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MIC101 Lecture 15

patience.almazan English 138 cards

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  1. 1What is the title of Lecture 15?Bacterial Infections
  2. 2Name the types of Bacteria we will be learning about todayStaphylococcus (S. aureus & S. epidermidis) & Neisseria (N.gonorrhoeae & N. meningitidis)
  3. 3What is the structure of Staphylococcus?Spherical cells typically clustered in grapelike arrangements.
  4. 4What is the physiology of Staphylococcus?Gram-positivie, facultatively anaerobic, salt tolerant, up to 10% NaCl
  5. 5What are the 2 species of Staphylococcus that are commonly associated with staphylococcal diseases in humans?S. aureus & S. epidermidis
  6. 6Describe S. aureus?More virulent, producing a variety of disease conditions & symptoms depending on the site of infection
  7. 7Describe S. epidermidispart of the normal microbiota of human skin, but is an opportunistic pathogen in immunocompromised patients or when introduced into the body via intravenous catheters or on prosthetic devices, such as artificial heart valves
  8. 8Which species of Staphylococcus is more virulent & produces a variety of disease conditions?S. aureus
  9. 9Which species of Staph is part of the normal microbiota of human skin?S. epidermidis
  10. 10How do Staph infections come about?Staph infections are a result of staphylococci breaching the body's physical barriers (skin or mucous membranes)
  11. 11What are 3 features of Staph that make it pathogenic?Structures that enable it to evade phagocytosis, production of enzymes, & production of toxins
  12. 12Describe Protein A of Staphinterferes with antibody immune responses by binding to the Fc portion of IgG antibodies, inhibits opsonization, & inhibits complement cascade
  13. 13Describe the Bound coagulase of Staphconverts the soluble blood protein fibrinogen into long, insoluble fibrin molecules, that form a blood clot around the bacteria
  14. 14Slime layersInhibit phagocytosis, facilitates attachment to artificial surfaces, such as catheters, shunts, artificial heart valves, & synthetic joints
  15. 15Which part of Staph interferes with antibody immune responses by binding to the Fc portion of IgG antibodies?Protein A
  16. 16Which part of Staph inhibits opsonization?Protein A
  17. 17Which part of Staph inhibits complement cascade?Protein A
  18. 18Which part of Staph converts blood protein fibrinogen into long, insoluble fibrin molecules, that form a blood clot around the bacteria?Bound coagulase
  19. 19Which part of Staph inhibits phagocytosis?Slime Layers
  20. 20Which part of Staph facilitates attachmnent to artificial surfaces, such as catheters, shunts, artificial heart valves, & synthetic joints?Slime Layers
  21. 21List the enzymes that S. aureus synthesize?Cell-free coagulase, Hyaluronidase, Staphylokinase, Lipases, & B-lactamase (penicillinase)
  22. 22What produces Cell-free coagulase, Hyaluronidase, Staphylokinase, Lipases, & B-lactamase (penicillinase)?S. aureus
  23. 23What enzymes are produced by S. epidermidis?Hyaluronidase & lipases
  24. 24What are Hyaluronidase & Lipases produced by?S. epidermidis
  25. 25Describe Cell-free coagulasetriggers blood clotting; only produced by S. aureus
  26. 26Describe HyaluronidaseBreaks down hyaluronic acid (Major component of the matrix between cells), enables bacteria to spread between cells throughout the body
  27. 27Describe StaphylokinaseDissolves fibrin threads in blood clots, allowing S. aureus to free itself from clots; produced by S. aureus
  28. 28Describe LipasesDigest lipids, allowing staphylococci to grow on the surface of the skin & in cutaneous oil glands
  29. 29Describe B-lactamase (penicillinase)Present in over 90% of S. aureus strains, Breaks down penicillin
  30. 30What enzyme triggers blood clotting?Cell-free coagulase
  31. 31Which enzyme breaks down hyaluronic acid (major component of the matrix between cells)?Hyaluronidase
  32. 32What is the major component of the matrix between cells?Hyaluronidase
  33. 33Which enzyme enables bacteria to spread between cells throughout the body?Hyaluronidase
  34. 34Which enzyme dissolves fibrin threads in blood clots, allowing S. aureus to free itself from clots?Staphylokinase
  35. 35What enzyme digests lipids, allowing staphylococci to grown on the surface of the skin & in cutaneous oil glands?Lipases
  36. 36What enzyme breaks down penicillin?B-lactamase (Penicillinase)
  37. 37Name the toxins of StaphylococcusCytolytic toxins, Exfoliative toxins, Toxic-shock syndrom (TSS) toxin (TSST-1), Enterotoxins
