Most common portals are respiratory, GI tracts § Inhaled through mouth, nose § Eaten - most killed by acid, bile § GU tract is portal for pathogens that cause STDs © 2013 Pearson Education, Inc. Skin § Largest organ, first line of defense § Unbroken skin is impenetrable to most microbes § Some gain access through openings in skin § Some fungi can infect skin directly © 2013 Pearson Education, Inc. Parental Route § Access through breaks in skin § From cuts, bites, drying § All microbes have preferred portal of entry § Some microbes have multiple portals of entry © 2013 Pearson Education, Inc. Numbers of Invading Microbes § Likelihood of disease increases as number of pathogens increase § Too few can be overwhelmed by immune system © 2013 Pearson Education, Inc. Numbers of Invading Microbes § Virulence of a disease expressed as ID50: infectious dose for 50% of the test population § Expression of relative virulence under experimental conditions – can be different for different portals § Bacillus anthracis has 3 portals of entry Portal of Entry ID50 Parenteral Route 10-50 endospores Inhalation 10,000-20,000 endospores Ingestion 250,000-1,000,000 endospores © 2013 Pearson Education, Inc. Numbers of Invading Microbes § Potency of toxin expressed as LD50: lethal dose for 50% of the test population Toxin LD50 in mice Botulinum toxin 0.03 ng/kg Shiga toxin 250 ng/kg Staphylococcal enterotoxin 1350 ng/kg © 2013 Pearson Education, Inc. Virulence Factors § Structures of molecules that a pathogen uses to cause disease § Many different virulence factors exist © 2013 Pearson Education, Inc. Adherence § Means of attachment § Necessary for pathogenicity in most pathogens § Interfere with binding, interfere with infection § Adhesins (ligands) bind to complementary receptors § Adhesins may be located on glycocalyx, surface structures § Adhesins usually glycoproteins, lipoproteins § Binding is specific for certain host tissues, receptors © 2013 Pearson Education, Inc. 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. © 2013 Pearson Education, Inc. How Pathogens Penetrate Host Defenses § Pathogens must penetrate tissue to cause disease § Several factors contribute to the ability of pathogens to invade a host © 2013 Pearson Education, Inc. Capsules § Capsules impair phagocytosis (being eaten) § Prevents binding to pathogen § Capsules do not mean a bacterium is virulent © 2013 Pearson Education, Inc. Cell Wall Components § Some cell walls contain chemicals that contribute to virulence § M protein resists phagocytosis § Streptococcus pyogenes § Opa protein inhibits T helper cells § Neisseria gonorrhoeae § Mycolic acid (waxy lipid) resists digestion § Mycobacterium tuberculosis © 2013 Pearson Education, Inc. Enzymes § Coagulase: coagulates fibrinogen § Kinases: digest fibrin clots § Hyaluronidase: hydrolyzes hyaluronic acid § Collagenase: hydrolyzes collagen § IgA proteases: destroy IgA antibodies © 2013 Pearson Education, Inc. Antigenic Variation § During pathogenesis, body produces antibodies to fight infection § Bind to antigens on surface of bacteria § Antigenic variation: ability to alter surface antigen § Changes slowly over time § By the time body produces antibodies, surface antigen has changed § Influenzavirus, N. gonorrhoeae, Trypanosoma brucei (African sleeping sickness) © 2013 Pearson Education, Inc. How Bacterial Pathogens Damage Host Cells § Bacteria can damage host by: § Using host’s nutrients § Direct damage § The production of toxins © 2013 Pearson Education, Inc. Using Host’s Nutrients § Siderophores: proteins that tightly bind iron § Iron is required for growth § Iron in human body is tightly bound § Some pathogens release siderophores to take away iron © 2013 Pearson Education, Inc. Direct Damage § A number of ways that microbes can damage cells § Grow within cells, multiply and rupture cell § Attach to host cell and cause damage as pathogen uses host for nutrients § Penetrate hosts by secreting enzymes © 2013 Pearson Education, Inc. Toxins § Toxins: poisonous substances that are produced by some microbes § Toxigenicity: ability of microbes to produce toxins § Two types of toxins § Endotoxins § Exotoxins © 2013 Pearson Education, Inc. Exotoxins § Exotoxins: protein toxins made inside bacterium and secreted to its surroundings § Many are enzymes, so small