Lecture 21 Campylobacter and helicobacter Flashcards

(35 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two flagella motility?

A

-Cj-Bipolar-darting

Hp-lophotrichous-penetration of mucous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the molecular mimicry of theses cells?

A

• LPS/LOS structures that mimic host glycosylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What genus of Campylobacter cause majority of foodborne bacterial infections?

A
  • C. Jejuni (most)
  • C. coli
  • low infectious dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can happen ifC Jejuni becomes extaintestinal?

A

– Biliary tract
– Bacteremia
– Meningitis
– Others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is C jejuni treated?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is C jejuni dx?

A
  • Cx (gold standard)
  • darting motility in stool sample
  • serum serology and PCR tests
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is cytolethal distending toxin (CDT)?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does Cj infection do?

A

promot colonization

  • increase inflammation
  • may promote immune evasion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

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
How is duodenal ulcer formed from H pylori?
Antral-predominant gastritis
26
How is gastric cancer caused by H pylori?
Corpus-predominant atrophic gastritis, intestinal metaplasia, dysplasia, gastric cancer
27
How is H pylori dx?
- Urea breath test (carbon isotope) - stool antigen test - serological tests (anti-H pylori IgG) - Endoscopy and biopsy (culture histology)
28
How is H pylori treated?
- no sx- don't treat -combination therapy -treatment failure can occur: resistance, pH effect on drugs, non-compliance
29
What can be used as combination therapy for H pylori?
– 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
What is the pathogenesis of H pylori?
- 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
What are the toxins of H pylori?
- Vac A- Cell damage - Nap -recruit immune cells - Cag A- subvert host cell signaling
32
What are the virulence factors of H pylori?
- adhesins (BabA, SAbA) - Molecular mimicry - Vac A (vaculolating cytotoxin) - Cag pathogenenicity island
33
What is Vac A in H pylori?
- 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
What is Cag pathogenicity island?
- associate with ulcer, cancer - Type IV secretion system - induce proinflammatory cytokines - Translocation of CAgA to host
35
What is an upside to H pylori?
immune modulation may protect against allergies and chronic inflammatory disorders