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Chp.15. Chp.15. Presentation Transcript

  • Chapter 15: Microbial Mechanisms of pathogenicity
    • Pathogen = microbe or virus able to produce disease
    • Pathogenicity = the ability of a microbe to cause disease in another organism
      • Ex. The host – usually human
    • Virulence = the power of an organism to cause disease
      • It is the degree of pathogenicity
      • Virulent organisms usually produce a violent, severe disease often leading to death
  • Chapter 15: Microbial Mechanisms of pathogenicity
    • Virulence cont.
      • Chickenpox, common cold viruses are pathogens not considered to be virulent
      • Yersinia pestis – bubonic plague, Ebola viruses – virulent pathogens
    • Virulence factors = pathogen produced molecules or structures that allow the cell to invade the host or evade your immune system and may result in disease in the host
  • How do microbes become established in a host
    • Step 1
    • Portal of entry – how pathogens get in or onto the body
      • Mucous membranes – line the conjunctiva of the eye, and the respiratory, Gastrointestinal and genital -urinary tracts
        • Respiratory tract is easiest and most frequently used route – cold, pneumonia, TB, flu, measles, smallpox
  • How do microbes become established in a host
    • Step1:Portal of entry: Mucous membranes
      • Gastrointestinal tract – contacted through food, water, fingers
        • May be destroyed by stomach acids and intestinal enzymes
        • Ex. Polio, hepatitis A, typhoid fever, amoebic dysentery, shigellosis (aka bacilliary dysentery), and cholera are transmitted through the GI tract
          • Pathogens leave (Portal of exit) through the feces to find a new host
  • How do microbes become established in a host
    • Step 1: Portal of entry : Skin
    • Most microbes can’t penetrate unbroken skin
      • Some can penetrate by entering through openings – hair follicles, sweat ducts
      • Fungi can grow in the keratin of the skin and infect the skin or nails
      • Exception to unbroken skin is hookworms
  • How do microbes become established in a host
    • Step 1: Portal of entry : Parenteral route
      • Microbes enter due to trauma to the skin and mucous membranes
      • Ex. Injections, punctures (tetanus), bites, cuts, wounds, or surgery
    • Microbes must enter your body from the preferred portal of entry to cause the disease
      • Ex. Smallpox – mucous membrane of respiratory tract, thru puncture of skin = slight inflammation of skin – immunity, vaccination
  • Portals of Entry “ Many organisms that cause one disease if they enter one body site are harmless if they enter another, e.g., various enteric urinary-tract pathogens.
  • How do microbes become established in a host
    • The ability of a pathogen to establish an infection and possible disease usually depends on the infectious dose which is the # of microbes taken into the body
    • A measure of virulence is the ID50 (infectious dose) = the number of microbes it takes to infect 50% of the population
      • Cutaneous anthrax ID50 = 10 endospores, inhalation anthrax ID50 = 10,000 endospores
    • The potency of a toxin is the LD50 or lethal dose to kill 50 % of a population
  • How do microbes become established in a host
    • Step 2: Adherence or attaching to the host
      • Pathogens attach to host cells by adhesins which are projections on the surface of the bacterium that adhere to complimentary receptors on the host cells
      • Adhesions are associated with fimbriae, glycocalyx, flagella
      • Parasitic worms use hooks, barbs, suckers
  • How do microbes become established in a host
    • Step 2: Adherence
    • Adherence is followed by colonization of the tissue and may involve invasion of the cells
      • Ex. Biofilms – microbes secrete a glycocalyx that aids in surface attachment and to each other
        • This allows them to share nutrients, and they are protected from antimicrobials and your immune system ex. Diphtheria – Corynebacterium diphtheriae
  • Adhesion to Host Tissues
    • For most pathogens, cells must adhere to tissues (and then colonize) before infection can take place, even if ultimately damage results from invasion or exotoxin production.
    • Bacteria typically employ proteins known as Adhesins to attach to host tissues, which usually are located on ends of fimbriae.
    • Alternatively, adhesins can consist of glycocalyx.
