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micro: bacteria Flashcards

1
Q

which three bacteria are glucose-fermenting? which ferments lactose? which produces H2S?

A

E. coli, shigella, salmonella
e. coli
salmonella

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2
Q

what is the most common cause of HUS? 2nd?

A

EHEC then Shigella dysenteriae

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3
Q

what is unique about the shigella bacteria? what does it do in response?

A

non-motile

spreads cell-to-cell using cellular actin polymerization (formins) to form membrane-bound protrusions

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4
Q

what is the role of antibiotics in treatment of shigella?

A

shortens course

ceftriaxone, ciprofloxacin, azithromycin

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5
Q

what’s the stereotypical mode of transmission of EHEC?

A

undercooked meat, esp. hamburgers

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6
Q

what are the two main pathogenic mechanisms of EHEC?

A
  • Locus of Enterocyte Effacement: type III secretion system delivers E. coli receptor to host cell with pedestal formation for attachment
  • Shiga toxin
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7
Q

how does the Shiga toxin work?

A

AB toxin

-inactivates 28s ribosomal RNA by cleaving adenine residue, stopping protein synthesis of cell

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8
Q

what serotype is the most common cause of EHEC and how is it differentiated in lab? how else may EHEC be diagnosed in lab?

A

O157:H7-doesn’t ferment sorbitol, so white on Sorbitol-MacConkey agar (other E. coli pink/red)
PCR/ELISA for Shiga toxin

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9
Q

what is the role of antibiotics in treatment of EHEC?

A

contraindicated: may predispose to HUS by inducing more Shiga toxin release

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10
Q

what is the species responsible for salmonellosis? how is it spread?

A

Salmonella enteritidis

  • dairy products, meat, poultry, eggs
  • pet lizards and reptiles (turtles)
  • human-to-human
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11
Q

what are complications of salmonellosis?

A

reactive arthritis

endovascular infection, endocarditis, osteomyelitis, aortic plaques

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12
Q

what is the role of antibiotics in salmonellosis?

A

fluoroquinolones for those at risk of disseminated/invasive infection

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13
Q

what are complications of shigellosis?

A

Reiter’s syndrome: reactive arthritis, conjuctivitis, urethritis
HUS (S. dysenteriae)

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14
Q

what causes Typhoid fever? what are characteristic of the 3 weeks of infection?

A

Salmonella enterica
1st week: relative bradycardia, for fever
2nd: ab pain, rose spots on trunk
3rd: hepatosplenomegaly, GI bleeding/perforation, secondary bacteremia +/- septic shock

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15
Q

what is different about the pathogenesis of Salmonella enteritidis and enterica?

A

enterica can disseminate into lymph nodes and RES

->hypertrophy of Peyer’s patches, hepatosplenomegaly

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16
Q

what is the role of antibiotics in treatment of typhoid fever?

A

ceftriaxone, ciprofloxacin, azithromycin

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17
Q

what is the most common bacterial enteric pathogen in developed countries (important cause of Traveler’s diarrhea)? what kind of diarrhea does it cause?

A

Campylobacter jejuni

-inflammatory (15% adults, >50% children become bloody)

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18
Q

how is campylobacter usually transmitted?

A

improperly cooked chicken

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19
Q

what is the role of antibiotics in treating Campylobacter?

A

azithromycin or ciprofloxacin, reserved for severe disease

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20
Q

what are 3 complications of Campylobacter infection?

A

Guillain-barre syndrome (most common cause)
reactive arthritis
erythema nodosum

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21
Q

how do the two C. diff toxins work? Toxin A (enterotoxin) and Toxin B (cytotoxin)?

A

glucosylate GTPases, stimulate IL-8 production (inflammation)
Toxin A: disrupts colonic mucosal cell adherence to BM and damages villous tips
Toxin B: depolymerization of actin with loss of cytoskeletal integrity->enterocyte apoptosis/death

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22
Q

what is the cardinal symptom of C. diff colitis? what are the 4 symptoms/signs of CDAD with colitis?

A

watery diarrhea

diarrhea, pain, low-grade fever, leukocytosis

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23
Q

what is the gold standard for diagnosis of C. diff? how else may it be diagnosed in lab?

A

cell culture cytotoxicity assay

PCR for toxin

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24
Q

what is the treatment for first time C. diff? recurrence? what else may be used?

A

metronidazole, vancomycin if severe
1st time: metronidazole again; 2nd time: extended course of vancomycin
fidaxomycin

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25
Q

how does Yersinia enterocolitica stain? where is it primarily found? what kind of diarrhea can it cause?

A

bipolar staining coccobacilli
Europe
inflammatory diarrhea

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26
Q

what is the main feature of Yersinia diarrhea? how does it present?

A

abdominal pain

can mimic acute appendicitis in young adults/teenagers

27
Q

what is the role of antibiotics in Yersinia?

A

treatment not usually needed

28
Q

what enteropathogenic bacteria can cause reactive arthritis?

A

Shigella, Salmonella, Yersinia, Campylobacter

29
Q

what is the pathogenesis of ETEC?

A

heat-labile toxin: stimulates adenylate cyclase (like cholera toxin)
heat-stable toxin: increases cGMP (same effect as cholera toxin)

30
Q

what group does EPEC cause diarrhea in?

A

children

31
Q

what is the pathogenesis of EPEC?

A

LEE: formation of pedestal-like structures

32
Q

which enteropathogenic bacteria is oxidase positive? how does it stain?

A

Vibrio

curved/comma-shaped gram-negative

33
Q

where is Vibrio typically found? what helps it grow more rapidly?

