Pathogens of the Gastro-intestinal tract Flashcards
(31 cards)
Gastroenteritis
Syndrome characterised by GI-symptoms including nausea, vomiting, diarrhoea and abdominal pain
Diarrhoea
Abnormal faecal discharge characterised by frequent and/or fluid stool. Associated with increased fluid and electrolyte loss- often disease of small intestine
Dysentery
Abnormal inflammation of GI-tract: often blood and pus in faeces and pain, fever, abdominal cramps- often disease of large intestine
Enterocolitis
Inflammation of mucosa of small and large intestine
Defences
Mouth Oesophagus Stomach Small intestine Large intestine
Defences - MOUTH
Flow of liquids
Saliva
Lysozyme
Normal bacterial flora
Defences - oesophagus
Flow of liquids
Peristalsis
Defences - stomach
Acid pH
Defences - small intestine
Flow of gut contents Peristalsis Mucus - bile Secretory IgA Lymphoid tissue (payer's patcheS) shedding and replacement of epithelium normal flora
Defences - LI
Normal flora
peristalsis
shedding and replication of epithelium
mucus
Food poisoning
Ingestion of toxins or poisons in food e.g bacterial or heavy metal
Bacteria grow and multiply in food
Cooking kills bacteria but toxin still active - intoxication
Food poisoning toxin sources
Staph aureus
Growth in food after human contamination
Products, cooked meats, prepacked sandwiches
50% of strains produce heat stable enterotoxins
Resistance to stomach acid and digestive enzymes - nasopharyngeal carriage
3-6hrs of severe vomiting - complete recovery
Botulism - clostridium botulinum
Heat stable toxin ingest din food, leads to flaccid paralysis and death covered in anaerobe lecture
infant most common
Bacillus cereus
Self limiting
Gram positive, spore former
The stomach
Gastric acid pH 1-2
Effective barrier to most infections
Many bacteria pass through before infecting lower GI
Helicobacter pylori - gastric ulcers
Infective cycle
Treatment
Produces urease
Protective cloud during transit to gastric mucin layer
Ammonia basis of breath test
Infection
Inflammation of gastric mucosa often asymptomatic
Produces ulcer - gastric inflammation may lead to duodenal or gastric ulcer
Severe complications can include perforated ulcer
Treatment now with proton-pump inhibitor PLUS metronidazole/ amoxicillin and Clarithromycin
Food associated infections
Mainly spread faeco-orally
Ingestion of contaminated food containing infectious dose of bacteria
Diarrhoeal treatment
Fluid and electrolyte replacement is essential
Antibiotic treatment often not successful and may worsen problem as it wipes out competing organisms or stimulates toxin production
Diarrhoeal disease - e. coli
Gram-negative motile rod
Major cause of diarrhoeal disease and gastroenteritis worldwide
Complications include HUS
Many genetically distinct disease causing strains
Some strains reside in normal commensal flora
Others infect urinary tract and cause meningitis
Diarrhoea: Ingested in food or via fecal-oral transmission route.
Genetic diversity dependent on plasmid, lysogenic phage and transposon encoded ‘pathogenicity islands’
Lab detection of E coli
Lactose fermentation
E.coli strains - EPEC
Features
Mechanism
Enteropathogenic
Bundle forming pili to attach
Type III secretion system injects proteins into host to manipulate cytoskeleton
Tir- translocated intimin receptor
Intimin - mediates intimate attachment to epithelial cells
Attaching and effacing lesion
Leads to watery diarrhoea
ETEC
Enterotoxigenic E.coli - toxin producing
Attach via adhesive pili
Produce Heat stable ST and Labile enterotoxins that cause diarrhoea
Common cause of Delhi Belly
EIEC - enteroinvasive
Invade and destroy epithelial cells
Bloody diarrhoea
EHEC
Attachment similar to EPEC- pedestals
Produce Vero-toxin (Also called Shigella-like toxin)- STx
STx (verotoxin) is a potent diarrhoeal toxin (and has receptor on kidney cells) acts via damaging cells directly
EHEC infections also cause hemorrhagic colitis- Bloody diarrhoea- destruction of mucosa>bleeding> spread to kidneys
HUS- Haemolytic Urinary Syndrome
- This may lead to kidney failure (15% cases) - O157:H7 strain most well known
2011 outbreak: O104:H4
- EHEC/EAEC strain: shiga-toxin, multi drug resistant, aggregative pili- Nasty!
Spring/summer 2011 - Outbreak focussed in Germany: 3,000 cases (857 HUS); 50 deaths
- Possible source- Fenugreek seeds from Egypt; raw beansprouts implicated also, WHO advises NOT eating raw.