Gastrointestinal infections 1 Flashcards

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1
Q

Bacterial agents in GI infection,

split into two groups according to mechanism by which they cause illness:

(1) - _______
= bacteria develop in ___ after ingestion of contaminated food

Examples: 3
[incubation time ?]

(2) - _________ (poisoning)
= bacteria grow in foods and produce _____

Examples: 2
[incubation time?]

A

Bacterial agents in GI infection,

split into two groups according to mechanism by which they cause illness:

(1) - Infection
= bacteria develop in gut after ingestion of contaminated food

Examples: salmonella, campylobacter, E.coli
[incubation time ~12hr]

(2) - Intoxication (poisoning)
= bacteria grow in foods and produce toxins

Examples: bacillus cereus, staph aureus
[short incubation as toxin already made]

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2
Q

Clinical terminology

Have a think about what each of these are and their symptoms:

Diarrhoea

Gastroenteritis

Dysentery

Enterocolitis

A

Clinical terminology

Diarrhoea

  • increased freq and fluid stool
  • fluid n electrolyte loss

Gastroenteritis

  • inflamm of stomach and intestines
  • nausea, vomiting, diarrhoea, ab discomfort

Dysentery

  • inflamm of large bowel
  • blood and pus in faeces
  • pain, fever, ab cramps

Enterocolitis

  • inflamm affecting small and large bowel
  • diarrhoea, nausea/vomting, ab cramps/pain, fever
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3
Q

Manifestations of GI infection

within GI tract

  • toxin effect
  • inflamm due to microbial invasion

outwith GI tract

  • systemic effects of toxins
  • invasive infection of GI tract with wider dissemination (spread)

Think of an example for each.

A

Manifestations of GI infection

within GI tract

  • toxin effect e.g. severe diarrhoea from cholera
  • inflamm due to microbial invasion e.g. shigellosis (shigella infection) [causes bloody diarrhoea]

outwith GI tract

  • systemic effects of toxins e.g. STEC (Shiga Toxin producing E.Coli)
  • invasive infection of GI tract with wider dissemination (spread)
    e. g. metastatic salmonella infection
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4
Q

Transmission of GI infection

  • faecal-oral

3Fs:

  • Food (farm to fork, cross-contamination in kitchen)
  • fluids (drinking water)
  • fingers (after toilet, preparing food)
  • person-to-person
A

Transmission of GI infection

  • faecal-oral

3Fs:

  • Food (farm to fork, cross-contamination in kitchen)
  • fluids (drinking water)
  • fingers (after toilet, preparing food)
  • person-to-person
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5
Q

Aetiological diagnosis of GI infection can be made from history alone.

True of false.

A

False.

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6
Q

Laboratory diagnosis of GI infection

There are many many normal flora.
Finding pathogen like needle in haystack.

3 approaches:

  • ________ ____ (?)
  • _________ ____ (?)
  • ________ ____ (?)

Best known example of _________ ____ is Salmonella and Shigella on non-lactose fermenter (NLF).

A

Laboratory diagnosis of GI infection

There are many many normal flora.
Finding pathogen like needle in haystack.

3 approaches:

  • Enrichment broth (contains nutrients for preferential growth of pathogen)
  • Selective media (suppress growth of background flora)
  • Differential media (distinguishes different microorgansims on the same plate using colour indicators)

Best known example of Differential media are Salmonella and Shigella on non-lactose fermenter (NLF).

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7
Q

Treatment of GI infections

General points:

  • most/mild GI infections resolve by _________
  • ______ maintenance is crucial

Antibiotics:

  • only for ______/______ symptoms
  • can be bad for it (can prolong/exacerbate symptoms and can be harmful e.g. in ____).
A

Treatment of GI infections

General points:

  • most/mild GI infections resolve by themselves
  • hydration maintenance is crucial

Antibiotics:

  • only for severe/prolonged symptoms
  • can be bad for it (can prolong/exacerbate symptoms and can be harmful e.g. in STEC).
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8
Q

Control of GI infections

  • many pathogens have animal/environmental reservoirs that cannot be eradicated
  • therefore need to ‘break chain’ of infection:

> ______ ____ (clean drinking water, proper sewage disposal)
________ __ ___ ______ (hand hygiene, avoid cross-contam, proper cooking)
___________ __ ___ ___ ____
________ ____ ___ _______ (wash it, peel it, cook it, forget it)

A

Control of GI infections

  • many pathogens have animal/environmental reservoirs that cannot be eradicated
  • therefore need to ‘break chain’ of infection:

> public health (clean drinking water, proper sewage disposal)
education in food hygiene (hand hygiene, avoid cross-contam, proper cooking)
pasteurisation of milk and dairy
sensible travel food practices (wash it, peel it, cook it, forget it)

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9
Q

Campylobacter

think what you know for each one.

