HB3 notecards-immuno.txt

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HB3 notecards-immuno.txt
2011-03-05 16:42:37
HB3 immunology

HB3 immunology
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  1. What bacterial enzyme does the positive indole test detect the presence of
  2. Catalase positive, Coagulase positive
    Staphylococcus aureus
  3. Catalase positive, Coagulase negative
    Staphylococcus epidermidis
  4. If catalase negative, what test do you do next
    Hemolysis on blood agar plate
  5. What are the two possible bacterial genera that are Gram positive, Catalase negative
    Streptococcus and enterococcus
  6. Catalase negative, alpha hemolysis, optochin sensitive, positive bile solubility test
    Streptococcus pneumoniae
  7. Catalase negative, alpha hemolysis, all other tests negative
    Viridans groupd streptococcus
  8. Catalase negative, Beta hemolysis, Bacitracin sensitive
    Group A Streptococcus pyrogenes
  9. Catalase negative, +CAMP test
    Group B streptococcus agalactiae
  10. Catalase negative, gamma hemolysis, Positive Bile esculin test, + Growth in 6.5% NaCl
    Group D enterococcus
  11. Catalase negative, gamma hemolysis, Positive bile esculin test, NO growth in 6.5% NaCl
    Group D streptococcus (Non-enterococcus)
  12. After bacteria has been shown to be Gram Negative, what is the next test to use?
    Oxidase test
  13. Gram negative, Oxidase positive
    Pseudomonas aeuruginosa
  14. Oxidase negative, grow on Mac Conkey agar-->turns media red, indole positive
    Escherichia Coli
  15. Oxidase negative, grown on Mac Conkey agar-->turns media red, indole negative, urea positive
    Kiebsella pneumoniae
  16. Oxidase negative, grow on Mac Conkey agar-->turns media red, indole negative, urease negative
    Enterobacter aerogenes
  17. 3 organisms that are oxidase negative, grown on Mac Conkey again-->turn media red
    Escherichia Coli, Kiebsella pneumoniae, Enterobacter aerogenes
  18. Oxidase negative, grown on Mac Conkey agar--> no color change, Black color for H2S production, Positive Indole test
    Proteus vulgaris
  19. Oxidase negative, grown on Mac Conkey agar--> no color change, Black color for H2S production, Negative Indole test
    Proteus Mirabeles
  20. Oxidase negative, grown on Mac Conkey agar--> no color change, No Black color because no H2S production, Positive citrate test
    Serratia Marcescens
  21. What two bacterium can transition between a metabolicaaly active and inactive form?
    Bacillus and Clostridium
  22. What is the Vegetative form of Clostridium and Bacillus?
    metabollically active
  23. What is the dormant form of Clostridium and Bacillus?
    metabolically inactive
  24. What is the process of transition from vegetative to spore?
  25. What is the process of transition from spore to vegetative?
  26. What compound binds the high concentration of Ca in a Bacillus or Clostridium spore?
    dipicolinic acid
  27. What type of reistance do spores exhibit?
    heat resistant, radiation resistant, resist starvation for hundreds of years and still germinate
