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Chapter 25: Microbial Infection and Pathogenesis

Alexandra Bozan Microbiology English 115 cards

Cards in this deck (115)

  1. 1infectiongrowth of microorganisms on or in the host
  2. 2diseaseactual tissue damage or injury that impairs host function
  3. 3Pathogens typically adhere to _____ _____epithelial cells
  4. 4adherenceenhanced ability of a microorganism to attach to a cell or a surface
  5. 5portal of entryhow pathogens gain access to host tissues
  6. 6portal of entry examplesmucous membranes, skin surface, puncture wounds, insect bites, cuts, or other abrasions
  7. 7pathogen that gains access to incompatible tissues is typically _____ineffective
  8. 8Receptor molecules coating the surfaces of both the pathogen and cells of its host are often critical foradhering the pathogen to host tissues
  9. 9the complementary nature of the pathogen and host cell receptors alerts the pathogen thatit has arrived on a suitable infection site
  10. 10adhesins- Receptors on the pathogen surface
    - composed of glycoprotein or lipoprotein
    - covalently bound to outer layer of the cell
  11. 11Host cell receptors are typically _____ or complex membrane _____- glycoproteins
    - lipids
  12. 12name some adherence structures of pathogensCapsules, Fimbriae, Pili, and Flagella
  13. 13Some adhesins form part of an outer cell surface structure that may or may not be covalently linked to components of the _____ _____cell wall
  14. 14capsule- contains specific receptors that facilitate adherence to host tissues
    - sticky nature assists in the overall attachment process
    - important for protecting pathogenic bacteria from host defenses
  15. 15_____ and _____ are bacterial cell surface protein structures that function in attachment- Fimbriae
    - pili
  16. 16Among the best-characterized fimbriae are the _____ ___ fimbriae of enteric bacteria- type I
  17. 17Pili- typically longer/fewer in # than fimbriae
    - used for attachment and some for conjugation
  18. 18Both pili and fimbriae function by specifically binding to host cell surface glycoproteins initiating _____- adherence
  19. 19_____ may also facilitate adherence of bacterial cells to host cells although their role is thought to be less important than that of fimbriae and pili.Flagella
  20. 20colonizationgrowth of a microorganism after it has gained access to host tissues
  21. 21colonization begins at _____, naturally exposed to harmless and necessary _____ and _____ that will serve as the initial normal microbiota- birth
    - bacteria
    - viruses
  22. 22Colonization typically begins at sites in the _____ _____mucous membranes
  23. 23Mucous membranes consist of _____ _____epithelial cells
  24. 24epithelial cells- tightly packed cells
    - interface with the external environment
    - found throughout body, lining urogenital, respiratory, and gastrointestinal tracts
  25. 25mucus- thick liquid secretion
    - contains water-soluble proteins and glycoproteins
    - retains moisture and naturally inhibits microbial attachment
  26. 26factors that influence the occurrence of infectious disease- Pathogenic Agents
    - Transmission
    - Host
    - Environment
  27. 27Invasion- ability of a pathogen to enter host cells or tissues, spread, and cause disease
    - Some remain localized after initial entry, multiplying and invading at a single focus of infection
  28. 28sometimes the pathogens enter the _____, from where they can travel to distant parts of the bodybloodstream
  29. 29bacteremia- presence of bacteria in the blood
  30. 30bacteremia is self-limiting becausebacterial cells do not grow in the bloodstream and thus the immune system quickly removes them
  31. 31bacteremia symptoms may bemild or none
  32. 32septicemia- bacteria multiply in the bloodstream
    - organism spreads systemically from an initial focus producing toxins or other poisonous substances
  33. 33Septicemia usually begins as an _____ in a specific organ and then spreads rapidly throughout the body from there- infection
  34. 34Septicemia symptoms are- major symptoms
