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STEP 1 Microbiology > GI/urinary- Bacteria and antibiotics > Flashcards

GI/urinary- Bacteria and antibiotics Flashcards

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1
Q

Enterobacter- Transmission

A

Nosocomial; multi-drug resistance

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2
Q

Serratia- Transmission

A

Nosocomial; multi-drug resistance

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3
Q

Klebsiella- Transmission

A

Nosocomial; multi-drug resistance; commonly affect alcoholics; common in cases of aspiration

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4
Q

Enterobacter- diagnosis

A

Lactose fermenter (pink colonies on McConkey agar)

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5
Q

Serratia- diagnosis

A

(Slow) Lactose fermenter (pink colonies on McConkey agar, but may appear negative at first); produces red pigment when cultured

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6
Q

Klebsiella- diagnosis

A

Lactose fermenter (pink colonies on McConkey agar)

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7
Q

Bacteria that ferment lactose

A

1) Enterobacter
2) Klebsiella
3) Serratia
4) E. coli

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8
Q

How is lactose fermentation observed?

A

Pink colonies on McConkey agar

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9
Q

Enterobacter- morphology

A

Gram-negative rods, facultative anaerobic, motile

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10
Q

Serratia- morphology

A

Gram-negative rods, facultative anaerobic, motile

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11
Q

Klebsiella- morphology

A

Gram-negative rods, oxidase-negative, urease-positive, prominent polysaccharide capsule (mucoid colonies), nonmotile

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12
Q

Klebsiella- presentation

A
  • Pneumonia with currant jelly sputum and abscesses (may mimic TB)
  • UTIs, struvite stones
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13
Q

Salmonella typhi- morphology

A

Gram-negative rods; facultative intracellular (within macrophages), motile

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14
Q

Salmonella enteritidis- morphology

A

Gram-negative rods; facultative intracellular (within macrophages), motile

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15
Q

Salmonella typhi- presentation

A
  • Typhoid fever
  • Rose-colored macules on abdomen (25%); osteomyelitis in sickle cell disease (#1 cause)
  • Constipation or “pea soup” diarrhea, GI ulceration/hemorrhage
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16
Q

Salmonella enteritidis- presentation

A

Inflammatory diarrhea

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17
Q

Salmonella typhi- diagnosis

A

H2S positive (black colonies on Hektoen agar), encapsulated, acid-labile (degraded in stomach)

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18
Q

Salmonella enteritidis- diagnosis

A

H2S positive (black colonies on Hektoen agar), encapsulated, acid-labile (degraded in stomach)

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19
Q

Salmonella typhi- treatment

A

Fluoroquinolone (i.e. cipro) or ceftriaxone

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20
Q

Salmonella enteritidis- treatment

A

None (antibiotics not indicated)

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21
Q

Salmonella enteritidis- transmission

A

Undercooked chicken (reservoir)

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22
Q

Which salmonella type has a vaccine? What type?

A

Salmonella typhi; live-attenuated

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23
Q

Salmonella- virulence

A

Type III secretion system detects eukaryotic cells (injectisome)

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24
Q

E. coli- morphology

A

Gram-negative rods; facultative anaerobic, encapsulated, catalase-positive

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25
Q

E. coli- diagnosis

A
  • Lactose fermenter (pink on McConkey agar)
  • Green on EMB agar
  • May have K antigen on capsule (serotyping)
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26
Q

E. coli- virulence (general)

A
  • Fimbriae (#1 cause of UTIs)

- LPS (#1 cause of gram-negative sepsis)

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27
Q

When can E. coli cause neonatal meningitis?

A

When it has the K antigen

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28
Q

EHEC- presentation

A

“Enterohemorrhagic,” bloody diarrhea; HUS (usually children under 10)

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29
Q

EHEC- transmission

A

Undercooked meat

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30
Q

How can EHEC be distinguished from other E. coli strains in a lab?

A

EHEC is the only one that does not ferment sorbitol

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31
Q

EHEC virulence

A

Shiga-like toxin inhibits ribosomes at 60S subunit

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32
Q

Hemolytic uremic syndrome pathogenesis in E. coli

A

Shiga-like toxin damages endothelial cells in capillaries of the glomerulus. Damaged lining becomes thrombogenic, causing platelets to adhere. Platelets lyse RBCs as they pass through the capillaries.

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33
Q

Serotype of EHEC that causes massive outbreaks

A

0157:H7 antigen

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34
Q

ETEC- presentation

A

Traveler’s diarrhea (watery)

35
Q

ETEC- virulence

A
  • Heat labile toxin increases cAMP

- Heat stable toxin increases cGMP

36
Q

Yersinia enterocolitica- morphology

A

Gram-negative rods; encapsulated

37
Q

Yersinia enterocolitica- transmission

A
  • Dog feces (commonly affects toddlers)
  • Contaminated milk products (resistant to cold)
  • Chitterlings
38
Q

Yersinia enterocolitica- diagnosis

A

Bipolar staining (“safety pin”)

39
Q

Yersinia enterocolitica- presentation

A

Bloody diarrhea, fever, leukocytosis, abscesses, intestinal perforation; mimics appendicitis (RLQ pain)

40
Q

Campylobacter jejuni- morphology

A

Curved Gram-negative rods; motile, oxidase-positive

41
Q

Campylobacter jejuni- presentation

A

Bloody diarrhea, bacteremia (invasive), Reiter syndrome, Guillain- Barre (ascending paralysis)

42
Q

Campylobacter jejuni- transmission

A

Thermophilic (42 degrees C); main reservoir is intestinal tract of animals (ie poultry); technically, fecal-oral route

43
Q

Vibrio cholerae- morphology

A

Curved Gram-negative rod (comma-shaped), oxidase-positive, acid-labile

44
Q

Vibrio cholerae- transmission

A

Endemic to developing countries; fecal-oral spread by water contamination

45
Q

Vibrio cholerae- presentation

A

Profuse, “rice-water” diarrhea

46
Q

Vibrio cholerae- virulence

A

Uses fimbriae to attach to ganglioside receptors in the intestinal wall; secretes cholera toxin Increases cAMP by constitutively activating adenylate cyclase (Gs pathway);

47
Q

How does cholera toxin work?

