First Aid: Microbiology

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First Aid: Microbiology
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2012-06-20 17:04:34
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First Aid Pharmacology Antimicrobials step microbiology
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First Aid: Microbiology: Pharmacology, pathology, etc.
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  1. What are the most common causes of meningitis in adults?
    • bacterial:
    • Strep. pneumoniae
    • Neisseria meningitidis

    viral:
  2. What are the most common causes of meningitis in HIV patients?
    • fungal:
    • Cryptococcus neoformans
  3. What are the most common causes of meningitis in neonates?
    Group B Strep. pyogenes

    gram(-) rods
  4. Identify:
    gram(-) rods
    oxidase (+)
    culture medium: produce pigment
    Pseudomonas aeruginosa

    water-based infections
  5. Which cytokines are increased in Toxic Shock Syndrome?
    (response to Staph aureus exotoxin: TSST-1)

    • "superantigen" activity:
    • (MHC-II) machrophages: TNF-a, IL-1
    • (TCR) T-cells: IL-2
  6. Which toxins are known to have "superantigen" activity?
    • Staph aureus: TSST-1 (toxic shock syndrome toxin)
    • Enterotoxins
    • Exfoliative toxins
  7. Identify:
    Pneumonia lung tissue specimen with macrophages filled with ovoid cells
    Histoplasma capsalatum
  8. Identify:
    Pneumonia lung tissue with multinucleate spherules packed with endospores
    Coccidioides immitis
  9. Identify:
    Pneumonia lung tissue with budding, encapsulated yeast forms
    Cryptococcus neoformans
  10. Identify:
    Paranasal sinus biopsy with noseptae hyphae branching at wide angels
    • (mucormycosis)
    • Mucor species
    • Rhizopus species
  11. Identify:
    Yeast that forms germ tubes after incubation
    Candida albicans
  12. What component does acid-fast testing identify?
    mycolic acid

    • Mycobacterium
    • Nocardia
  13. What are examples of polysaccharide vaccines?
    • Strep. pneumoniae
    • Neisseria meningitidis
    • Haemophilus influenzae
  14. Which antibiotics are useful for gram (+) infections?
    "CCC, there's no r-u in L-V"

    • Cephalosporins
    • Clindamycin
    • Chloramphenicol
    • Linezolid
    • Macrolides
    • Penicillin
    • Quinolones
    • Sulfonamides
    • Tetracycline
    • Vancomycin
  15. Which antibiotics are useful in atypical infections?
    "MQ CAT"

    • macrolides
    • quinolones
    • cloramphenicol
    • aminoglycosides
    • tetracycline
  16. Which antibiotics are useful in anaerobic coverage?
    "Quinn Cleaned Metro Cars with Clorox and a Broad Pen"

    • quinolones
    • clindamycin
    • metronidazole
    • carbapenems
    • chloramphenicol
    • broad spectrum penicillins
  17. Which antibiotics are useful in gram (-) coverage?
    • broad spectrum penicillins
    • cephalosporins (excepth 1st generation)
    • aminoglycosides
    • macrolides
    • quinolones
    • monobactams
    • sulfonamide/trimethoprim
    • carbapenems
    • chloramphenicol
  18. Which antimicrobials are useful against Pseudomonas?
    • ciprofloxacin (quinolone)
    • aminoglycosides (e.g. gentamicin)
    • 4th gen. and some 3rd gen. cephalosporins
    • broad spectrum penicillins
    • carbapenems
  19. What are the spore forming bacteria and what are their features?
    • Clostridium
    • Bacillus
    • B. cereus
    • Coxiella burnetii

    • features:
    • dipicolinic acid
    • resistance to heat, dehydration, and chemicals
    • found in soil
  20. Which bacteria's cell wall is made of mycolic acid?
    Mycobacteria (tuberculosis, leprae)
  21. Which bacteria does not have a cell wall?  What antibiotics would it be immune to?
    Mycoplasma

    • antibiotic immunity: cell-wall disrupters
    • penicillins
    • beta-lactams
    • cephalosporins
  22. Which microbes are detected using silver stain?
    • Fungi (e.g. Pneumocystis)
    • Legionella
  23. Which microbes generally do not gram stain well?
    "These Rascals May Microscopically Lack Color"

