Microbio Chp 23-27

  1. what are the 2 Gram (+) cocci?
    staphlococci and micrococci
  2. what are the 2 gram (+) pleomorphic rods?
    propionbacterium acnes and cornyebacterium xerosis
  3. what does lipophilic mean?
    takes sebum and breaks it down to an acid that blocks the duct on the skin
  4. what is yeast?
    malassezia furfur
  5. what element causes a decrease in yeast growth?
    selenium
  6. what are the 4 diseases caused by Staphylococcus aureus?
    folliculitis, scalded skin syndrome, wound infections, impetigo
  7. what oxygen level does S. aureus need?
    facultative anaerobe
  8. what is the apperance of S. aureus on agar?
    round, raised, yellow color
  9. what is another name for a boil?
    furuncle
  10. what is folliculitis?
    small red bump or pimple
  11. what is a carbuncle from a hair follicle infection?
    large area of redness, swelling, and pain with several pustule sites
  12. where can hair follicle infection systemically spread to?
    heart, bones, brain
  13. hair follicle infections can spread to what layer of skin that causes what?
    subcutaneous layer and leads to an abcess
  14. how are hair follicle infections transmitted?
    usually by hands
  15. what are S. aureus strains resistant to?
    penicillin
  16. how do you prevent/treat hair follicle infections?
    anti-staphylococcal creams and soaps that decrease the carrier state
  17. how do you treat furuncles and carbuncles?
    surgical draining
  18. what is the main symptom of staphylococcal wound infections?
    pyogenic - causes production of pus
  19. what are the 2 causative agents of S. wound infections?
    S. aureus and S. epidermis
  20. what is the pathogenesis of S. wound infections?
    coagulase, alpha toxin, protein A
  21. what is the superantigen of S. wound infections called?
    TSST-1
  22. how are the S. wound infections spread?
    nasal carriers
  23. who are at risk for getting S. wound infections? 3 of them
    elderly, immunosuppressed, prolonged post hospital stays
  24. the vancomycin resistant strain for S. wound infections was identified when?
    1997
  25. what are 2 symptoms of scalded skin syndrome?
    dehydration and large blisters filled with clear fluid
  26. what is the pathogenesis of scalded skin syndrome?
    exfoliation toxin that causes a split in the cellular layer of the epidermis
  27. scalded skin syndrome normally affects who?
    newborns and elderly
  28. how is scalded skin syndrome transmitted?
    person to person
  29. how do you prevent scalded skin syndrome?
    isolation to reduce risk of secondary infections
  30. how do you treat scalded skin syndrome?
    getting rid of the dead skin
  31. what are the 2 disesases caused by strepococcus pyogenes?
    impetigo and necrotizing fascitis
  32. what does streptococcus pyogenes secrete?
    hemolysins
  33. what color does beta hemolytic streptococci give around the colony?
    clear
  34. what color does alpha hemolytic streptococci give around the colony?
    green
  35. what is alpha hemolytic?
    incomplete destruction of RBCs
  36. what is beta hemolytic?
    complete destruction of RBCs
  37. what is gamma hemolytic?
    no hemolysis of RBCs
  38. what is the Lancefield system based on?
    cell wall carbohydrates
  39. what is a classic sign of impetigo?
    blisters that break and weep found mostly around the mouth with a golden formation of crust
  40. what is the pathogenesis of impetigo?
    enters though minor breaks and M protein the intereferes with phagocytosis
  41. what is the epidemiology of impetigo?
    direct contact, insects, fomites
  42. what are the symptoms of flesh eaters?
    swelling, confusion, blood leakage
  43. what is the pathogenesis of flesh eaters?
    fibronectin binding protein that produces a toxin that gets into the blood stream
  44. what is the epidemiology of flesh eaters?
    direct contact, nose and throat discharge, people with underlying conditions like diabetes, cancer, drugs
  45. what is the treatment for flesh eaters?
    surgery to remove dead skin and maybe amputation
  46. what does pyocyanin do in pseudomonas aerguinosa?
    turns tissue green
  47. what is a symptom of clostridial myonecrosis?
    bloody or brownish fluid and gas leaks from wound, mottled black
  48. what is the pathogenesis of gas gangrene?
    grows in poorly oxygenated tissue that releases an alpha toxin
  49. what is the epidemiology of gas gangrene?
    wounds from war, high risk populations
  50. how do you treat gas gangrene?
    hyperbaric chamber
  51. what are the signs of chicken pox?
    pustules, itchy, blisters, latent infections leads to shingles
  52. what is the causative agent of chicken pox?
