Lecture 21 Campylobacter and helicobacter Flashcards

1
Q

What are some shared characteristics?

A

-Gram-negative helical rods
-Epsilonproteobacteria
-common bacterial pathogens, but only recently discovered
-microaerophilic and fastidious
-infect GI tract of humans and animals
flagellar motility
-molecular mimicry

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2
Q

What are the two flagella motility?

A

-Cj-Bipolar-darting

Hp-lophotrichous-penetration of mucous

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3
Q

What is the molecular mimicry of theses cells?

A

• LPS/LOS structures that mimic host glycosylation

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4
Q

What genus of Campylobacter cause majority of foodborne bacterial infections?

A
  • C. Jejuni (most)
  • C. coli
  • low infectious dose
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5
Q

What are some sx of C jejuni dx?

A

• Enteritis: diarrhea (sometimes bloody - dysentery), fever, abdominal pain, inflammation

  • 1-7 days after exposure
  • self limiting
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6
Q

What can happen ifC Jejuni becomes extaintestinal?

A

– Biliary tract
– Bacteremia
– Meningitis
– Others

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7
Q

How is C jejuni treated?

A

-fluids electrolytes
-in severe cases abx
-resistance problem
Ciprofloxacin, azithromycin

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8
Q

How is C jejuni dx?

A
  • Cx (gold standard)
  • darting motility in stool sample
  • serum serology and PCR tests
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9
Q

What are the cases of C jejuni?

A

most sporadic zoonosis

  • poultry
  • pets

some can cause outbreaks, Raw milk, untreated water in warmer months

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10
Q

What is the pathogenesis of C jejuni?

A
  • Adheres to intestinal epithelial
  • Cytolethal distending toxin
  • cell cycle arrest, growth but do not divide
  • Endocytosis/transcytosis (immune evasion, gain access to underlying tissues, requires Tubulin not actin)
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11
Q

What are the virulence factors of C jejuni?

A
  • Motility (polar flagellum, darting)
  • Chemotaxis- mucins and glycoproteins, repelled by bile
  • Adhesion and invasion (zipper trigger)
  • capsule
  • iron uptake
  • stress respones
  • antimicrobial resistance
  • LPS/LOS
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12
Q

What is cytolethal distending toxin (CDT)?

A

-AB2 type toxin
-found in gram -
activates ATM, causing apoptosis

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13
Q

What does Cj infection do?

A

promot colonization

  • increase inflammation
  • may promote immune evasion
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14
Q

What is Cuillain-Barre syndrome?

A
  • ascending paralysis caused by C jejuni
  • anti-GM1 and anti GD1a IgG (expressed in nervous system)
  • serotype O:19 and O:41 responsible
  • 90 percent recover
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15
Q

What is reactive arthritis?

A
  • caused by C Jejuni
  • Caused by enteric pathogens like Slamonella, Shigella, or chlamydial infection
  • molecular mimicry
  • treatments for sx,
  • 2/3 self limited, chronic arthritis in unresolved
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16
Q

What is C fetus?

A

extraintestinal disease causing

  • in cattle, sheep, reptiles
  • can cause diarrheal illness, but more associated with invasive disease
  • S- layer resistant to complement
  • infection during pregnancy can cause fetal loss, neonatal sepsis (also in C jejuni infection)
17
Q

When and how was H pylori discovered?

A

100 years ago as spirochetes in canine gastric mucosa, cannot compete in lower level tract, only in stomach

18
Q

What are some distinguishing things about H. pylori?

A
  • originally part of campylobacter, then helicobacter was created
  • Bacterial carcinogen (Stomach cancer)
  • occurs early in life and can persist
  • infects humans and non-human primates
  • no known environmental reservoir
  • gastro to oral
19
Q

what are H pylori diseases?

A
  • asymptomatic gastritis
  • ulcers (gastric, duodenal)
  • gastric adenocarcinoma
  • MALT lymphoma
20
Q

What is H pylori gastritis?

A
  • asymptomatic
  • parietal cells depleted (secrete HCl acid for stomach)
  • neutrophils infiltrate
  • pro inflammatory cytokines
21
Q

What can H pylori cause in the stomach?

A

ulcers

22
Q

What are two types of cancers caused by H pylori?

A
  • gastric adenocarcinoma

- MALT lymphoma

23
Q

How is a gastric ulcer formed from H pylori?

A

Corpus predominant atrophic gastritis

24
Q

How is a MALT lymphoma formed from H pylori?

A

Nonatrophic pangastritis

25
Q

How is duodenal ulcer formed from H pylori?

A

Antral-predominant gastritis

26
Q

How is gastric cancer caused by H pylori?

A

Corpus-predominant atrophic gastritis, intestinal metaplasia, dysplasia, gastric cancer

27
Q

How is H pylori dx?

A
  • Urea breath test (carbon isotope)
  • stool antigen test
  • serological tests (anti-H pylori IgG)
  • Endoscopy and biopsy (culture histology)
28
Q

How is H pylori treated?

A
  • no sx- don’t treat
    -combination therapy
    -treatment failure can occur:
    resistance, pH effect on drugs, non-compliance
29
Q

What can be used as combination therapy for H pylori?

A

– 2 antibiotics (tetracycline, metronidazole, clarithromycin, amoxicillin)
– drug to reduce acid (ranitidine, cimetidine, famotidine, omprazole, pantoprazole, lansoprazole, bismuth)
• improve symptoms
• increase efficacy of antibiotics
– Bismuth
• Promotes mucosal healing • Has antibacterial properties

30
Q

What is the pathogenesis of H pylori?

A
  • Majority of bacteria in mucus layer overlying gastric epithelium
  • Urease enzyme to locally buffer acid
  • flagellar motility to get epithelium
  • adherence to epithelium
  • toxins
31
Q

What are the toxins of H pylori?

A
  • Vac A- Cell damage
  • Nap -recruit immune cells
  • Cag A- subvert host cell signaling
32
Q

What are the virulence factors of H pylori?

A
  • adhesins (BabA, SAbA)
  • Molecular mimicry
  • Vac A (vaculolating cytotoxin)
  • Cag pathogenenicity island
33
Q

What is Vac A in H pylori?

A
  • auto transporter
  • isolates have different alleles with different activities
  • induces cells to fill up with big vacuoles-cytostatic
  • increase permeability of epithelium
  • can induce apoptosis via interaction with mito
  • inhibits T cells
34
Q

What is Cag pathogenicity island?

A
  • associate with ulcer, cancer
  • Type IV secretion system
  • induce proinflammatory cytokines
  • Translocation of CAgA to host
35
Q

What is an upside to H pylori?

A

immune modulation may protect against allergies and chronic inflammatory disorders