    • Treponema: too thin
    • Rickettsia: intracellular
    • Mycobacteria: high lipid in cell wall (acid-fast)
    • Mycoplasma: no cell wall
    • Legionella pneumophila: intracellular
    • Chlamydia: intracellular, no muramic acid in cell wall 
  24. Which microbes have significant intracellular phases?
    • Chlamydia
    • Rickettsia
    • Legionella pneumophila
    • Malaria
  25. What microbes are detected using fluorescent antibody staining and darkfield microscopy?
    Treponemes
  26. Which microbes stain with Giemsa stain?
    • Borrelia
    • Plasmodium
    • Trypanosomes
    • Chlamydia
  27. Which microbes stain with periodic acid Schiff (PAS)? Why?
    Tropheryma shippelii (Whipple's disease)

    • stains:
    • glycogen
    • mucopolysaccharides 
  28. Which microbes stain with Ziehl-Neelsen (carbol fuschin)?
    • acid-fast microbes:
    • Mycobacteria
    • Nocardia 
  29. Which microbes stain with India ink?
    • mucicarmine polysaccharide capsule:
    • Cryptococcus neoformans
  30. What is a partially acid fast microbe?  What is its main association?
    Cryptosporidium (protozoa)

    #1 cause of HIV-related diarrhea 
  31. What is the Thayer-Martin (VPN) media and what is it used to grow?
    • V = vancomycin: inhibits gram (+)
    • P = pilomyxin: inhibits gram (-)
    • N = nystatin: inhibits fungi

    • grows: N. gonorrhea
    •  
  32. What does H. influenzae grow on?
    • chocolate agar 
    • requires factors V and X 
  33. What grows on Bordet-Gengou (potato) agar?
    Bordetella pertussis

    "Bordet for Bordatella" 
  34. What does corynebacterium diptheria grow on?
    • Tellurite plate
    • Loffler's media 
  35. What does M. tuberculosis grow on?
    Lowenstein-Jensen agar
  36. What grows on Eaton's sugar?
    Mycoplasma pneumoniae
  37. What grows on MacConkey's agar?  What do the colonies look like?
    • grows lactose fermenting enterics 
    • i.e. grows gram (-) rods
    • colonies turn pink from acid release
    •  
  38. What is eosin-methylene blue agar used for?
    • grow E. coli
    • blue-black colonies with metallic sheen
  39. What grows Legionella?
    charcoal yeast extract agar with cystein and iron
  40. What is Sabouraud's agar used for?
    grow fungi
  41. What are the obligate aerobes?
    "Nagging Pests Must Breathe"

    • Nocardia
    • Pseudomonas
    • Mycobacteria
    • Bacillus
  42. Why does reactivated TB prefer the lung apices?
    • higher PO2
    • Mycobacteria = obligate aerobe 
  43. What are the obligate anaerobes?
    "Can't Breathe Aire"

    • Clostridium
    • Bacteriodes
    • Actinomyces
  44. What is a feature of obligate anaerobes?
    • require O2-free environment
    • lack catalase and/or superoxide dismutase
    • susceptible to oxidative damage
    • foul smelling (short-chain fatty acids)
    • difficult to culture
    • produce gas in tissue (H2, CO2) 
  45. What are prominent intracellular microbes?
    • obligate (can't make own ATP):
    • Rickettsia
    • Chlamydia

    • facultative:
    • Salmonella
    • Neisseria
    • Brucella
    • Mycobacterium
    • Listeria
    • Francisella
    • Legionella
    • Yersinia pestis

    "Some Nasty Bugs May Live FacultativeLY" 
  46. What are the encapsulated bacteria?  What test is used to detect them?
    • Neisseria meningtitis
    • Strep. pneumonia
    • Strep. agalactae (Group B)
    • H. influenzae
    • Salmonella
    • Kleibsiella 

    "SHiN SKiS"

    test: Quellung reaction (antisera: capsular swelling)
  47. Why are asplenic individuals more susceptible to encapsulated bacteria?
    asplenic: decreased ability to opsonize capsules
  48. What are encapsulated vaccines made of?
    • capsule + conjugated protein = antigen
    • conjugated protein required for T-cell recognition/class switching

    (N. meningitis, S. pneumonia, H. influenzae)
  49. What disease is particularly susceptible to invasion by catalase (+) bugs?
    • chronic granulomatous disease
    • catalase (+) bugs degrade limited H2O2

    deficiency: NADPH oxidase deficiency

  50. What are some catalase (+) organisms?
    • Staph
    • Serratia
    • Pseudomonas
    • Actinomyces
    • Candida
    • E. coli
  51. What would happen if a capsular polysaccharide vaccine was NOT conjugated to a protein prior to injection?
    no conjugated protein = no T-cell recognition = no class switching of antibodies

    only IgM present: no longterm immunity

    EXCEPTION: Pneumovax = Strep. pneum. vaccine 
  52. What are the urease (+) bugs?
    "K-PUNCH"

