HB3 notecard- all.txt

  1. MIC is within the therapeutic window of _______ drugs
  2. MBC is within the therapeutic window of _______ drugs
  3. Post antibiotic effect
    Still some bacteriostatic killing after removal of the drug, concentration independent activity
  4. Concentration independent activity
    Maintaining steady serum levels above MBC over time results in maximum killing
  5. DNA synthesis inhibitors
    Fluorquinolones, Sulfonamides, Trimethoprim
  6. Protein Synthesis inhibitors
    Aminoglycosides, Tetracyclines, Macrolidea
  7. Cell Wall Synthesis Inhibitors
    Beta lactams, Glycopeptides, Polypeptides
  8. Mechanism of resistance for P. aeruinosa to many B-lactams
    decreased permeabiltiy of outer membrane=decreased access of drug to target site
  9. Mechanism of resistant for S. aureus against B-lactams?
    alterations in PBP= alteration of target, production of B-lactamase=inactivation of antibiotic
  10. 3 main mechansims for bacterial resistance against drugs
    Decreased access of drug to target, alteration of target, inactivation of antibiotic by bacterial enzyme
  11. Mechanism of Isoniazid= inhibit mycolic acids synthesis= mycoplasma cell wall
    • Prodrug activated by mycobacterial catalase peroxidase that inhibits enoyl-ACP reductase of fatty acid synthesis
    • R and I are the CYP inducers
    • I and E are disrupted by antacid
  12. How does Acyclovir work
    Blocks TK, fraudulent nucleotide

    • Amphotericin B and Azoles cover:
    • Histoplasmosis, Blastomycosis, Coccidioides
  13. Amphotericin B + Flucytosine
    Cryptococcus Neoformans (fungal meningitis)
  14. Echinocandins
    Blocks at the wall, doesn't do CRYPTOCOCCUS NEOFORMANS
  15. Kernig sign
    Can't extend knee when hip is flexed
  16. Neurocysticercosis
    Histo demonstration from biopsy, cystic lesions on CT/MRI,subcutaneous nodules, subcutaneous parasitesmTreat with albendazole
  17. What has erythema nodosum
    Coccidioides and Atypical Pneumonia
  18. What binds to sialic acid
    Tetanus (AB toxin), Influenza (binds to sialic acid on epithelial)
  19. What is the best treatment for community acquired native valve infectious endocarditis?
    Nafcillin+Pencillin (bactericidal) + Gentamicin (bacteristatic)
  20. What is the best treatment for infectious endocarditis in IV drug users?
    Vancomycin + Gentamycin (treat agents that cover MRSA and MRSE too)
  21. What is the best treatment for prosthetic valve infectious endocarditis?
    Vancomycin + Gentamycin + Rifampin (antimycobacterial)
  22. What do B-lactam antibiotics inhibit?
    transpeptidase (penicillin binding protein)- two fold attack because also tricks autolytic enzyme into thinking it is undergoing division
  23. What are the classes of B-lactams?
    Penicillins, monobactams, carbapenems, Cephalosporins
  24. What drugs are sensitive to B-lactamase (ie: subject to resitance)
    Penicillins, cephalosporins, 2nd generation extended spectrum (amoxicillin and ampicillin), 3rd and 4th generation extended spectrum (Ticarcillin, Piperacillin)
  25. Penicillin G and V
    1st generation penicillins, narrow spectrum, mainly G+ (not S. aureus), few G- (N. meninitidis), G is acid labile (IV) and V is acid stable (oral)
  26. Antistaphylococcal penicillins
    Nafcillin, Oxacillin, Dicloxacillin, narrow spectrum mainly G+ (includes S. aureus), B-lactamase resistance!