    - massive inflammation
    - septic shock (sepsis)
    - death
  35. 35Viremiaviruses present in the bloodstream
    i.e. measles
  36. 36pathogenicitythe overall ability to cause disease
  37. 37virulenceThe measure of pathogenicity
  38. 38Pathogenicity and virulence are not _____ properties of a given pathogenuniform
  39. 39Host damage in an infectious disease is mediated by ______ _____virulence factors
  40. 40virulence factors- toxic or destructive substances produced by the pathogen
    - directly or indirectly enhances invasiveness and host damage by facilitating and promoting infection
  41. 41Virulence is a _____ _____, especially if a pathogen is lethal and an experimental animal model is availablequantifiable entity
  42. 42LD₅₀- lethal dose
    - # of pathogen/virion cells that kills 50% of the animals in a test group
  43. 43Highly virulent pathogens frequently show little difference in the number of cells required to kill 100% of a test group of animals as compared with the _____LD₅₀
  44. 44Attenuationis the decrease or loss of virulence of a pathogen
  45. 45attenuatedStrains that have either a reduced virulence or are no longer virulent
  46. 46Attenuation is thought to occur becausenonvirulent or weakly virulent mutants grow faster than virulent strains in laboratory media where virulence has no selective advantage
  47. 47if an attenuated culture is reinoculated into an animal, the organism may _____ its original virulence as more-virulent strains are _____ _____- regain
    - naturally selected
  48. 48Attenuated strains are often used for the production of _____vaccines
  49. 49attenuated viruses are “live” in the sense that, unlike “killed” strains, they could ...become once again active and replicate
  50. 50_____ virus vaccines typically show greater efficacy and generate an overall stronger immune response than do _____ virus vaccines- live
    - killed
  51. 51The virulence of a pathogen may be encoded by firmly entrenched _____ genes or by highly mobile genetic elements like _____- chromosomal
    - plasmids
  52. 52pathogenicity islands- distinct genetic elements on the chromosomes of a large number of bacterial pathogens
    - in both gram (+) and (-)
  53. 53pathogenicity islands encode various _____ _____ and are normally absent from non-pathogenic strains of the same or closely related species- virulence factors
  54. 54pathogenicity islands are considered to be a subclass of genomic islands that are acquired by ...horizontal gene transfer via transduction, conjugation and transformation
  55. 55nosocomial infectionshealthcareassociated infections
  56. 56opportunistic pathogensmicrobes that cause disease only in the absence of normal host resistance
  57. 57bacterial pathogens damage host tissues (or the entire host) in two major ways:- secreting tissue-destructing enzymes
    - secreting or shedding toxins that target specific host tissues or the entire host
  58. 58In contrast to bacterial pathogens, most viral pathogens damage host tissues by _____ cells directly. some are _____ and instead introduce genes into host cells that may eventually harm the host- lysing
    - lysogenic
  59. 59_____ follows adherence, colonization, and infection by a pathogeninvasiveness
  60. 60invasiveness requires the breakdown of _____ _____ and access to _____ released from host cells- host tissues
    - nutrients
  61. 61pathogens can produce enzymes both as - offensive weapons to ... - defensive weapons to ...- destroy host tissues
    - destroy or inactivate offensive weapons of the host
  62. 62Enzymes increases the _____ of the pathogen & allows it to ultimately extract more _____ from its host.- invasiveness
    - resources
  63. 63Toxicityability of an organism to cause disease by means of a toxin that inhibits host cell function or kills host cells
  64. 64Exotoxins- toxic proteins released from the pathogen as it grows
    - toxins travel from a site of infection and cause damage at distant sites
    - some are enterotoxins
  65. 65enterotoxins- toxic proteins whose site of action is the small intestine
