Bacteriology- Pathogenic Bacteria Part 1.txt

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  1. Virulence factor of bacillus anthracis that prevents phagocytosis; not immunogenic.
    capsule polypeptide (polyglutamic acid)
  2. Capsule polypeptide (polyglutamic acid) of Bacillus anthracis is coded in _________.
  3. Vegetative cells that are antigenically distinct.
  4. 3 factors (proteins) that make up the exotoxin complex of Bacillus anthracis.
    Factor I edema factor, factor II protective antigen, factor III lethal factor
  5. The factor I edema factor of Bacillus anthracis is _________ in its inactive form and _________ when activated.
    adenylcyclase; calmodulin
  6. Factor II protective Ag of Bacillus anthracis is the _______________ for factors I and III.
    binding and delivery device
  7. Factor III lethal factor of Bacillus anthracis is a _________ that ____________, which is a key molecular switch that controls a cell's internal communications.
    protease; digests MAPKK
  8. The toxin synergism of Bacillus anthracis factors I + II lead to ___________.
  9. The toxin synergism of Bacillus anthracis factors II + III lead to ___________.
  10. How do you prevent disease caused by Bacillus anthracis?
    destroy spores, vaccinate, antibiotic txt for post-exposure prophylaxis
  11. How can you diagnose Bacillus anthracis infection?
    large gram + rods; subterminal spore formation is activated by high temp and air
  12. How can you treat disease caused by Bacillus anthracis?
    early diagnosis- antibiotic (amoxi, doxy, penicillin, cyprofloxacine), peptide antitoxin
  13. The _________ of Bacillus anthracis is extremely resistant and bacteria ___________, which present problems for treatment.
    endospore; grow too rapidly
  14. What are the 3 kinds of botulism?
    foodborne botulism, wound botulism, infant botulism
  15. Clotridium botulinum produces a __________ that inhibits ____________.
    neurotoxin; acetylcholine release
  16. Botulism causes _________ of all muscles; C. botulinum produces ____ serotypes of toxin.
    flaccid paralysis; 7
  17. What are the virulence factors of C. botulinum?
    botulism A-B type toxin, blockade neurotransmitter release, endospore
  18. The botulism toxin is an ____________.
  19. What are host factors that permit C. botulinum infection?
    infant intestinal tract (don't have full range of beneficial bacteria), deep wounds (allow bacteria to germinate)
  20. How can you prevent botulism? (3)
    properly prepare canned food, don't feed young babies honey, immunization with type specific toxoid
  21. How do you diagnose botulism? (3)
    inject patient serum/stool into mice and look for signs; gram-positive rods, obligate anaerobes
  22. How do you treat botulism?
    administer antitoxin
  23. What are the problems with misdiagnosis of botulism?
    misdiagnose symptoms as Guillain-Barre syndrome, stroke, intoxication
  24. What are the two general types of Clostridium other than C. botulinum?
    potent toxin-forming, non-invasive, does not lyse cell; less potent, toxin-forming, tissue invading, lyse cell and necrotize
  25. What is the habitat of Clostridium tetani?
    intestine and soil
  26. How does C. tetani enter the body to cause disease?
    through a wound, castration, docking, shearing, parturition
  27. C. tetani produces a __________ that inhibits a __________________.
    neurotoxin; neurotransmitter glycine and gamma-animobutyric acid in CNS
  28. Tetanus is characterized by...
    prolonged spasmic contractions of muscles
  29. Clostrdium hemolyticum causes ________________; it has an enzyme, ___________, that causes ____________.
    bovine bacillary hemoglobinuria; lecithinase; intravascular hemolysis
  30. Clostridium chauvoei causes _________ and leads to _____________.
    blackleg in cattle; myonecrosis with gas
  31. Clotridium novyi causes _______________; there is subcutaneous ______________, which causes _______________.
    ovine and bovine infectious necrotic hepatitis; venous congestion (Black disease)
  32. Clostridium perfringens causes _____________ and ______________; also known as ______________.
    enterotoxemia; gas gangrene; overeating disease
  33. Clostridium septicum causes _____________.
    ovine and bovine malignant edema
  34. Staphylococcus aureus causes _____________ infections, including... (11)
    suppurative (pus-forming); skin lesions, pneumonia, mastitis, phlebitis, meningitis, osteomyelitis, endocarditis, food poisoning, nosocomial (hospital-acquired) infection, bovine mastitis, and toxic shock syndrome
  35. What are 2 antiphagocytic virulence factors of staph aureus?
    polysaccharide capsule, protein A
  36. What are 5 exotoxins associated with staph aureus?
    hemolysins, leukotoxins, enterotoxins, exfoliatin, toxic shock syndrome toxin 1
  37. The superantigen exotoxin of staph aureus is __________.
    toxic shock syndrome toxin 1
  38. Extracellular enzymes that are virulence factors of staph aureus. (2)
    coagulase, hyaluronidase
  39. What is the extracellular enzyme that is a virulence spreading factor of staph aureus?
  40. What are 3 host factors that permit staph aureus to cause disease?
    wound, dermatitis, invasive procedures
  41. How does staph aureus usually enter the body to cause disease?
    breaks mucous membrane, usually by a wound
  42. How can you diagnose staph aureus? (4)
    gram-positive cocci, grape-like clusters, facultative anaerobe, catalase-positive
  43. The cell wall of S. aureus contains _____________, whereas the cell walls of S. hyicus and S. intermedius contain ______________.
