4. Bacterial and Viral Infections of the Gastrointestinal Tract Flashcards
What damage can be caused by GI pathogens?
Local inflammation
Ulceration / perforation of mucosal epithelium
Disruption of normal microbiota
Pharmacological action of bacterial toxins
Invasion to blood or lymphatics
Why is the lining of the epithelium perforated?
Due to untreated ulcers
Name 6 bacterial diarrhoea pathogens
Gram neg: • Vibrio cholerae • Escherichia coli • Campylobacter jejuni • Salmonella spp. • Shigella spp.
Gram pos:
• Listeria monocytogenes
V. cholerae: Structure? Characteristics? Serotypes based on? Vaccines?
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
Pathogenesis of V. cholerae: Dosage? Main barrier`? Colonisation in SI requires? Produces? Results in?
- 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
What is the structure of the cholera toxin (CTx)?
What does it cause?
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.
5 potential consequences of cholera infection?
- Fluid loss of up to 1 litre/hour
- Electrolyte imbalance leading to dehydration, metabolic acidosis and hypokalemia
- Hypovolaemic shock
- 40-60% mortality
- <1% mortality if given fluid/electrolytes (ORT)
Structure of E.coli?
Gram neg
Bacillus
Normal GI microbiota, however, strains with virulence factors (e.g. toxins) enabling them to cause disease
Mode of action of E. coli enterotoxins
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
C. jejuni:
Structure?
Consequences?
Transmission?
Structure:
- Gram neg
- Helical bacillus
Consequences:
- Food associated diarrhoea
- Mucosal inflammation nd luid secretion
Transmission: Consumption of raw/undercooked meat, contaminated milk
Histological appearance of c. jejuni infection?
- Inflammation involves entire mucosa
- Villous atrophy
- Necrotic debris in crypts
- Thickening of basement membrane
Salmonella spp.: Structure? Consequences? Transmission? Key species?
Structure:
- Gram neg
- Bacilli
Consequences: Food associated diarrhoea
Transmission: Consumption of raw / undercooked meat, contaminated eggs and milk
Key species:
- S. typi
- S. paratyphi
What are the stages of a Salmonella infection?
- Ingestion of large numbers of bacteria
- Absorption to epithelial cells in terminal section of small intestine
- Penetration of cells and migration to lamina propria
- Multiplication in lymphoid follicles
- Inflammatory response mediates release of prostaglandins
- Stimulation of cAMP
- Release of fluid and electrolytes causing diarrhoea
S. typhi and S. paratyphi: Cause which enteric fevers?
Role of macrophages?
Cause which enteric fevers? Typhoid and paratyphoid
Macrophages are the site of multiplication and transport around body
What are the two options for typhoid vaccine?
Oral: Live attenuated (booster after 5 years)
Parenteral: Capsular polysaccharide (Booster after 2 years)
Shigella spp.:
Structure?
Results in?
4 species?
Structure: Bacillus Causes shigellosis (bacillary dysentery) 4 species: -S. dysenteriae (most serious) -S. flexneri -S. boydii -S. sonnei
Stages of shigella infection?
- Attaches to mucosal epithelium of distal ileum
and colon - Causes inflammation and ulceration
- Rarely invasive
- Produces Shiga toxin
- Diarrhoea watery initially, later can contain blood and mucus
- Disease usually self-limiting
L. monocytogenes:
- Structure?
- Condition caused?
- Population at risk?
- Presents as?
Structure: Coccobaccilus Condition caused: Listeriosis Population at risk: -Pregnant women] -Immunosuppressed individual -The elderly Presents as: Meningitis
3 viral diarrhoea pathogens?
Rotavirus
Norovirus
Enteric adenovirus
Rotavirus:
Structure?
Common patient?
Transmission?
Structure: Wheel, 11 separate segments of double-stranded RNA
Common: Children <2 years olds
Transmission: Faeco-oral, but may also be faeco-respiratory
Pathogenesis of rotavirus infection?
- Incubation period of 1-2 days
- Replication of virus in small intestinal epithelial cells at tips of villi
- Resultsinvillousatrophy
- Damage caused to infected cells leaving immature cells with reduced absorptive capacity for sugar, water and electrolytes
- Onset of vomiting, diarrhoea lasting 4 –7 days
What is the rotavirus vaccine?
RotaRix, RotaTeq
- Oral administration
- 2-3 doses
- First dose at 6-10 weeks of age
- Live,attenuated virus
Norovirus:
AKA?
Transmission?
Vaccine?
aka winter vomiting disease
Transmission: Faeco-oral, contaminated water / shellfish, fomites
No vaccine
Enteric adenovirus:
Presentation?
Presentation:
- Asymptomatic infections common
- Mild, but prolonged diarrhoea
What is antibiotic associated diarrhoea?
Drugs involved?
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
Helicobacter pylori.:
- Structure?
- Assoication to disease?
Structure:
- Gram neg
- Spiral
- Flagellated
- Microaerophilic
Disease associations:
- Duodenal ulcers
- Gastric ulcers
- Gastro-oesophageal reflux disease
- Non-ulcer dyspepsia
Key features of H. pylori?
• 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
Treatment of H. pylori associated Gastritis?
1 week triple therapy
Option 1. Proton pump inhibitor (PPI) + clarithromycin + amoxycillin
OR
Option 2: PPI + clarithromycin + metronidazole
What is food poisoning?
Syndrome is restricted to diseases caused by toxins elaborated by contaminating bacteria in food before it is consumed
4 ingredients in ORS?
- Glucose (anhydrous)
- Sodium chloride
- Potassium chloride
- Trisodium citrate dihydrate
Characteristics of typhoid patients
Blanching rash
Rose spots
In faeces for several weeks after recovery\1-3% become chronic carriers
Public health concern