Overview: 
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Clinical pres:
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-
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-

A

Campylobacter

Overview:

  • gram -ve bacilli (rods)
  • microaerophilic + thermophilic (42degrees)
  • culture on Campylobacter selective agar
  • C. jejuni most important species

Epidemiology:

  • commonest foodborne bacteria in UK (70% raw chicken)
  • large animal reservoir (poultry, cattle, sheep etc)
  • spread with contaminated food, person-to-person transmission rare

Patho:

  • inflamm, ulceration and bleeding in small+large bowel due to bacterial invasion
  • bacteraemia can occur
  • rarely Guillain-Barre (‘post-infectious demyelination syndrome’ characterised by ascending paralysis)

Clinical:

  • incubation 2-5 days
  • bloody diarrhoea
  • ab cramps/pain
  • fever
  • lasts 2-10 days
  • vomiting not usually a feature

Treatment:

  • fluids
  • clarithromycin for severe
  • quinolone (e.g. ciprofloxacin) or aminoglycoside (gentamicin) for invasive disease

Control points:

  • reduce raw poultry contam
  • fully cook
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10
Q

Salmonella

Think what you know for each one.

Overview:
-
-
-
-
Epidemiology:
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-
-

Clinical pres:
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-
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A

Salmonella

Overview:

  • gram -ve bacilli
  • member of enterobacteriaceae
  • culture on non-lactose fermenters (NLF)
  • XLD agar

Epidemiology:

  • many animal carriers
  • only two not in animals are S.Typhi and S.Paratyphi (cause typhoid fever and paratyphoid fever [these make up enteric fever] )
  • food-borne, in contaminated meat n dairy
  • secondary person-to-person transmission

Patho:

  • diarrhoea due to invasion of epithelial cells in distal small intestine, which also causes inflamm
  • bacteraemia can occur
  • distant organs may establish metastatic foci of infection e.g. osteomyelitis, septic arthritis, meningtis

Clinical pres:

  • incubation 12-72hours
  • watery diarrhoea
  • vomiting common
  • fever (more assoc with invasive disease)
  • lasts 2-7 days

Treatment:

  • fluids usually sufficient
  • antibiotics for severe and bacteraemia (b-lactams, quinolones, aminoglycosides)

Control points:
- immunisation of poultry reduced S.Enteritidis (salmonella. Enteritidis) dramatically

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11
Q

Shigella

Think about what you know for each.

Overview:
- 
-
-
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Epidemiology:
- 
-
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- 

-
-

Clinical pres:
- 
-
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-
-

-
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A

Shigella

Overview:

  • gram -ve bacilli
  • member of enterobacteriaceae
  • 4 species: sonnei (mild), boydii (mod), flexneri (mod), dysenteriae (severe)
  • culture on non-lactosing fermenters (NLF)
  • XLD agar

Epidemiology:

  • diarrhoeal disease common in children
  • humans only reservoir
  • does not persist in environment (unlike V.cholerae)
  • person-to-person spread via faecal oral route (more common and important)
  • contaminated food and water less important

Patho:

  • bacteria attach and colonise mucosal epithelium of terminal ileum and colon
  • systemic invasion is not a feature
  • S.dysenteriae produces Shiga toxin –> damages glomerular endothelium as well as intestinal epith, causes renal failure as part of haemolytic-uraemic syndrome (HUS)

Clinical pres:

  • dysentery (diarrhoea with blood or mucus)
  • incubation 1-3 days
  • duration 2-7 days
  • initially watery diarrhoea followed by bloody diarrhoea
  • marked ab cramps/pain
  • vomiting is uncommon
  • fever

Treatment:

  • fluids
  • usually self-limiting though
  • some S.dysenteriae infection will require renal failure treatment

