Exam 3 Lecture 22 Flashcards

1
Q

Describe the gram stain of Campylobacter and Helicobacter

A

gram-negative helical rods

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2
Q

Campylobacter and Helicobacter are part of which broad group?

A

Epsilonproteobacteria

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3
Q

True or false: though they were discovered in the last 50 years, Campylobacter and Helicobacter are common bacterial pathogens

A

True

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4
Q

Campylobacter and Helicobacter are _____ and ____

A

microaerophilic; fastidious

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5
Q

Campylobacter and Helicobacter infect the __ ___ of humans and other animals

A

GI tract

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6
Q

True or false: Campylobacter and Helicobacter do not have flagellar motility

A

False

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7
Q

C. jejuni has ____ flagella, which contributes to what kind of motility?

A

bipolar; darting motility

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8
Q

Lophotrichous flagella

A

Multiple flagella found at one end of the bacterium

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9
Q

H. pylori has ____ flagella, which allows for:

A

lophotrichous; penetration of mucus (which likely attributes to its ability to get into the tissue and cause infection)

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10
Q

How do Campylobacter and Helicobacter have molecular mimicry?

A

Their LPS/LOS structures mimic host glycosylation, which can induce autoantibodies (those that mistakenly target the host)

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11
Q

How many species of Campylobacter do we know of? How many subspecies?

A

32 species; 9 subspecies

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12
Q

True or false: Campylobacter is the major cause of foodborne bacterial infections in developed nations

A

True (more than Salmonella, E. coli, Shigella combined)

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13
Q

Does Campylobacter cause disease via low or high inoculum?

A

Low (400-500 sufficient to cause infection)

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14
Q

Most Campylobacter infections are caused by:

A

C. jejuni

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15
Q

C. coli attributes to -% of Campylobacter infections

A

1-25%

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16
Q

True or false: Campylobacter can commonly colonize domestic animals where it doesn’t cause much disease.

A

True

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17
Q

C. jejuni causes ____, which consists of what symptoms?

A

Enteritis; symptoms = diarrhea; sometimes bloody, fever, abdominal pain, inflammation

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18
Q

C. jejuni symptoms usually appear in __-__ hours. The range is - days.

A

24-48 hours; 1-7 days

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19
Q

True or false: C. jejuni enteritis usually is self-limiting and resolves within a week

A

True

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20
Q

Sometimes, C. jejuni infection can become _____, which can lead to other diseases, such as:

A

extraintestinal; biliary tract, bacteremia, meningitis, others

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21
Q

How is C. jejuni infection treated?

A

fluids and electrolytes, antibiotics for severe infections

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22
Q

True or false: antibiotic resistance is a problem when treating C. jejuni

A

True - presumably due to resistance having developed in livestock

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23
Q

Which antibiotics are used for treating C. jejuni?

A

Azithromycin, Ciprofloxacin

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24
Q

True or false: For diagnosing C. jejuni, culture via selective media is the gold standard

A

True

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25
Q

Besides culture, what are some other ways to diagnose C. jejuni?

A
  1. looking for darting motility in fresh stool samples

2. serum serology and PCR

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26
Q

Most cases of C. jejuni are due to ____ ____

A

sporadic zoonosis

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27
Q

You can contract C. jejuni infection through: (2; hint - one is rare)

A
  1. contaminated/undercooked poultry

2. (rare) pets, contact with farm animals, person to person

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28
Q

True or false: raw milk or untreated water can cause outbreaks in C. jejuni

A

True

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29
Q

C. jejuni cases peak during ___ ___

A

warmer months

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30
Q

What are the four steps of C. jejuni pathogenesis?

A
  1. adheres to intestinal epithelial cells
  2. induced toxin-mediated cell damage
  3. uses cytolethal distending toxin to induce cell cycle arrest
  4. performs endocytosis and transcytosis (which is thought to be important for immune evasion)
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31
Q

True or false: C. jejuni flagella are required for infection

A

True (darting motility)

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32
Q

Regarding C. jejuni flagella, FlaA and FlaB expression can be turned on or off due to ___ ____, which is controlled by ___-___ ____

A

phase variation; slip-strand mispairing

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33
Q

Which flagellin monomers make up the C. jejuni flagella?

