copyright © 2010 pearson education, inc. microbial mechanisms of pathogenicity chapter 15
TRANSCRIPT
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MICROBIAL MECHANISMS OF PATHOGENICITY
Chapter 15
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Mechanisms of Pathogenicity
Pathogenicity: The ability to cause disease
Virulence: The extent of pathogenicity, the amount of “damage” done
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Portals of Entry
Mucous membranes- nose/ mouth/ lungs/ intestines
Skin
Parenteral route- injection/ IV/ wound
Preferred portal of entry
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Portals of Entry
Streptococcus pneumoniae if inhaled can cause pneumonia if enters the G.I. Tract, no disease
Salmonella typhi if enters the G.I. Tract can cause Typhoid Fever if on skin, no disease
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Portal of Entry ID50
Skin 10–50 endospores
Inhalation 10,000–20,000 endospores
Ingestion 250,000–1,000,000 endospores
Bacillus anthracis
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Portal of Entry ID50
Botulinum 0.03 ng/kg
Shiga toxin 250 ng/kg
Staphylococcal enterotoxin 1350 ng/kg
Toxins
Shiga:1/160th of human hair
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Adherence
Adhesins/ligands bind to receptors on host cells Glycocalyx: Streptococcus mutans Fimbriae: Escherichia coli M protein: Streptococcus pyogenes
Form biofilms
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Adherence
Figure 15.1
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Adherence
Figure 15.1
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Adherence
Figure 15.1
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Capsules
Prevent phagocytosis Streptococcus pneumoniae Haemophilus influenzae Bacillus anthracis
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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
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Enzymes
Coagulase: Coagulates fibrinogen
Kinases: Digest fibrin clots
Hyaluronidase: Hydrolyzes hyaluronic acid
Collagenase: Hydrolyzes collagen
IgA proteases: Destroy IgA antibodies
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Membrane Ruffling
Figure 15.2
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Antigenic Variation
Alter surface proteins
Figure 22.16
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Invasins Salmonella
alters host actin to enter a host cell
Use actin to move from one cell to the next Listeria
Penetration into the Host Cell Cytoskeleton
Figure 15.2
Salmonella
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Direct Damage
Disrupt host cell function
Produce waste products
Toxins
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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
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Exotoxins and Endotoxins
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Exotoxins
Specific for a structure or function in host cell
Figure 15.4a
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Membrane-Disrupting Toxins
Lyse host’s cells by Making protein channels in the plasma
membrane– Leukocidins– Hemolysins– Streptolysins
Disrupting phospholipid bilayer
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Superantigens
Cause an intense immune response due to release of cytokines from host cells
Symptoms: fever, nausea, vomiting, diarrhea, shock, and death
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Endotoxins and the Pyrogenic Response
Figure 15.6
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LAL Assay
Limulus amoebocyte lysate assay
Amoebocyte lysis produces a clot
Endotoxin causes lysis
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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
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Pathogenic Properties of Fungi
Ergot toxin Claviceps
Aflatoxin Aspergillus
Mycotoxins Neurotoxins: Phalloidin, amanitin
Amanita
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Pathogenic Properties of Protozoa
Presence of protozoa
Protozoan waste products may cause symptoms
Avoid host defenses by Growing in phagocytes Antigenic variation
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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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Pathogenic Properties of Algae
Paralytic shellfish poisoning Dinoflagellates Saxitoxin
Figure 27.13
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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
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Mechanisms of Pathogenicity
Figure 15.9