    - massive secretion of fluid into the intestinal lumen, resulting in vomiting and diarrhea
  66. 66Exotoxins fall into three categories- AB toxins
    - cytolytic toxins
    - superantigen toxins
  67. 67AB toxins (i.e. Diphtheria Exotoxin)- has two subunits, A and B
    - subunit B binds to host cell surface
    - subunit B cleaved from subunit A
    - subunit A crosses cytoplasmic membrane and stops protein synthesis
  68. 68_____ molecule(s) of Diphtheria AB toxin is enough to kill one cellone
  69. 69Neurological Exotoxins (i.e. Botulinum and Tetanus Toxins)- AB exotoxins that function as neurotoxins
    - block the release of neurotransmitters that control muscle activities,
  70. 70Botulinum Toxins- most potent biological substances known
    - composed of seven related AB toxins
    - two are encoded on lysogenic bacteriophages specific for C. botulinum
  71. 71Botulinum Toxins- prevents muscle contraction
    - causes flaccid paralysis
  72. 72Botulinum Toxins acts at the motor end plate to prevent release of _____ from vesicles, resulting in a lack of stimulus to the _____ _____, irreversible relaxation of the muscles, and _____ _____- acetylcholine
    - muscle fibers
    - flaccid paralysis
  73. 73Tetanus Toxins- prevents muscle relaxation
    - outcome in a case of tetanus is a twitching, spastic paralysis
  74. 74C. tetani grows in deep wounds that become _____ (punctures); it's transported thru motor neurons to the spinal cord, where it binds to interneurons resulting in the continual release of _____ and uncontrolled _____ of the muscle fibers- anoxic
    - acetylcholine
    - contraction
  75. 75Cholera enterotoxin- disrupts normal ion flow in the intestine
    - results in potentially life-threatening diarrhea
  76. 76Cytolytic and superantigen exotoxins function by destroying _____ _____ or by triggering a massive _____ _____- host cells (activity of hemolysins)
    - immune response (toxic shock syndrome)
  77. 77CYTOTOXINS, CYTOLYTIC EXOTOXINS- soluble proteins secreted by a variety of pathogens
    - damage the host cytoplasmic membrane, causing cell lysis and death
  78. 78CYTOTOXINS, CYTOLYTIC EXOTOXINS hemolysinsalso lyse cells other than erythrocytes
  79. 79CYTOTOXINS, CYTOLYTIC EXOTOXINS Some hemolysins affect the _____ of the cytoplasmic membrane,sterols
  80. 80CYTOTOXINS, CYTOLYTIC EXOTOXINS Leukocidinslyse white blood cells decreasing the immune response
  81. 81CYTOTOXINS, CYTOLYTIC EXOTOXINS Staphylococcal a-toxinkills nucleated cells and lyses erythrocytes through the creation of pores
  82. 82pyrogenic feverinduced from an internal source, typically a small immune system protein called a cytokine, or from an external substance such as endotoxin
  83. 83SUPERANTIGEN EXOTOXINS- produced by many viruses/bacteria that interact with T cell receptors
    - overstimulation of immune system
    - can lead to shock and death
    - generally due to a localized infection, but with systemic effects
    - Fever, shock, death
  84. 84SUPERANTIGEN EXOTOXINS Superantigen poisoning can be triggered by ...- certain types of food poisoning
    - pyrogenic fever
    - and toxic shock syndrome
  85. 85Reactions to superantigen poisoning are _____ and can even be _____- severe
    - fatal
  86. 86Toxic shock syndromeresults from exposure to any of a series of exotoxins secreted during infection by certain strains
  87. 87Endotoxins- toxic lipopolysaccharides found in the cell walls of most gram-negative Bacteria
    - are not proteins but are structural components of the gram-negative outer membrane
  88. 88In contrast to exotoxins, which are the _____ _____ of living cells, endotoxins are _____ _____ and released in toxic amounts only when the cells ______- secreted products
    - cell bound
    - lyse
  89. 89A major component of the gram-negative cell outer membrane is _____- lipopolysaccharide (LPS)
  90. 90LPS is made of 3 units- membrane-distal O-specific polysaccharide
    - membrane-proximal core polysaccharide
    - and lipid A—a phosphoglycolipid and the membraneanchoring portion of LPS
  91. 91The _____ ___ portion of LPS is responsible for toxicity- lipid A