Control points:
- only in humans so good hygiene

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12
Q

Vibrio cholerae / V.cholerae

Overview:
-
-
-
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Epidemiology:
-
-
-
-

-

-
-

-

OTHER pathogenic Vibrio species

Vibrio parahaemolyticus is a halophilic (likes high salt) bacteria that can cause diarrhoeal disease - contaminated fish in warm coastal waters

A

Vibrio cholerae / V.cholerae

Overview:

  • gram -ve bacilli
  • comma-shaped
  • serotypes defined based on ‘O’ antigens, main ones: O1 and O139
  • culture on sucrose-fermenter (use thiosulphate bile sucrose as differential media)

Epidemiology:

  • causes cholera (severe watery diarrhoea)
  • only infects humans
  • can live in fresh water
  • spreads via contaminated food or water

Patho:

  • flagellae and mucinase facilitate penetration of intestine
  • diarrhoea due to potent protein exotoxin

Clinical pres:

  • severe non-bloody diarrhoea (rice water stool)
  • profound dehydration causes hypokalaemia, metabolic acidosis, hypovolaemic shock and cardiac failure
  • 30-40% mortality in untreated

Treatment:

  • oral or IV rehydration (reduces mortality to <1%)
  • tetracycline (e.g. doxycycline) can reduce duration of shedding

Control point:
- no animal reservoir, only humans, so clean water and sanitation (clean drinking water and disposal of sewage)

OTHER pathogenic Vibrio species

Vibrio parahaemolyticus is a halophilic (likes high salt) bacteria that can cause diarrhoeal disease - contaminated fish in warm coastal waters

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13
Q

Escherichia coli / E.coli

Overview:

  • gram __, ______
  • member of _____________ family (important gut flora members in man and animal, although some strains can cause infection)

SIX DIFFERENT DIARRHOEAL GROUPS OF E.COLI:

- 
-
-
-
-
-

These will be discussed individually on other cards.

Memory aid:
if you take the second letter of each one (e.g. ET-EC would be T) then you can spell ‘pad thai’ (includes D and A from DA-EC)

A

Escherichia coli / E.coli

Overview:

  • gram -ve bacilli
  • member of enterobacteriaceae family (important gut flora members in man and animal, although some strains can cause infection)

SIX DIFFERENT DIARRHOEAL GROUPS OF E.COLI:

  • EP-EC = enteropathogenic E.coli
  • ET-EC = enterotoxigenic E.coli
  • EH-EC = Enterohaemorrhagic E.coli
  • EI-EC = Enteroinvasive E.coli
  • EA-EC = Entero-aggregative E.coli
  • DA-EC = diffuse aggregative E.coli

These will be discussed individually on other cards.

Memory aid:
if you take the second letter of each one (e.g. ET-EC would be T) then you can spell pad thai (includes D and A from DA-EC)

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14
Q

____ = _____________ E.coli

  • diarrhoea in infants and children and traveller’s
  • adherence via pili followed by “attaching and effacing” / A/E lesion which is mediated by intimin protein binding to Tir (translocated intimin receptor)
  • causes disruption of intestinal microvilli
  • incubation 1-2 days, lasts weeks
  • watery diarrhoea with ab pain and vomiting
  • fever
A

EPEC = Enteropathogenic E.coli

  • diarrhoea in infants and children and traveller’s
  • adherence via pili followed by “attaching and effacing” / A/E lesion which is mediated by intimin protein binding to Tir (translocated intimin receptor)
  • causes disruption of intestinal microvilli
  • incubation 1-2 days, lasts weeks
  • watery diarrhoea with ab pain and vomiting
  • fever
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15
Q

____ = ___________ E.coli

  • major bacterial cause of diarrhoea in infants and children and traveller’s
  • diarrhoea due to plasmid-encoded toxins:
    > LT (heat-labile toxin) - analogous to cholera toxin
    > ST (heat-stable toxin) - similar mode of action
  • incubation 1-7 days, duration 2-6 days
  • watery diarrhoea with ab pain and vomiting
  • no fever
A

ETEC = Enterotoxigenic E.coli

  • major bacterial cause of diarrhoea in infants and children and traveller’s
  • diarrhoea due to plasmid-encoded toxins:
    > LT (heat-labile toxin) - analogous to cholera toxin
    > ST (heat-stable toxin) - similar mode of action
  • incubation 1-7 days, duration 2-6 days
  • watery diarrhoea with ab pain and vomiting
  • no fever
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16
Q

