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Flashcards

Enterics I

Kerra Washington English 87 cards

Cards in this deck (87)

  1. 1entericsfacultative gram-negative, rod-shaped bacteria common to or occuring as pathogens in the intestinal tract
  2. 2What are the families of enteric bacteria?Enterobacteriaceae and Vibrionaceae
  3. 3facultative anaerobesorganisms capable of aerobic and anaerobic metabolism
  4. 4medically important genera of the EnterobacteriaceaeEscherichia
    Salmonella
    Shigella
    Yersinia
  5. 5What body sites do Enterobacteriaceae infect?any body site
  6. 6What are the common community-acquired infections of Enterobacteriaceae?enteritis/colitis
    cystitis/pyelonephritis
  7. 7enteritisinflammation of the small intestine
  8. 8colitisinflammation of the large intestine
  9. 9cystitisinflammation of the bladder
  10. 10pyelonephritisinflammation of the kidney
  11. 11What are the general physical features of Enterobacteriaceae?gram-negative rods
    motile (peritrichous flagella)
  12. 12peritrichous flagellamultiple flagella emanating from all aspects of the cell periphery
  13. 13polar flagellaflagella localized to one end of the cell
  14. 14What are general biochemical/metabolic features of Enterobacteriaceae?facultative anaerobes
    ferment glucose
    oxidase negative
  15. 15What family is oxidase negative?Enterobacteriaceae
  16. 16What families are oxidase positive?Vibrios
    Campylobacter
  17. 17What are the type of antigens used for serotyping?O, H, and K
  18. 18O-antigenlipopolysaccharide
  19. 19H-antigenflagellum
  20. 20K-antigencapsule
  21. 21What is the selective agent of MacConkey?bile salts
  22. 22What is MacConkey medium differentiate for?lactose
  23. 23lac positivecells that ferment lactose
  24. 24lac negativecells that do not ferment lactose
  25. 25What are the prominent lac negative enterics?Salmonella
    Shigella
    Yersina
    Proteus
  26. 26fecal coliformslac negative enterics, primarily E. coli, indicative of fecal contamination
  27. 27What bacteria is part of the normal commensal flora of the intestines?E. coli
  28. 28What is the most abundant facultative anaerobes in the gut?E. coli
  29. 29What vitamin does E. coli produce?K2
    (humans cannot produce this vitamin)
  30. 30How has pathovars of commensal E. coli evolved?horizontal gene transfer of mobile genetic elements, pathogenicity islands, plasmids, and phages (containing virulence genes)
  31. 31What is the clinical significance of E. coli pathovars?1. pathovars have distinct pathogenic mechanisms and can have variable clinical presentations
    2. future physicians will be treating, and should be alert to the appearance of, new and/or atypical enteric infections
  32. 32What does ETEC stand for?Enterotoxigenic E. coli
  33. 33What is the most common E. coli pathovar?ETEC
  34. 34What are the disease symptoms of ETEC?- mild to severe watery diarrhea
    - vomiting (common)
    - fever (rare)
  35. 35What are the clinical syndromes associated with ETEC?- weanling diarrhea in developing nations
    - traveler's diarrhea in developed nations
  36. 36weanling diarrheaa collection of diseases in the infant, described as a syndrome, associated with weaning from the breast; it is attributed to the introduction of other food and loss of the protective properties of breast milk
  37. 37How is ETEC transmitted?contaminated food and water
    *high dose is required*
  38. 38What toxins do ETEC produce?LT and/or ST
  39. 39What does LT stand for?heat labile toxin
  40. 40What does ST stand for?heat stable toxin
  41. 41What are the types of adhesion factors of ETEC?CFA/I and CSI-22 antigens
  42. 42What is CFA/I?colonizing factor antigen of ETEC
  43. 43What is CSI-22?coli surface antigen of ETEC
  44. 44How is ETEC diagnosed?- based on presence of CFA/CS, LT and ST antigens or genes
    - no convenient or commercially available diagnostic
  45. 45What is the treatment of ETEC?- self-limiting (3-4 days); rehydration
    - empiric antibiotic treatment of traveler's diarrhea
  46. 46What are preventative measures for ETEC?- improved sanitation and water treatment
    - vaccine development in progress
    - CFA/CS and LT antigens (cholera toxin B subunit cross-protects)
  47. 47What does EHEC stand for?Enterohemorrhagic E. coli
  48. 48What disease is caused by EHEC?hemorrhagic colitis
  49. 49What are the disease symptoms of EHEC?- watery, progressing to grossly bloody diarrhea
    - abdominal cramping
    - fever rare/low grade
  50. 50What is the life-threatning sequela infection of EHEC?HUS
  51. 51What does HUS stand for?hemolytic uremic syndrome
  52. 52What is the most prominent EHEC disease causing serotype?O157:H7
  53. 53What is the animal reservoir for EHEC?cattle and other ruminants
  54. 54What is the transmission route of EHEC?fecal to oral