A

Increases cAMP by constitutively activating adenylate cyclase (Gs pathway). cAMP stimulates Cl- secretion by CFTR. Sodium and water follow.

48
Q

Vibrio cholerae- treatment

A

Oral rehydration therapy

49
Q

Vibrio cholerae

A

Grows on alkaline media

50
Q

Where are Vibrio vulnificus and Vibro parahemolyticus found?

A

Seafood contamination (especially oysters)

51
Q

Helicobacter pylori- morphology

A

Curved Gram-negative rod; urease-positive, oxidase positive

52
Q

Helicobacter pylori- transmission

A

Duodenal ulcers, gastric adenocarcinoma, MALT lymphoma (usually goes away by treating H. pylori)

53
Q

Helicobacter pylori- treatment

A

Triple therapy:

1) PPi
2) Amoxycillin
3) Macrolide (Clarithromycin)

54
Q

Helicobacter pylori- treatment

A

Triple therapy:

1) PPi
2) Amoxycillin
3) Macrolide (Clarithromycin)

55
Q

Helicobacter pylori- virulence

A

Urease reduces acidity of environment for invasion of stomach

56
Q

How does urease work?

A

Splits urea into ammonium and CO2

57
Q

How does urease work?

A

Splits urea into ammonium and CO2

58
Q

Pseudomonas- morphology

A

Gram-negative rods; encapsulated, obligate aerobe, oxidase-positive, catalase-positive

59
Q

Pseudomonas- presentation

A
  • Hot tub folliculitis (pruritic, papular, pustular)
  • Nosocomial pneumonia
  • Respiratory failure in cystic fibrosis
  • Osteomyelitis in IV drug users and diabetics (due to neuropathy)
  • Infection in burn patients (often lethal)
  • Indwelling catheter infections/UTIs
  • Ecthyma gangrenosum (black, necrotic lesions on skin in sepsis)
  • Otitis externa
60
Q

Pseudomonas- diagnosis

A
  • Blue-green pigment on plate, due to pyocyanin and pyoverdin (may even turn wounds blue)
  • Fruity, grape-like odor
61
Q

Pseudomonas- virulence

A

Exotoxin A (similar to diphtheria toxin; inactivates EF-2 by ribosylation)

62
Q

Pseudomonas- treatment

A
  • Piperacillin + Tazobactam
  • Aminoglycosides
  • Fluoroquinolones (especially UTIs)
63
Q

Pseudomonas- transmission

A

Thrives in aquatic environments

64
Q

Proteus mirabilis- morphology

A

Gram-negative; urease-positive

65
Q

Proteus- presentation

A
  • Struvite stones

- UTIs

66
Q

Proteus mirabilis- diagnosis

A
  • Swarming motility when plated

- Fishy odor

67
Q

Proteus mirabilis- virulence

A

Urease needed to form staghorn calculi (alkaline environment from ammonia and CO2)

68
Q

What are struvite stones composed of?

A

Ammonia, magnesium, phosphate

69
Q

Proteus mirabilis- treatment

A

Sulfonamides

70
Q

Bacillus anthracis- morphology

A

Large Gram-positive rods in chains; obligate aerobe, encapsulated (made of poly-D glutamate, rather than polysaccharide), spore-forming

71
Q

Bacillus cereus- morphology

A

Gram-positive rods in chains; facultative anaerobic, motile, beta-hemolytic, spore-forming

72
Q

Bacillus anthracis- presentation

A
  • Black eschar
  • Pulmonary anthraw (Woolsorter’s disease), which starts as a dry cough but can migrate to mediastinal lymph nodes and cause hemorrhagic mediastinitis (widened mediastinum on X-ray)
73
Q

Bacillus cereus- presentation

A

Fried rice syndrome (vomiting)

74
Q

Bacillus cereus- transmission

A

Eating reheated fried rice

75
Q

Is Bacillus anthracis beta-hemolytic?

A

No

76
Q

Is Bacillus cereus beta-hemolytic?

A

Yes

77
Q

Clostridium difficile- morphology

A

Gram-positive rods in pairs/short chains; anaerobic, motile, spore-forming

78
Q

Clostridium difficile- presentation

A

Nosocomial diarrhea

79
Q

Clostridium difficile- virulence

A
  • Exotoxin A (“apple”), which binds to brush border, causing inflammation, cell death, and watery diarrhea
  • Exotoxin B (“black licorice”), which disrupts the cytoskeleton by depolymerizing actin, causing enterocyte death and necrosis; forms pseudomembrane (yellow-gray) that covers colonic mucosa
80
Q

Clostridium difficile- treatment

A
  • ORAL vancomycin
  • Fidaxomicin
  • Metronidazole
81
Q

Antibiotic classically associated with C. diff

A

Clindamycin

82
Q

Clostridium difficile- diagnosis

A
  • PCR/assay for toxin
  • Direct visualization of the pseudomembrane
  • Characteristic odor
83
Q

What type of infection is classically observed in patients with colonic carcinoma?

A

Streptococcus bovis

84
Q

Streptococcus bovis- morphology

A

Gram-positive cocci in chains; group D strep, oxidase-negative, catalase-negative

STEP 1 Microbiology (22 decks)

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