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BHCS3003 > Gram- Curved Rods > Flashcards

Gram- Curved Rods Flashcards

1
Q

List the Gram- Curved Rods.

A

Vibrio cholera
Campylobacter Jejuni
Helicobacter pylori

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2
Q

Outline features of V. Cholera

A
  • Curved bacterium natural habitat salt water
  • Facultative anaerobe, Gram –ve bacteria
  • Respiratory & fermentative metabolism
  • Pathogens include: Vibrio cholera, V. parahaemolyticus, V. vulnificus
  • Some of these pathogens are bioluminescent.
  • Broad temperature & pH range for growth on media
    • 18-37C, pH 7.0 - 9.0 (useful for enrichment)
  • Most other Vibrio are halophiles
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3
Q

What are some symptoms of V. Cholera infection/disease it causes?

A

V. Cholera causes cholera.

Symptoms include:
Dehydration, diarrhoea, stomach cramps, etc.

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4
Q

Explain the Pathogenesis of V. Cholera and VF

A
  • Usually aquatic reservoir (Biofilm formation)
  • GbpA protein colonisation factor
  • Ingestion & Colonisation of epithelial cells
  • Mucinase complex (Sialidase) hydrolyses mucus
  • Removes sialic acid to reveal GM1 receptor
  • CTX binds to GM1 on enterocyte
  • Proteases HapA, VesA, and VesB cleave toxin
  • Cholera toxin enters the enterocytes
  • Induces a secretory diarrhoea!
  • Late stage of infection, HapA degrades GbpA.

VF:

  • Toxins (serogroup O1 or O139 cause the most severe pathology)
    • CTX Cholera toxin hypersecretion of electrolytes & water ADP ribosylating.
      • Cholera toxin, by acting as a classical A-B type toxin,leads to ADP-ribosylation of G protein, and constitutive activation of AC, thereby giving rise to increased levels of cyclic AMP within the host cell. (Explored in the ‘Pathogenesis of Cholera’)
  • Adhesins
    • Co-regulated Pilus adherence to mucosal cells
    • Accessory Colonisation Factors Adhesin
  • Proteases
    • Haemagglutination (Mucinase)
    • Induces intestinal inflammation
  • Siderophores
    • Iron sequestration
  • Neuraminidase
    • Increase toxin receptors
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5
Q

Discuss the methods of diagnosis/diagnostic tools to identify V. Cholera

A

Laboratory diagnosis of V. cholerae

  • Clinical sample- stool or vomit
  • Microscopy- Gram stain

Culture:

  • Thiosulphate citrate bile salt sucrose (TCBS) agar plates
    • No autoclaving required
    • Green agar- yellow bacterial colonies (sucrose fermentation)
  • TTGA is a selective agar (Taurocholate tellurite gelatin agar)
    • not commercially available, small colonies
    • Potassium tellurite increases selectivity
    • Gunmetal grey colonies- reduction of tellurite
  • Maconkeys agar- pink colonies
  • Dipstick tests, rapid tests- not accurate for routine diagnosis
  • Dipsticks (Crystal VC® dipstick) should be performed with culture
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6
Q

Discuss the treatment options/prevention of V. Cholera

A
  • Untreated: 60% fatality; Treated: <1% fatality
  • Rehydration & supportive therapy
  • Oral
    • Sodium chloride (3.5 g/L)
    • Potassium chloride (1.5 g/L)
    • Rice flour (30-80g/L)
    • Trisodium citrate (2.9 g/L)
  • Intravenous (IV)
    • Antibiotics: Doxycycline or tetracycline
  • Water purification, sanitation & sewage treatment
  • Vaccines- Oral vaccine
    • Inactivated and attenuated

Alternative potential therapy: Phages:

Benefits

  • Fast acting
  • Targeting is specific
  • Kills drug resistant strains

Drawbacks

  • Again, resistance to phage therapy noted – mutation in phage receptors
  • Only tested in animal models
  • Doesn’t fully stop infection
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7
Q

Outline features of C. Jejuni

A
  • Common cause of food poisoning
  • Gram-negative, Helical & pleomorphic
  • Characteristics that facilitate penetration and colonization
  • Microaerophilic
  • Neither ferment nor oxidize carbohydrates
  • Found in animal faeces
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8
Q

What are some symptoms of C. Jejuni infection/disease it causes?