  55. 55What are the transmission vehicles of EHEC?ground beef, spinach, unpasteurized milk, lettuce, apple cider, radish sprouts, water (municipal, swimming), animal contact (farms, petting zoos), person to person
  56. 56What is the infectious dose of EHEC?10-100 bacteria
  57. 57What principle can be deduced from the low infectious dose of EHEC?- stomach acid provides a strong barrier to intestinal infection; therefore, acid resistant intestinal pathogens have a lower infectious dose
    - they can withstand the acidic pH of the stomach
  58. 58What is HUS?sequela of infection with EHEC and other Shiga toxin producing bacteria
  59. 59What are the clinical features of HUS?- microangiopathic hemolytic anemia
    - thrombocytopenia
    - glomerular thrombotic microangiopathy
  60. 60What is the incidence of HUS?~ 15% of children below the age of 10
    also, elderly are more susceptible
  61. 61How is EHEC infection diagnosed?1. culture for detection of O157
    2. test Sorb-neg for O157 antigen
    3. detection of Stx protein gene
    4. test for other non-O157 antigens
  62. 62What is the treatment for EHEC?- self-resolving in 5-8 days
    - supportive therapy, particularly for HUS
    - experimental strategies (i.e. Gb3 receptor analogs and immunization against Stx)
  63. 63What is antibiotic use controversial for the treatment of EHEC?the bacteria responds by excising the lambda phage from the bacteria which causes an increase production of toxin and a subsequent increase in infection
  64. 64What does EAEC stand for?Enteroaggregative E. coli
  65. 65What are the disease symptoms of EAEC?- acute or persistent watery diarrhea (sometimes with blood and mucus)
    - abdominal pain
    - nausea
    - vomiting
    - low grade fever
  66. 66What are the clinical syndromes associated with EAEC?- traveler's diarrhea (2nd most common cause)
    - pediatric diarrhea world-wide
    - food borne outbreaks
  67. 67How is EAEC transmitted?contaminated food and water
  68. 68What does EPEC stand for?Enteropathogenic E. coli
  69. 69What is unique about EPEC?utilize diffuse adhesion
  70. 70What does EIEC stand for?Enteroinvasive E. coli
  71. 71What are the disease symptoms of EIEC?produces watery diarrhea occasionally progressing to dysentery
  72. 72What are the microbiological features of the genus Shigella?- gram negative rods
    - falcultative anaerobes
    - oxidase negative
    - lactose negative
    - nonmotile
  73. 73What diseases are caused by the genus Shigella?- Shigellosis
    - bacillary dysentery
  74. 74dysenterytriad of symptoms includine
    1. abdominal cramps
    2. tenesmus
    3. frequent, small-volume bloody, mucoid discharge
  75. 75tenesmusstraining to have a bowel movement
  76. 76What are the clinical symptoms of a Shigella infection?- mild to severe, initial watery diarrhea
    - subsequent abdominal cramping
    - fever
    - bloody, mucoid discharge with prominent fecal leukocytes
  77. 77What is the significance of fecal leukocytes?invasive enteric pathogens, Shigella, Salmonella, Yersinia and Campylobacter, provoke inflammatory response resultsing in high fecal leukocyte count
  78. 78What is the primary reservoir for Shigella?humans
  79. 79What is the infectious dose of Shigella?< 200 bacteria
  80. 80What are the 5 F's of Shigella transmission?food, fingers, feces, flies, and formites
  81. 81What is the US incidence of Shigella?~ 15,000 reported cases/year
    > 70% caused by S. sonnei
    ~ 60% in children <15 years old
    outbreaks in daycare & institutional settings
    traveler's diarrhea
  82. 82What is the global incidence of Shigella?~150 million cases/year
    S. flexneri is the most common cause
    epidemics caused by S. dysenteriae
  83. 83How is Shigella isolated and identified?1. plate fecal specimen on selective differential media
    2. biochemical tests for lac negative isolates
    3. determine serotype
    4. sensitivity profile
  84. 84What are the treament practices and prevention methods for Shigella?- supportive therapy in conjunction with antimicrobial therapy (severe cases?)
    - antimicrobial therapy shortens course of disease and fecal shedding in developing nations
    - antimicrobial resistance problematic
    - scrupulous hygiene to prevent spread
    - limited homologous immunity - vaccine?
    - improved sanitation infrastructure and water treatment in developing nations
  85. 85What are the sequelae infections of Shigella?- HUS
    - reactive arthritis (Reiter's syndrome)
  86. 86HUS in Shigella infectionrelated to Shiga toxin production
    only S. dysenteriae type I has stx gene
  87. 87reactive arthritis (Reiter's syndrome)clinical triad post-dysentery or postvenereal infection includes
    1. arthritis
    2. urethritis
    3. conjunctivitis
    6-30% of invasive enteric infections

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Flashcards on Enterics I, created by Kerra Washington on 05/11/2018.
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