  92. 92Endotoxins cause a variety of physiological effects:fever, diarrhea, increased heart rate, a rapid decrease in the numbers of lymphocytes and platelets, and generalized inflammation, activation of the complement cascade
  93. 93Large doses of endotoxin can cause death from _____ _____ and _____ _____- hemorrhagic shock
    - kidney failure
  94. 94_____ are generally less toxic than most _____ and rarely cause symptoms that can lead to death in an otherwise healthy individual- endotoxins
    - exotoxins
  95. 95EXOTOXIN VS ENDOTOXIN chemistry - exotoxin- Proteins, secreted by certain gram(+) or gram(-) Bacteria
    - generally heat-labile
  96. 96EXOTOXIN VS ENDOTOXIN chemistry - endotoxin- Lipopolysaccharide–lipoprotein complexes, released on cell lysis as part of the outer membrane of gram-negative Bacteria
    - extremely heat-stable
  97. 97EXOTOXIN VS ENDOTOXIN Mode of action; symptoms - exotoxin- Specific
    - usually binds to specific cell receptors or structures
    - either cytotoxin, enterotoxin, or neurotoxin with defined, specific action on cells or tissues
  98. 98EXOTOXIN VS ENDOTOXIN Mode of action; symptoms - endotoxin- General
    - fever, diarrhea, vomiting
  99. 99EXOTOXIN VS ENDOTOXIN Toxicity - exotoxinOften highly toxic in picogram to microgram quantities, sometimes fatal
  100. 100EXOTOXIN VS ENDOTOXIN Toxicity - endotoxinModerately toxic in tens to hundreds of microgram amounts, rarely fatal
  101. 101EXOTOXIN VS ENDOTOXIN Immune response - exotoxins- Highly immunogenic
    - stimulate the production of neutralizing antibody (antitoxin)
  102. 102EXOTOXIN VS ENDOTOXIN Immune response - endotoxins- Relatively poor immunogen
    - immune response not sufficient to neutralize toxin
  103. 103EXOTOXIN VS ENDOTOXIN Toxoid potentiala - exotoxinHeat or chemical treatment may destroy toxicity, but treated toxin (toxoid) remains immunogenic
  104. 104EXOTOXIN VS ENDOTOXIN Toxoid potential - endotoxinNone
  105. 105EXOTOXIN VS ENDOTOXIN Fever potential - exotoxinNonpyrogenic; does not produce fever in the host
  106. 106EXOTOXIN VS ENDOTOXIN Fever potential - endotoxinPyrogenic; often induces fever in the host
  107. 107EXOTOXIN VS ENDOTOXIN Genetic origin - exotoxinOften encoded on extrachromosomal elements or lysogenic bacteriophages
  108. 108EXOTOXIN VS ENDOTOXIN Genetic origin - endotoxinEncoded by chromosomal genes
  109. 109hyaluronidase (Streptococcus pyogenes)- breaks down polysaccharide hyaluronic acid
    - causes host cells to slough apart, allowing pathogens at initial colonization site to spread between host cells to attack subsurface tissues
  110. 110polysaccharide hyaluronic acid- component of the extracellular matrix
    - functions as a type of “intercellular cement” in animal tissues
    - maintain organization of individual cells
  111. 111collagenase- destroys collagen
    - enables bacteria to gain access to deeper host tissues and spread through the body
    - allows anaerobes pathogen to reach less
    oxic conditions & use destroyed tissues as source of nutrients
  112. 112collagenmajor protein of connective tissues i.e. muscle
  113. 113streptokinase- dissolve fibrin clots and make further invasion possible
    - activates the host to produce plasmin, an
    enzyme that degrades fibrin blood clots
  114. 114coagulase (Staphylococcus aureus)- promotes formation of fibrin clots
    - clots protect pathogen
    - converts fibrinogen to fibrin, resulting
    in clotting of blood and the formation of fibrin surrounding pathogen
    - seen in boils and pimples
  115. 115Virulence factorsmolecules produced by microbes that add to their effectiveness like: colonization of a niche, attachment to cells, evasion of host's immune response
    i.e. toxins, surface coats that inhibit phagocytosis, and surface receptors that bind to host cells, etc.

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Microbiology (Exam III) Flashcards on Chapter 25: Microbial Infection and Pathogenesis, created by Alexandra Bozan on 18/04/2020.
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