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MD3002 Week 3 > 4. Bacterial and Viral Infections of the Gastrointestinal Tract > Flashcards

4. Bacterial and Viral Infections of the Gastrointestinal Tract Flashcards

1
Q

What damage can be caused by GI pathogens?

A

Local inflammation
Ulceration / perforation of mucosal epithelium
Disruption of normal microbiota
Pharmacological action of bacterial toxins
Invasion to blood or lymphatics

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2
Q

Why is the lining of the epithelium perforated?

A

Due to untreated ulcers

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3
Q

Name 6 bacterial diarrhoea pathogens

A 
Gram neg:
• Vibrio cholerae
• Escherichia coli
• Campylobacter jejuni 
• Salmonella spp.
• Shigella spp.

Gram pos:
• Listeria monocytogenes

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4
Q 
V. cholerae:
Structure?
Characteristics?
Serotypes based on?
Vaccines?
A

Structure:
• Gram negative
• Comma-shaped rod
• Flagellated

Characteristics:
• Characterised by epidemics and pandemics
• Human-only pathogen
• Flourishes in communities with no clean drinking water / sewage disposal

Serotypes:
-Based on O antigens

Vaccines:

  • Parenteral vaccine: low protective efficiency
  • Oral vaccine: Effective and suitable for travellers
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5
Q 
Pathogenesis of V. cholerae:
Dosage?
Main barrier`?
Colonisation in SI requires?
Produces?
Results in?
A
  • Only infective in large doses
  • Many organisms killed in stomach
  • Colonisation of small intestine involving flagellar motion, mucinase, attachment to specific receptors
  • Production of multicomponent toxin
  • Loss of fluid and electrolytes without damage to enterocytes
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6
Q

What is the structure of the cholera toxin (CTx)?

What does it cause?

A

Structure of cholera toxin:
Oligomeric complex and 6 protein subunits.
- 1 x copy of A subunit (enzymatic)
- 5 x copies of B subunit (receptor binding)

Release of cAMP –> Lost of fluid and electrolytes.
Responsible for the characteristic, watery cholera diarrhoea. Acts as secretogogue.

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7
Q

5 potential consequences of cholera infection?

A
  1. Fluid loss of up to 1 litre/hour
  2. Electrolyte imbalance leading to dehydration, metabolic acidosis and hypokalemia
  3. Hypovolaemic shock
  4. 40-60% mortality
  5. <1% mortality if given fluid/electrolytes (ORT)
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8
Q

Structure of E.coli?

A

Gram neg
Bacillus
Normal GI microbiota, however, strains with virulence factors (e.g. toxins) enabling them to cause disease

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9
Q

Mode of action of E. coli enterotoxins

A

Enterotoxins secreted into the gut. E. coli has two of them, LT and STa
LT leads of cAMP ==> fluid loss
STa= leads to production of GMP

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10
Q

C. jejuni:
Structure?
Consequences?
Transmission?

A

Structure:

  • Gram neg
  • Helical bacillus

Consequences:

  • Food associated diarrhoea
  • Mucosal inflammation nd luid secretion

Transmission: Consumption of raw/undercooked meat, contaminated milk

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11
Q

Histological appearance of c. jejuni infection?

A
  1. Inflammation involves entire mucosa
  2. Villous atrophy
  3. Necrotic debris in crypts
  4. Thickening of basement membrane
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12
Q 
Salmonella spp.:
Structure?
Consequences?
Transmission?
Key species?
A

Structure:

  • Gram neg
  • Bacilli

Consequences: Food associated diarrhoea

Transmission: Consumption of raw / undercooked meat, contaminated eggs and milk

Key species:

  • S. typi
  • S. paratyphi
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13
Q

What are the stages of a Salmonella infection?

A
  1. Ingestion of large numbers of bacteria
  2. Absorption to epithelial cells in terminal section of small intestine
  3. Penetration of cells and migration to lamina propria
  4. Multiplication in lymphoid follicles
  5. Inflammatory response mediates release of prostaglandins
  6. Stimulation of cAMP
  7. Release of fluid and electrolytes causing diarrhoea
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14
Q

S. typhi and S. paratyphi: Cause which enteric fevers?

Role of macrophages?

