Microbiota 1,2,3 Flashcards

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1
Q

define microbiota

A

assemblage of MOs present in a defined environment

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2
Q

define the human microbiota

A

The total microbial community that resides both on and within us.

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3
Q

what is the bacteria: host cell ratio?

A

1.3:1

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4
Q

does the bacteria: host cell ratio vary?

A

yes depending on when you’ve been to the toilet

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5
Q

explain the sterile womb hypothesis?

A

the initial host colonisation
human womb is sterile- no microbes unless there’s a complication
acquisition occurs during the birth process
vaginal microbiota and/or skin and surrounding environment is involved in the initial colonisation

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6
Q

is the womb sterile?

A

yes unless there’s complications

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7
Q

what’s involved in initial colonisation of children?

A

vaginal and/or skin microbiota from mother

surrounding environment

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8
Q

what is the alternative theory to sterile womb hypothesis?

A

in utero colonisation

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9
Q

what is in utero colonisation

A

womb isn’t sterile and is colonised by gram negative bacteria- likely to be contaminants

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10
Q

what evidence is there for in utero colonisation

A

enterobacter and escherichia DNA found in amniotic fluid

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11
Q

when does the microbiota reach a climax community?

A

3 years of age

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12
Q

what is development of the microbiota based on?

A

environment e.g. sun exposure
diet- breast milk or formula?
antibiotic exposure in infancy

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13
Q

TF: microbiota acts as a metabolic organ?

A

true

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14
Q

2 most important phyla in the GIT?

A

Fimicutes and bacterodetes

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15
Q

do people all have the same amounts of Fimicutes and bacterodetes

A

no- large sis

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16
Q

3 ROLES OF GUT MICROBIOTA IN HEALTH?

A
  1. induction of intestinal angiogenesis
  2. colonisation resistance
  3. metabolism of carbohydrates and proteins
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17
Q

what is induction of intestinal angiogenesis?

A

development of villus capillary network

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18
Q

example of a bacteria which contributes to induction of intestinal angiogenesis?

A

bacteroides thetaiotaomicron

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19
Q

explain 3 ways in which bacteria in the colon contribute to colonisation resistance

A

takes up the available surface meaning that any new pathogens cant attach and cause complications

also use food for energy- use up nutrients so there’s less for invading pathogens

change the pH- make organic acids which can infer growth inhibition for pathogens

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20
Q

explain the role of bacteria in carbohydrate and protein metabolism

A

simple sugars can be non digestible so need bacteria to digest

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21
Q

example of non-digestible carbohydrates?

A

cellulose, resistant starch, inulin

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22
Q

what type of foods make it to the later stages of the gut?

A

greens

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23
Q

where are simple carbohydrates broken down by bacteria?

A

in the early stages of the gut- this is where the necessary bacteria reside

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24
Q

examples of short chain fatty acids produced by the bacteria? what effects do these have?

A

butyrate
propionate
acetate

anti-inflammatory and anti-carcinogenic

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25
Q

summary of link between microbiota and obesity in mice?

A
  • Gut microbiota of obese phenotype (Ob) associated with fewer Bacteroidetes phylum- balance was more in favour of finicetes. But when compared to lean phenotype (Ln) it was more 50:50
  • Co-habitation of Ln and Ob mice altered metabolic profile to a lean-like state. Why?
  • Mice are coprophagic- eat their own poo- so if you put them on the same diet in a mixed cage. The Ob was consuming the Ln faeces- colonising itself which altered metabolic profile to a lean like state.
  • Increasing the Bacteroidetes in the diet= reduction in its food consumption. The altered gut microbiota was changing the amount of food the mouse needed.
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26
Q

in the obese phenotype mice, which was more prevalent: bacteroidetes or finicetes?

A

BACTEROIDETES

27
Q

in the lean phenotype which was more prevalent: bacteroidetes or finicetes?

A

50:50

28
Q

why did co-habition of Ln and Ob mice alter the metabolic profile of the Ob to the lean- like state?

A

mice are coprophagic- eat their own poo

the Ob was consuming the Ln faeces- colonising itself with altered its profile to the lean like state

29
Q

increasing bacteroidetes in the diet does what to food consumption?

A

reduces its food consumption

30
Q

could you eat a diet of fast food and then introduce the lean phenotype microbiota?

A

no, still need a balanced diet- as the bacteria associated with the lean phenotype needs the indigestible carbohydrates from the diet

31
Q

what is the effect of introducing SC fatty acids to someone?

