Gastrointestinal infections Flashcards

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1
Q

Intoxication

A

microbial intoxication does not require ingestion microbes: just their biologically active toxins. These are usually protein exotoxins

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2
Q

Infection

A

disease due to ingestion of live microbes

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3
Q

Diarrhoea definition

A
  • Abnormal frequency and/or fluid stool
  • Usually indicates small bowel disease
  • Causes fluid and electrolyte loss
  • Severity varies widely from mild self-limiting to severe/fatal
    a. Virulence of organism
    b. Degree of compromise of the host
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4
Q

Gastroenteritis definition

A

Nausea, vomiting, diarrhoea and abdominal discomfort

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5
Q

Dysentery definition

A

inflammatory disorder of the large bowel
blood and pus in faeces
Pain, fever, and abdominal cramps

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6
Q

Enterocolitis

A

inflammatory process affecting small and large bowel

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7
Q

Where can GI infections arise

A

Within GI tract (GIT)

  • Toxin effects e.g. cholera
  • Inflammation due to microbial invasion e.g. shigellosis

Outwith GIT

  • Systemic effect of toxins e.g. STEC
  • Invasive infection of GIT with wider dissemination e.g. metastatic salmonella infection
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8
Q

Transmission of GI infection

A

3 F’s

  • Food (contaimination farm to fork, cross contaimination: domestic kitchen)
  • Fluids (water, juice)
  • Fingers (importance of washing hands, after toileting)

Person-person transmission (infectious dose, ability to contaminate and persist in the environment)

Faecal-oral (any means by which infectious organisms from human/animal faecces can gain access to GIT of another susceptible host)

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9
Q

Diagnosis of GI infection

A

History

  • Aetiological diagnosis cannot be made from history alone
  • However may get useful clues
    a. Vomiting, abdominal pain, diarrhoea, frequency and nature of symptoms, travel history, food history, other affected individuals, speed of onset of illness, blood in stools

Examination
-Abdominal, fever, features of dehydration

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10
Q

Laboratory diagnosis of GI infection

A

Enrichment media
-Liquid culture media containing nutrients that promote preferential growth of the pathogen

Selective media
-Liquid or solid media that suppress growth of background flora while allowing growth of the pathogen being sought

Differential media
-Solid media which distinguishes mixed microorganisms on the same plate. Uses biochemical characteristics of microorganisms growing in presence of specific nutrients combined with an indicator that changes colour. Best known examples are Salmonella and Shigella species which are non-lactose fermenters (NLF).

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11
Q

Campylobacter microbiology

A

Gram negative bacilli

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12
Q

Campylobacter transmission

A

Contaiminated food (poultry), milk or water

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13
Q

Campylobacter epidiemiology

A

Commonest bacerial foodbourne infection in UK

Peak in may and september

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14
Q

Pathogenesis of Campylobacter

A
  1. inflammation and ulceration and bleeding of large and small bowel
  2. bactermeia can occur - spread into bloodstream
  3. post infectious demyelination syndrome e.g Guillian barre syndrome, characterised by ascending paralysis
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15
Q

Clinical features of campylobacter

A

Bloody diarrhoea
Cramping abdominal pain
Vomiting is not usually a feature
Fever

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16
Q

Incubation period and duration of campylobacter

A

2-11 days

duration 3 days - 3 weeks

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17
Q

Treatment of campylobacter

A

Symptomatic
-adequate fluid replacmeent

Severe/persistent
-clarithromycin

Invasive
-quinolone (ciprofloxaine) or aminoglycoside (gentamicin) or invasive

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18
Q

Salmonella microbiology

A

Gram negative bacilii (member f enterobacteriacae)

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19
Q

Transmission of salmonella

A

Contaiminated food, pork, poultry and other meat

Secondary - via person-person

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20
Q

Pathogenesis of salmonella

A
  1. Diarrhoea due to invasion of epithelial cells in the distal small intestine, and subsequent inflammation
  2. Bacteraemia -spread into the bloodstream (extremes of age, immunocompromised)
  3. Bacteraemia causes -. osteomyelitis, septic arthritis, meningitis etc.
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21
Q

Clinicall features of salmonella

A

Watery diarrhoea
Vomiting is common
Fever can occur, and is usually associated with more invasive disease

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22
Q

Incubation period and duration of salmonella

A

incubation - 6hrs-2 days

duration 2-7 days

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23
Q

Treatment of salmonella

A

Symptomatic
-fluid replacement

Severe infections and bacteraemia
-beta lactams, quinolones or aminoglycosides

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24
Q

Shigella micro

A

Gram negative bacilli (memmber of the enterobacteriacae

4 species
mild- s . sonnei
moderate-severe - S boydii, S flexneri
most severe - S. dysenteriae

