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
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