Microorganisms in the GI Tract in Health and Disease Flashcards

1
Q

what type of bacteria is ‘good’ bacteria

A

commensal

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2
Q

how does a baby receive microbiota from its mother

A

through breastfeeding
contact with skin
from vagina through passage through the birth canal

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3
Q

what can inhibit microbiota passage between a baby and a mother

A

bottle feeding
casaerian section
early/extensive bathing
early life antibiotics

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4
Q

what does our microbiota do for us

A

nutrient extraction from food
terminal postnatal differentiation of mucosal structures
physical barrier function
immune system development
regulation of metabolism
colonisation resistance against pathogens

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5
Q

what do human do for the microbiota

A

supply nutrients and growth
provide protected habitat
provide means for dispersal

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6
Q

what are the two main forms of microbe found in the colon

A

firmicutes - ~55%
bacteroidetes - ~33%

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7
Q

name 4 commensal microbes which are found in the colon that can becomes opportunistic pathogens

A

chlostidium spp.
enteroccocus faecium
bacteroides fragilis
e. coli

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8
Q

def. of pathogen

A

need to cause disease to transmit between hosts (and survive evolutionarily)

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9
Q

do pathogens need to cause symptoms

A

no
can be asymptomatic or mild disease

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10
Q

examples of gut pathogens

A

e. coli
shigella dysenteriae
salmonella typhi
campylobacter jejuni/coli

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11
Q

if zoonotic or environmental pathogens/commensals cause disease is this accidental or necessary for evolutionary survival

A

accidental

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12
Q

what protective factors does the gut have against microbes

A

low pH
low oxygen
flow rate caused by peristalsis
bile salts and digestive enzymes
mucus from goblet cells
intestinal microbiota
tight junctions between epithelial cells
adaptive immune cells

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13
Q

what conditions and drugs can damage the protective factors of out gut against pathogens

A

anatacid drugs - raise pH
appendicitis - stops peristalsis
antibiotics - kills commensal bacteria which makes space for pathogen colonisation
sepsis - causes leakage in epithelium
immunosuppression - suppressive immune response

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14
Q

what is required for an opportunistic pathway to cause infection

A

damage to GI protective mechanisms due to illness or drugs
the pathogen can’t cause damage itself

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15
Q

what mechanisms do obligate pathogens have to overcome the host defences

A

adherence mechanisms
motility
resistance to bile salts and digestive enzymes
toxin production to break through barrier
invasion
avoidance of immune system surveillance (e.g. capsule)

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16
Q

definition of diarhhoea

A

> 3x a day
more than 80% water
300g per 24 hours

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17
Q

what types of diarrhoea are possible as a result of infection

A

secretory
inflammatory

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18
Q

what types of stimulus can cause vomiting

A

neuronal or hormonal

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19
Q

what is secretory diarrhoea

A

secretion or lack of reabsorption of water and electrolytes

20
Q

what is inflammatory diarrhoea

A

release of proteins, blood, WBC, mucus due to inflammation of the epithelium

21
Q

where does helicobacter pylori live

A

(pylorus of) stomach

22
Q

what three adaptations does helicobacter pylori have to allow it to survive in the stomach

A

microaerophile - it doesn’t require much oxygen
motility - spiral shape to corkscrew through to stomach
urease activity - produces ammonia which buffers the H+ and lowers stomach pH

23
Q

what effect does h.pylori have on the stomach

A

causes inflammation - gastritis
and ulcers
chronic inflammation can lead to carcinoma

24
Q

investigation of h.pylori

A

biopsy and histology with gastroscopy - invasive
urea breath test
antigen in stools

25
Q

treatment of h.pylori

A

antibiotics

26
Q

rice water diarhhoea is a sign of

A

vibrio cholerae

27
Q

how is v.cholerae transmitted

A

contaminated water or seafood

28
Q

where does v.cholerae live

A

small intestine

29
Q

v.cholerae virulence factors

A

pili to adhere to mucosa
toxin secretion

30
Q

clinical features of v.cholerae

A

secretory watery diarrhoea (rice water stools)
severe dehydration

31
Q

how is v.cholerae diagnosed

A

clinical picture and stool culture

32
Q

treatment of v.cholerae

A

rehydration (IV if possible)
sometime antibiotics

33
Q

where does shigella spp live

A

large intestine

34
Q

how is shigella transmitted

A

contaminated water or food

35
Q

which has a higher infectious load - cholerae or shigella

A

cholerae - very high
shigella - very low

36
Q

main species of shigella is

A

s.dysenteriae

37
Q

what effect does shigella have on gut

A

it is invasive so causes lots of inflammation of the epithelium

38
Q

clinical features of shigella

A

bacterial dystentery

bloody diarhhoea
abdominal cramps
fever

39
Q

diagnosis of shigella

A

stool culture

40
Q

treatment of shigella

A

supportive
antibiotics

41
Q

how is c.difficile transmitted

A

spores - often in healthcare settings

42
Q

c.difficile virulence factors

A

toxin production

43
Q

clinical features of c.difficile

A

a spectrum of
- asymptomatic carriage
- diarrhoea
- simple colitis (inflammation)
- pseudomembranouse colits
- fulminant colitis
- explosive (inflammatory) diarrhoea

44
Q

diagnosis of c.difficile

A

clinical picture and
stool analysis (toxin, bacteria and culture)

45
Q

c.difficile treatment

A
  • specific antibiotics (metronidazole or vancomycin or fidaxomicin) - can’t use broad Abx as would kill other bacteria and allow c.difficile to take over
  • faecal transplants
  • immunotherapy
46
Q

how can we prevent c.difficile infections

A

infection control - removal of spores from hospital environment
antibiotic stewardship - restriction of antibiotics known to precipitate c.difficile infection