Establishment of InfectionPortals of entryPowerPoint PresentationSlide 4Slide 5Slide 6Slide 7Slide 8Slide 9Slide 10Slide 11Damage to the HostBacterial Damage to Host CellsSlide 14Slide 15Slide 16Slide 17Slide 18Slide 19Slide 20Slide 21Mechanisms of Viral PathogenesisSlide 23Mechanisms of Eukaryotic PathogenesisSlide 25Slide 26Portals of ExitSlide 28Establishment of Infection•In order to cause disease pathogen must follow a series of steps–Gain entrance to host –Adherence–Colonization –Avoid Host Defenses –Cause host damagePortals of entry1. Mucus membranes•Respiratory tract •Gastrointestinal tract•Genitourinary tract•Placenta 2. Skin3. Parenteral route•Bite, puncture, injection, wound•Most microbes have a preferred portal of entry–Streptococci when inhaled may cause pneumonia; when ingested they do not •A few microbes cause illness no matter how they enter–May cause different illness based on portal–Plague has 2 forms; bubonic and pneumonic–Anthrax has 3 forms•Adherence (adhesion)–Critical Step–Bacteria use adhesins (ligands)–Viruses has surface attachment proteins –Binding to host cells receptors is highly specific•Colonization–Organism must multiply in order to colonize–New organisms must compete with established organisms for nutrients and space–May form biofilms•Virulence factors–Structural or physiological characteristics that aid in penetrating or avoiding host defenses•Capsules–Avoid phagocytosis; Prevents dessication; aids attachment •Incomplete phagocytosis –Escape the phagosome–Prevent fusion with lysozome–Survive inside phagolysozome•Fimbrae –Attachment •Components of cell wall –M proteins of Streptococcus–Mycolic acid of Mycobacteria and Norcardia –Outer membrane of Gram- bacteria•Extra-cellular enzymes (exoenzymes)–Coagulases –Kinases–Hyaluronidase•Dissolves hyaluronic acid–Collagenase–IgA proteases –Leukocidins•Antigenic variation–Avoid antibodies by altering surface antigens –Neisseria varies pili type•Penetration into host cytoskeleton –Manipulate actin to penetrate cells and to move between cells–Some pathogens induce non-phagocytic cells into endocytosis–Disruption of cytoskeleton may cause membrane rufflingDamage to the Host•In order to cause disease pathogen must cause damage–Damage facilitates dispersal of organisms•Vibrio cholerae causes diarrhea•Bordetella pertussis causes coughing–Damage can be direct result of pathogen such as toxin production or indirect via immune responseBacterial Damage to Host Cells•Use host cell’s nutrients•Binding to and invading host cells•Induce hypersensitivity reactions (allergies)•Production of toxins (Toxigenicity) –May be exotoxins or endotoxins–Exotoxins –Produced by G+ bacteria•Produced as part of their metabolism•Secreted externally or released following cell lysis•Proteins–Enzymatic nature –Highly soluble–Heat Liable–Among most lethal substances –Toxoids •Inactivated exotoxins•Induce antitoxins that provide immunity–Antibodies against a specific toxin•Passive immunity in form of antitoxin can be given as treatment–Grouped into functional categories•Neurotoxins•Enterotoxins•Cytotoxins•Staphylococcus aureus –enterotoxin – may be heat stable –exofoliatin toxin•Scalded skin syndrome–Toxic Shock Syndrome (cytotoxin) •Vibrio cholera–cholera enterotoxin•Clostridium botulinum –botulinum neurotoxin•Clostridium perfringens–Gas gangrene•Clostridium tetani –tetanus neurotoxin•Endotoxins –part of the outer portion of the G- cell wall–lipopolysaccharides (LPS) •lipid portion (lipid A) –Released when cells die and cell walls lyse –Antibiotics used to treat diseases can lyse cells•May cause an immediate worsening of symptoms–All endotoxins produce the same symptoms•Chills, fever, weakness, aches•May activate blood clotting proteins •May cause septic shock that can be fatal – Heat stable; not suitable for use as toxoids•Do not cause formation of antitoxins–Antibodies may enhance action of toxins–Salmonella typhi, Proteus spp. and Neisseria meningitidis•Cytopathic effects•Avoiding immune responses•Antibodies interact with extracellular viruses only•Viruses can remain intracellular by forcing neighboring cells to fuse in the formation of syncytium•Viruses can outpace body’s capacity to produce antibodyMechanisms of Viral Pathogenesis•Some virus-infected cells release interferons to warn neighbor cells–Anti-viral proteins –Helps limit viral replication–Some viruses encode specific proteins to interrupt activity of interferonsMechanisms of Eukaryotic Pathogenesis•Fungi–Generally opportunistic–Most serious fungal infections caused by dimorphic fungi–Some produce mycotoxins•Claviceps; Ergot toxin•Aspergillus; Aflatoxin•Amanita; Neurotoxins•Parasites–Most live within intestinal tract or enter body via bite of an arthropod–Use host nutrients–Presence of parasite interferes with host function–Parasite's metabolic waste can cause symptoms•Algae–A few species produce neurotoxins•Alexandrium produces toxin that causes paralytic shellfish poisoning •Produces symptoms similar to botulismPortals of Exit•Respiratory and gastrointestinal tracts–Most common •Genitourinary tract•Skin/wounds •Biting insects •Contaminated needles and