  27. What is the mechanism of resistance against anti-staphylococcal penicillins?
    resistance due to expression of PBP2-->MRSA
  28. 2nd generation Extended Spectrum Penicillin
    Amoxicillin (oral) and Ampicillin (oral or IV), G+ identical to Penicillin, more G- coverage and enterococci, good anaerobe coverage
  29. 3rd generation Extended Spectrum Penicillin
    Ticarcillin (IV), G+ identical to Penicillin, G- activity >2nd generation (including P. aeruginosa), good anaerobe coverage
  30. 4th generation Extended Spectrum Penicillin
    Piperacillin (IM or IV), G+ identical to Penicillin, G- activity >2nd generation (including P. aeruginosa), good anaerobe coverage
  31. What has anti-Pseudomonal activity
    3rd and 4th generation penicillins (Ticarcillin and Piperacillin), Monobactams (Aztreonam)
  32. Monobactams
    Aztreonam (IV, IM, inhalational), narrow spectrum, NO G+ activity, G- activity (including P. aeruginosa), aerobes only, intermediate resistance to B-lactamase
  33. Carbapenems
    Broad spectrum, good G+ (includes S. aureus), G- including P. aeruginosa, Good anaerobe coverase, resistance to most B-lactamases, SAVE THESE GUYS!
  34. How many generations of Cephalosporins are there?
  35. Which generation of Cephalosporin has the most G- activity
    5th generation
  36. Which generation of Cephalosporin has the most G+ activity
    1st generation
  37. 1st generation Cephalosporin
    Cefazolin (IV), broad spectrum, most G+ cocci (Kiebsiella, E.Coli), intermediate resistance to B-lactamase
  38. 2nd generation Cephalosporin
    Cefuroxime (IV, oral), most G+ cocci (Kiebsiella, E.Coli), some G- (weak enterobacter coverage), intermediate resistance to B-lactamase
  39. 3rd generation Cephalosporin
    Cefotaxime, most G+ cocci (Kiebsiella, E.Coli), most G- (including P. aeruginosa), enhanced enteric coverafe, mixed activity against MDR, resistance to B-lactamase
  40. 4th generation Cephalosporin
    Cefepime, most G+ cocci (Kiebsiella, E.Coli), most G- (including P. aeruginosa), enhanced enteric coverafe, mixed activity against MDR, resistance to B-lactamase
  41. 5th generation Cephalosporin
    Ceftobiprole and Ceftaroline (IV), G+ similar to 3rd/4th but extended coverage of enterococci and MRSA), G- similar to 3rd/4th, resistance to B-lactamase
  42. What bacterial enzyme does the positive indole test detect the presence of
  43. Catalase positive, Coagulase positive
    Staphylococcus aureus
  44. Catalase positive, Coagulase negative
    Staphylococcus epidermidis
  45. If coagulase negative, what test do you do next
    Hemolysis on blood agar plate
  46. What are the two possible bacterial genera that are Gram positive, Catalase negative
    Streptococcus and enterococcus
  47. Catalase negative, alpha hemolysis, optochin sensitive, positive bile solubility test
    Streptococcus pneumoniae
  48. Catalase negative, alpha hemolysis, all other tests negative
    Viridans groupd streptococcus
  49. Catalase negative, Beta hemolysis, Bacitracin sensitive
    Group A Streptococcus pyrogenes
  50. Catalase negative, +CAMP test
    Group B streptococcus agalactiae
  51. Catalase negative, gamma hemolysis, Positive Bile esculin test, + Growth in 6.5% NaCl
    Group D enterococcus
  52. Catalase negative, gamma hemolysis, Positive bile esculin test, NO growth in 6.5% NaCl
    Group D streptococcus (Non-enterococcus)