NO animal reservoir

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25
Q

Transmission of shigella

A

person to person via faecal-oral route

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26
Q

Epidemiology of shigella

A

Diarrhoeal disease in children

Humans only reservoir

Large outbreaks

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27
Q

Control of shigella

A

humans, so good standards of sanitation and personal hygiene

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28
Q

Pathogenesis of shigella

A
  1. organisms attach to and colonise mucosal epithelium of terminal ileum and colon
  2. systemic invasion not a feature
    3, S dysenteriae - produces a potent exotoxin (Shiga toxin) which not only damages intestinal epithelium but in some patients targets glomerular endothelium causing renal failure as part of haemolytic-uraemic syndrom (HUS)
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29
Q

Clinical features of shigella

A

Inital watery diarrhoea followed by bloody diarrhoea
Marked, cramping abdominal pain
Vomitting is uncommon
Fever is usually present

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30
Q

Incubation period and duration of shigella

A

Incubation 1-4 days

Duration 2-3 days

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31
Q

Treatment of shigella

A

usually self-limiting

Symptomatic treatment with fluid replacement

Some cases of S dysenteriae infection with require treament of renal failure

32
Q

Vibrio cholera microbiology

A

Comma-shaped gram ngative bacilli

Serotypes defned on basis of O-antigens

33
Q

Transmssion of vibrio cholera

A

food and water

lives in freshwater

only infects humans

34
Q

Epidiemiology of vibrio cholera

A

Eoedemic and pandemic cholera

35
Q

Pathogeneiss of vibrio cholera

A
  1. polar flagellae and mucinance penterate intestinal mucous
  2. attachment to mucosa by specific receptors
  3. diarrhoea due to production of a potent protein exotoxin
36
Q

Clinical features of virio cholera

A

Severe, profuse, non-bloody, watery diarrhoea (rice water stool)

Profound fluid loss & dehydration precipitates hypokalaemia, metabolic acidosis, hypovolaemic shock and cardiac failure

Untreated mortality 30-40%

37
Q

Treatment of vibrio cholera

A

oral or intravenous rehydration is lifesaving

Tetracycline antibiotics may have a role in shortening duration f shedding only

38
Q

Specific control point of vibrio cholera

A

Clean drinking water supply and proper sanitation key preventative measures

39
Q

Escherichia coli microbiology

A

Gram-negative bacilli
members of the enterobacteiaea

Six different diarrhoeagenic groups of E.coli have been described

Different serogroups and serotypes are described on the basis of “O” and “H” antigens

40
Q

Epidemiology of EPEC

A

Sporadic cases & outbreaks of diarrhoea in infants & children
Cause of some cases of “traveller’s” diarrhoea

41
Q

Pathogeneis of EPEC

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

42
Q

Clinical features of EPEC

A

Watery diarrhoea with abdominal pain and vomiting

Often accompanied by fever

43
Q

Incubation period and duration of EPEC

A

incubation 1-2 days

duration several weekes

44
Q

Microbiology of Enterotoxigenic E coli (ETEC)

A

Differential routine media unavailable

Test liquid cultures for production of toxins by immunoassays

45
Q

Epidiemiology of ETEC

A

The major bacterial cause of diarrhoea in infants & children in developing world
The major cause of “travellers” diarrhoea

46
Q

Pathogeneis 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

47
Q

Clinical features of ETEC

A

Watery diarrhoea with abdominal pain and vomiting

No associated fever

48
Q

Incubation period and duration of ETEC

A

Incubation 1-7 days

Duration 2-6 days

49
Q

Microbiology of EHEC (enterohaemorrhagic Ecoli)

A

More than 100 serotypes
Best known is E.coli O157:H7
O157 is a non-sorbitol fermenter. Sorbitol MacConkey agar (SMAC)

50
Q

Epidiemiology of EHEC

A

Outbreaks & sporadic cases worldwide (~250 cases/year in Scotland)
Large animal reservoirs (esp. cattle & sheep)
Persistent in environment

51
Q

Transmission of EHEC

A

Consumption of contaminated food, water and dairy products & direct environmental contact with animal faeces e.g. petting zoos
Secondary person-to-person spread important (associated with low infectious dose)

52
Q

Pathogenesis of EHEC

A
  1. Attaching and effacing lesion (similar to EPEC)
  2. 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
53
Q

Clinical features of EHEC

A

Bloody diarrhoea with abdominal pain and vomiting

No associated fever

Haemolytic uraemic syndrome (5-10% of cases)

  • Microangiopathic haemolytic anaemia
  • Thrombocytopaenia
  • Acute renal failure

E.coli O157 infection is the commonest cause of acute renal failure in children in the UK