    • Klebsiella
    • Proteus
    • Ureaplasma
    • Nocardia
    • Cryptococcus
    • H. pylori
    •  
  53. What bacteria produces yellow pigment?
    • Actinomyces israelii
    • yellow sulfur granules = filaments in pus 

    Staph. aureus 
  54. What bacteria produces blue-green pigment?
    Pseudomonas
  55. What bacteria makes red pigment?
    Serratia marcescens
  56. How does S. aureus evade the host immune reponse?
    • Protein A:
    • binds Fc region of Ig
    • prevents opsonization
    • prevents phagocytosis 
  57. How does Group A Strep. evade the host immune reponse?
    • M protein:
    • prevents phagocytosis 
  58. Which organisms evade host immune response by IgA protease production?
    "SHiN"

    • Strep. pneum.
    • H. influ. type B
    • Neisseria

    IgA protease: helps colonize respiratory mucosa 
  59. Which organisms produce endotoxin?  What are typical examples?
    • gram (-)
    • Listeria: only gram (+) with endotoxin

    • typical:
    • Meningococcemia
    • sepsis with gram (-) rods 
  60. What are examples of exotoxin producing organisms?  What are typical presentations?
    • certain gram (+)
    • certain gram (-)

    • typical:
    • Tetanus
    • botulism
    • diptheria 
  61. Which are more heat stable: exotoxins or endotoxins?
    endotoxins: stable at 100 C for 1 hr

    (exotoxins: destroyed rapidly at 60 C except staph. enterotoxin)
  62. How does C. diptheria toxin work? Typical presentation?
    • exotoxin: diptheria toxin
    • ADP-ribosylation inactivates EF-2 (elongation factor) 

    • typical:
    • pharyngitis
    • pseudomembrane in throat
    • "bull neck"
    •  
  63. How does Pseudomonas aeur. pathogenicity work?  Typical presentation?
    • exotoxin: exotoxin A
    • inactivates elongation factor EF-2

    • typical:
    • host cell death (apoptosis/necrosis) 
  64. Which microbes inactivate 60S ribosome by cleaving rRNA via an exotoxin?
    • Shigella (shiga toxin, ST)
    • EHEC (shiga-like toxin, SLT)
  65. Which microbes' pathogenicity is related to an exotoxin that inactivated EF-2?
    • Pseudomonas (exotoxin A)
    • C. diptheria (diptheria toxin)
  66. How does the Shigella spp. exhibit pathogenicity? Typical presentation?
    • exotoxin: shiga toxin, ST
    • inhibits 60S ribosome via rRNA cleavage 

    • typical:
    • GI mucosal damage (invasive)
    • diarrhea/dysentery
    • enhances cytokine release: HUS
  67. What is the pathogenicity of EHEC? Typical presentation
    • (enterohemorrhagic e. coli)
    • exotoxin: shiga-like toxin, SLT

    • typical: 
    • enhances cytokine release: HUS
    • diarrhea (non-invasive)
  68. What is the difference between Shigella spp. and EHEC?
    • exotoxins: shiga vs shiga-like toxin
    • EHEC: does NOT invade GI mucosal cells

    both cause diarrhea
  69. Which bugs have exotoxins that cause increased fluid secretion in the gut as the mechanism of diarrhea?
    • E. coli:
    • ETEC
    • Yersinia enterocolitica
    • Bacillus anthracis
    • Vibrio cholerae
  70. Which microbes have an exotoxin that prevents phagocytosis? Typical presentation?
    • Bordetella pertussis
    • exotoxin: pertussis toxin
    • disables Gi: overactivated adenylate cyclase: increased cAMP 

    • presentation:
    • Whooping cough
    • hard cough, "whoops" on inspiration 
  71. Which microbe has both a heat-labile and heat-stable toxin? What do they do?
    • Enterotoxigenic E. coli (ETEC)
    • both cause increased GI fluid secretion: diarrhea

    HL: overactivate adenylate cyclase: increase cAMP: increase Cl secretion in GI: increase water efflux

    HS: overactivate guanylate cyclase: increase cGMP: decrease NaCl and water absorption 

    "Labile in the Air, Stable on the Ground"
  72. Which bugs have a heat-stable toxin?  How does it work? How do they differ in presentation?
    • ETEC
    • Yersinia enterocolitica