  28. What are Petechiae, splinter hemorrhages and Osler nodes symptoms of?
    infectious endocarditis
  29. What are the criteria for diagnosing infective endocarditis?
    new murmur, positive Echocardiogram, Positive blood culture
  30. Most common cause of acute, native valve community acquired infectious endocarditis
    Staphylococcus aureus
  31. Most common cause of subacute, native valve community acquired infectious endocarditis
    Streptococci viridans
  32. Most common cause of infectious endocarditis in IV drug users
    Staphylococcus aureus
  33. Most common cause of prosthetic valve acquired infectious endocarditis
    S. epidermidis
  34. Why is S. epidermidis good at colonizinf articifical surface (prosthetic valve, catheters, etc)?
    Biolfim (slime layer), polysaccharide matrix protects them from defense mechanisms that would normally eliminate them
  35. What are opportunistic pathogens?
    patheogens that are normally part of the natural flora, can cause infection when immunocompromised or when they get somewhere they aren't supposed to be
  36. What are strict pathogens?
    microbes with relatively potent or multiple virulense factors, almost always cause disease
  37. What is the function of Protein A and where do you find it?
    On bacteria, binds to antibody, prevents the antibody from binding to the cell and completing phagocytosis
  38. What are the 3 pathways of complement activation?
    Alternative pathway, Lecin-mediated, Classical Pathway
  39. What is the function of Properdin
    Protein in the system that stabilizes the C3bBb membrane convertase complex
  40. What inactivates membrane bound C3b?
    Factor H and I, convert C3b to iC3b
  41. What symptoms would you have if you had deficiency in Factor I?
    cant inhibit C3b from forming, you'd run out of it, Prone to infection of the upper respiratory, urinary systems, ear
  42. What protects the self's own cells from immune system?
    DAF and MCP inactivated C3bBb (membrane convertase) quickly
  43. What are the consequences of DAF or MCP deficiency?
    Paroxysmal noctrunal hemoglobinuria (self lyses own blood cells)
  44. What are the consequences of C1INH deficiency?
    Hereditary Angioneurotic Edema, classical pathway of complement is overactive, produce large amountf of C2a, vasoactive peptide and bradykinin
  45. What are the consequences of C3 deficiency?
    susceptibiltiy to encapsulated bacteria
  46. What are the consequences of C5-C9 deficiency?
    can't form MAC's susceptibility to Neisseria
  47. What are the consequences of C1,2,4 deficiency?
    immune complex disease
  48. What Gram Positive Cocci are strrictly anaerobic?
  49. What is the way to classify streptococcus based on serologic data?
    Lancefield groups A-->W
  50. What are the types of hemolytic patterns you can get on blood agar Hemolysis test?
    Alpha, Beta, Gamma
  51. What does alpha hemolysis indicate
    partial hemolysis, green on agar plate
  52. What does Beta hemolysis indicate
    total hemolysis, clear on agar plate
  53. What is the serologic group and hemolysis group for S. pneumoniae
    None, alpha hemolysis
  54. How does S. pneumoniae usually cluster?
  55. How does S. pneumoniae colonize the oropharynx?
    surface adhesion proteins
  56. What does Gamma hemolysis indicate
    No hemolysis
  57. What is the main virulence factor for Strep pneumoniae that is responsible for the ability to avoid phagocytosis?
    Polysaccharide capsule
  58. How does pneumolysin in S. pneumoniae causes complement activation?
    lyses ciliated epithelial cells and activates complement via the classical pathway producing C3a and C5a, teichoic and peptidoglycan fragments activate complement via alternative pathway
  59. What soluble substances do macrophages secrete that promote further inflammation?
    IL1 and TNF alpha
  60. How does Strep pneumoniae defend against phagocytosis?
    Polysaccharide capsule, Pneumolysin inhibits phagocytic oxidative burst, phosphocholine binds to recptors on leukocytes, platelets and ECs allowing bacteria to enter cells and bloodstream
  61. How does the adaptive immune system override the resistance to phagocytosis of bacterium's polysaccharide capsule?
    antibodies directed at capsular polysaccharide
  62. Why does Pneumonia produce Low grade fever in older people
    They do not have the high functioning immune system, decreased number of cytokines, lower immune response
  63. What are the age related changes of Pneumonia in elderly?
    Decreased mucociliary clearance, increased colonization of oropharynx with pathogen, proliferation of bacteria in gastric contents (less stomach acid), increased aspiration
  64. What is the CURB-65 Criteria for prognosis in Pneumonia?
    Confusion, Urea (BUN>20 mg/dL), Respiratory rate (>30 breaths/min), Blood pressure (systolic < 90, diastolic < 60), Age >65
