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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
Transmission of shigella
person to person via faecal-oral route
26
Epidemiology of shigella
Diarrhoeal disease in children Humans only reservoir Large outbreaks
27
Control of shigella
humans, so good standards of sanitation and personal hygiene
28
Pathogenesis of shigella
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)
29
Clinical features of shigella
Inital watery diarrhoea followed by bloody diarrhoea Marked, cramping abdominal pain Vomitting is uncommon Fever is usually present
30
Incubation period and duration of shigella
Incubation 1-4 days | Duration 2-3 days
31
Treatment of shigella
usually self-limiting Symptomatic treatment with fluid replacement Some cases of S dysenteriae infection with require treament of renal failure
32
Vibrio cholera microbiology
Comma-shaped gram ngative bacilli Serotypes defned on basis of O-antigens
33
Transmssion of vibrio cholera
food and water lives in freshwater only infects humans
34
Epidiemiology of vibrio cholera
Eoedemic and pandemic cholera
35
Pathogeneiss of vibrio cholera
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
Clinical features of virio cholera
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
Treatment of vibrio cholera
oral or intravenous rehydration is lifesaving Tetracycline antibiotics may have a role in shortening duration f shedding only
38
Specific control point of vibrio cholera
Clean drinking water supply and proper sanitation key preventative measures
39
Escherichia coli microbiology
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
Epidemiology of EPEC
Sporadic cases & outbreaks of diarrhoea in infants & children Cause of some cases of “traveller’s” diarrhoea
41
Pathogeneis of EPEC
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
Clinical features of EPEC
Watery diarrhoea with abdominal pain and vomiting | Often accompanied by fever
43
Incubation period and duration of EPEC
incubation 1-2 days | duration several weekes
44
Microbiology of Enterotoxigenic E coli (ETEC)
Differential routine media unavailable | Test liquid cultures for production of toxins by immunoassays
45
Epidiemiology of ETEC
The major bacterial cause of diarrhoea in infants & children in developing world The major cause of “travellers” diarrhoea
46
Pathogeneis 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
47
Clinical features of ETEC
Watery diarrhoea with abdominal pain and vomiting | No associated fever
48
Incubation period and duration of ETEC
Incubation 1-7 days | Duration 2-6 days
49
Microbiology of EHEC (enterohaemorrhagic Ecoli)
More than 100 serotypes Best known is E.coli O157:H7 O157 is a non-sorbitol fermenter. Sorbitol MacConkey agar (SMAC)
50
Epidiemiology of EHEC
Outbreaks & sporadic cases worldwide (~250 cases/year in Scotland) Large animal reservoirs (esp. cattle & sheep) Persistent in environment
51
Transmission of EHEC
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
Pathogenesis of EHEC
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
Clinical features of EHEC
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
Treatment of all ecoli infections
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
Staph aureus Micro biology
gram-positive cocci | Grow well on routine media
56
Epidemiology & pathogeneiss of staph aureus
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
Clinical features of staph aureus
Profuse vomiting and abdominal cramps | No fever and no diarrhoea
58
Incubation period and duration of staph aureus
Incubation 15 minutes – 6 hours | Duration 12 hours - 1 day
59
Treatment of staph aureus
self-limiting
60
Bacillus cerus micro
Aerobic, spore-forming gram positive bacilli
61
Pathogeneis bacillus cereus
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
Clinical features of bacills cereus
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
Treatment of bacillus cerus
self-limiting
64
Clostridium perfringes micro
Anaerobic, spore-forming gram-positive bacilli
65
Epidiemiology and pathogenesis of clostriudium perfringes
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
Clinical features of clostridium perfringens
Watery diarrhoea and abdominal cramps | No fever and no vomiting
67
Incubation period and duration of clostridium perfringens
Incubation 8 hours -1 day | Duration 12 hours - 1 day
68
Treatment of clostrium perfringens
self-limiting
69
Clostridium botulinium micro
Anaerobic, spore-forming Gram-positive bacilli | Laboratory diagnosis based upon toxin detection
70
Pathogeneis of Colstridium botulinum
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
Clinical features of clostrium botulinum
Neuromuscular blockade results in flaccid paralysis & progressive muscle weakness Involvement of muscles of chest/diaphragm causes respiratory failure High mortality if untreated
72
Treatment of clostridium botulinum
urgent intensive supportive care due to difficulties breathing and swallowing
73
Listeria monocytogenes micro
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
Pathogeneis of listeria monocytogenes
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
Clinical features of listeria monocytogenes
Initial flu-like illness, with or without diarrhoea Majority of cases present with severe systemic infection - Septicaemia - Meningitis
76
Incubation period and duration of monocytogenes
Median incubation period 3 weeks | Duration of illness 1-2 weeks
77
Treatment of listeria
Intravenous antibiotics (usually Ampicillin and synergistic gentamicin) is required

Microbiology (21 decks)

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