Patho Exam 3 part 3

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  1. What does Shigella cause ?
    bacillary dysentry (severe bloody and muscous diarhea; have no adherence factors.
  2. In the colon and rectum Shigella _________ thru epithelial barrier via __ cells invading resident macrophages, escape from the phagosomes into cytoplasm, where they multiply and induce rapid cell death.
    translocate , M cells
  3. Released 4rm dead macrophages _______ than infect other epithelial cells using a "trigger mechanism of entry."
  4. When Shigella come into contact with epithelial cells, the ______________________ is stimulated & delivers effectors (IcsB) into host cells which play roles in camouflage against phagocytic recognition.
    Type 2 Secretion system (TTSS)
  5. What delivers effectors (IcsB) into the host cells ?
    Type 2 secretion system (TTSS)
  6. Bacterial toxins is some of the well known virulence factors on the ________ .
  7. What is the mode of action/targets of toxins? (3)
    • protein synthesis stopped 
    • cell wall integrity affected 
    • nerve impulses interrupted
  8. C. botulinum toxin is produced when....?
    in food prior to ingestion.

    • bacteria form spores, pass thru GI tract and don't colonize GI tract / enter tissue.
    • toxin attacks neuron causing paralysis and death (collapse of respiratory system)
  9. What is the natural source of C. botulinum?
  10. What are 2 bacterias that do not have toxin genes that are part of their normal components of the bacterial genome?
    C. botulinum (C&D) & Corynebacterium diphtheriae

    (carried on lysogenic bacteriophage / plasmids) 
  11. Where are the toxin genes in C. botulinum and Corynebacterium diphtheriae?
    lysogenic bacteriophage / plasmids
  12. What is exotoxin ?
    accumulated and released toxins on cell lysis.


    injected directly into host cells therefore bypassing extracellular phase.
  13. What are the 7 criterias for the naming system ?
    1. cytotoxins: can have a more general action & attack a variety of cell types. 

    2. 4rm disease / bacteria: cholera, shiga, dipherthia, tetanus 

    • 3. Type of cell or organ affected: neurotoxin (brain), leukotoxin (WBC), hepatotoxin (liver), cardiotoxin ()
    • 4. Activity: adenylate cyclase, (Bordetella pertussis - whooping cough)
    • -lecithinase (C. perfringens - gangrene)

    • 5. Immunological cross-reactivity 
    • -Botulinum - A-G

    • 6. Letter designation:
    • -Exotoxin A(P. aeruginosa)

    • 7. Multiple names: 
    • -E. coli 0157:H7 - shiga-like, verotoxin (culture cells)
  14. 7 Criteria for naming system
    • Cytotoxins
    • 4rm disease/bacteria
    • Type of cell/organ affected 
    • Activity 
    • Immunological cross-reactivity
    • Letter designation
    • Multiple names
  15. Endotoxin vs. Enterotoxin
    Endotoxin-structure of Gram (-) cell wall, recognized by immune sys (LPS)

    Enterotoxin specific for toxins in small intestine producing diarrhea/vomiting ex: enteric symptoms
  16. What are example pathogens that cause food poisoning ?
    Sty. aureus, C. perfringens, B. cereus, Camp. jejuni 
  17. What are example of intestinal pathogens?
    Vibrio cholera, E. coli, Salmonella enteritidis
  18. Campylobacter jejuni is now the leading cause of ... ?
    bacterial food poisoning, most often spread by contact with raw/undercooked poultry. 

    symptoms: diarrhea(bloody), fever(typical fever), ab pain, cramping, nausea, vomit
  19. What is the 1st step in action of toxins?
    binding to target cells
  20. What are Type I Toxins?
  21. What do Type I Superantigens bind to?
    host surface but not translocated into cell.

    ex: Superantigens bind to marcophages & T-cells and stimulate large amt of toxic cytokines.
  22. Over-secretion of cytokines can trigger a dangerous syndrome known as a ... ?
    cytokine storm
  23. Cytokine storm deaths were weighted more heavily towards people with _________ due to its ability to produce stronger immune responses, like increasing cytokine levels.
    healthy immune systems

    • -nausea, vomit, malasie, and fever
    • Staphylococcus aureus (enterotoxin) and Streptococcal infections
  24. Type II toxins are... ?
    cytolytic / membrane disrupting
  25. What are the 2 types of Type II toxins?
    1. Proteins that form channels in membrane 