  65. What is the most cause of atypical community acquired pneumonia?
    Mycoplasma pneumoniae
  66. What is the mechanism that antibodies overcome the effects of S.pneumoiae capsule?
    antibody has Fc portion that is usually coated on the outside, macrophages have receptors for Fc, complement mediated killing
  67. Where does Pneumococcal pneumonia accumulate?
    alveolar spaces, often localized in the lower lobe
  68. What are the symptoms of pneumococcal pneumonia?
    fever (102-103F), coughing, production of blood tinged sputum, chest pain
  69. What is common treatment for S. pneumoniae infection
    Lovofloxacin (FQN), broad spectrum, orally, long half life allows daily dosing, little resistance (1.1%)
  70. What is common combination treatment for S. pneumoniae infection
    B-lactam (Cefpodoxime, Cefuroxime, Ceftriaxone) + macrolide, broad spectrum, oral or IV, poor bioavailability
  71. Which B-lactam has problems with discordant therapy?
  72. What macrolide is used to treat S. pnuemoniae?
    Azithromycin, Clarithromycin, broad spectrum, rapid absorption but poor bioavailability, hepatic excretion, side effect= QT prolongation
  73. What is the most common cause of nosocomial pneumonia?
    Gram negative rods (P. aeruginosa, E. coli, H. influenzae)
  74. What is a double sickening pattern associated with upper respiratory disease usually indicative of?
  75. What is the typical symptoms of upper respiratory infection?
    headache, shore throat, rhinorrhea
  76. What is the typical symptoms of lower respiratory infection?
    persistent cough, purulent sputum, shortness of breath
  77. What kind of cough is associated with atypical vs. acute pneumonia?
    non-productive for atypical, productive for acute
  78. What timeline is associated with atypical vs. acute pneumonia?
    atypical is insidious onset (over a week) acute pneumonia is rapid onset (2-3 days)
  79. What causative agent of atypical pneumonia produces a high cold agglutinin titer?
    Mycoplasma pneumoniae
  80. What is the most common cause of bacterial phayrngitis?
  81. What is the most common cause of pharyngitis, viral or bacterial?
  82. What is the serologic (Lancefield) group and type of hemolysis exhibited by Streptococcus pyogenes?
    A, Beta hemolysis
  83. Group A streptococcus (GAS) has what major type protein on its surface?
    M protein, two polypeptide chains complexed in alpha helix, anchored to membrane and extend through cell wall
  84. What are the main virulense factors for S. pyogenes?
    Hyaluronic acid capsule (blocks phagocytosis), M protein (inhibits complement C3b), C5a peptidase (inactivated complement C5a), adhesins, streptolysins, streptokinases, DNAases
  85. What is the function of DNAases as virulence factors?
    depolymerizae free DNA in pus, reduce viscosity & facilitate spread of bacteria
  86. What is the function of Streptolysins S & O as virulence factors?
    lyse leukocytes, erythrocytes, and platels (streptolysin S= B hemolysis)
  87. What is the function of Streptokinases A & B as virulence factors?
    degrade blood clots and fibrin deposites--facilitates spread of bacterium
  88. What is responsible for the progression of S. pyrogenes to Scarlet Fever?
    Pyrogenic Exotoxins (SpeA, SpeB, SpeC, SpeF), superantigens that stimulate macrophages and T helper cells