  • Step 3: Penetrating and surviving host defenses
    • Capsules – aid in resistance to phagocytosis
      • Streptococcus pneumoniae causes pneumococcal pneumonia – some strains have capsules and are therefore virulent and produce disease and some strains don’t have capsules and are avirulent and don’t cause disease
  • Avoidance of Phagocytosis Capsules are Involved in avoidance of phagocyte-mediated recognition and attachment.
  • Step 3: Penetrating and surviving host defenses
    • Cell wall components – aid in resisting phagocytosis and in adherence of microbes
      • Waxes in cell wall – Mycobacterium tuberculosis resist digestion by macrophages
      • M protein produced by Streptococcus pyogenes aids in attachment to epithelial cells and resistance to phagocytosis by WBCs
  • Step 3: Penetrating and surviving host defenses
    • Enzymes – extracellular enzymes are able to lyse cells, dissolve the material between cells and form or dissolve blood clots
      • Coagulases – enzymes produced by some Staphylococcus – converts fibrinogen to fibrin which causes clotting – the clots protect against phagocytosis
  • Step 3: Penetrating and surviving host defenses
      • Kinases – Staphylococcus and Streptococcus – digests the fibrin thus dissolving the clots formed by the body to isolate the infection
        • Streptokinase – used to remove some blood clots due to heart attack
      • Hyaluronidase – Streptococcus , Staphylococcus, Clostridium – digests hyaluronic acid of connective tissue
  • Step 3: Penetrating and surviving host defenses
      • Collagenase – Clostridium sp. – dissolves collagen framework of muscles – aids in the spread of gas gangrene
      • IgA proteases – destroys host’s defense IgA antibodies
      • Antigenic variation – microbes are able to change their surface antigens ( causes Ab formation)
      • - the immune system recognizes antigens (pathogens) and produces Abs specific for that Ag
  • How Pathogens cause disease or damage
    • Using the hosts nutrients – pathogens need iron to grow
      • Iron in the host’s cell is tightly bound to iron transport proteins such as hemoglobin
      • Some microbes secrete proteins called siderophores which take the iron away from the iron transport proteins and form iron – siderophore complexes. These complexes bind with siderophores receptors on the bacterial surface where the iron is brought into the bacterium either as the whole complex or free iron
      • Cell lysis caused by pathogens can also release iron
  • How Pathogens cause disease or damage
    • Toxins – are poisonous substances produced by some microbes. If toxins are found in the blood = toxemia
    • Exotoxins are proteins usually secreted by Gram + bacteria
      • They are among the most lethal substances known
      • They are specific to a cell type ex. Neurotoxin
  • How Pathogens cause disease or damage
    • Exotoxins cont.
      • The body can produce Abs called antitoxins that provide immunity to exotoxins
      • Toxoids are altered exotoxins that allow the host immune system to produce antitoxins without causing any side effects
        • Can be vaccines ex. Diphtheria, tetanus
  • How Pathogens cause disease or damage
    • Types of exotoxins
      • A-B toxins – most are exotoxins, consists of 2 parts
        • A is the active part that inhibits protein synthesis and kills the host cell
        • Part B is the binding part and binds to host cell
      • Membrane disrupting toxins – cause lysis of host cells by disrupting their plasma membranes
        • Leukocidins – white blood cell killers
        • Hemolysins – target red blood cells
  • How Pathogens cause disease or damage
    • Types of exotoxins cont.
      • Superantigens – provoke an intense immune response
        • Stimulate the proliferation of T cells which in turn release large amounts of cytokines
        • Cytokines are small proteins that regulate immune responses and in high concentrations can cause many sxs – fever, nausea, vomiting, diarrhea, shock and even death
  • How Pathogens cause disease or damage
    • Some exotoxins
      • Diphtheria toxin – Corynebacterium diphtheriae – A-B toxin, bacteria has to be infected by lysogenic phage (prophage) carrying the tox gene
      • Erythrogenic toxin- Streptococcus pyogenes –is a superantigen that damages plasma membranes of capillaries under the skin and produces red skin rash ex. Scarlet fever
  • How Pathogens cause disease or damage
    • Some exotoxins cont.
