Ch 15 – Microbiology – Flashcards
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5 keys to success for a pathogen |
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-ability to contact host cells -ability to adhere to host cells and resist physical removal -ability to invade host cells -ability to complete for iron and other nutrients -ability to resist immune defenses |
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ability to contact host cells |
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-Helicobacter pylori swim with flagella thorugh mucous layer of stomach and adhere to epithelial cells of the mucous membranes |
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ability to adhere to host cells and resist physical removal |
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-pili (vibrio cholerae) -adhesins (steptococcus pyogenes) -capsules (streptococcus mutans) |
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ability to invade host cell |
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-invasins activate host cell's cytoskeletal machinery enabling bacterial entry into the cell by phagocytosis -Shigella |
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ability to compete for iron and other nutrients |
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-Neiserria |
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ability to resist immune defense (phagocytosis and complement) |
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-Streptococcus pneumonia is able to initially evade phagocytosis and cause infections such as pneumococcal pneumonia, sinusitis, otitis, and meningitis because of its capsule |
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Entry of microorganisms into the host |
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-mucous membranes -skin -parenteral route |
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mucous membrane entry |
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-respiratory tract as airborne particles (water droplets) -gastrointestinal tract (food, water, contaminated objects, fomites-esp. in nosocomial infections) -genitourinary tract (sexual contact) -conjunctiva (airborne particles, abrasion) |
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examples of microorganisms that enter resp., gastro, genital, conj. |
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-respiratory-Bordetella pertussis, influenza virus, Mycobacterium tuberculosis -gastrointestinal- Vibrio cholerae, Mumps virus, Trichinella spiralis -genital-N. gonorrhea, HIV-1, Treponema pallidum -conjuctiva-Herpes simplex virus, staphlococcus, streptococcus |
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entry through skin |
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-insect/animal bites, wounds, injections -Rickettsia rickettsii, Plasmodium, Rabies virus |
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entry thorough parenteral route |
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-tissue beneath skin or into mucous membranes -insect/animal bites, wounds, intraveinous fluids, blood transfusions, catheterization -HIV-1, HBV, Clostridium tetani |
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adherence |
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-attachment of microorganism to host cell mediated by adhesins -results in the production of biofilms (dental plaque) |
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N. gonorrhea uses _____ to attach to ______ |
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-fimbraie -receptors on cells of the genitourinary tract, eyes, and pharynx |
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Treponema pallidum uses _____ to attach to host cells |
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-tapered end as a hook |
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virulence factors |
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-toxins -capsules -cell wall components -enzymes |
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exotoxins |
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-proteins secreted from bacterial cell into surrounding environment -very potent-small amount are necessary to cause -solube-can diffuse into blood -produced by G+ and G- -very specific action on host -converted into toxoids, can be used as vaccine |
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3 types of exotoxins |
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-A-B toxins -membrane disrupting toxins -superantigens |
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A-B toxins |
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-most exoxins -2 parts -active component and binding component |
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Steps of exotoxin (Diptheria) |
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-bacterium produces and releases exotoxins -B-component attaches to host cell receptor -A-B exotoxin enters host by endocytosis -A-B exotoxin enclosed in pinched off portion of plasma membrane of plasma membrane during pinocytosis -A-B components seperate-A alters cell function by inhibiting protein synthesis. B is released |
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membrane disrupting toxins |
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-cause host cells to lyse by -forming pores in plasma membrane (S. aureus) -disrupting phospholipid portion (Clostridium perfringens) -Hemolysin destroys RBCs -Leokocidins kill phagocytic leukocytes |
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superantigens |
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-non-specifically stimulate Th-cells to release large amount of cytokines -results in fever, nausea, vomiting, diarrhea, shock and death |
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Endotoxins |
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-part of G- cell wall (Lipid A) -small amount escape into surrounding fluids when ingested by phagocytes -stimulate macrophages to release high concentrations of cytokines -more general effects on host (shock, fever, diarrhea) |
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Steps of Endotoxins |
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-macrophage ingest G- bacteria -it is degraded in a vacuole releasing endotoxins and stimulating release of cytokines -cytokines are released into bloodstream by macrophages and travel to hypothalmus -induces production of prostaglandins which cause fever |
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capsules |
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-polysaccharides or polypeptides found on surface of bacteria -block attachment of phagocytic cells to bacteria -inhibit phagocytosis -Strep. pneumoniae, Haemophilus influenzae, Bacillus anthracis, Yersinia petsis |
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cell wall components |
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-strep. pyogenes produces M protein found on the cell surface and fimbriae -enhances attachment to host epithelial cells and protects from phagocytosis |
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enzymes |
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-coagulases -kinases -hyaluronidase -collagenase -IgA protease |
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coagulases |
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-coagulate fibringoen present in blood -fibrin clot may protect bacterium from phagocytosis -Staphlococcus |
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kinases |
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-break down fibrin and digest blood clots formed by body to isolate infection -s. pyogens -s. aureus |
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hyaluronidase |
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-digests and damages connective tissues -helps microorganism spread -s. pyogenes -c. perfringens |
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collagenase |
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-breaks down collagen that forms connective tissues of organs, tissues, and muscle -Clostridium |
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IgA protease |
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-Neisseria produces this to destroy IgA (mucosal surfaces) |
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invasins |
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-class of proteins that rearrange actin filaments of host cytoskeleton -enables penetration into the host cell -Salmonella and E. coli |
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Siderophores |
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-proteins released into the medium and take the iron away from iron-transport proteins -iron is a nutritional requirement for most pathogenic bacteria -free iron is very scare in human body -iron is mainly bound to hemoglobin, lactoferrin, transferrin, ferritin |
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pathogenic properties of viruses |
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-evasion of host immune defenses -cytopathic effect |
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evasion of host immune defenses |
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-viruses can grow inside host cells |
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cytopathetic effect |
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-visible effects of viral infection -may result in cell death (cytocidal) -may damage without killing |
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cytopathic effect examples |
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-arrest of synthesis of macromolecules (HSV stops mitosis) -release of cell's lysosomes contents -formation of inclusion bodies (nuclear and/or cytoplasmic aggregates) -formation of syncytium (fusion of adjacent infected cells) -change in the host cell's function (measles virus makes host cell produce IL-12) -production of interferons by infected cells -induction of antigenic changes on host cell -chromosomal changes in infected cell -loss of contact inhibition (unregulated growth) |
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pathogenic properties of fungi |
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-toxins -proteases -capsules |
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fungi toxins |
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-trichothecenes are fungal toxins that inhibit protein synthesis in eukaryotic cells (Fusarium and Stachybotrys) -ergot is a toxin thats grows on grain (alkaloid that causes ergotism-hallucinations (LSD)) -also constricts capillaries and prevents proper blood circulation in limbs -Aflatoxin is produced by Aspergillus flavins (grow on plants-peanuts) -Mycotoxins-phalloidin and amanitin are produced by Amanita phalloides-neurotoxins |
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proteases |
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-Candida albicans-produces a protease that modifies host cell membrane to allow its attachment |
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capsules |
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-Crytococcus neoformans produces a capsule that protects it from phagcytosis |
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Plasmodium |
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invade and reproduce within host cells -lysis |
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Toxoplasma |
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prevents normal acidification and digestion inside the phagocytic vacuoles of the macrophages it infects |
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Giardia lamblia |
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-attaches to the host cell and digests the cells and tissue fluids |
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Trypanosoma and Giardia |
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use antigenic variation |
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exit of microorganisms from host |
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-resp tract- talking, breathing, singing, shouting, coughing, sneezing -dead cells from skin -feces and urine -blood -milk -secretions from vagina and penis |