Helicobacter Flashcards

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1
Q

Helicobacter disease is gram _____

A

negative

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2
Q

Helicobacter is ____ shape

A

Helical shaped

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3
Q

Helicobacter disease is found where?

A

found in the stomach

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4
Q

Helicobacter disease is what type of bacterium?

A

gram negative miicro-aerophilic bacterium

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5
Q

How many people are infected by Helicobacter?

A

significant portion (possibly 50%) of population is infected

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6
Q

Helicobacteria is present in patients with what?

A
  • chronic gastritis and

- gastric ulcers

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7
Q

What are the symptoms of Helicobacter disease?

A
  • Dyspepsia (indigestion)
  • stomach pains
  • nausea
  • bloating
  • belching
  • sometimes vomiting
  • sometimes black stool
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8
Q

Helicobacter can be possible causes of what?

A
  • Gastric ulcers
  • duodenal ulcers
  • gastric cancer (carcinoma)
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9
Q

Helicobacter pylori is originally classified as ____

A

C. pyloridis

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10
Q

Helicobacter pylori infects how much of the population?

A

significant portion (possibly 50%) of the population infected

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11
Q

How do the flagella of H. pylori help adhesion?

A

the flagella help burrow in the mucus layer and to reach epithelial layer.

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12
Q

What does BabA stand for?

A

blood-group antigen binding adhesion

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13
Q

What does SabA stand for?

A

Sialic acid binding adhesion

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14
Q

What do the antigens SabA and BabA in H. pylori do?

A

they trigger inflammation and help Helicobacter with adhesion

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15
Q

What does urease from H. pylori help colonization?

A

It produces ammonia and buffers acid pH; triggers apoptosis (death of cells)

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16
Q

H. pylor can modifiy what? how is this a virulence factor?

A

by modifying its peptidoglycan which helps immune evasion

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17
Q

How does H. pylori’s LPS play a role in virulence?

A

It binds to toll like receptors which can activate B cells and reduce pathology.

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18
Q

What are people with TLR (toll like receptor) at higher risk for when infected with H, pylori as well?

A

more prone to tissue damage and cancer

19
Q

What toxin of H. pylori that causes tissue damage?

A

CagA (cytoxin associated gene A)

20
Q

What type of secretion in H. pylori is involved in injecting CagA into gastric cells?

A

Type 4

21
Q

cagA is a virulence of H. pylori located where?

A

on a pathogenicity island

22
Q

CagA is a virulence of H. pylori that is associated with what?

A

gastric carcinoma

23
Q

What does cagA do with several host genes?

A

Interacts

24
Q

What is Tip-alpha

A

Tumor Necrosis factor alpha inducing protein; virulence of H. pylori

25
Q

What is Tip-alpha associated with?

A

carcinogensis; hy. pylori virulence

26
Q

Vaculoating cytotoxin A (vacA) is a virulence factor if H. pylori that causes what?

A

vacuole formation (large vesicles in host cells)

27
Q

VacA targets what?

A

the mitochondria

28
Q

VacA can induce what

A

apotosis

29
Q

what is apotosis?

A

the death of cells

30
Q

The vac A virulence is a major contributor to what? Why?

A

Gastric cancer; because of the increased occurences of mutation due to direct damage of DNA (free radicals primarliy ROS, NOS) and a deficient repair of mutations

31
Q

How is H. pylori diagnosed

A
  • based on symptoms of chronic gastritis, GERD (gastroesophageal reflex disease)
  • blood antigen
  • 13C urea breath teast (urease test)
  • antigen in stool
  • Endoscopy, tissue staining with immunostain
32
Q

How is H. pylori r treated?

A

triple/ quadruple therapy

33
Q

What is triple/quadruple therapy in regards to H. pylori ?

A

Treatment in which Mentronidazole + tetracycline + Bismuth sulphate is used and sometimes also a proton pump inhibito (omeprazole) to allow healing

34
Q

what are toll like recpetors?

A

a class of proteins that play a key role in innate immune system

35
Q

H. pylori adhesin has what type of binding?

A

apical binding; apical colonization and signaling to known and unknown receptors on gastric epithelium

36
Q

H. pylori directs what?

A

signal transduction

37
Q

Upregulation of H. pylori transcription factors such as _____ leads to production of what?

A

upregulation of transcription factors such as NF-kB leads to the production of pro-inflammatory cytokines and chemokines

38
Q

Secretion of mediators at the basolateral surfaces does what?

A

attracts immune cells to the site of infection

39
Q

Upon host cell contact, H. pylori assembles what? Resulting in what?

A

T4SS (type 4 secretion) pili at the surface enabling (allowing) delivery of molecules from bacterial cytoplasm into host cells

40
Q

What molecules at the surface of host cells are enabled into the host via T4SS?

A

Cag A and peptidoglycan

41
Q

cag PAI proteins include

A
  • CagA
  • CagI
  • CagL
  • CagY
42
Q

Cag PAI proteins interact with _____

A

integrin receptors

43
Q

Interactions with phosphatidyserine (PS) and cholesterol in lipid rafts are inolved in ____ processing

A

T4SS

44
Q

T4SS and CagA are involved in _____

A

numerous cellular effects including:

  • disruption of cell-to-cell junctions (tight junctions and adherence junctions)
  • Cytoskeletal rearrangement
  • nuclear signaling