A

FlaA and FlaB

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34
Q

True or false: generally, bacterial flagella are normally glycosylated

A

False

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35
Q

C. jejuni flagellin glycosylation is important for _______ and _____ _____

A

autoagglutination; microcolony formation

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36
Q

Besides making up the flagellar structure, what else is the basal body in C. jejuni responsible for?

A

Exporting other proteins, such as FlaC, Cia proteins, and FspA

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37
Q

Generally, flagella are made via what type of secretion system?

A

(Modified) T3SS

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38
Q

Name the C. jejuni virulence factors (7)

A
  1. motility
  2. chemotaxis
  3. adhesion and invasion
  4. capsule
  5. iron uptake
  6. biofilm formation and antibiotic resistance
  7. LPS/LOS
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39
Q

Describe the chemotaxis of C. jejuni

A

attracted to mucus, glycoproteins of mucus, nutrients

repelled by bile

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40
Q

C. jejuni adheres to host ____ via what proteins?

A

CadF and FlpA

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41
Q

Which protein of C. jejuni binds to host heat shock protein?

A

JlpA

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42
Q

True or false: C. jejuni flagella are thought to be important for adhesion to host cells.

A

True

43
Q

True or false: in addition to FlaA/FlaB expression, C. jejuni turns capsule biosynthesis on/off via slip-strand mispairing

A

True

44
Q

C. jejuni capsule is important for:

A

survival, adherence, immune evasion

45
Q

How many serotypes exist in C. jejuni?

A

over 100

46
Q

What serotypes are associated with GBS?

A

Serotypes O19 and O41

47
Q

What type of toxin is CDT?

A

AB2

48
Q

CdtB gene codes for? And what functions does this protein product have?

A

A subunit of the CDT toxin; has DNase and phospholipase activity

49
Q

What do CdtA and CdtC genes code for?

A

binding subunits of the AB2 CDT toxin

50
Q

CdtA and CdtC bind to ____-rich regions on the host cell membrane and drives internalization of the toxin via _____-____ __

A

cholesterol; clathrin-coated pits

51
Q

True or false: the CDT toxin is unique solely in C. jejuni

A

False - found in many Gram negative organisms, such as E. coli, H. ducreyi, Helicobacter spp, S. Typhi, Shigella

52
Q

How does C. jejuni CDT cause cell cycle arrest/apoptosis?

A

B subunit migrates into the nucleus, induces double strand breaks; also activates ATM, p53

53
Q

What does GBS syndrome cause?

A

ascending paralysis

54
Q

Approximately _/___ patients develop GBS after C. jejuni infection

A

1/1000

55
Q

True or false: GBS correlates with presence of anti-GM1, anti-GD1a, IgG (antibodies against host proteins)

A

True - this attributes to paralysis

56
Q

In GBS, antibodies that are produced attack the ___ and assemble complement, essentially destroying the ___

A

nerves

57
Q

In addition to causing GBS, C. jejuni can also cause ____ ____

A

reactive arthritis

58
Q

C. fetus major reservoir

A

animals such as cattle, sheep, reptiles

59
Q

C. fetus grows optimally at __ºC

A

37ºC

60
Q

C. fetus can cause ____ and ___ ___

A

diarrhea; fetus loss

61
Q

True or false: C. fetus was the first Campylobacter characterized

A

True

62
Q

____ grows more slowly than Campylobacter

A

Helicobacter

63
Q

True or false: there is a correlation between H. pylori and peptic cancer

A

True

64
Q

H. pylori infection occurs ___ in life and can ____ for life

A

early; persist

65
Q

What is the H. pylori reservoir?

A

stomach

66
Q

H. pylori is ____ transmitted within families. As such, there is a strong ____ ____ to the genetic variation of Helicobacter spp.