    2. Enzymes that disrupt the membrane phospholipid
  26. What are 3 examples of proteins that form channels in the membrane ?
    • Streptococcal Streptolysin O
    • -affects sterols of host cytoplasmic membrane 

    • Staphylococcal Leukocidins 
    • -lyse WBCs 

    • Staphylococcal α-toxin
    • -disrupt smooth muscle in blood vessels but also toxic to many cell types
  27. What is a convenient test for testing toxins (ex: phospholipase, hemolysin, cytotoxin)?
    blood agar assay
  28. What cleaves at other sites to destabilize the cell membrane?
  29. Enzymes that disrupt membrane phospholipid (2nd type of type II toxins) rather than make "holes" some enzymes just _________________ group of lipid portion of molecule that normally acts to stabilize lipid bilayer of cytoplasmic membrane -cell lysis.
    remove charged head group
  30. What toxin can enter bloodstream and damage kidneys?
    C. perfringens α-toxin
  31. Type III toxins (A-B) are... ?
    protein inhibitor toxins
  32. Type iii toxins (A-B) protein inhibitor toxins consist of 2 components...?
    Active (enzymatic) (A) and Binding (B) portions
  33. When does proteolytic cleavage occur ?
    when the A portion is internalized and activated when disulphide bonds are broken. 
  34. Which portion of Type III toxin is more specific? A or B?
    (B) portion is very specific [binds to carbohydrate moiety of a host cell glycoprotein/ glycolipid] 

    (A) portion = less specific and can kill several types of cell if it can gain entry into cytoplasm
  35. What happens in Type III toxins when binding (B) occurs?
    leads to A being translocated thru host membrane into cytoplasm .
  36. What results in A becoming active and exerts its toxic effect?
    endocytosis / direct translocation 
  37. Although diff cells may be attacked, the mode of action of toxin is the same... what is the mode of action ?
    protein inhibition
  38. How does Scalded Skin Syndrome begin?
    w/ a fever and redness of skin, followed by formation of fluid-filled blister that ruptures easily. Eventually, top layer of skin may peel off in sheets 
  39. What does Dipheria toxin do?
    acts on elongation factor-2; normally brings an amino charged tRNA to ribosome -- prevents protein synthesis
  40. What does Cholera-toxin (Enterotoxin) do?
    ADP- ribosylates an enzyme that controls AMP and ion flow leading to massive water loss (diarrhea)
  41. What occurs in Shiga toxin ?
    (A) subunit cleaves a host cell rRNA molecule, which prevents ribosome carrying out translocation of proteins.

    -protein synthesis is terminated
  42. Endotoxins (nonprotein toxins) consists of what ? What are they a part of?
    polysaccharide (immunogenic) and lipid part of LPS, is Lipid A which is toxic component.

    Endotoxins are part of outer portion of cell wall of Gram negative bacteria 
  43. Cytokines also induce ____________ Complex and __________________ systems.
    Alternative Complex, Coagulation systems
  44. What is factor XII?
    activate blood-clotting proteins
  45. Factor XII (activate blood-clotting protein) lead to ?
    blood clots in small blood vessels. 

    aka Disseminated intravascular coagulation (DIC)
  46. What does disseminated intravascular coagulation (DIC) result in ?
    -acute respiratory distress syndrome 
  47. Another example of nonprotein toxin is ?
    membrane blebs (Bordetella pertussis - Whooping cough) ex of a pathogen that releases part of their cell wall 
  48. What is mycolactone toxins?
    lipid-like toxins - cytotoxic and immunosuppressive properties 

    • ex: mycobacterium ulcerans
    • -emerging human pathogen
    • reversoir - aquatic insects 

    • ex: buruli ulcer
    • destructive effects on skin, soft tissues, and bones (central, west africa, central and south america, asia and australia)
  49. What are 2 examples of mycolactone toxins?
    • ex: mycobacterium ulcerans
    • emerging human pathogen
    • reversoir - aquatic insects 
    • ex: buruli ulcer-
    • destructive effects on skin, soft tissues, and bones (central, west africa, central and south america, asia and australia)
  50. What is an negative impact of Buruli ulcer ?
    lifelong disfigurement! (but little inflammation and pain)
  51. What is a cluster of 3 giant biosynthetic genes?
    polyketide synthases
  52. What does infection of subcutaneous fat result in?
    focus of necrotic (dead) fat containing myriads of mycobacteria in characteristic spherules formed w/in dead fat cells.
  53. What's the secondary event of getting an infection of subcutaneous fat?
    skin ulceration 
  54. What is a toxin mediated disease?
    Diphtheria (III A-B toxin)

