GI infections Flashcards
Name the two mechanisms by which bacteria that cause GI infections can be classified into
Infection - bacterial pathogens develop in the gut after the ingestion of contaminated food e.g. salmonella
Intoxication - bacterial pathogens grow in food and produce toxins e.g. bacillus cereus
Diarrhoea
o Abnormal frequency and/or fluid stool o Usually indicates small bowel disease o Causes fluid and electrolyte loss o Severity varies widely from mild self-limiting to severe/fatal Virulence of organism Degree of compromise of the host
Gastroenteritis
o Nausea, vomiting, diarrhoea and abdominal discomfort
Dysentery
o Inflammatory disorder of the large bowel
o Blood and pus in faeces
o Pain, fever and abdominal cramps
Enterocolitis
o Inflammatory process affecting small and large bowel
how is campylobacter infection spread
via contaminated food
Describe the campylobacter bacteria
gram-negative bacilli. They are microaerophillic and thermophillic.
Give the clinical effects of campylobacter infection
o Incubation 2-5 days o Bloody diarrhoea o Cramping abdominal pain o Vomiting is not usually a feature o Fever o Duration 2-10 days
Describe pathogenesis of campylobacter infection
o Inflammation, ulceration & bleeding in small and large bowel due to bacterial invasion. Can cause a bacteraemia (elderly and immunocompromised)as well as Guillan barré syndrome
How would you treat campylobacter infection
Fluids, clarithromycin in severe/resistant cases. You would give quinolones or an aminoglycoside if the disease was invasive.
what species causes the majority of salmonella infection
Salmonella enterica
Describe the salmonella bacteria
Gram negative bacilli. Non-lactose fermenters
How is Salmonella generally acquired
through ingestion of infected food stuffs (especially pork, poultry and meat). Waterborne infection if less common.
Can have large outbreaks as can multiply in food.
Describe pathogenesis of salmonella infection
o Diarrhoea due to invasion of epithelial cells in the distal small intestine, and subsequent inflammation
o Bacteraemia can occur (extremes of age, immunocompromised)
o Distant organs may become seeded to establish metastatic foci of infection e.g. osteomyelitis, septic arthritis, meningitis etc.
Clinical features of salmonella infection
o Incubation 12-72 hours o Watery diarrhoea o Vomiting is common o Fever can occur, and is usually associated with more invasive disease o Duration 2-7 days
Treatment of Salmonella
o Fluid replacement is sufficient in most cases
o Antibiotics reserved for severe infections and bacteraemia
o Beta-lactams, quinolones or aminoglycosides may be used
o Antibiotics and antimotility agents prolong excretion of salmonellae in the faeces
Describe the shigella bacteria
Gram negative bacilli. Non-lactose fermenters. Has four species.
How is shigella transmitted?
faecal-oral route is the most common. Humans are only reservoir and large outbreaks can occur. Associated with a low infectious dose.
Pathoegenesis of shigella
o Organisms attach to and colonise mucosal epithelium of terminal ileum & colon
o Systemic invasion is not a feature
o S.dysenteriae produces a potent protein exotoxin (Shiga toxin) which not only damages intestinal epithelium, but in some patients targets glomerular endothelium causing renal failure as part of haemolytic-uraemic syndrome (HUS)
Four types of shigella
Shigella sonnei associated with milder infections
Shigella boydii & S.flexneri associated with more severe disease
Shigella dysenteriae associated with most severe disease
Clinical features of shigella infection
o Dysentery o Incubation 1-3 days o Duration 2-7 days o Initially watery diarrhoea followed by bloody diarrhoea o Marked, cramping abdominal pain o Vomiting is uncommon o Fever is usually present
Treating shigella
o Usually self-limiting
o Fluid replacement is usually sufficient
o Some cases of S.dysenteriae infection will require treatment of renal failure
o Specific control points
o Only found in humans, so good standards of sanitation and personal hygiene are key measures
Describe the Cholera bacteria
gram negative bacilli, sucrose-fermenter.
Classified on the basis of their O antigens.
How does cholera spread?
Spreads via contaminated food or water. Can cause pandemics. Is endemic in parts of SE Asia, S America
Person to person transmission is uncommon
Pathogenesis of cholera
o Flagellae and mucinase facilitate penetration of intestinal mucous
o Attachment to mucosa by specific receptors
o Diarrhoea due to production of a potent protein exotoxin
Clinical features of cholera
o Severe, profuse, non-bloody, watery diarrhoea (rice water stool)
o Profound fluid loss & dehydration precipitates hypokalaemia, metabolic acidosis, hypovolaemic shock and cardiac failure
o Untreated mortality 30-40%
treatment of cholera
o Prompt oral or intravenous rehydration is lifesaving (mortality reduced to <1%)
o Tetracycline antibiotics may shorten duration of shedding
Describes the pathogenesis of enteropathogenic E.coli
Initial adherence via pili, followed by formation of characteristic “attatching & effacing” lesion mediated by intimin protein and Tir (translocated intimin receptor) with disruption of intestinal microvilli
What is a major bacterial cause of diarrhoea in infants & children in developing world and travellers diarrhoea?
ETEC
Summaries pathogenesis of ETEC
Diarrhoea due to action of 1 or 2 plasmid-encoded toxins
Heat-labile (LT). Structural and functional analogue of cholera toxin
Heat-stable (ST). Produced in addition to or instead of LT. Similar mode of action
Describe the pathogenesis of EHEC
o Attaching and effacing lesion (similar to EPEC)
o Production of Shiga-like toxins. Structural and functional analogue of Shigella dysenteriae toxin (sometimes strains called STEC [shiga-toxin producing EC] or VTEC [verotoxin-producing EC] because toxins are toxic for cultured vero cells
Clinical features of EHEC
o Incubation 1-7 days o Duration 5-10 days o Bloody diarrhoea with abdominal pain and vomiting o No associated fever o Haemolytic uraemic syndrome (5-10% of cases) Microangiopathic haemolytic anaemia Thrombocytopaenia Acute renal failure
Describe pathogenesis of S.aureus in GI infection
50% of S.aureus produce enterotoxins (types A-E)
Heat stable and acid-resistant protein toxins
Food is contaminated by human carriers
Especially cooked meats, cakes and pastries
Bacteria multiply at room temperature and produce toxins
Describe the two types of disease you can develop from B.cereus
Emetic - commonly results from the re-cooking of rice that has already been boiled. The spores survive the initial boiling and then have time to germinate, multiple and re-sporulate. As they resporulate they produce enterotoxin which survives any subsequent frying.
Diarrhoeal disease - Spores survive cooking and then germinate in the food. They are then ingested and produce a heat-labile toxin in the gut which has a similar action to cholera toxin
Describe the bacillus cereus bacteria
aerobic, spore-forming gram-positive bacilli.
Describe the clinical effects of the two types of B.cereus
Emetic - profuse vomiting with abdominal cramps. Incubation: 30 minutes -6 hours. Duration: 12 -24 hours.
Diarrhoeal - watery diarrhoea with crampy abdominal pain. No vomiting.
Incubation 8 -12 hours
Duration 12 -24 hours
Describe the C.diff bacteria
anaerobic, gram-positive and spore forming bacilli.
Treatment of C.diff
If no severity markers - metronidazole
If 1 or more severity markers - oral vancomycin.
How would you treat a H.pylori infection
triple therapy - PPI, clarithromycin and metronidazole.