A

vertically; ethnogeographic signature

67
Q

Most cases of H. pylori are ____ ____

A

asymptomatic gastritis

68
Q

H. pylori can cause what type of ulcers?

A

gastric and duodenal ulcers

69
Q

H. pylori can also cause ___ ___ ___ ___, which resolves upon eradication of infection.

A

Mucosa Associated Lymphoid Tissue

70
Q

Asymptomatic gastritis is characterized by? (3)

A
  1. neutrophil infiltration
  2. proinflammatory cytokines (increases acid)
  3. can progress to atrophic gastritis (loss of parietal cells, less acid)
71
Q

Parietal cells

A

epithelial cells that line the stomach and secrete HCl

72
Q

What does H. pylori gastritis look like?

A

bumpy lining, hyperplasia, loss of parietal cells, immune cells infiltrate, inflammation

73
Q

How does H. pylori survive the acidic environment of the stomach?

A

secretes urease

74
Q

True or false: patients with gastric cancer know early on that they have it

A

False - often is silent until tumor grows so large that it becomes hard to eat

75
Q

True or false: MALT lymphoma is rare

A

True

76
Q

H. pylori gastric cancer ___ doesn’t match ___. Ex: China

A

incidence; prevalence

77
Q

H. pylori diagnosis (4)

A
  1. urea breath test (carbon isotope)
  2. stool antigen test
  3. serological test (anti-H. pylori IgG)
  4. endoscopy and biopsy (for culture and histology purposes)
78
Q

Do we treat H. pylori if there are no symptoms?

A

No

79
Q

If there are symptoms or cancer risk, treat H. pylori with:

A

Combination therapy

  • 2 antibiotics
  • drug to reduce acid
  • bismuth to promote mucosal healing
80
Q

True or false: H. pylori treatments rarely fail

A

False- it can happen so we are wary of it due to resistance, pH effect on drugs, non-compliance due to long course of treatment

81
Q

Majority of H. pylori live in:

A

mucus layer overlying the gastric epithelium

82
Q

Urease has two main functions, which are:

A
  1. buffers stomach acid via cleaving urease to make NH3

2. changes rheological properties of mucin to make it easier to swim through

83
Q

H. pylori uses ___ ___ and ____ __ __ to get to epithelium

A

flagellar motility; helical cell shape

84
Q

H. pylori toxins (3)

A

VacA, Nap, CagA

85
Q

VacA

A

vacuolating cytotoxin

86
Q

Nap

A

recruit immune cells

87
Q

CagA

A

subvert host cell signaling

88
Q

H. pylori uses adhesins __ and __ to bind to? (respectively)

A

BabA and SabA; lewis antigens; sialyl-lewis antigens

89
Q

True or false: there is molecular mimicry with H. pylori due to Lewis antigens on LPS

A

true

90
Q

VacA has different ___ ___ ___ which can lead to higher/lower levels of its expression and binding ability

A

signal sequence polymorphisms

91
Q

VacA induces cells to fill up with big ____, which is ____. It also increases the ____ of the epithelium

A

vacuoles; cytostatic; permeability

92
Q

VacA can induce apoptosis via interaction with?

A

mitochondria

93
Q

VacA can inhibit _-___

A

T- cells

94
Q

Cag is coded within _____ ___

A

pathogenicity island

95
Q

Cag is associated with ___ and ___

A

ulcer and cancer

96
Q

Cag is displaced into a host cell via what secretion system?

A

T4SS

97
Q

Cag induces _____ ___

A

proinflammatory cytokines

98
Q

translocation of CagA into host does what two things?

A
  1. activate growth receptor signaling pathways

2. induce cell shape changes and motility

99
Q

True or false: Cag pathogenicity island is found in all strains of H. pylori

A

False - only in some strains, but found in those associated with causing ulcers/cancer

100
Q

CagA has ___ motifs. East Asians in particular have the _ motif which binds ___ much more tightly.

A

EPIYA; D; SHP-2

101
Q

SHP-2 binds to what specifically?

A

Phosphorylated Y within EPIYA

102
Q

True or false: Kids who have H. pylori are much more likely to have asthma and other allergic conditions

A

False: less likely

103
Q

Regarding H. pylori, protection against allergies/chronic inflammatory disorders is mediated through ____ _ ___

A

regulatory T cells