    Corynebacterium diptheriae (Gram (+), non-sporeforming, non-motile, aerobic, club-shaped rod)
  55. What's the epidemiology and pathology of Corynebacterium diphtheriae?
    severe respiratory condition that usually infects children, but due to immunization its now shifted towards elderly. (but PREVENTABLE AND TREATABLE)
  56. Humans are the only known reservoir for what?
  57. Inhalation of air-borne droplets starts with what?
    colonization of throat and tonsils
  58. What is pseudomembrane ?
    grayish membrane, dead host cells, inflammatory cells and bacteria forms in throat extending to lungs.
  59. Pseudomembrane may block passage of air, so how does death occur?
    combination of partial suffocation and tissue destructions by toxin
  60. Even tho bacteria remain in the throat, toxin enters .... ?
  61. A-B toxin proteins consists of 3 functional regions, what are they?
    • B consists of 2 subunits
    • receptor binding region
    • translocation region

    • catalytic region
  62. What is the host cell receptor that Toxin B subunit binds to?
    heparin-binding epidermal growth factor (HB-EGF) and it gets taken up in an endocytic vesicle
  63. How does the heparin-binding epidermal growth factor (HB-EGF) get taken up?
    an endocytic vesicle
  64. 5% of total protein consists of?
  65. Endocytosis is an important step in what?
    toxin activation 
  66. how many toxin molecules can kill a host cell?
  67. Toxin catalyzes the ____________ of EF-2.
  68. What is a diagnostic trait of  failure?
    difficulty in swallowing
  69. What is governed by the number of cell receptors?
    difference in susceptibility 
  70. Toxin production stimulated by low iron concentration and regulated by a repressor... what is the protein used?
    Diphtheria toxin regulation (DtxR) protein

    activated by presence of high-iron concentrations--binds to toxin gene operon and prevents toxin production
  71. Iditarod is the toughest ____ on Earth..

    related to Diphtheria antitoxin bc only route to get more antitoxin was the Iditarod Trail; normally takes 13 days but made a record of 6 days
  72. C. diphtheriae is isolated from ______ and cultured in lab.

    nasal/throat swabs used in inoculate Blood Agar and Loeffler's medium (inhibits most other respiratory pathogens)
  73. During an infection, what can be used to neutralize toxin (passive immunization) ?
  74. What is the highly effective vaccine DTaP?
    • Diptheria
    • Tetanus
    • Acellular 
    • Pertussis
  75. Cholera is a _______ toxin.
    III A-B toxin
  76. Organism for cholera is?
    • vibrio cholerae
    • (Gram(-) curved rod)
    • sever diarrheal disease

    epidemiology and pathology (contaminated H2O, raw shellfish and raw vegetables)
  77. Diagnosis and Prevention of cholera...?
    • Examination of "rice-stool" and presence of bacteria 
    • Adequate water treatment/safe drinking water
  78. What's the treatment for cholera?
    electrolyte replacement therapy, intravenous / oral liquid
  79. Botulism is what type of toxin?
    III A-B toxin
  80. What organism is in botulism ?
    Clostridium botulinum (Gram(+), sporeforming, obligative anaerobic rod)

    • normally found in soil and lake sediments 
    • cause death in humans in small doses (0.05-0.1 μg)

    • Epidemiology and Pathology:
    • -food poisoning, fatal: paralysis of lungs (suffocation) and heart muscle
  81. Normally, how do you get botulism?
    ingestion of foods not cooked correctly after processing