A

See notion figure

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9
Q

Explain the Pathogenesis of C. Jejuni and VF

A
  • Innate immune response to Campylobacter jejuni in humans
  • Not fully characterised… however;
  • Causes IL-8 production via circumventing mucus layer
  • C. jejuni binds to, and is internalized by, epithelial cells.
  • The induction of IL-8 causes cell recruitment
  • dendritic cells (DC), macrophages and neutrophils,.
  • pro-inflammatory response
    (DRAW FROM NOTION)

VF: (more detail?)

Flagella

  • •Motility

Adhesins

  • Attachment to mucosa & invasins

Toxins

  • •LPS (endotoxin) and exotoxins

Superoxide dismutase

  • Removes reactive oxygen species

Siderophores

  • •Iron sequestration
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10
Q

Discuss the methods of diagnosis/diagnostic tools to identify C. Jejuni

A

Laboratory diagnosis of C. jejuni

  • Clinical specimen- Stool, rectal swabs (avoid oxygen exposure)

Culture:

  • Selective Agar: CAMP, 35-37 & 42 °C or Skirrow’s medium

Microscopy:

  • Gull-wing appearance in Gram stain
  • Darting motility in fresh stool
  • Faecal leukocytes

Biochemical Identification:

  • Hippurate hydrolysis (C. jejuni is positive)
  • Susceptibility to nalidixic acid
  • Oxidase positive
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11
Q

Discuss the treatment options/prevention of C. Jejuni

A
  • Self-limiting; Replace fluids and electrolytes
  • Abx can shorten the excretion period;
    • Erythromycin;
    • fluoroquinolone resistance
    • Azithromycin
  • Control should be directed at domestic animal reservoirs
    • interrupting transmission to humans
  • Guillain-Barre Syndrome (GBS)
  • Favourable prognosis with optimal supportive care
  • Intensive-care unit for 33% of cases
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12
Q

Outline features of H. Pylori

A
  • Ulcers stomach bacterium
  • Gram-negative, Helical & pleomorphic
  • Penetrates mucosal linings
  • Blunted/rounded ends in gastric biopsy specimens;
  • Cells become rod-like and coccoid on prolonged culture
  • Produce urease, mucinase, and catalase
  • H. pylori tuft (lophotrichous) of 4-6 sheathed flagella
  • Smooth cell wall with unusual fatty acids
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13
Q

What are some symptoms of H. Pylori infection/disease it causes?

A
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14
Q

Explain the Pathogenesis of H. Pylori and VF

A
  • oral – oral/ Faecal-oral spread
  • Poverty and overcrowding predisposes
  • Causes mild to acute gastritis
  • Gastric antrum - causes gastric metaplasia
  • Colonizes overlying mucosa but do not invade mucosa
  • Burrows into the mucus lining of the stomach using flagella
  • Uses chemotaxis to move to less acidic pH
  • Produces Urease to neutralise acid
  • Produces CO2 and ammonia
    (DRAW FROM NOTION)

VF:

  • Corkscrew motility
    • Adhesins:
    • Mucinase
  • Urease production
  • Vacuolating cytotoxin VacA
  • Epithelial cell damage
  • Protection from phagocytosis
    • Superoxide dismutase
    • Catalase
  • Pathogenicity island: cag
  • Type IV secretion
  • LPS
  • Cag+ HP is much more associated with peptic ulcer disease than Cag(–) HP.
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15
Q

Discuss the methods of diagnosis/diagnostic tools to identify H. Pylori

A

Laboratory diagnosis of H. Pylori

  • Recovered from or detected in endoscopic/ gastric biopsy material;
    • Multiple biopsies are taken

Culture

  • Chocolate agar
  • Campylobacter (CAMP) media
  • Grows under Microaerophilic conditions
  • With presence of 5 – 20% CO2
  • Oxidase Positive
  • Catalase Positive
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16
Q

Discuss the treatment options/prevention of H. Pylori

A
  • Bismuth salts
    • Ingestion of Bismuth subsalicylate
  • Antibiotics
    • Tetracycline’s and metronidazole for two weeks
    • Use of Omeprazole
    • Clarithromycin
  • Do not treat for Asymptomatic colonization
  • Antibiotic resistance is a growing problem

BHCS3003 (11 decks)

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