  53. After bacteria has been shown to be Gram Negative, what is the next test to use?
    Oxidase test
  54. Gram negative, Oxidase positive
    Pseudomonas aeuruginosa
  55. Oxidase negative, grow on Mac Conkey agar-->turns media red, indole positive
    Escherichia Coli
  56. Oxidase negative, grown on Mac Conkey agar-->turns media red, indole negative, urea positive
    Kiebsella pneumoniae
  57. Oxidase negative, grow on Mac Conkey agar-->turns media red, indole negative, urease negative
    Enterobacter aerogenes
  58. 3 organisms that are oxidase negative, grown on Mac Conkey again-->turn media red
    Escherichia Coli, Kiebsella pneumoniae, Enterobacter aerogenes
  59. Oxidase negative, grown on Mac Conkey agar--> no color change, Black color for H2S production, Positive Indole test
    Proteus vulgaris
  60. Oxidase negative, grown on Mac Conkey agar--> no color change, Black color for H2S production, Negative Indole test
    Proteus Mirabeles
  61. Oxidase negative, grown on Mac Conkey agar--> no color change, No Black color because no H2S production, Positive citrate test
    Serratia Marcescens
  62. What two bacterium can transition between a metabolicaaly active and inactive form?
    Bacillus and Clostridium

    • What is the Vegetative form of Clostridium and Bacillus?
    • metabollically active
  63. What is the dormant form of Clostridium and Bacillus?
    metabolically inactive
  64. What is the process of transition from vegetative to spore?
  65. What is the process of transition from spore to vegetative?
  66. What compound binds the high concentration of Ca in a Bacillus or Clostridium spore?
    dipicolinic acid
  67. What type of reistance do spores exhibit?
    heat resistant, radiation resistant, resist starvation for hundreds of years and still germinate
  68. What are Petechiae, splinter hemorrhages and Osler nodes symptoms of?
    infectious endocarditis
  69. What are the criteria for diagnosing infective endocarditis?
    new murmur, positive Echocardiogram, Positive blood culture
  70. Most common cause of acute, native valve community acquired infectious endocarditis
    Staphylococcus aureus
  71. Most common cause of subacute, native valve community acquired infectious endocarditis
    Streptococci viridans
  72. Most common cause of infectious endocarditis in IV drug users
    Staphylococcus aureus
  73. Most common cause of prosthetic valve acquired infectious endocarditis
    S. epidermidis
  74. 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
  75. 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
  76. What are strict pathogens?
    microbes with relatively potent or multiple virulense factors, almost always cause disease
  77. 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
  78. What are the 3 pathways of complement activation?
    Alternative pathway, Lecin-mediated, Classical Pathway
  79. What is the function of Properdin
    Protein in the system that stabilizes the C3bBb membrane convertase complex
  80. What inactivates membrane bound C3b?
    Factor H and I, convert C3b to iC3b
  81. 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
  82. What protects the self's own cells from immune system?
    DAF and MCP inactivated C3bBb (membrane convertase) quickly
  83. What are the consequences of DAF or MCP deficiency?
    Paroxysmal noctrunal hemoglobinuria (self lyses own blood cells)