____ = ____________ E.coli

  • over 100 serotypes but best known is E.coli ____
  • large animal reservoirs
  • persistent in evironment
  • on contaminated food/water/dairy
  • secondary person-to-person spread also
  • ‘attaching and effacing’ lesion (similar to ____)
  • production of ____-like toxin (sometimes strains are called ____)
  • incubation 1-7 days, duration 5-10 days
  • bloody diarrhoea with ab pain and vomiting
  • Haemolytic Uraemic Syndrome (HUS) - triad of _ _ _
  • commonest cause of acute renal failure in children
A

EHEC = enterohaemorrhagic E.coli

  • over 100 serotypes but best known is E.coli 0157(!!)
  • large animal reservoirs
  • persistent in evironment
  • on contaminated food/water/dairy
  • secondary person-to-person spread also
  • ‘attaching and effacing’ lesion (similar to EPEC)
  • production of Shiga-like toxin (sometimes strains are called STEC = shiga toxin producing E.coli)
  • incubation 1-7 days, duration 5-10 days
  • bloody diarrhoea with ab pain and vomiting
  • Haemolytic Uraemic Syndrome (HUS) - triad of anaemia, thrombocytopenia (low platelets) and renal failure. Shiga-like toxin binds to glomerular epithelium and causes clotting which shreds RBCs.
  • commonest cause of acute renal failure in children
17
Q

More on E.coli infections

____ and ____ are key causes of diarrhoea in children and the developing world. ____ can mimic cholera clinically.

____, ____ and ____ - true extent is unclear.

General treatment:

  • ________
  • ________ not indicated, and even increases risk of HUS in __EC
  • anti-motility agents (ones that slow bowel movements e.g. _________ [______] ) also increase HUS risk
A

More on E.coli infections

EPEC and ETEC are key causes of diarrhoea in children and the developing world. ETEC can mimic cholera clinically.

EIEC, EAEC and DAEC - true extent is unclear.

General treatment:

  • rehydration
  • antibiotics not indicated, and even increases risk of HUS in EHEC
  • anti-motility agents (ones that slow bowel movements e.g. loperamide [Imodium] ) also increase HUS risk
18
Q

Staphylococcus aureus

-

Patho:
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Clinical pres:
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-

A

Staphylococcus aureus

Overview:

  • gram +ve cocci
  • looks like grape bunches

Patho:

  • 50% of s.aureus produce enterotoxins (types A-E)
  • toxins are heat stable and acid-resistant
  • food is contaminated by human carriers
  • affects meats, cakes and pastries
  • bacteria multiply at room temp and produce toxins

Clinical pres:

  • incubation 30mins-6hrs
  • duration 12-24 hrs
  • profuse vomiting and ab cramps
  • no fever, no diarrhoea

Treatment:
- self limiting disease

Control points:

  • Hygienic food prep
  • refrigeration
19
Q

Bacillus cereus

-

Patho:
- 
2 types of disease:
-
-

Clinical pres:

A

Bacillus cereus

Overview:

  • gram +ve bacilli
  • aerobic and spore forming

Patho:
- spores and vegetative cells contaminate food
2 types of disease:
- Emetic disease (fried rice, spores survive boiling and produce heat stable toxin during storage - which survives further frying)
- Diarrhoeal disease (spores multiply in food and survive cooking, heat labile toxin [one that is inactivated by high temps] is produced in the gut)

Clinical pres:

  • Emetic disease = incubation 30min-6hrs, duration 12-24hrs, profuse vomiting and ab cramps with watery diarrhoea, no fever
  • Diarrhoeal disease = incubation 8-12 hrs, duration 12-24hrs, watery diarrhoea with ab cramps but no vomiting and no fever

Treatment:
- self-limiting

20
Q

Clostridium difficile / C.diff

Overview:
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(^all clostridiums the same for first two)
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Patho:
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Clinical pres:
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Treatment:
-
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Pics in folder for c.diff

A

Clostridium difficile / C.diff

Overview:
- gram +ve bacilli
- anaerobic, spore forming
(^all clostridiums the same for first two)
- spores resistant to heat/drying/disinfection/alcohol
- clinical features due to toxins A and B

