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Exam 2 MIM Microbiology > Enterics > Flashcards

Enterics Flashcards

1
Q

What defines enterics?

A

1) rod-shaped
2) gram-negative
3) occuring in the GI tract
4) facultative anaerobes

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2
Q

What are three main enteric bacteria?

A

1) Shigella
2) Salmonella
3) Escherichia

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3
Q

Which sites do enteric bacteria infect?

A

Any site!

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4
Q

What are some common community-acquired enteric infections?

A

enteritis or colitis. cystitis, pyelo

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5
Q

What does nosocomial infection mean?

A

infection originating in the hospital

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6
Q

What is a major nosocomial infection?

A

Opportunistic Klebsiella pneumoniae infection

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7
Q

What is the average size of bacteria of Enterobacteriaceae?

A

0.5-2.0 microns

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8
Q

How are Enterobacteriaceae microbes motile?

A

peritrichous flagella

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9
Q

What are the two non-motile species of Enterobacteriaceae?

A

1) Klebsiella

2) Shigella

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10
Q

What is the most common selective media for enterics?

A

MacConkey agar

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11
Q

What is an important distinction for selective isolation of enterics?

A

Lactose fermentation

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12
Q

How are Enterobacteriaceae species identified?

A

biochemical reactions

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13
Q

How are subtypes of Enterobacteriaceae bacteria identified?

A

serotyping of antigens

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14
Q

What are the three antigens of enterics?

A

O antigen
H antigen
K antigen

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15
Q

What is the O antigen?

A

O polysaccharide of LPS

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16
Q

What is the H antigen?

A

flagella

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17
Q

What is the K antigen?

A

capsule

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18
Q

What is the exception to K antigen?

A

Vi-antigen of Salmonella

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19
Q

Where can you find E.coli?

A

As part of the normal commensal flora of the Gi tract

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20
Q

How are E.coli turned into pathogens?

A

Through the uptake of pathoenicity-associated islands, phages, and plasmids

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21
Q

How have pathovars of E.coli evolved?

A

through HGT!

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22
Q

What is EHEC?

A

Enterohemorrhagic E.coli

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23
Q

What is the most abundant facultative anaerobe in the gut?

A

E. coli

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24
Q

What does EHEC produce?

A

hemorrhagic colitis

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25
Q

Why is the primary infection of EHEC not of real concern?

A

it is usually self-resolving and not fatal

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26
Q

What do 15% of EHEC infections evolve into?

A

hemolytic uremic syndrome

27
Q

What can hemolytic uremic syndrome lead to?

A

CNS manifestations and acute renal failure

28
Q

Where is the incidence of EHEC the greatest?

A

developed countries

29
Q

Is O157:H7 the only serotype which causes hemorrhagic colitis?

A

no!

30
Q

What is the primary reservoir of EHEC?

A

cattle

31
Q

Is EHEC pathogenic in cattle?

A

no

32
Q

How do you transmit EHEC?

A

fecal-oral route

33
Q

What is the infectious dose of EHEC and what is significant about this?

A

10-100 bacteria, which is very low

34
Q

Is stomach acid a strong barrier to intestinal infection?

A

Yes.

35
Q

Can a lack of stomach acid lead to a higher susceptibility to infection?

A

Yes.

36
Q

What is a pathogenic feature of EHEC?

A

A/E lesions

37
Q

What are A/E lesions?

A

Attaching and effacing lesions. These are parts of the intestinal epithelium which the bacteria uses to inject in proteins and take over the cells

38
Q

How does pathogenic E. coil promote diarrhea?

A

1) tight junction disruption

2) loss of absorptive surface area

39
Q

What does Shiga toxin bind?

A

Gb3 receptors

40
Q

Why is Shiga toxin called Shiga-like toxin in E.coli?

A

It shares similarity to Shiga toxin produced in virulent strains of Shigella

41
Q

Which is the more potent of the Shiga-like toxins?

A

Stx-2

42
Q

What encodes for Stx in E.coli?

A

lambda phage

43
Q

Why is the treatment of EHEC with abx controversial?

A

Because it leads to larger release of Shiga toxin and thus worse symptoms.

44
Q

Why are there systemic sequela from EHEC?

A

Stx binds globotriaosylceramide receptors which are prominent in the endothelium of the various organs, especially the kidneys

45
Q

How does Shiga or Shiga-like toxin work?

A

deadenylates 60S rRNA subunit

46
Q

What are the classic triad of symptoms of dysentery?

A

1) abdominal cramping
2) tenesmus
3) frequent, small-volume, bloody, mucoid discharge

47
Q

What is tenesmus?

A

Urge to defecate without or without actual production of fecal matter

48
Q

How do the strains of Shigella line up in terms of pathogenicity?

A

sonnei < flexneri &laquo_space;dyseneteriae

49
Q

What is the fatality rate in S. dyseneteriae epidemics?

A

5-15%

50
Q

What is Shigella thought to be a pathovar of?

A

E.coli

51
Q

What is the significance of fecal leukocytes?

A

invasive enteric pathogens provoke an inflammatory response resulting in high fecal leukocyte count

52
Q

What are the predominant Shigella infections in the US?

A

S. sonnei

53
Q

What is the primary reservoir for Shigella?

A

humans

54
Q

What is the infectious dose for Shigella and is it high or low?

A

<200 bacteria, low!

55
Q

What is the US incidence of Shigella infections?

A

~15k/year

56
Q

What are the primary targets of Shigella infections?

A

1) travelers

2) children in day care

57
Q

How many global infections of Shigella are there?

A

150 million per year

58
Q

Which is the most common strain of Shigella in the world?

A

Flexneri

59
Q

How does Shigella infect the intestines?

A

Phagocytosis by the M cell, and then makes its way to the basolateral membrane. It then replicates intracellularly and spreads through the actin cytoskeleton.

60
Q

Which strain has Shiga toxin?

A

Shigella dysenteriae Type 1

61
Q

What is the difference between EHEC and Shiga toxin in Shigella?

A

The gene for Shiga toxin in Shigella is in the bacterial genome rather than a phage

62
Q

What differentiates Salmonella from the other Enterobacteriaceae species?

A

1) produces H2S

2) phase variably motile

63
Q

Which types of infections are worse: broad host-range or narrow host-range?

A

Narrow host-range

64
Q

What are the two clinical presentations of Salmonella infections?

A

1) gastroenteritis

2) Typhoid fever

Exam 2 MIM Microbiology (5 decks)

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