A

saltwater

warm months: causes more disease

34
Q

what is the main reservoir for Vibrio cholerae? 2nd?

A

humans then marine shellfish

35
Q

what are the 2 pathogenic mechanisms of Vibrio cholerae?

A
  • secretes mucinase: dissolves glycoprotein covering of intestinal cells, allowing adherence to brush border
  • AB cholera toxin: ADP-ribosylates Gs protein->adenlyate cyclase activation
36
Q

what is unique about the diarrhea of cholera? what is unique about symptoms?

A

rice water stools: fleck with mucous and fishy odor

abdominal pain is absent

37
Q

how is cholera diagnosed in lab?

A

colorless colonies on MacConkey agar

38
Q

how should cholera be treated?

A

oral rehydration salts

39
Q

what is the most common cause of foodborne illness in Japan? why/how is it transmitted?

A

Vibrio parahemolyticus

-transmitted by raw/undercooked seafood/shellfish

40
Q

what severe complication can Vibrio parahemolyticus cause?

A

wound infection from marine activities leading to severe cellulitis in patients with liver disease or diabetes

41
Q

what is the role of antibiotics in Vibrio parahemolyticus?

A

doxycycline in severe disease

42
Q

what bacteria causes severe skin and soft tissue infections? what type of lesions? who usually gets it? what is the fear that it leads to?

A

Vibrio vulnificus
bullous lesions
shellfish handlers: infection of open wounds
rapidly fatal septicemia in underlying liver disease, alcoholism, diabetes

43
Q

what is the role of antibiotics in Vibrio vulnificus?

A

doxycycline+cefotaxime or ceftriaxone

44
Q

what is the pathogenesis of S. aureus gastroenteritis? what is unique about the gastroenteritis it causes

A

enterotoxin is heat-stable, superantigen

ingestion of toxin leads to symptoms within 1-6 hours

45
Q

how is S. aureus gastroenteritis usually spread? classic way?

A

potato salad/picnic
food contaminated by food handler sits are room temperature before being eaten so organisms multiply and make lot of toxin

46
Q

what is the pathogenesis of emetic syndrome caused by Bacillus cereus? how is it usually transmitted?

A

cereulide toxin: heat stable, emetic toxin
causes comiting withing 1-5 hours, 1/3 have diarrhea
rice dishes

47
Q

what other syndrome can Bacillus cereus cause? what is pathogenesis?

A

diarrheal syndrome

diarrheal enterotoxin, vomiting uncommon

48
Q

what is the predominant organism in the colon? how does it stain? what is its pathogenesis?

A

Bacteroides fragilis
gram negative rod
polysaccharide antiphagocytic capsule

49
Q

what sort of infections does Bacteroides fragilis cause? exception?

A

below the diaphragm: intra-abdominal abscesses or peritonitis
25% of lung abscesses

50
Q

what is the treatment for Bacteroides fragilis?

A

metronidazole, carbapenem, beta-lactam/beta-lactamase inhibitor combos
-resistant to penicillin

51
Q

what disease does Prevotella melaninogenica causes?

A

above the diaphragm:

  • oral/periodontal/periorbital abscesses
  • pulmonary abscesses/emyemas
  • sinusitis
52
Q

what is the only anaerobic, endospore-forming bacteria?

A

Clostridia

53
Q

what bacteria is the 3rd most common foodborne illness in US? what kind of illness does it cause? what is pathogenesis?

A

Clostridia perfringens
watery diarrhea with cramps
heat-resistant spores survive cooking, germinate at lower temps, produce enterotoxin in GI tract

54
Q

“skin popping” by drug abusers is a risk for what infection?

A

Clostridia tetani

55
Q

what is the toxin for C. tetani and how does it work? what is the result?

A

tetanus toxin/tetanospasmin: AB neurotoxin

  • enters at NMJ, retrograde transport to ganglia
  • cleaves SNARE, blocking release of inhibitory neurotransmitters: GABA and glycine
  • disinhibition of excitatory impulses->increased muscle tone, spasms, autonomic instability
56
Q

what is the overall clinical picture of tetanus? what are 3 classic manifestations? what can cause death?

A 
spastic paralysis
trismus: lockjaw
risus sardonicus: characteristic grimace
opisthotonos: arching of back
-respiratory failure
57
Q

what are 3 ways to treat tetanus? why is vaccination so important?

A

wound debridement to clear spores
human tetanus immune globulin (HTIG): neutralize toxin
metronidazole
-infection does not confer immunity

58
Q

what is the pathogenesis of C. botulinum and the resulting clinical picture? how can it kill?

A

AB toxin cleaves SNARE, preventing Ach release

  • symmetric, descending flaccid paralysis
  • with decreased parasympathetics
  • can cause respiratory failure
59
Q

what are the two classic ways of transmitting C. botulinum?

A

classic: foodborne->canned foods
infant: raw honey or spores in carpet

60
Q

why does cooking not prevent botulism but reheating does?

A

spores are resistant to cooking, but after germinating at lower temperatures, produce heat-labile toxin

61
Q

what is the role of antibiotics in botulism?

A

only in wound botulism

contraindicated in classic or infant: release of more toxin

62
Q

how should botulism be treated?

A

mechanical ventilation
horse anti-toxin if >1 y/o
-human-derived botulism immune globulin (BIG-IV) for infants
do NOT give antibiotics to classic or infant botulism

63
Q

which bacteria is microaerophilic?

A

Helicobacter pylori

64
Q

what are the 4 pathogenic mechanisms of H. pylori?

A

urease
CagA: rearranges cytoskeleton
Type III secretion system
VacA: vacuolating cytotoxin

GI (5 decks)

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