    ribital teichoic acid; glycerol teichoic acid
  44. What is a major problem with the treatment of S. aureus?
    widespread drug resistance (MRSA)
  45. Staphylococcus hyicus causes _________________.
    porcine exudative epidermitis (greasy pig disease)
  46. Staphylococcus intermedius causes ____________.
    canine pyoderma
  47. What are 2 types of diseases caused by Streptococcus pyogenes?
    suppurative-pyogenic, non-suppurative complication
  48. What are 3 results of suppurative-pyogenic infection with Streptococcus pyogenes?
    strep throat, scarlet fever, impetigo (skin)
  49. What are the 3 results of non-suppurative complication after acute infection with S. pyogenes?
    glomerulonephritis, rheumatic fever, endocarditis
  50. What are the 2 theories for the pathogenesis of S. pyogenes infection?
    serum sickness reactions mediated by complement, autoimmune disease because of cross-reaction b/w S. pyogenes and self- tissue Ag
  51. Infections of S. pyogenes that infects the deep layer of tissue (fascia).
    necrotizing faciitis
  52. M-protein of S. pyogenes
    Antigenic ___
    Protective Ab ___
    Anti-phagocytic ___
    Role in virulence ___
    • Antigenic +
    • Protective Ab +
    • Anti-phagocytic +
    • Role in virulence +
  53. 3 surface structures of S. pyogenes that are antigenic.
    Gp carbohydrate, M-protein, lipoteichoic acid
  54. What surface structure of S. pyogenes induces production of protective Ab?
  55. What 2 surface structures of S. pyogenes are anti-phagocytic?
    hyaluronic acid, M-protein
  56. What 3 surface structures of S. pyogenes have a role in virulence?
    hyaluronic acid, M-protein, lipoteichoic acid
  57. Surface structure of S. pyogenes that extend through the capsule to the outermost surfaces as hair-like fimbriae; type-specific.
  58. Soluble toxin of S. pyogenes that is antigenic, induces production of protective Ab against rash of scarlet fever, and increases capillary fragility.
    erythrogenic toxin
  59. Enzyme of S. pyogenes that is leukotoxic; O2 labile stable hemolysin.
    streptolysin O
  60. Enzyme of S. pyogenes that is leukotoxic; O2 stable hemolysin.
    Streptolysin S
  61. Enzyme of S. pyogenes that is a "spreading factor" that leads to cellulitis.
  62. How do you diagnose S. pyogenes? (3)
    gram + cocci arranged in pairs or chains, facultative anaerobe, catalase-negative
  63. Cell wall antigens of S. pyogenes that are branched polymers that confers 25 Lancefield group-specific antigen.
    "C" carbohydrate
  64. Group A carbohydrate cell wall Ag is used to diagnose streptococcus _________.
  65. Group B carbohydrate cell wall Ag is used to diagnose streptococcus _________.
    agalactiae- sepsis in newborn infants
  66. Group C carbohydrate cell wall Ag is used to diagnose streptococcus _________.
    equi- strangles
  67. Alpha hemolysis associated with S. pyogenes causes...
    a partial zone of hemolysis around colony
  68. Beta hemolysis associated with S. pyogenes causes...
    a complete zone of hemolysis around the colony
  69. Gamma hemolysis associated with S. pyogenes causes...
    no hemolysis around the colony
  70. How do you treat disease caused by S. pyogenes?
    β-lactam antibiotics
  71. Streptococcus agalactiae causes _____________.
    bovine mastitis
  72. Streptococcus equi subsp. equi causes ___________; what is a pathognomonic lesion for this disease?
    strangles; abscess formation in the retropharyngeal lymph nodes
  73. Streptococcus equi subsp. zooepidemicus causes....
    equine neonatal streptococcal infections, associated with endometritis
  74. Describe the manifestation of the disease caused by mycobacterium.
    tuberculosis- latent for long periods of time, disease progresses slowing, chronic disease
  75. Mycobacterium bovis causes disease in...
    bovines, man, dog, cat
  76. How does Mycobacterium enter the body to cause disease?
    inhalation of organisms
  77. A __________ response is activated in response to infection with Mycobacterium.
    cell-mediated immune
  78. __________ formation by mycobacterium stimulations formation of _____________, which localizes and walls off the infectious agent.
    Mycolic acid; granuloma (tubercle)
  79. What type of lesion is pathognomonic for Mycobacterium infection?
    tubercles (granuloma) in lymph nodes
  80. _______ is associated with Mycobacterium infection because macrophages are activated release mediators that interfere with lipid and energy metabolism.
  81. What are 2 virulence factors associated with Mycobacterium?
    mycolic acid, facultative intracellular parasitism
  82. 2 molecules of mycolic acid esterified to the disaccharide trehalose, giving rise to a pattern of growth in serpentine cords; confers adherence in Mycobacterium.
    cord factor
  83. Component of mycolic acid produces by Mycobacterium that interferes with fusion of phagosome with lysosome.
  84. Many symptoms of tuberculosis result from ________________ of the host.
    immunological hypersensitivity reactions
  85. ______________ hosts develop acute active tuberculosis.
  86. Mycobacterium is highly _____________; how do you control it in cattle?
    resistant; testing and slaughtering cattle (national bovine tuberculosis eradication program)
  87. How do you diagnose tuberculosis?
    Mycobacterium is acid fast, tuberculin skin test
  88. How do you treat tuberculosis?
  89. What is the complication with treating/controlling tuberculosis?
    multi-drug resistance
  90. Mycobacterium avium subsp. paratuberculosis causes _____________; it enters the body by __________; it causes....
    Johne's disease; ingestion; chronic diarrhea and emaciation and proliferative enteritis
  91. What is a pathognomonic lesion for Johne's disease?
    proliferative enteritis (no granuloma)
Card Set:
Bacteriology- Pathogenic Bacteria Part 1.txt
2015-04-03 01:02:32
vetmed bacteriology

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