A

Cause which enteric fevers? Typhoid and paratyphoid

Macrophages are the site of multiplication and transport around body

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15
Q

What are the two options for typhoid vaccine?

A

Oral: Live attenuated (booster after 5 years)

Parenteral: Capsular polysaccharide (Booster after 2 years)

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16
Q

Shigella spp.:
Structure?
Results in?
4 species?

A 
Structure: Bacillus
Causes shigellosis (bacillary dysentery)
4 species:
-S. dysenteriae (most serious)
-S. flexneri
-S. boydii
-S. sonnei
17
Q

Stages of shigella infection?

A
  1. Attaches to mucosal epithelium of distal ileum
    and colon
  2. Causes inflammation and ulceration
  3. Rarely invasive
  4. Produces Shiga toxin
  5. Diarrhoea watery initially, later can contain blood and mucus
  6. Disease usually self-limiting
18
Q

L. monocytogenes:

  • Structure?
  • Condition caused?
  • Population at risk?
  • Presents as?
A 
Structure: Coccobaccilus
Condition caused: Listeriosis
Population at risk:
-Pregnant women]
-Immunosuppressed individual
-The elderly
Presents as: Meningitis
19
Q

3 viral diarrhoea pathogens?

A

Rotavirus
Norovirus
Enteric adenovirus

20
Q

Rotavirus:
Structure?
Common patient?
Transmission?

A

Structure: Wheel, 11 separate segments of double-stranded RNA

Common: Children <2 years olds

Transmission: Faeco-oral, but may also be faeco-respiratory

21
Q

Pathogenesis of rotavirus infection?

A
  1. Incubation period of 1-2 days
  2. Replication of virus in small intestinal epithelial cells at tips of villi
  3. Resultsinvillousatrophy
  4. Damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes
  5. Onset of vomiting, diarrhoea lasting 4 –7 days
22
Q

What is the rotavirus vaccine?

A

RotaRix, RotaTeq

  • Oral administration
  • 2-3 doses
  • First dose at 6-10 weeks of age
  • Live,attenuated virus
23
Q

Norovirus:
AKA?
Transmission?
Vaccine?

A

aka winter vomiting disease

Transmission: Faeco-oral, contaminated water / shellfish, fomites

No vaccine

24
Q

Enteric adenovirus:

Presentation?

A

Presentation:

  • Asymptomatic infections common
  • Mild, but prolonged diarrhoea
25
Q

What is antibiotic associated diarrhoea?

Drugs involved?

A

Does not involve ingestion of pathogen or toxin
Can arise from disruption of gut microbiota following antibiotic therapy.

Drugs:
• Tetracycline-allows colonisation by Staphylococcus aureus & Candida sp.
• Clindamycin suppresses gut microbiota and allows Clostridium difficile to multiply
• C. difficile infection. is now associated with resistance to vancomycin

26
Q

Helicobacter pylori.:

  • Structure?
  • Assoication to disease?
A

Structure:

  • Gram neg
  • Spiral
  • Flagellated
  • Microaerophilic

Disease associations:

  • Duodenal ulcers
  • Gastric ulcers
  • Gastro-oesophageal reflux disease
  • Non-ulcer dyspepsia
27
Q

Key features of H. pylori?

A

• Acid-inhibiting protein: Survival in
stomach
• Urease – neutralisation of acid pH
• Adhesins – binding to gastric epithelium
• Cytotoxin – damage to gastric epithelium
• Flagellum – movement through gastric mucus layer

28
Q

Treatment of H. pylori associated Gastritis?

A

1 week triple therapy
Option 1. Proton pump inhibitor (PPI) + clarithromycin + amoxycillin
OR
Option 2: PPI + clarithromycin + metronidazole

29
Q

What is food poisoning?

A

Syndrome is restricted to diseases caused by toxins elaborated by contaminating bacteria in food before it is consumed

30
Q

4 ingredients in ORS?

A
  • Glucose (anhydrous)
  • Sodium chloride
  • Potassium chloride
  • Trisodium citrate dihydrate
31
Q

Characteristics of typhoid patients

A

Blanching rash
Rose spots
In faeces for several weeks after recovery\1-3% become chronic carriers
Public health concern

MD3002 Week 3 (8 decks)

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