54
Q

Treatment of all ecoli infections

A

Adequate rehydration important
Antibiotics not indicated, and in the case of EHEC may increase risk of HUS
Antimotility agents also increase HUS risk with EHEC

55
Q

Staph aureus Micro biology

A

gram-positive cocci

Grow well on routine media

56
Q

Epidemiology & pathogeneiss of staph aureus

A
  1. 50% of S.aureus produce enterotoxins (types A-E)
  2. Heat stable and acid-resistant protein toxins
  3. Food is contaminated by human carriers
  4. Especially cooked meats, cakes and pastries
  5. Bacteria multiply at room temperature and produce toxins
    `
57
Q

Clinical features of staph aureus

A

Profuse vomiting and abdominal cramps

No fever and no diarrhoea

58
Q

Incubation period and duration of staph aureus

A

Incubation 15 minutes – 6 hours

Duration 12 hours - 1 day

59
Q

Treatment of staph aureus

A

self-limiting

60
Q

Bacillus cerus micro

A

Aerobic, spore-forming gram positive bacilli

61
Q

Pathogeneis bacillus cereus

A

2 types of disease

Emetic disease
- “fried rice”- survive initial boiling, if rice is cooked and stored prior to frying, the spore germinate, multiply and re-sporulate

Diarrhoeal disease

  • spores in food survive cooking, germinate and orgnisms multiply in food
  • ingested organisms produce a heat-labile toxin in teh gut with similar mode of action to cholera
62
Q

Clinical features of bacills cereus

A

Emetic disease

  • Incubation 15 minutes - 4 hours
  • Duration 12 hours-2 days
  • Profuse vomiting with abdominal cramps and watery diarrhoea
  • No fever

Diarrhoeal

  • Incubation 8-12 hours
  • Duration 12 hours-1 day
  • Watery diarrhoea with cramping abdominal pain, but no vomiting
  • No fever
63
Q

Treatment of bacillus cerus

A

self-limiting

64
Q

Clostridium perfringes micro

A

Anaerobic, spore-forming gram-positive bacilli

65
Q

Epidiemiology and pathogenesis of clostriudium perfringes

A
  1. Spores & vegetative cells ubiquitous in soil and animal gut
  2. Contaminated foodstuff (usually meat products)
  3. Often involves bulk-cooking of stews, meat pies
  4. Spores survive cooking, germinate and organisms multiply in cooling food
  5. Food inadequately re-heated to kill organisms
  6. Organisms ingested & sporulate in large intestine with production of enterotoxin
66
Q

Clinical features of clostridium perfringens

A

Watery diarrhoea and abdominal cramps

No fever and no vomiting

67
Q

Incubation period and duration of clostridium perfringens

A

Incubation 8 hours -1 day

Duration 12 hours - 1 day

68
Q

Treatment of clostrium perfringens

A

self-limiting

69
Q

Clostridium botulinium micro

A

Anaerobic, spore-forming Gram-positive bacilli

Laboratory diagnosis based upon toxin detection

70
Q

Pathogeneis of Colstridium botulinum

A
  1. spores and vegetative cells ubiquitos in soil and animal GIT
  2. Produces powerful heat-labile toxin protein neurotoxin
  3. Absorbe toxins spread via the blood stream and enter peripheral nerve
  4. Block Ach and causes descending paralysis
71
Q

Clinical features of clostrium botulinum

A

Neuromuscular blockade results in flaccid paralysis & progressive muscle weakness
Involvement of muscles of chest/diaphragm causes respiratory failure
High mortality if untreated

72
Q

Treatment of clostridium botulinum

A

urgent intensive supportive care due to difficulties breathing and swallowing

73
Q

Listeria monocytogenes micro

A

Gram-positive coccobacilli
Selective culture media available for culture from suspect foods
Can be grown on standard laboratory media from blood and CSF samples

74
Q

Pathogeneis of listeria monocytogenes

A
  1. Widespread among animals and the environment
  2. Pregnant women, elderly and immunocompromised
  3. Overall number of cases small, but mortality high
  4. Infection associated with contaminated foods, especially unpasteurised milk and soft cheeses, pate, cooked meats, smoked fish, and coleslaw
  5. Outbreaks occur associated with contaminated ready to eat foods and produce
  6. Can multiply at 4oC
  7. Invasive infection from GIT results in systemic spread via bloodstream
75
Q

Clinical features of listeria monocytogenes

A

Initial flu-like illness, with or without diarrhoea

Majority of cases present with severe systemic infection

  • Septicaemia
  • Meningitis
76
Q

Incubation period and duration of monocytogenes

A

Median incubation period 3 weeks

Duration of illness 1-2 weeks

77
Q

Treatment of listeria

A

Intravenous antibiotics (usually Ampicillin and synergistic gentamicin) is required