amounts harmful § Can act over and over again Exotoxin: toxic substances released Clostridium botulinum, an outside the cell example of a gram-positive bacterium that produces exotoxins © 2013 Pearson Education, Inc. Exotoxins § Soluble in body fluids, can be transported all over body § Diseases caused by bacteria that produce toxins are a direct result of toxin § Staphylococcal food poisoning is an intoxication § Antitoxins: antibodies produced by the body that provide immunity to toxins © 2013 Pearson Education, Inc. Types of exotoxins § A-B toxins: consist of two parts, “A” and “B” § A part is active (enzyme) component § B part is the binding component § Diptheria toxin is A-B toxin © 2013 Pearson Education, Inc. Membrane Disrupting Toxins § Lyse host cells by making protein channels in the plasma membrane – Leukocidins – Hemolysins – Streptolysins § Disrupts phospholipid bilayer © 2013 Pearson Education, Inc. Superantigens § Provoke very intense immune response § Stimulate proliferation (division) of T cells § Release chemicals, cytokines, that regulate immune response § Too many cytokines in blood à fever, shock, death © 2013 Pearson Education, Inc. Endotoxins § Part of cell wall of gram-negative bacteria § LPS portion of outer membrane § Endotoxin is the lipid portion, called Lipid A Exotoxins are proteins, Endotoxins are lipids © 2013 Pearson Education, Inc. Endotoxins § Endotoxins are released when Gram-negative bacteria die and cells lyse § Liberates endotoxins § Antibiotics can cause lysis à release LPS Endotoxins: toxins composed of lipids Intact cell that are part of the Dead cell cell membrane © 2013 Pearson Education, Inc. Endotoxins § All endotoxins produce the same signs and symptoms § Chills, fever, weakness, aches, shock, death § Disseminated intravascular clotting § Shock: life threatening drop in blood pressure § Endotoxic shock: shock produced by Gram- negative bacterial endotoxin © 2013 Pearson Education, Inc. Endotoxins Endotoxins cause fever (by inducing the release of cytokines) and shock © 2013 Pearson Education, Inc. Plasmids and Pathogenicity § R factors carry antibiotic resistance genes § Others can carry virulence factors § Toxins – tetanus neurotoxin, staphylococcal enterotoxin § Fimbriae, adhesins, enzymes (coagulase) © 2013 Pearson Education, Inc. Lysogeny and Pathogenicity § Prophage: phage DNA incorporated into bacterial chromosome § Prophage can provide new properties to bacteria § Lysogenic conversion: change in characteristics due to a prophage § Diptheria toxin, staphylococcal toxin, capsule of S. pneumoniae are encoded by prophages § Can transfer virulence genes to nonpathogenic strains © 2013 Pearson Education, Inc. Figure 13.12 The lysogenic cycle of bacteriophage λ in E. coli. 1 Phage attaches 5 Occasionally, the prophage may excise Phage DNA to host cell and from the bacterial chromosome by another (double-stranded) injects DNA. recombination event, initiating a lytic cycle. Bacterial chromosome Many cell divisions Lytic Lysogenic cycle cycle 4A Cell lyses, releasing 2 Phage DNA circularizes and enters 4B Lysogenic bacterium phage virions. lytic cycle or lysogenic cycle. reproduces normally. Prophage OR 3A New phage DNA and 3B Phage DNA integrates within the proteins are synthesized bacterial chromosome by and assembled into virions. recombination, becoming a prophage. © 2013 Pearson Education, Inc. Pathogenic Properties of Viruses § Viruses have a number of mechanisms to evade immune system § Can grow inside of host cells § Some can “hide” attachment sites - HIV has attachment sites too small for antibodies to bind § Some attack immune cells - HIV © 2013 Pearson Education, Inc. Cytopathic Effects of Viruses § Cytopathic effects (CPE): visible effects of viral infection § CPE used to diagnose many viral infections © 2013 Pearson Education, Inc. Figure 15.7 Some cytopathic effects of viruses. Inclusion body Cytoplasmic mass Nuclei © 2013 Pearson Education, Inc. Figure 15.8 Transformed cells in culture. © 2013 Pearson Education, Inc. Cytopathic Effects of Viruses © 2013 Pearson Education, Inc. Pathogenic Properties of Fungi § Fungal waste products may cause symptoms § Chronic infections provoke an allergic response § Tichothecene: toxins that inhibit protein
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