    varcella which a a double stranded DNA
  53. how does chicken pox enter the body?
    through respiratory route then to the blood then skin
  54. T/F humans are the only reservoir of the varicella virus
    true
  55. what kind of vaccine is used for varicella and what is the name of it?
    attenuated (live) and zovarix
  56. how old can children be to get the chicken pox virus?
    around 1
  57. what is the sign of rubeola?
    koplik spots
  58. what are koplik spots?
    white patchy dots on infected areas of the mouth associated with rubeola
  59. how does measles enter the body?
    respiratory route
  60. what are the signs of rubella?
    rash build-up on skin, enlarged lymph nodes
  61. how does rubella enter the body?
    respiratory route and multiplies in the nasopharynx
  62. how is rubella and rubeola transmitted?
    human to human contact
  63. what is tinea capitis?
    ringworm of the scalp
  64. who does tinea capitis affect the most?
    elementary children the most
  65. what is tinea cruris?
    ringworm of the groin
  66. what is tinea cruris associated with?
    jock itch
  67. what is tinea pedis?
    ringworm of the feet
  68. what is tinea pedis associated with?
    athletes foot
  69. what is the pathogenesis of the fungal diseases of the skin?
    excessice mositure allows invasion of the keratinized layers of the tissue
  70. what do dermatophytes produce?
    keratinase
  71. what are the 5 leading causes of meningitis?
    • group B streptococcus,
    • listeria monocytogenes,
    • streptococcus pneumoniae,
    • nisseria meningitidis,
    • haemophilus influenzae
  72. who does haemophilus influenzae meningitis affect?
    children between 6 months to 4 years
  73. where is haemophilus influenzae found?
    normal flora in the throat
  74. what kind of capsule does haemophilus influenzae have?
    antigen type B
  75. where does neisseria meningtidis begin?
    throat infection and then a rash
  76. what is the most common type of neisseria meningitis?
    serotype B
  77. what is a sign of meninococcal meningitis?
    petechia- ruptured capillary beds on skin that appear as tiny dots on the surface
  78. T/F bacterial is better than viral when it comes to meningins
    false
  79. what causes virulence in streptococcus agalactiae?
    capsule
  80. who does streptococcus agalactiae affect?
    newborns
  81. how does newborns get streptococcus agalactiae?
    the bacteria colonizes in the vagina then baby passes through the gential tract
  82. T/F can listeriosis be transmitted to the fetus?
    true
  83. where is listeriosis usually found?
    food normally kept around 4o C (fridge temp)
  84. how long is the incubation period for listerosis?
    a few days to 2-3 months
  85. what is hansens disease also known as?
    leprosy
  86. what are the symptoms of leprosy?
    skin lesions, deformed face, loss of fingers or toes
  87. how long is the incubation period for hansens disease?
    3 months to 20 years
  88. what is the pathogenesis of leprosy?
    invasion of small nerves of skin that produces nerve damage
  89. what is the epidemiology of leprosy?
    direct contact
  90. what is the main symptom of botulism?
    generalized paralysis
  91. what is the pathogenesis of botulism?
    endospores germinate in food and releases a neurotoxin
  92. how do you get botulism?
    home-canning or food not heated enough
  93. what is the main sign of tetanus?
    painful uncontrollable muscle spasms that beings in the jaw muscle
  94. what is tetanus resulted from?
    tetanospasmin- an exotoxin produced by the bacterium
  95. how do you get tetanus?
    dirty or puncture wounds
  96. what are the causative agents of viral meningitis?
    small, non-enveloped RNA enteroviruses
  97. how are the enteroviruses in viral meningitis transmitted?
    fecal-oral route
  98. viral meningitis is also assiocated with?
    mumps
  99. what are the symptoms of virl meningitis?
    disorientation, seizures, localized paralysis, coma
  100. what id the causative agent of viral menigitis?
    arboviruses- viruses transmitted by insects, mites, or ticks
  101. T/F there is no accepted treatment for arboviral encephalitis
    true
  102. what is the main sign of polio?
    shrinking of muscles and bones not developing fully
  103. what is the characteristic sign of rabies?
    tingling or twitching sensation of site of viral entry along with muscle spasms of mouth and throat
  104. what does the rabies virus look like?
    bullet shaped
  105. how do you get rabies?
    bite of a rabid animal or inhalation
  106. is there effective treatment for rabies once symptoms begin?
    no
Author
coronagirl415
ID
74190
Card Set
Microbio Chp 23-27
Description
Bacterial/Viral skin and nervous system
Updated