    HS: overactivate guanylate cyclase increase cGMP: decrease NaCl and water absorption

    • presentation:
    • ETEC: watery diarrhea
    • Yersinia: bloody diarrhea/dysentery (invasive)
  73. What bug produes edema factor?  How does it work?
    • edema factor = Bacillus anthracis
    • mimics adenylate cyclase enzyme: increased cAMP
    • induces fluid secretion

    causes edematous borders of black eschar in cutaneous anthrax
  74. How does Vibrio cholerae work?
    • exotoxin: cholera toxin
    • induces GI fluid secretion
    • permanently activates Gs: overactivated adenylate cyclase: increased cAMP: increased Cl secretion: increased water efflux
  75. Which bugs use an exotoxin that inhibits release of neurotransmitters?
    • Clostridium:
    • C. botulinin: botulinum toxin
    • C. tetani: tetanospasmin

    cleaves SNARE protein required for neurotransmitter release

    • C. botulinin: inhibits Ach release
    • C. tetani: inhibits GABA and glycine release

     
  76. Which bugs use exotoxins to lyse cell membranes?
    • Clostridium perfringens: Alpha toxin
    • Streptococcus pyogenes: Streptolysin O
  77. What do ASO titers reveal?
    • antibodies to Streptolysin O 
    • recent infection with Strep. pyogenes
  78. What is the pathogenicity of Clostridium perfringens?  Typical presentation?
    • exotoxin: Alpha toxin
    • lecithinase/phospholipase degrades cell membranes/tissue

    • presentation:
    • myonecrosis: gas gangrene
    • hemolysis: double zone on blood agar
  79. What produces a "double zone" of hemolysis on blood agar?
    Alpha toxin: C. perfringens
  80. What is the pathogenicity of Strep. pyogenes?  Typical presentation?
    • exotoxins:
    • Streptolysin O: degrades cell membrane: RBC lysis
    • Exotoxin A: super antigen: toxic shock syndrome 
  81. How do superantigens work?  What bugs produce them?
    superantigen: brings MHC II and TCR in proximity: high release of IFN-g and IL-2: induces shock syndrome

    Strep. pyogenes: Exotoxin A: toxic shock

    Staph. aureus: TSST-1: toxic shock, scalded skin, food poisoning
  82. What is endotoxin?
    • endotoxin:
    • lipopolysaccharide found in outer membrane (Lipid A)
    • gram (-) organisms only (except Listeria) 
    • heat-stable
  83. What are the main pathogenicities of endotoxin (especially Lipid A)?
    • 1. activates alternate complement pathway:
    • increases C3a: hypotension, edema
    • increases C5a: neutrophil chemotaxis

    • 2. activates macrophages: 
    • increases IL-1: fever
    • increases TNF-a: fever, hemorrhagic tissue necrosis
    • increases nitric oxide: hypotension, shock

    • 3. activates Hageman factor
    • activates coagulation cascade: DIC 
  84. During which phase of the bacterial growth curve does spore formation occur?
    • stationary phase:
    • when nutrient depletion slows growth 
  85. During which phase of the bacterial growth curve do cell-wall inhibitor antibiotics have the greatest efficacy?
    • exponential growth phase:
    • time of rapid cell division (peptidoglycan required)
  86. What is transformation and which bacteria prominently use it?
    • transformation = ability to take up (any) DNA from envrironment
    • a.k.a. competence

    • Strep. pneum.
    • H. influ.
    • Neisseria

    "SHiN"
  87. What separates conjugation from transformation?
    • conjugation: 2 types of transfer
    • F+: plasmid DNA only (i.e. no chromosomal DNA), sex pilus transfer
    • F-: plasmid and chromosome DNA, incorporate into host

    transformation: any DNA, absorbed from environment
  88. What is the difference between F+ and F- bacteria?
    • conjugation process
    • F+: have required gene for conjugation
    • F-: incorporated into bacterial chromosomal DNA
  89. What is transposition?
    • form of transfering bacterial genetic material
    • segment of DNA can "jump" from plasmid to chromosome and vice versa 
  90. What is generalized transduction?
    • = packaging event
    • lytic phage infects bacterium: cleavage of bacterial DNA and synthesis of viral proteins: parts of bacterial DNA packaged into viral capsid: phage infects another bacterium and transfers DNA 
  91. What is specialized transduction?
    • = excision event
    • lysogenic phage infects bacterium: viral DNA incorporated into bacterial chromosome: during viral DNA excision, some flanking bacterial genes can also be cut: DNA packaged into phage viral capsid 
  92. Which bacterial toxins exhibit specialized transduction features?
    = genes encoded in a lysogenic phage