Patho:

  • spores and vegetative cells ubiquitous in environment
  • many asymptomatic carriers
  • infection requires disruption of normal gut flora
  • antibiotics risk this and PPIs can contribute too
  • mainly affects elderly
  • major cause of healthcare associated infections

Clinical pres:

  • ab pain
  • pseudomembranous colitis (colon inflamm)
  • severe n sudden cases can dilation and perforate colon (can be fatal)
  • relapse common

Treatment:

  • stop precipitating antibiotics
  • oral metronidazole (foltate synth inhib) for mild
  • oral vancomycin for severe
  • faecal transplant for reccurrent disease

Pics in folder for c.diff

21
Q

Clostridium perfringens

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(^all clostridiums the same for first two)

Patho:
-
-
-
-

-

A

Clostridium perfringens

Overview:
- gram +ve bacilli
- anaerobic and spore forming
(^all clostridiums the same for first two)

Patho:

  • spores an vegetative cells ubiquitous in soil and animal gut
  • contaminated foods, often meat
  • spores survive cooking, then germinate to form organism which multiply in cooling food
  • organisms ingested and produce enterotoxin in large intestine

Clinical pres:
- incubation 6-24hrs, duration 12-24hrs, watery diarrhoea and ab cramps , no fever no vomiting

Treatment:
- self limiting

Control:

  • rapid chilling/freezing of bulk cooked foods
  • thorough re-heating
22
Q

Clostridium botulinum

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(^all clostridiums the same for first two)

Patho:
-
-
-
3 types:
-
-
-

-
-

-

Control points:
-
-
-
-
A

Clostridium botulinum

Overview:
- gram +ve bacilli
- anaerobic, spore-forming
(^all clostridiums the same for first two)

Patho:
- uncommon in UK
- spores and vegetative cells ubiquitous in soil and animal gut
- heat labile toxin neurotoxin (A,B,E cause human disease)
3 types:
- foodborne botulism = pre-formed toxin in food (common with improperly processed canned foods)
- infant botulism = organisms germinate in gut of babies and then toxins produced in gut
- wound botulism = organism produce toxin in wound which travels in bloodstream to block neuromuscular junction in peripheral nerves

Clinical pres:

  • flaccid paralysis and muscle weakness
  • respiratory failure if involvement of diaphragm
  • high mortality in untreated

Treatment:

  • intensive supportive care to continue breathing
  • antitoxin

Control points:

  • proper manufacturing in canned foods
  • hygienic food prep
  • proper cooking
  • refrigeration
23
Q

Listeria monocytogenes

Patho:
-
-
-
-

-
-

-

-

A

Listeria monocytogenes

Overview:
- gram +ve coccobacilli

Patho:

  • widespread in animals and environment
  • small cases, high mortality
  • contaminated food (milk, soft cheese, meats, fish, coleslaw)
  • can go from gut to systemic infection

Clinical pres:

  • incubation 3 weeks, duration 1-2 weeks
  • initial flu-like illness, may or may not have diarrhoea
  • majority of cases present with severe systemic infection –> septicaemia and meningitis

Treatment:

  • IV antibiotics
  • usually ampicillin [penicillin] and synergistic gentamicin [aminoglycoside]

Control points:

  • use by dates
  • wash raw fruit and veg to avoid cross-contamination
24
Q

Helicobacter pylori / h.pylori

Overview:
-
-
-
- diagnosis:
Patho:
-
-
-
-
-

-
-

-

A

Helicobacter pylori / h.pylori

Overview:

  • gram -ve spiral shaped bacilli
  • microaerophilic [need oxygen, but are poisoned by high levels]
  • urease enzymes
  • diagnosis: faecal antigen or urea breath test

Patho:

  • one of the most common bacterial infections in the world
  • 70% developing, 30-40% developed world
  • faecal-oral or oral-oral
  • humans are only reservoir
  • life long infection unless treated

Clinical pres:

  • infection asymptomatic unless peptic ulceration develops
  • causes most duodenal ulcers and most gastric ulcers
  • gastric cancer risk

Treatment:

  • combined treatment: PPI and antibiotic (clarithromycin [a macrolide, protien synth inhib] and metronidazole [folate synth inhib]
  • these eradicates carriage and facilitates ulcer healing