  89. What heart condition can result from Rheumatic Fever?
    Endocarditis (vegetations), myocarditis, pericarditis= PANCARDITIS
  90. What is Molecular Mimicry and what disease is an example of it?
    Host and invading microorganism share antigenic determinant, ex: Rheumatic Fever
  91. What tests are most useful in confirming Rheumatic heart disease?
    ASO (abs against streptolysin O), Anti-DNAse (abs agains streptococcal DNAse), Anti hyaluornidase (abs to hyaluronidase)
  92. What are the virulence factors of B. pertussis
    Adhesins, pertussis toxin, tracheal cytotoxin
  93. What is a toxoid?
    detoxififed toxin
  94. What are the 3 stages of infection with Bordatella Pertussis
    Incubation: 7-10 d, Catarrhal stage: 1-2 weeks, Paroxysmal stage 2-3 weeks, Convalescence stage: 3-4 weeks
  95. What is the major virulence factor for C. diptheriae
    Diphtheria toxin, A-B exotoxin actively excreted by bacterium stops protein synthesis
  96. What are the symptoms of C. Diptheriae infection
    Incubation: 2-4 days, sudden onset of malaise, low grade fever, exudative pharyngitis, sore throat, thick pseudomembrane, can progress to myocarditis and neuropathy
  97. What are icosahedral capsids?
    nearly spherical with 20 faces, 12 symmetrical pentamers
  98. What are icosadeltahedral capsids
    larger, more complex version of icosahedral capsids, 12 pentamers + hexamer subunits (soccerball)
  99. What are helical capsids
    cylindrical appearance, usually RNA genomes if helical virus infects human
  100. What are the capsid properties of non-enveloped viruses?
    very tough capsid, disease they cause do not require direct contact for transmission, virus can survive outside of host, harder to inactivate
  101. What is the structure of viral envelope?
    phospholipids, proteins and glycoproteins, membranous (lipid bilayer) derived from host cell membrane but modified by virus
  102. What is the purpose of Glycoproteins in viral envelopes?
    extend like spikes, serve as viral attachment proteins (VAPs), bind to receptor on surface of host cell
  103. What is the transmission of enveloped viruses?
    Not easily transmitted via fecal oral, fomites, air, usually transmitted in secreted body fluids or blood-blood transfer
  104. Wht are the steps of viral infection?
    attachment, penetration, uncoating, macromolecular synthesis, assembly, release
  105. What is a host range?
    range of species a virus can infect
  106. What is tropism?
    range of tissue types a virus can infect
  107. How do most non-enveloped viruses penetrate host cell?
    Endocytosis (viropexis= 3D conformational change of capsid, is less common)
  108. How do most enveloped viruses penetrate host cell?
    Fusion at cell surface (Fusion with endosome membrane= entire virion brought into cell viral envelope fuses with endosome)
  109. Where does replication for all DNA viruses occur?
    nucleus (exception= Pox virus)
  110. Where does replication for all RNA viruses occur
    cytoplasm (exception= retrovirus and orthomyxovirus)
  111. Does DNA virus use its own DNA-dependent RNA polymerase to synthesize viral mRNAs?
    No, it uses host cells, enzyme doesnt know the different between host cell and viral DNA
  112. Does DNA virus use its own DNA binding proteins to synthesize viral mRNAs?
    simple DNA viruses rely on host cell, complicated DNA viruses encode theis own DNA bps
  113. What are the requirements for DNA replication of DNA viruses
    Nuclear factor (host cell or virus provides), DNA-dependent DNA polymerase (host cell or virus provide), Primer (virus provides)
  114. What does the RNA virus need early on for copying RNA?
    RNA dependent RNA polymerase, virus must carry enzymes in virion or code for their production shortly after entry
  115. How do (+) sense strand ss-RNA viruses replicate?
    viral genome binds to host cell ribosomes and directs production of viral proteins, codes for RNA dependent RNA polymerase first, makes (-) sense strand to be template for multiple (+) strands
  116. How do (-) sense strand ss-RNA viruses replicate?
    bring RNA dependent RNA polymerase with them, makes (+) strand mRNAs to make protein using host cell ribosomes, makes multiple (-) strands with RNAdepRNApoly
  117. How are nonenveloped viruses released from host cell?
  118. How are enveloped viruses released from host cell?
    lysis, budding or exocytosis
  119. What is the most likely causative agent of Croup?
    Parainfluenza viruses
  120. What is the most likely causative agent of common cold?
  121. What is the most likely causative agent of viral conjunctivitis?
    Adenovirus (types 3 & 7)
  122. What are the glycoproteins on the envelope of parainfluenza virus?
    F (fusion) protien, and HN (hemagglutinin nuramidase) protein
  123. Why does parainfluenza virus cause seal bark cough?
    rapid replication results in giant cells and extensive cell lysis, inflammation of the airway and edema
  124. What does tachypnea and wheezing indicate, upper or lower respiratory infection?
    lower respiratory