GI infections Flashcards

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1
Q

Name the two mechanisms by which bacteria that cause GI infections can be classified into

A

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

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2
Q

Diarrhoea

A
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
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3
Q

Gastroenteritis

A

o Nausea, vomiting, diarrhoea and abdominal discomfort

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4
Q

Dysentery

A

o Inflammatory disorder of the large bowel
o Blood and pus in faeces
o Pain, fever and abdominal cramps

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5
Q

Enterocolitis

A

o Inflammatory process affecting small and large bowel

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6
Q

how is campylobacter infection spread

A

via contaminated food

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7
Q

Describe the campylobacter bacteria

A

gram-negative bacilli. They are microaerophillic and thermophillic.

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8
Q

Give the clinical effects of campylobacter infection

A
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
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9
Q

Describe pathogenesis of campylobacter infection

A

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

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10
Q

How would you treat campylobacter infection

A

Fluids, clarithromycin in severe/resistant cases. You would give quinolones or an aminoglycoside if the disease was invasive.

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11
Q

what species causes the majority of salmonella infection

A

Salmonella enterica

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12
Q

Describe the salmonella bacteria

A

Gram negative bacilli. Non-lactose fermenters

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13
Q

How is Salmonella generally acquired

A

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.

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14
Q

Describe pathogenesis of salmonella infection

A

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.

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15
Q

Clinical features of salmonella infection

A
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
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16
Q

Treatment of Salmonella

A

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

17
Q

Describe the shigella bacteria

A

Gram negative bacilli. Non-lactose fermenters. Has four species.

18
Q

How is shigella transmitted?

A

faecal-oral route is the most common. Humans are only reservoir and large outbreaks can occur. Associated with a low infectious dose.

19
Q

Pathoegenesis of shigella

A

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)

20
Q

Four types of shigella

A

 Shigella sonnei associated with milder infections
 Shigella boydii & S.flexneri associated with more severe disease
 Shigella dysenteriae associated with most severe disease

21
Q

Clinical features of shigella infection

A
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
22
Q

Treating shigella

A

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

23
Q

Describe the Cholera bacteria

A

gram negative bacilli, sucrose-fermenter.

Classified on the basis of their O antigens.

24
Q

How does cholera spread?

A

Spreads via contaminated food or water. Can cause pandemics. Is endemic in parts of SE Asia, S America
Person to person transmission is uncommon

25
Q

Pathogenesis of cholera

A

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

26
Q

Clinical features of cholera

A

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%

27
Q

treatment of cholera

A

o Prompt oral or intravenous rehydration is lifesaving (mortality reduced to <1%)
o Tetracycline antibiotics may shorten duration of shedding

28
Q

Describes the pathogenesis of enteropathogenic E.coli

A

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

29
Q

What is a major bacterial cause of diarrhoea in infants & children in developing world and travellers diarrhoea?

A

ETEC

30
Q

Summaries pathogenesis of ETEC

A

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

31
Q

Describe the pathogenesis of EHEC

A

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

32
Q

Clinical features of EHEC

A
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
33
Q

Describe pathogenesis of S.aureus in GI infection

A

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

34
Q

Describe the two types of disease you can develop from B.cereus

A

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

35
Q

Describe the bacillus cereus bacteria

A

aerobic, spore-forming gram-positive bacilli.

36
Q

Describe the clinical effects of the two types of B.cereus

A

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

37
Q

Describe the C.diff bacteria

A

anaerobic, gram-positive and spore forming bacilli.

38
Q

Treatment of C.diff

A

If no severity markers - metronidazole

If 1 or more severity markers - oral vancomycin.

39
Q

How would you treat a H.pylori infection

A

triple therapy - PPI, clarithromycin and metronidazole.