    (toxin absorbed 4rm intestines into bloodstream; specific for neurons attacking peripheral nerve endings)
  82. What are the 2 forms of botulism that do involve the organism?
    • Transient Colonization and
    • Infant Botulism : infant intestinal tract often lacks both protective bacterial flora and clostridium-inhibiting bile acids found in normal adult intestinal tract, 
  83. Wound Botulism enables growth of organism prior to
    toxin production
  84. Out of the 8 most potent biological Botulinum toxins A-H, which 2 causes more infections?
    Types A and B
  85. What are the 3 components produced in Type A Botulinum toxin?
    • Botulinum toxin (Botox) - neurotoxin
    • C2 and C3 toxins (ADP-ribosylation) - protein synthesis 
    • Nontoxigenic components (may act to protect 4rm stomach acid and proteases and mediate binding to mucosal surfaces)
  86. Botulinum toxin have protein complexes called ...
    progenitor toxin 
  87. Once the Botulinum toxin is processed it's called ?
    derivative toxin: consists of heavy and light chains
  88. Amino terminus of "H" chain causes formation of an endocytic vesicle in neuronal membrane allowing which chain to enter the cell?
    "light chain"
  89. Toxin binds to presynaptic membranes on termini of stimulatory motor neurone at neuromuscular junction which does what?
    blocks releasing of Acetylcholine (Neutrotransmitter)
  90. Nerves received excitatory signal but contraction is prevented. What does this cause?
    flaccid paralysis 
  91. What are neurotransmitters?
    chemicals used to relay, amplify and modulate electrical signals btwn a neuron and another cell.
  92. What organism makes up Tetanus?
    • Clostridium tetani (Gram(+), motile, sporeforming, anaerobic rod)
    • found in soil (and GI tract of animals)

    • Epidemiology and Pathology:
    • -life threatening, preventable by immunization.
  93. What is Lockjaw, and what is it a diagnostic trait of?
    muscles of face and jaw first affected; Tetanus 

    (death results 4rm respiratory failure)
  94. What is the prevention and treatment of Tetanus?
    • "booster" tetanus shot;antitoxin made in horses, neutralizes toxin as it is released. 
    • Toxoid vaccine is very effective.
  95. Opposite to botulism rather than flaccid, what does the toxin of tetanus do?
    • a rigid/"spastic" paralysis ensues(come afterward).
    • [contracted muscles cannot relax]
  96. What are the 2 toxins of tetanus ?
    • oxygen labile hemolysin (tetanolysin
    • plasmid borne, heat labile neurotoxin (tetanospasmin)
  97. What does the toxin do?
    • On contact with CNS, toxin is transported through the motor neurons back to the spinal cord.
    • Binds to ganglioside lipids at the terminus of the inhibitory interneurons,
    • Cleaves synaptobrevin, blocks release of glycine.
    • Inhibitory neurotransmitter (glycine), binds to receptors on the motor neurons and allows relaxation of muscle.
  98. Morphology of Clostridium perfringens ..
    Gram (+), bacilli, anaerobic, sporeforming

    (found in intestinal tracts of humans and animals, nature)
  99. C. perfringens is a major cause of .... ?
    food poisoning; CPE released upon cell lysis in final stage of sporulation
  100. C. perfringens is anaerobic but C. septicum is aerotolerant and infects what?
    normal, healthy tissue (may be deadlier of the 2 Clostridia)
  101. Clostridium perfringens has how many toxins produced?
  102. What happens during Food Poisoning ?
    growth of vegetative cell, alkaline conditions of small intestine stimulates Sporulation, triggering production of enterotoxin

    • Toxin also kills cells producing anaerobic condition to allow spores to germinate
  103. What occurs during food poisoning?
    -enterotoxin binds to brush border of small intestine, inserts into membrane leading to altered permeability -loss of fluids and ions, the exotoxin acts as superantigen stimulating T-lymphocytes.
  104. What is the diagnostic trait of food poisoning?
    abdominal cramps and watery diarrhea, but no fever, nausea / vomiting
  105. Low temperature inhibits C. perfringens.. how to do this?
  106. What is used to detect enterotoxin in stools (feces) ?
    direct-enzyme-linked immunosorbant assay (ELISA)
  107. What is debridement?
    • removal a dead tissue
    • problem: even with a skilled surgeon, damage to non-infected (live) tissue is a consequence -- treat w/ Hyperbaric oxygen treatment: oxygenates blood, kills anaerobic bacteria and reduces ability of surviving bacteria to produce toxin.
  108. A consequence of debridement is non-infected tissue damage, what is used to help this?
    Maggot Therapy
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Patho Exam 3 part 3
2015-11-01 23:23:09
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