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GIT 303 > Bacteria affecting the GIT > Flashcards

Bacteria affecting the GIT Flashcards

1
Q

Define Gastroenteritis

A

Syndrome characterised by GI-symptoms including nausea, vomiting, diarrhoea and abdominal pain

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2
Q

Define Diarrhoea

A

Abnormal faecal discharge characterised by frequent and/or fluid stool. Associated with increased fluid and electrolyte loss- often disease of small intestine

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3
Q

Define Dysentery

A

Abnormal inflammation of GI-tract: often blood and pus in faeces and pain, fever, abdominal cramps- often disease of large intestine

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4
Q

Define Enterocolitis

A

Inflammation of mucosa of small and large intestine

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5
Q

Defences of the mouth?

A

Flow of liquids
saliva
lysozyme
normal bacterial flora

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6
Q

Defences of the oesophagus?

A

flow of liquids

peristalsis

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7
Q

Defences of the stomach?

A

Gastric Acid pH 1-2

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8
Q

Defences of the small intestine?

A 
flow of gut contents
peristalsis
mucus, bile
secretory IgA
lymphoid tissue
shedding and removal of epi
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9
Q

Defences of the large intestine?

A

Normal flora
peristalsis
shedding and replication of epi
mucus

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10
Q

What is food poisoning?

A

Ingestion of toxins or poisons in food: e.g. bacterial toxins or heavy metals
Bacteria grow and multiply in food
Cooking kills bacteria but toxin still active – intoxication

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11
Q

Staphylococcus aureus in food poisoning?

A

Growth in food after human contamination> mainly dairy, cooked meats
50% of strains produce heat stable enterotoxins - resistant to stomach acid and digestive enzymes
3-6hrs of severe vomiting
Complete recovery

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12
Q

Botulism: Clostridium botulinum in food poisoning?

A

Heat stable toxin ingested in food, leads to flaccid paralysis and death
Infant botulism most common

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13
Q

What is bacillus cereus in?

A

Fried rice - gram positive, heat resistant spore former

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14
Q

What bacteria infects the lower GIT?

A

Ones that resist the low pH of the stomach

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15
Q

What causes gastric ulcers?

A

Helicobacter pylori

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16
Q

How is helicobacter pylori resistant to stomach acid?

A

Produces urease - turns urea to ammonia and co2
= Protective cloud during transit to gastric mucin layer
Ammonia basis of breath test

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17
Q

How to treat diarrhoea?

A

Fluid and electrolyte replacement

Antibiotic treatment often not successful and may worsen problem

18
Q

Why may antibiotic treatment worsen diarrhoea?

A

They wipe out competing organisms or stimulates toxin production

19
Q

Diarrhoea - E.coli features?

A

Gram-negative motile rod
Major cause of diarrhoeal disease and gastroenteritis worldwide
Complications include HUS
Many genetically distinct disease causing strains
Some strains reside in normal commensal flora
Others infect urinary tract and cause meningitis
Diarrhoea: Ingested in food or via fecal-oral transmission route.
Genetic diversity dependent on plasmid, lysogenic phage and transposon encoded ‘pathogenicity islands’

20
Q

How to detect E.coli?

A

Lactose fermentation - MacConkey agar

PCR/antigen tests for serotypes

21
Q

EPEC features?

A

Bundle-forming pili important in attachment
Type III secretion system injects proteins into host to manipulate cytoskeleton:

Tir- translocated intimin receptor
Intimin- mediates intimate attachment to epithelial cells

Attaching and effacing lesion
Leads to watery diarrhoea

22
Q

How does ETEC work?

A

Attach via adhesive pili

Produce Heat Stable (ST) and Labile (LT) enterotoxins (cholera like) that cause diarrhoea

23
Q

What does ETEC commonly cause?

A

Travellers diarrhoea OR Delhi Belly! (No blood) (cholera like in some cases)

24
Q

What does EIEC do? What does it cause?

A

Invade and destroy epithelial cells

Causes bloody diarrhoea

25
Q

EHEC features?