  84. 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
  85. What are the consequences of C3 deficiency?
    susceptibiltiy to encapsulated bacteria
  86. What are the consequences of C5-C9 deficiency?
    can't form MAC's susceptibility to Neisseria
  87. What are the consequences of C1,2,4 deficiency?
    immune complex disease
  88. What Gram Positive Cocci are strrictly anaerobic?
  89. What is the way to classify streptococcus based on serologic data?
    Lancefield groups A-->W
  90. How does pseudomonas increase its resistance to B-lactams?
    decreasing porin channels-decreased amount of antibiotic gets in
  91. What are the types of hemolytic patterns you can get on blood agar Hemolysis test?
    Alpha, Beta, Gamma
  92. What does alpha hemolysis indicate
    partial hemolysis, green on agar plate
  93. What does Beta hemolysis indicate
    total hemolysis, clear on agar plate
  94. What is the serologic group and hemolysis group for S. pneumoniae
    None, alpha hemolysis
  95. How does S. pneumoniae usually cluster?
  96. How does S. pneumoniae colonize the oropharynx?
    surface adhesion proteins
  97. What does Gamma hemolysis indicate
    No hemolysis
  98. What is the main virulence factor for Strep pneumoniae that is responsible for the ability to avoid phagocytosis?
    Polysaccharide capsule
  99. 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
  100. What soluble substances do macrophages secrete that promote further inflammation?
    IL1 and TNF alpha
  101. 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
  102. How does the adaptive immune system override the resistance to phagocytosis of bacterium's polysaccharide capsule?
    antibodies directed at capsular polysaccharide
  103. 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
  104. 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
  105. 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
  106. What is the most cause of atypical community acquired pneumonia?
    Mycoplasma pneumoniae
  107. 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
  108. Where does Pneumococcal pneumonia accumulate?
    alveolar spaces, often localized in the lower lobe
  109. What are the symptoms of pneumococcal pneumonia?
    fever (102-103F), coughing, production of blood tinged sputum, chest pain
  110. What is common treatment for S. pneumoniae infection
    Lovofloxacin (FQN), broad spectrum, orally, long half life allows daily dosing, little resistance (1.1%)
  111. What is common combination treatment for S. pneumoniae infection
    B-lactam (Cefpodoxime, Cefuroxime, Ceftriaxone) + macrolide, broad spectrum, oral or IV, poor bioavailability
  112. Which B-lactam has problems with discordant therapy?
  113. What macrolide is used to treat S. pnuemoniae?
    Azithromycin, Clarithromycin, broad spectrum, rapid absorption but poor bioavailability, hepatic excretion, side effect= QT prolongation
  114. What is the most common cause of nosocomial pneumonia?
    Gram negative rods (P. aeruginosa, E. coli, H. influenzae)
  115. What is a double sickening pattern associated with upper respiratory disease usually indicative of?
  116. What is the typical symptoms of upper respiratory infection?
    headache, shore throat, rhinorrhea
  117. What is the typical symptoms of lower respiratory infection?
    persistent cough, purulent sputum, shortness of breath
  118. What kind of cough is associated with atypical vs. acute pneumonia?
    non-productive for atypical, productive for acute
  119. What timeline is associated with atypical vs. acute pneumonia?
    atypical is insidious onset (over a week) acute pneumonia is rapid onset (2-3 days)
  120. What causative agent of atypical pneumonia produces a high cold agglutinin titer?
    Mycoplasma pneumoniae
  121. What is the most common cause of bacterial phayrngitis?
  122. What is the most common cause of pharyngitis, viral or bacterial?
  123. What is the serologic (Lancefield) group and type of hemolysis exhibited by Streptococcus pyogenes?
    A, Beta hemolysis
  124. 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
  125. 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
  126. What is the function of DNAases as virulence factors?
    depolymerizae free DNA in pus, reduce viscosity & facilitate spread of bacteria
  127. What is the function of Streptolysins S & O as virulence factors?
    lyse leukocytes, erythrocytes, and platels (streptolysin S= B hemolysis)
  128. What is the function of Streptokinases A & B as virulence factors?
    degrade blood clots and fibrin deposites--facilitates spread of bacterium
  129. 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
  130. What heart condition can result from Rheumatic Fever?
    Endocarditis (vegetations), myocarditis, pericarditis= PANCARDITIS
  131. What is Molecular Mimicry and what disease is an example of it?
    Host and invading microorganism share antigenic determinant, ex: Rheumatic Fever
  132. 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)
  133. What are the virulence factors of B. pertussis
    Adhesins, pertussis toxin, tracheal cytotoxin
  134. What is a toxoid?
    detoxififed toxin
  135. 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
  136. What is the major virulence factor for C. diptheriae
    Diphtheria toxin, A-B exotoxin actively excreted by bacterium stops protein synthesis
  137. 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
  138. What are icosahedral capsids?
    nearly spherical with 20 faces, 12 symmetrical pentamers
  139. What are icosadeltahedral capsids
    larger, more complex version of icosahedral capsids, 12 pentamers + hexamer subunits (soccerball)
  140. What are helical capsids
    cylindrical appearance, usually RNA genomes if helical virus infects human
  141. 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
  142. What is the structure of viral envelope?
    phospholipids, proteins and glycoproteins, membranous (lipid bilayer) derived from host cell membrane but modified by virus