      • Botulinum toxin – Clostridium botulinum –
      • A-B neurotoxin that causes flaccid paralysis when ingested
      • -- Tetanus toxin – Clostridium tetani – A-B neurotoxin aka tetanospasmin which blocks the relaxation pathway of muscle control causing spasmodic contraction = tetanus
      • ex. Lockjaw-mouth, opisthotonos – back ms
      • pg.648 fig. 22.6
  • How Pathogens cause disease or damage
    • Some exotoxins cont
      • Vibrio enterotoxin – Vibrio cholerae –A-B enterotoxin (aka cholera toxin) that causes the release of large amounts of fluids and electrolytes (ions) that result in severe diarrhea ex. Cholera
      • Staphylococcus enterotoxin – S. aureus – superantigen that affects the intestines the same way as cholera toxin
  • How Pathogens cause disease or damage
    • Endotoxins = lipid A which is the lipid portion of LPS (outer membrane) of G- cell wall
      • Not secreted but is released upon death and lysis of the bacteria or during multiplication of bacteria
      • They stimulate macrophages to release large amounts of cytokines which are toxic at high concentrations
      • Lab test for endotoxins = Limulus amoebocyte lysate (LAL) assay
        • Uses WBCs (amoebocytes) of horseshoe crab ( Limulus polyphemus ) which lyse if endotoxins are present releasing a clotting protein
        • Draw chart
  • Pathogenic Properties of Viruses
    • Cytopathic Effects (CPE) = visible damage to host cell
      • Cytocidal effects kill the cell
      • Noncytocidal effects damage cell – not lethal
    • A virus can produce one or more of the following CPE
      • Stops the synthesis of macromolecules
      • Cause cell’s lysosomes to release their enzymes and lyse themselves
    • CPE cont. pg 466
      • Inclusion bodies = granules found in the cytoplasm (rabies virus) or nucleus (herpes virus) if some infected cells
      • Syncytium = adjacent infected cells fuse to form a multinucleated cell
      • Change in fx but otherwise no visible change ex. Decreased hormone production
      • Cell produces interferon which protects neighboring, uninfected cells from the virus
  • Pathogenic Properties of Viruses
    • CPE cont.
      • Antigenic changes on the surface of infected cells that target the cells for destruction by the immune system
      • Chromosomal changes in the host cell, oncogenes may be activated
      • Cancer causing viruses transform host cells resulting in abnormal cell shape and a loss of contact inhibition which causes unregulated cell growth
  • Pathogenic properties of fungi, protozoa, helminths and algae
    • Protozoa and helminths grow on host tissues causing cellular damage
      • Their waste products may contribute to sxs of disease
    • Algae (dinoflagellates) produce neurotoxins called saxitoxin and people become ill after eating mollusks that feed on the algae
  • Pathogenic properties of fungi, protozoa, helminths and algae
    • The toxin ergot is associated with some fungi and cause ergotism which can result in LSD type hallucinations
      • Ergot is contained in resistant mycelia called sclerotia in Claviceps purpurea – fungi that grow on grains
      • Ergot can constrict blood capillaries and cause gangrene in extremities
  • Pathogenic properties of fungi, protozoa, helminths and algae
    • Aflatoxin is produced by the mold Aspergillus flavus and can cause cancer in the liver of animals
    • Amanita phalloides (deathcap) is a toxic mushroom which contains the mycotoxins phalloidin and amanitin.
      • These neurotoxins are so potent that ingestion may cause death
  • Portals of exit
    • To complete the cycle of infectious disease and to allow transmission to new hosts, pathogens require a portal of exit
    • In some cases the portal of exit relates to the area of the body infected
    • Infections of the respiratory tract pathogens exit through the nose (sneezing) or mouth (coughing)
    • Pathogens of GI tract exit – saliva, feces
    • Pathogens of genitourinary tract exit - secretions