  38. 38Describe Cytolytic toxinsalpha, beta, gamma, & delta toxins disrupt the cytoplasmic membranes of a variety of cells, Leukocidin lyses leukocytes
  39. 39Exfoliative toxinscauses the dissolution of epidermal desmosomes (intracellular bridge proteins that hold adjoining cytoplasmic membranes together), causing the patient's skin cell to separate from each other & slough off the body
  40. 40Describe Toxic-shock syndrome (TSS) toxin (TSST-1)Causes toxic-shock syndrome (discussed later) & functions as a superantigen
  41. 41Describe enterotoxinsStimulate the intestinal muscle contractions, nausea, & intense vomiting associated with staphylococcal food poisoning, heat stable, remaining active @ 100 degrees C for up to 30 min, functions as superantigen
  42. 42What toxin disrupts the cytoplasmic membranes of a variety of cells & leukocidin lyses leukocytes?Cytolytic toxins
  43. 43What toxin causes dissolution of epidermal desmosomes?Exfoliative toxins
  44. 44What are desmosomes?intercellular bridge proteins that hold adjoining cytoplasmic membranes together
  45. 45Which toxin causes the patients skin cells to separate from each other & slough off the body?Exfoliative Toxins
  46. 46Which toxin causes toxic-shock syndrome?Toxic-shock syndrome toxin
  47. 47What toxin functions as a superantigen?Toxic-shock syndrome toxin & Enterotoxins
  48. 48What toxin stimulates the intestinal muscle contractions, nausea, & intense vomiting associated with staphylococcal food poisoning?Enterotoxins
  49. 49Which heat stable, remaining active at 100 degrees C for up to 30 minutes?Enterotoxins
  50. 50What do superantigens do?Crosslink MHC class 2 & the TCR, which stimulates release of cytokines (IL1, IL2, TNF, & INF- gamma)
  51. 51Describe how Staphylococcus aureus EnterotoxinProtein is cooked to kill bacteria, but contaminated by worker with staph on hands. The organisms incubate in food long enough to form & release toxins. Reheating will eliminate staphylococci but not the toxin. Food containing toxins is eaten. In 1-6 hrs, intoxication occurs.
  52. 52What does INF-gamma do?activates macrophages
  53. 53What does TNF?Cause inflammation
  54. 54Where is S. epidermidis be found?all over the human skin
  55. 55Where is S. aureus found?Only on moist skin folds
  56. 56Where do both staphyloccus grow?grow in upper respiratory, gastrointestinal, & urogenital tracts of humans
  57. 57What grows in the upper respiratory, GI, & Urogenital tracts of humans?Both species of Staph
  58. 58Where are both staph species transmitted?through direct contact b/t individuals as well as fomites such as contaminated clothing, bed sheets, & medical instruments
  59. 59What is transmitted through direct contact b/t individuals as well as fomites such as contaminated clothing, bed sheets, & medical instruments?Both species of Staph
  60. 60How can you prevent contamination of both Staph species?Proper hand washing & aseptic techniques are essential
  61. 61what is prevented by using Proper hand washing & aseptic techniques?Both species of Staph
  62. 62List the types of Staphylococcal Disease?Noninvasive, Cutaneous, & Systemic
  63. 63What are Noninvasive, Cutaneous, & Systemic examples of?Staphylococcal Diseases
  64. 64Name a Noninvasive DiseaseFood intoxication
  65. 65What is food intoxication?a form of food-borne illness caused by ingesting exotoxins made by organisms such as bacteria
  66. 66Name a cutaneous staphylococcal diseasePyogenic lesions
  67. 67Name Systemic Staphylococcal DiseasesToxic-shock syndrome, Bacteremia, Endocarditis, Pneumonia, & Osteomyelitis
  68. 68What category of disease are pyogenic lesions under?Cutaneous Staphyloccal Diseases
  69. 69What foods are commonly affected that lead to food intoxication?processed meats, custard pastries, potato salad, & ice cream
  70. 70How do you inactivate enterotoxins?You can't inactivate by warming or reheating foods because enterotoxins are heat stable
  71. 71What are the symptoms of food intoxication?Nausea, severe vomiting, diarrhea, headache, sweating, & abdominal pain
  72. 72When do symptoms of food intoxication occur?within 4 hours following ingestion
  73. 73How long does food intoxication last?24 hrs or less because consumed staph stop producing toxins
  74. 74Describe the 4 types of Pyogenic lesionsStaphylococcal scalded skin syndrome, Impetigo, Folliculitis, & Furuncle (boil)
  75. 75What is Staphylococcal scalded skin syndrom caused by?S. aureus exotoxin exfoliatin
  76. 76What is Staphylococcal scalded skin syndrome look like?Reddening of the skin that typically begins near the mouth & spreads over the entire body. Followed by large blisters.