A

reduced appetite

32
Q

how can you ensure the SCFA’s make it to the end of. the gut to be broken down?

A

tag it to inulin

33
Q

can microbiota composition influence host response to a drug?

A

yes, enzymatic alteration of drug structure may affect toxicity, F or bioactivity

34
Q

example: how can the microbiota affect levodopa treatment?

A

Ldopa is made into dopamine by decarboxylase enzymes
Decarboxylase mediated drug metabolism by Enterococcus faecalis- can generate a bacterial decarboxylase enzyme- drug was being converted into dopamine before crossing BBB- so there were side effects
- Reduced drug availability and cardiac/GI complications- cardiac arrythmias

35
Q

what is dysbiosis

A

imbalance in the normal host microbiota- can be caused by environmental stress which deters the normal community

36
Q

what does dysbiosis lead to a loss of?

A

commensal microbiota

loss of bacterial diversity

37
Q

gram stain and shape of C.diff

A

gram positive rods

38
Q

TF: C.diff is spore forming

A

yes which can persist for days- years

39
Q

C.diff respiration?

A

obligate anaerobe- doesn’t like oxygen which is good for living in the distal intestine

40
Q

C.diff gut commensal % in adults and children

A

adults: 3%
children: 75%

41
Q

when does the children’s composition of C.diff start to change?

A

tends to decrease after the year of 5

42
Q

what is C.diff the major identifiable cause of?

A

AB associated diarrhoea

43
Q

clinical manifestations of C.diff

A

mild to severe diarrhoea

pseudomembranous colitis in rare cases

44
Q

what can pseudomembranous colitis lead to?

A

toxic mega colon

45
Q

main risk factors of C.diff?

A

over 65

AB consumption

46
Q

what type of AB is heavily associated with C.diff onset

A

3rd generation cephalosporins

47
Q

mechanisms by which the commensal bacteria stop C.diff growth?

A

breakdown and cleaving of sugars which produces silica acids and SCFAs for nutrients for their growth
taking primary bile acids and converting them to secondary bile acids which inhibit C.diff growth

48
Q

why does +AB cause C.diff growth

A

loss of commensal microbiota yet there’s still members producing SCFAs and silica acid which C.diff can use to grow
no secondary bile acid production- loss of antimicrobial factor
increased primary bile acids

49
Q

what affect does the increased primary bile acids have on C.diff

A

known to promote spore germination- BAD

50
Q

effect of C.diff on epithelial integrity?

A

produces toxins which is endocytose into the cell and causes breakdown of Tight junctions and decreases integrity

51
Q

why are tight junctions important in the GIT

A

stop movement of components between the cell layer- no longer selective

52
Q

what toxin does virulent C.diff produce? what does this do?

A

binary toxin- affects actin polymerisation
Taken up by endocytosis and enzymatically target actin P, this is needed for cytoskeleton- changes cell shape- protrusions on the cell surface which are rich in fibronectin- increases adherence of C.diff to the surface of the host cell

53
Q

affect of binary toxin?

A

affects actin polymerisation

54
Q

what is pseudomembranous colitis? what is it a result of

A

inflammation of the colon
dead cells accumulate on the surface and form yellowy pseudomembranes
result of epithelial damage

55
Q

how is pseudomembrane colitis diagnosed?

A

detection of C.diff toxins

colonoscopy in more rare cases

56
Q

symptoms of psudomembranous colitis

A

diarrhoea- bad smell due to toxin
abdominal pain
fever

57
Q

what is SIGHT?

A

prevention!
Suspect that a case is infective- coiuld be non-infective diarrhoea due to laxatives etc
Isolation
Gloves and aprons- barrier precautions
Hand washing- alcohol hand gel doesn’t affect spores
Test stool for toxin

58
Q

management of C.diff in mild disease?

A

don’t always need ABs
manage the effects of dehydration
if need AB: metronidazole 400mg TDS

59
Q

mild disease AB If needed?

A

metronidazole 400MG TDS

60
Q

moderate disease treatment?

A

oral metronidazole 400-500mg TDS

61
Q

severe disease treatment?

A

oral vancomycin 125mg QDS

fidaxomicin

62
Q

non AB strategies against C.diff?

A

decal microbiota transplant- uncommon in UK

probiotics

63
Q

Success of FMT

A

92% of cases

64
Q

problems with FMT?

A

lacks standardised approach

long term health indications?