A

Attachment similar to EPEC- pedestals
Produce Vero-toxin (Also called Shigella-like toxin)- STx
STx (verotoxin) is a potent diarrhoeal toxin (and has receptor on kidney cells) acts via damaging cells directly
EHEC infections also cause hemorrhagic colitis- Bloody diarrhoea- destruction of mucosa>bleeding> spread to kidneys
HUS- Haemolytic Urinary Syndrome
-This may lead to kidney failure (15% cases)
- O157:H7 strain most well known

26
Q

Shigella features?

A

Shiga toxin producing (similar to EHEC)
Shigella dysenteriae
– bacillary dysentry, Bloody stools
Shigella sonnei and flexneri
milder forms
Low infectious dose 10-100 cells – sometimes ID50
Non-lactose fermenters (Maconkey agar, Hektoen enteric- green no H2S)
Common in poorer countries
Spread fecal-orally, often via water contamination

27
Q

Salmonella features?

A

Historically most common food-associated pathogen in UK- FORMER NO.1 CAUSE IN UK
Spread from food- mainly chicken and dairy products, but also person to person
Invade M-cells then spread to surrounding epithelium
Usually a severe but self-limiting diarrhoea and enterocolitis

Salmonella enterica subsp. Cause uncomplicated diarrhoea

  • typhimurium
  • enteritidis
28
Q

Lab detection of salmonella?

A

MacConkey agar

Non-lactose fermenter

29
Q

S.typhi features?

A

Cause of typhoid fever
Infection initiates in the intestine
Spreads systemically- transported in macrophages around body
seed many organs before further spread
causes increasing fever over 14 days&raquo_space; GI symptoms
Pre-antibiotics 12-16% died
Complications:
GI lesions and haemorrhage
toxaemia- endocarditis
Meningitis
Vi antigen vaccine recommended for travel
1 – 3 % become carriers &raquo_space; gall-bladder

30
Q

What is the number 1 cause of food poisoning in the UK?

A

Campylobacter spp.

31
Q

Campylobacter spp. features? (also known as helicobacter pylori)

A

Gram-negative micro-aerophiles
Campylobacter jejuni most common
Acquired by ingestion of contaminated food
Major reservoir in Chickens> 75% of all we buy have colonisation
Symptoms like Shigellosis and Salmonellosis:
- ulceration (jejunum), diarrhoea up to 10 movements per day…
- longer lasting illness- up to 3 weeks!
- complications: Guillame Barre and reactive arthiritis

32
Q

What is the number 1 cause of food poisoning worldwide?

A

Cholera

33
Q

What causes cholera?

A

Caused by motile Gram-negative comma-shaped bacterium

34
Q

Cholera prevalence?

A

Estimated 1.3-4 million cholera cases and 21000–140 000 deaths due to cholera every year- mainly developing countries

35
Q

How does the cholera toxin work regarding water flow?

A

ADP-ribosylation of G-protein signalling pathways causes increased secretion of Chloride ions
This prevents influx of Sodium ions into cells
Results in rapid loss of water from tissue- massive diarrhoea
= rapid fluid loss of 1-3 litres per hour

36
Q

How to treat cholera?

A

Rapid fluid and electolyte replacement required or dehydration and death result

37
Q

Symptoms of cholera when severely dehydrated?

A 
Unconscious, floppy
Sunken and dry eyes
Absent tears
V dry mouth and tongue
Drinks poorly or cannot drink 
Skin pinch - goes back very slowly
38
Q

How to prevent cholera?

A

Unsuccessful vaccine

Improve water system and sanitation

39
Q

Where are viral causes of GI infections most likely? How are they spread?

A

Developing countries

Mainly oral-fecal spread

40
Q

Rotavirus features?

A 
Wheel-like viral particle
 Diarrhoea caused by tissue  damage in small intestine
 Dehydration main risk
 Very low-infectious dose
 Very contagious
 V resistant to celaining products
41
Q

Winter virus features?

A

Norovirus (Norwalk viruses) - not cultivated
Chills, headache, fever, nausea, vomiting, v-low infectious doses (10).
recovery in 24 – 48 hours
Common in hospital settings …. Hard to clean away

42
Q

How is the cholera toxin produced?

A

Vibrio cholerae ingested
Large doses needed to cause disease unless on antibiotics and acholorhydric
Sensitive to stomach acid
Small intestine colonisation depends on: motility, production of mucinase attachment to specific receptors
Toxin production
Massive loss of fluid and electrolytes

GIT 303 (2 decks)

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