    • ShigA-like toxin (EHEC)
    • Botulinum (certain strains)
    • Cholera toxin
    • Diptheria toxin
    • Erythrogenic toxin of Strep. pyogenes
  93. Which bacteria form clear areas of hemolysis on blood agar?
    = beta-hemolytics

    • Staph. aureus
    • Strep (Groups A and B) 
    • Listeria monocytogenes 
  94. Which bacteria features tumbling motility?  Where is it found?
    • Listeria monocytogenes:
    • tumbling motility
    • endotoxin

    • source: unpasteurized milk
    •  
  95. What is the mode of antibiotic resistance of MRSA?
    • altered penicillin-binding proteins
    • resistance to beta-lactams 
  96. What are common presentations of Staph aureus infection?
    • skin infections
    • organ abscesses
    • pneumonia
    • toxic shock syndrome (TSST)
    • scalded skin syndrome (exfoliative toxin)
    • rapid-onset food poisoning (preformed enterotoxin) 
    • nosocomial infection (MRSA) 
  97. Where is Staph. epidermidis found?
    normal skin flora

    • infects (via biofilm): 
    • prosthetic devices 
    • intravenous catheters
    • blood culture (contamination) 
  98. What does Strep. pneum. commonly cause?
    "MOPS"

    • Meningitis
    • Otitis media (children)
    • Pneumonia
    • Sinusitis 

    • associations:
    • "rusty" sputum
    • sepsis in patients with sickle cell anemia and asplenia 
  99. What is the common presentation of Strep. viridans?
    normal flora: oropharynx

    • infections: 
    • subacute bacterial endocarditis on damaged valves
    • dental caries 
  100. What differentiates Strep. viridans from Strep. pneum.?
    • S. viridans: optochonin resistant, grows in bile
    • S. pneum.: optochonin sensitive, bile soluble
  101. What produces CAMP factor and what does it do?
    • Strep. agalactiae (Group B)
    • CAMP factor enlarges area of hemolysis formed by S. aureus
  102. What antibody should pregnent women be screened for to prevent neonatal meningitis?  What treatment would you recommend?
    screen for Strep. agalactiae (Group B) antigen

    positive culture: treat with intrapartum penicillin prophylaxis 
  103. What are the main features of Group D Streptococci/enterococci?  Where are they found?
    • Group D = C carbo on cell wall, variable hemolysis
    • enterococci: Penicillin G resistant, grow in 6.5% NaCl and bile
    • streptococci: cannot grow in 6.5% NaCl


    • enterococci:
    • normal gut flora
    • cause UTI
    • nosocomial infection: VRE

    • streptococci:
    • S. bovis: normal colon flora
    • endocarditis in colon cancer patients 
  104. What are the "ABCDEFG" of Corynebacterium diptheriae?
    • ADP-ribosylation
    • Beta prophage
    • Corynebacterium
    • Diptheriae
    • Elongation
    • Factor-2
    • Granules
  105. What is the common presentation of C. diptheriae?  How is it diagnosed?
    • pseudomembranous pharyngitis
    • gray pharyngeal exudate
    • lymphadenopathy 

    • diagnosis:
    • gram (+) rods
    • metachromatic (red, blue) granules
    • Elek test: toxin 
  106. What are the general features of spores?
    • made during stationary phase of bacterial growth
    • dipicolinic acid core
    • no metabolic activity
    • need autoclave to sterilize: heat resistent
    • commonly found in soil
  107. What is the autoclave sterilization protocol for spores?
    steaming at 121 C for 15 minutes
  108. What are common spores found in soil?
    • Bacillus anthracis
    • Clostridium perfringens
    • C. tetani
  109. What are the Clostridia species with exotoxins?
    • C. botulinin: botulinin toxin
    • C. tetani: tetanospasmin
    • C. difficile: Toxin A (enterotoxin), Toxin B (cytotoxin)
    • C. perfringens: alpha toxin, lecithinase/phospholipase 
  110. What is the pathogenicity of C. perfringens?  Treatment?
    • Toxin A: enterotoxin binds to brush border
    • Toxin B: cytotoxin destroys cytoskeleton of enterocytes
    • causes pseudomembranous colitis

    common cause:  antibiotic use (esp. clindamycin, ampicillin)

    treatment: metronidazole, vancomycin 
  111. What is the pathogenicity of Bacillus anthracis?  Common presentation?
    • only bacterium with polypeptide capsule (D-glutamate)
    • lethal factor
    • edema factor