  143. 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
  144. 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
  145. Wht are the steps of viral infection?
    attachment, penetration, uncoating, macromolecular synthesis, assembly, release
  146. What is a host range?
    range of species a virus can infect
  147. What is tropism?
    range of tissue types a virus can infect
  148. How do most non-enveloped viruses penetrate host cell?
    Endocytosis (viropexis= 3D conformational change of capsid, is less common)
  149. 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)
  150. Where does replication for all DNA viruses occur?
    nucleus (exception= Pox virus)
  151. Where does replication for all RNA viruses occur
    cytoplasm (exception= retrovirus and orthomyxovirus)
  152. 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
  153. 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
  154. 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)
  155. 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
  156. 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
  157. 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
  158. How are nonenveloped viruses released from host cell?
  159. How are enveloped viruses released from host cell?
    lysis, budding or exocytosis
  160. What is the most likely causative agent of Croup?
    Parainfluenza viruses
  161. What is the most likely causative agent of common cold?
  162. What is the most likely causative agent of viral conjunctivitis?
    Adenovirus (types 3 & 7)
  163. What are the glycoproteins on the envelope of parainfluenza virus?
    F (fusion) protien, and HN (hemagglutinin nuramidase) protein
  164. Why does parainfluenza virus cause seal bark cough?
    rapid replication results in giant cells and extensive cell lysis, inflammation of the airway and edema
  165. What does tachypnea and wheezing indicate, upper or lower repsiratory?
    lower respiratory
  166. If gram negative coccus from ear exudate, what is the likely cause of the infection?
    Moraxella catharrhalis
  167. What are the 3 Gram negative cocci?
    Moraxella catarrhalis, Neisseria gonorrheae, Neisseria meningitidis
  168. Epididymitis
    inflammation of the epididymis, symptoms: tender scrotal swelling with erythema, dyuria and urethral discharge, pain in scrotum
  169. Orchitis
    inflammation of the testes, may be unilateral or bilateral, acute symptoms= testicular pain and swelling, inguinal lymphadenompathy, nausea, vomiting
  170. Cervicitis
    inflmmation of the cervis, usually asymptomatic or mild, severe cases cause mucopurulent discharge, pelvic painm dyspareunia
  171. What are the properties of enterobacteriaceae ("enteric bacteria")
    facultative anaerobes, ferment glucose, catalase positive, oxidase negative
  172. what are the most significant genera of GU enteric bacteria?
    Escheriae, Klebsiella, Proteus
  173. what are the most significant genera of GI enteric bacteria?
    Salmonella, Shigella, Yersinia
  174. What are the virulence factors of enteric bacteria?
    endotoxin (lipid A portion of LPS), Capsule, Type III secretion systems, drug resistance
  175. What are unicellular fungi
  176. How do yeasts reproduce
  177. What are multicellular fungi?
  178. How do molds embed into surface
  179. What is an example of specialized mycelium
  180. Candida are dimorphic and can be both ____ and ______
    yeasts and molds
  181. What is responsible for different class of Ig functions
    Heavy chain- constant region
  182. IgM
    Has more carbohydrate on heavy chain, Has 4 globular domains on heavy chain, Efficient at activating complement (classical and alternative), Secreted IgM is pentamer held together by J (joining chain)
  183. IgA
    Has monomer and dimer forms Has 3 globular domain on heavy chain + HINGE region Both are good at neutralizing pathogen Dimerc version is two monomer held together by J chain DIMERIC VERION: Secreted in MILK, saliva, sweat, tears, gut DIMERIC VERSION: Made in MALT (mucous associated lymphoid tissue),IgE, Has 4 globular domains on heavy chain, Very low levels in serum, High affinity for mast cells, eosinophils, basophils, Responds to parasites and allergens
  184. IgD
    Has 3 globular domains +HINGE region,Very low levels in serum,Function not known
Card Set
HB3 notecard- all.txt
HB3 exam1