Microorganisms in the GI Tract in Health and Disease Flashcards

(46 cards)

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
treatment of h.pylori
antibiotics
26
rice water diarhhoea is a sign of
vibrio cholerae
27
how is v.cholerae transmitted
contaminated water or seafood
28
where does v.cholerae live
small intestine
29
v.cholerae virulence factors
pili to adhere to mucosa toxin secretion
30
clinical features of v.cholerae
secretory watery diarrhoea (rice water stools) severe dehydration
31
how is v.cholerae diagnosed
clinical picture and stool culture
32
treatment of v.cholerae
rehydration (IV if possible) sometime antibiotics
33
where does shigella spp live
large intestine
34
how is shigella transmitted
contaminated water or food
35
which has a higher infectious load - cholerae or shigella
cholerae - very high shigella - very low
36
main species of shigella is
s.dysenteriae
37
what effect does shigella have on gut
it is invasive so causes lots of inflammation of the epithelium
38
clinical features of shigella
bacterial dystentery bloody diarhhoea abdominal cramps fever
39
diagnosis of shigella
stool culture
40
treatment of shigella
supportive antibiotics
41
how is c.difficile transmitted
spores - often in healthcare settings
42
c.difficile virulence factors
toxin production
43
clinical features of c.difficile
a spectrum of - asymptomatic carriage - diarrhoea - simple colitis (inflammation) - pseudomembranouse colits - fulminant colitis - explosive (inflammatory) diarrhoea
44
diagnosis of c.difficile
clinical picture and stool analysis (toxin, bacteria and culture)
45
c.difficile treatment
- 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
how can we prevent c.difficile infections
infection control - removal of spores from hospital environment antibiotic stewardship - restriction of antibiotics known to precipitate c.difficile infection