    • cutaneous anthrax: direct contact, bacteremia, death
    • pulmonary anthrax: inhale spores, flulike, pulmonary hemorrhage, mediastinits, shock
    • black skin lesions: black eschar surrounded by edematous ring
  112. What are the main features of Listeria monocytogenes?  Presentation? Mode of transmission?  Treatment?
    • features:
    • facultative intracellular microbe
    • tumbling motility

    • presentation:
    • amnionitis
    • septicemia
    • spontaneous abortion
    • granulomatosis infantiseptica
    • meningitis (immunocompromised)
    • mild gastroenteritis (healthy)

    • treatment:
    • healthy adults: self-limited
    • infants/immunocompromised: ampicillin 
    •  
  113. Which gram (+) bacteria form long branching filaments that resemble fungi? How are they distinguished?
    Actinomyces israelii: anaerobe, normal oral flora, oral/facial abscesses, tx = penicillin

    Nocardia: acid-fast, in soil, pulm. infection in immunocompromised, tx = sulfa
  114. What does a negative PPD test mean?
    • 1. no current or previous infection with M. tuberculosis
    • 2. not enough immune reserve to mount Type IV hypersensitivty reaction
    • (steroids, malnutrition, immunocompromised) 
  115. What are common sequelae of reactivation of disseminated tubercle bacilli of M. tuberculosis?
    • Pott's diesease: vertebral body
    • lymphadenitis
    • renal
    • GI
    • CNS: tuberculoma or meningitis
    • lungs: fibrocaseous cavitary lesion (upper lobes) 
  116. What are the different lung manifestations of primary vs secondary TB?
    primary TB: Gohn complex (hilar lymph nodes + Gohn focus), presents in lower lobes

    secondary TB: caseating granuloma, presents in upper lobes
  117. What is a common cause of disseminated disease in AIDS patients that is acid fast?  How is it prevented?
    • Mycobacterium avium
    • prophylaxis: azithromycin 
  118. What are the general symptoms of TB?
    • hemoptysis
    • "B symptoms": night sweats, weight loss, fever
  119. What are treatments for leprosy?  Common side effects?
    dapsone: methoglobinemia, hemolysis

    • rifampin
    • clofazimine + dapsone 
  120. Which antibiotics are gram (-) bacteria restistant to and why?
    gram (-) bacteria are resistant to Penicillin G and vancomycin

    outer membrane layer inhibits entry 
  121. What are the lactose-fermenting enteric bacteria and what are they grown on?
    MacConkey's agar

    • Citrobacter
    • Kelbsiella
    • E. coli (beta-galactosidase)
    • Enterobacter
    • Serratia

    "MaConKEES" 
  122. Which E. coli virulence factor is associated with pyelonephritis?
    fimbriae
  123. Which E. coli virulence factor is associated with cystitis?
    fimbriae
  124. Which E. coli virulence factor is associated with pneumonia?
    K capsule
  125. Which E. coli virulence factor is associated with neonatal meningitis?
    K capsule
  126. Which E. coli virulence factor is associated with septic shock?
    LPS endotoxin
  127. How is EHEC differentiated from other toxic E. coli?
    does NOT ferment sorbitol
  128. What is the pathology of hemolytic uremic syndrome related to EHEC?
    O157:H7 exotoxin: inflammation and necrosis

    • mechanical hemolysis: 
    • endothelium swells: lumen narrows: reduced GFR: endothelium "consumes" platelets
  129. What is the classic triad of HUS?
    • (hemolytic) anemia
    • thrombocytopenia
    • acute renal failure
  130. What is the toxin/mechanism of EIEC?  Presentation?
    • No toxins:
    • invasive: microbe invades intestinal mucosa
    • causes necrosis

    • presentation:
    • similar to Shigella
    •  dysentery
  131. What is the toxin/mechanism of ETEC?  Presentation?
    • exotoxin: heat-stable and heat-labile forms
    • causes secretory diarrhea

    • presentation:
    • no inflammation or invasion
    • Traveler's/watery diarrhea
  132. What is the toxin/mechanism of EPEC?  Presentation?
    • No toxin: 
    • adheres to apical surface
    • flattens villiprevents absorption

    • presentation:
    • pediatric diarrhea 

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