Lecture 3 part 2 Flashcards

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1
Q

Order: Campylobacterales
General morphological and biochemical characteristics

A

family Campylobacteraceae

  • 3 genera (Campylobacter, Helicobacter)
  • Gram negative spiral shaped
  • Microaerophilic (<5% O2)
  • Oxidase positive; they have cytochrome c
  • Catalase positive
  • Nitrate reductase positive
  • G+C%: 30-40%; genome size 1.5 – 1.7 M
    bases
  • Optimum growth (30 - 42˚C)
  • motile (Campylobacter - single polar
    flagella; Helicobacter – sheathed, 2-5 polar
    flagellum)

Both genera have reduced metabolic capability compared to members of Enterobacteriaceae

  • Campylobacter spp. - very sensitive to external
    conditions (UV light, heat, salt etc); unable to
    multiply and thrive outside the host’s body
  • Helicobacter spp. - fastidious microorganisms
    (require complex growth media (e.g. blood,
    serum) with additional amino acids)
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2
Q

What is the most frequent bacterial cause of foodborne illness in the developed
world?

A

Campylobacter jejuni- causes more foodborne illness than any other bacteria
(500,000 cases per year in the UK alone)

22 species, C. jejuni and C. coli
cause most human disease
(self-limiting gastroenteritis with
systemic complications)

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3
Q

C. jejuni infection and pathogenesis

A

Clinical symptoms:
day 1 → 3 ; fever, vomiting, headaches
day 3 → watery/bloody diarrhoea with
abdominal pain; stools contain
inflammatory cells and colonic biopsies
show diffuse inflammatory colitis

very different to grow in labs as they cannot tolerate atmospheric oxygen

Steps in infection:
1. ingestion of bacteria
2. reaches small intestine
3. (mucosal damage)
4. invades via transcellular and
paracellular routes
5. provokes an immune
response
6. virulence gene expression
7. eventually cleared from host

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4
Q

C. jejuni virulence factors

A
  • Motility
    (e.g. major flagella protein (FlaA), structural/export apparatus protein (FlhA)
  • Lipooligosaccharide (LOS) and capsule
    (e.g. LOS resembles human neuronal gangliosides → molecular mimicry thought
    to lead to autoimmune disorders)
    (e.g. capsule provides protection from host immune system, aids adhesion)
  • Colonization and invasion
    (e.g. outer membrane adhesins: CadF, DocA, VirB11 etc)
  • Toxin production
    (e.g. cytolethal distending toxin (CdtABC) causes doublestranded breaks in DNA → cell death)
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5
Q

Main reservoir of Campylobacter spp.

A

poultry and poultry products due to the temperature

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6
Q

What is the most frequent bacterial infection world-wide?

A

Helicobacter pylori
(~50% of worlds’ population are infected !)

H. pylori is classified by WHO as a Class
1 (definite) carcinogen

> 20 species, H. pylori is the main human pathogen

main cause of chronic
gastritis, gastric cancer
and peptic ulcer disease

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7
Q

Helicobacter pylori: disease and
prevalance

A

Humans: predominant reservoir;

Disease: 80% asymptomatic / 10-20% gastric hyperacidity & ulcers / <0.5% gastric cancer

Prevalence is highest:
Africa (79.1%)
Latin America & the
Caribbean (63.4%)
Asia (54.7%)
Prevalence is lowest:
Northern America (37.1%)
Oceania (24.4%).

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8
Q

H. pylori infection and pathogenesis

A

Route: oral, mainly spread by intrafamilial transmission

Key aspects of bacterial colonization involve flagellar motility, urease
activity, adhesion and damage to gastric epithelium via vacuolisation.

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9
Q

H. pylori virulence factors

A
  • Urease production
    7 gene cluster including ureA/B, which enables organism to cope with low pH of stomach. Mechanism: at low pH, urea entry across periplasm results in production of
    ammonium, which is believed to neutralise excess protons- this allows bacteria to deal with low pH of the stomach
  • Flagella / motility
    40 gene cluster including structural components FlaA, FlaB. The sheathed
    flagellum may help ‘hide’ the apparatus from detection by immune system
  • Adhesins
    e.g. Blood-antigen binding protein A (BabA), sialic acid-binding adhesin (SabA)
  • Toxins
    e.g. Cytotoxin-associated gene A (CadA) located on cag pathogenicity island;
    alters host cell signalling leading to disruptions in host cytoskeleton, inflammatory mediators etc- pathogenicity island allows bacteria to hop between genomes
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