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Microbiology > Microbiota 1,2,3 > Flashcards

Microbiota 1,2,3 Flashcards

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
summary of link between microbiota and obesity in mice?
* 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.
26
in the obese phenotype mice, which was more prevalent: bacteroidetes or finicetes?
BACTEROIDETES
27
in the lean phenotype which was more prevalent: bacteroidetes or finicetes?
50:50
28
why did co-habition of Ln and Ob mice alter the metabolic profile of the Ob to the lean- like state?
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
increasing bacteroidetes in the diet does what to food consumption?
reduces its food consumption
30
could you eat a diet of fast food and then introduce the lean phenotype microbiota?
no, still need a balanced diet- as the bacteria associated with the lean phenotype needs the indigestible carbohydrates from the diet
31
what is the effect of introducing SC fatty acids to someone?
reduced appetite
32
how can you ensure the SCFA's make it to the end of. the gut to be broken down?
tag it to inulin
33
can microbiota composition influence host response to a drug?
yes, enzymatic alteration of drug structure may affect toxicity, F or bioactivity
34
example: how can the microbiota affect levodopa treatment?
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
what is dysbiosis
imbalance in the normal host microbiota- can be caused by environmental stress which deters the normal community
36
what does dysbiosis lead to a loss of?
commensal microbiota | loss of bacterial diversity
37
gram stain and shape of C.diff
gram positive rods
38
TF: C.diff is spore forming
yes which can persist for days- years
39
C.diff respiration?
obligate anaerobe- doesn't like oxygen which is good for living in the distal intestine
40
C.diff gut commensal % in adults and children
adults: 3% children: 75%
41
when does the children's composition of C.diff start to change?
tends to decrease after the year of 5
42
what is C.diff the major identifiable cause of?
AB associated diarrhoea
43
clinical manifestations of C.diff
mild to severe diarrhoea | pseudomembranous colitis in rare cases
44
what can pseudomembranous colitis lead to?
toxic mega colon
45
main risk factors of C.diff?
over 65 | AB consumption
46
what type of AB is heavily associated with C.diff onset
3rd generation cephalosporins
47
mechanisms by which the commensal bacteria stop C.diff growth?
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
why does +AB cause C.diff growth
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
what affect does the increased primary bile acids have on C.diff
known to promote spore germination- BAD
50
effect of C.diff on epithelial integrity?
produces toxins which is endocytose into the cell and causes breakdown of Tight junctions and decreases integrity
51
why are tight junctions important in the GIT
stop movement of components between the cell layer- no longer selective
52
what toxin does virulent C.diff produce? what does this do?
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
affect of binary toxin?
affects actin polymerisation
54
what is pseudomembranous colitis? what is it a result of
inflammation of the colon dead cells accumulate on the surface and form yellowy pseudomembranes result of epithelial damage
55
how is pseudomembrane colitis diagnosed?
detection of C.diff toxins | colonoscopy in more rare cases
56
symptoms of psudomembranous colitis
diarrhoea- bad smell due to toxin abdominal pain fever
57
what is SIGHT?
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
management of C.diff in mild disease?
don't always need ABs manage the effects of dehydration if need AB: metronidazole 400mg TDS
59
mild disease AB If needed?
metronidazole 400MG TDS
60
moderate disease treatment?
oral metronidazole 400-500mg TDS
61
severe disease treatment?
oral vancomycin 125mg QDS | fidaxomicin
62
non AB strategies against C.diff?
decal microbiota transplant- uncommon in UK | probiotics
63
Success of FMT
92% of cases
64
problems with FMT?
lacks standardised approach | long term health indications?

Microbiology (19 decks)

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