  77. 77What happens after 2 days when someone is infected with Staphylococcal scalded skin syndrome?the affected out layer of skin (epidermis) peels off in sheets
  78. 78Describe Impetigosmall flattened, red patches on the face & limbs that develop into pus-filled vesicles that eventually crust over
  79. 79What is the pus of Impetigo filled with?Bacterial & white blood cells
  80. 80Who is Impetigo most common in?Children with immune systems that are not fully developed
  81. 81What is Folliculitis?An infection of a hair follicle in which the base of the follicle becomes red, swollen, & pus filled.
  82. 82What is Folliculitis called when it occurs at the base of the eyelid?Sty
  83. 83What is a Furuncle or boil?A large, painful, raised nodular extension of folliculitis into surrounding tissue.
  84. 84What happens when several furuncles coalesce?They form a carbuncle, which extends deeper into the tissues, triggering the fever & chills that are characteristic of innate immunity.
  85. 85What is Toxic-shock syndrome caused by?Caused when strains of Staphylococcus produce TSST-1. This funtions as a superantigen through activation of T cells by cross-linking MHC class 2 molecules with T cell receptors.
  86. 86How is the toxin in Toxic-shock syndrome put into the body?Toxin is absorbed into the blood & causes TSS
  87. 87What are the symptoms of Toxic-shock syndrome?fever, vomiting, red rash, extremely low bld pressure, loss of sheets of skin
  88. 88When does Toxic-shock syndrome become fatal?Fatal to 5% of patients when their blood pressure falls so low that the brain, heart & other vital organs have an inadequate supply of oxygen.
  89. 89Describe BacteremiaAfter staph enter the blood from a site of infection, they travel to other organs of the body, which may become infected
  90. 90When does Endocarditis occur?When S. aureus attacks the lining of the heart (including its valves)
  91. 91What are symptoms of Endocarditis?nonspecific, flulike symptoms, but their condition quickly deteriorates as the amount of blood pumped from the heart drops precipitously.
  92. 92What is the mortality rate of Endocarditis?About 50% of patients die
  93. 93Describe PneumoniaInflammation of the lungs in which alveoli (air sacs) & bronchioles (smallest airway) become filled with fluid
  94. 94When does Pneumonia occur?When staph in the blood invades the lungs
  95. 95When does Osteomyelitis occur?When staph invade a bone either thru a traumatic wound or via the blood
  96. 96What is Osteomyelitis?Inflammation of the bone marrow & the surrounding bone
  97. 97What are symptoms of Osteomyelitis?characterized by pain in the infected bone accompanied by high fever
  98. 98How do you diagnose a Staph disease?detect grapelike arrangements of Gram positive bact. isolated from pus, blood, or other fluids. If they are able to clot blood, then they are coagulase-positive S. aureus. Negative=s. epidermidis.
  99. 99If you isolate grape-like arrangements of Gram + bact & they clot blood, what are they?coagulase-positive S. aureus
  100. 100If you isolate grape-like arrangements of Gram + bact & they do not clot blood, what are they?S. epidermidis (Coagulase-negative)
  101. 101How do you treat Staph infections?Only 5% of staph species are susceptible to penicillin. Doctors then tried semisynthetic forms of penicillin, methicillin, what are not inactivated by B lactamase, but S. aureus are now methicillin-resistant. Vancomycin is used to treat MRSA infections, but there are S. aureus that are resistant to this as well.
  102. 102What percentage of Staph species are susceptible to penicillin?Only 5%
  103. 103Describe the structure of NeisseriaArranged in diplococci, have fimbria, have capsules, contain lipooligosaccharide (LOS)
  104. 104Describe the physiology of NeisseriaGram-negative, nonmotile, aerobic, oxidase positive, fastidious in growth
  105. 105what does it mean that Neisseria is Oxidase positive?electron transport chains contain the enzyme cytochrome oxidase
  106. 106What does it mean that Neisseria contain LOS?Lipooligosaccharide, which is composed of Lipid A & sugar molecules, which enable bacteria to attach to & invade human cells
  107. 107What enables Neisseria bacteria to attach to & invade human cells?Lipooligosaccharide (LOS) which contains lipid A & sugar molecules
  108. 108Why do Neisseria have fastidious growth?Cultured on blood agar plates. Thay-Martin medium contains antimicrobials that inhibit the growth of most other organisms.
  109. 109Name the 2 species of Neisseria that are pathogenic to humans.Neisseria gonorrhoeae & Neisseriameningitidis
  110. 110Describe Neisseria gonorrhoeaeCauses gonorrhea, an STD. "Clap"
  111. 111Describe NeisseriameningitidisCauses a type of meningitis & life-threatening diseases when it invades the blood or cerebrospinal fluid
  112. 112In what animals does Neisseria gonorrhoeae occur?humans only (mostly in female adolescents)
  113. 113Describe the pathogenicity of N. gonorrhoeaeadhere via their fimbriae & capsules to epithelial cells of the mucous membranes lining the genital, urinary, & digestive tracts of humans. Secrete a protease that cleaves secretory IgA in mucus. Endocytosed bacteria survive & multiply within neutrophils.
  114. 114How many cells (N. gonorrhoeae) cause disease?As few as 100 pairs of cells can cause disease
  115. 115Describe the Epidemiology of N. gonorrhoeae in men.Insufferably symptomatic. Acute inflammation occurs 2-5 days after infection in the urethra of the penis, causing extremely painful urination & a pus-filled discharge.
  116. 116Describe the epidemiology of N. gonorrhoeae in women.Often asymptomatic. Neisseria cannot attach to cells lining the vagina. Most commonly infect the cervix of the uterus. Can infect deep in the uterus & the Fallopian tubes by "hitchhiking" on sperm to which they attach by means of fimbriae or LOS. In the uterine tubest they can trigger inflammation, fever, & abdominal pain (pelvic inflammatory disease).
  117. 117Can you explain the general epidemiology of N. gonorrhoeaeGonococcal infection of a child during birth can result in inflammation of the cornea, ophthalmia neonatorum, or blindness
  118. 118How do you diagnose N. gonorrhoeae?In symptomatic men, the presence of Gram-negative diplococci in pus from an inflamed penis. In asymptomatic cases, commercially available genetic probes provide direct, accurate, rapid detection. Bacterium can be cultured on Thayer-Martin agar.
  119. 119How do you treat N. gonorrhoeae?It is resistant to penicillin, tetracycline, erythromycin, & aminoglycosides. Current txt is broad-spectrum cephalosporins. Long-term specific immunity doesn't develop due to highly variable surface antigens.
  120. 120Why is N. gonorrhoeae immune to many treatments?It has highly variable surface antigens. Promiscuous people can be infected again. Antigenic variation: alter the antigen on their outer surface.
  121. 121How do you prevent N. gonorrhoeae?Sexual abstinence. Monogamy with an uninfected, faithful partner, consistent & proper use of condom.
  122. 122Describe the pathogenicity of Neisseria miningitidisCauses life-threatening diseases when it invades the blood or erebrospinal fluid
  123. 123What does much of the damage from N. meningitidis come from?Results from blebbing (a process in which the bacterium sheds extrusions of outer membrane).
  124. 124What are the symptoms of N. meningitidis?The lipid A component of LOS that is released into extracellular spaces triggers fever, vasodilation, inflammation, shock, & disseminated intravascular coagulation (DIC).
  125. 125Describe the epidemiology of N. meningitidis.Part of normal microbiota in upper respiratory tracts of up to 40% of healthy ppl. More prevalent in children & young adults from lower economic groups. Transmitted by respiratory droplets among people living in close contact.
  126. 126How is N. meningitidis transmitted?Transmitted by respiratory droplets among people living in close contact.
  127. 127Describe the disease N. meningitidis.involve abrupt sore throat, headache, stiff neck, vomiting, convulsions. Can progress rapidly that death results within six hours of the initial symptoms.
  128. 128Why is meningococcal septicemia is life threatening?LOS may trigger shock, devastating blood coagulation & petechiae (minute hemorrhagic skin lesions) on the trunk & lower extremities.
  129. 129How do you diagnose N. meningitidis?Identify Gram-negative diplococci within cerebrospinall phagocytes. Perform spinal tap.
  130. 130What occurs during a spinal tap?a sample of cerebrospinal fluid using a needle inserted into the lower spinal canal.
  131. 131What can N. meningitidis ferment?maltose
  132. 132What is the difference between N. meingitidis & N.gonorrhoeae?N. meningitidis can ferment maltose
  133. 133How do you treat N. meningitidis?Intravenously administer penicillin is the drug of choice
  134. 134How do you prevent N. meningitidis?Prophylactic txt with ceftriaxone or rifampin to anyone exposed to individuals with meningococcal disease.
  135. 135What does ceftriaxone do?inhibits bacterial cell wall synthesis
  136. 136What does ciprofloxacin do?Inhibits bact. DNA gyrase
  137. 137What does Rifampin do?inhibits bacterial DNA-dependent RNA polymerase
  138. 138Are there vaccines against N. meningitidis?Clinically relevant serogroups are A, B, C, W-135, & Y

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Flashcards on MIC101 Lecture 15, created by patience.almazan on 28/05/2015.
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