Microorganisms in the GI Tract in Health and Disease Flashcards
what type of bacteria is ‘good’ bacteria
commensal
how does a baby receive microbiota from its mother
through breastfeeding
contact with skin
from vagina through passage through the birth canal
what can inhibit microbiota passage between a baby and a mother
bottle feeding
casaerian section
early/extensive bathing
early life antibiotics
what does our microbiota do for us
nutrient extraction from food
terminal postnatal differentiation of mucosal structures
physical barrier function
immune system development
regulation of metabolism
colonisation resistance against pathogens
what do human do for the microbiota
supply nutrients and growth
provide protected habitat
provide means for dispersal
what are the two main forms of microbe found in the colon
firmicutes - ~55%
bacteroidetes - ~33%
name 4 commensal microbes which are found in the colon that can becomes opportunistic pathogens
chlostidium spp.
enteroccocus faecium
bacteroides fragilis
e. coli
def. of pathogen
need to cause disease to transmit between hosts (and survive evolutionarily)
do pathogens need to cause symptoms
no
can be asymptomatic or mild disease
examples of gut pathogens
e. coli
shigella dysenteriae
salmonella typhi
campylobacter jejuni/coli
if zoonotic or environmental pathogens/commensals cause disease is this accidental or necessary for evolutionary survival
accidental
what protective factors does the gut have against microbes
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
what conditions and drugs can damage the protective factors of out gut against pathogens
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
what is required for an opportunistic pathway to cause infection
damage to GI protective mechanisms due to illness or drugs
the pathogen can’t cause damage itself
what mechanisms do obligate pathogens have to overcome the host defences
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)
definition of diarhhoea
> 3x a day
more than 80% water
300g per 24 hours
what types of diarrhoea are possible as a result of infection
secretory
inflammatory
what types of stimulus can cause vomiting
neuronal or hormonal
what is secretory diarrhoea
secretion or lack of reabsorption of water and electrolytes
what is inflammatory diarrhoea
release of proteins, blood, WBC, mucus due to inflammation of the epithelium
where does helicobacter pylori live
(pylorus of) stomach
what three adaptations does helicobacter pylori have to allow it to survive in the stomach
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
what effect does h.pylori have on the stomach
causes inflammation - gastritis
and ulcers
chronic inflammation can lead to carcinoma
investigation of h.pylori
biopsy and histology with gastroscopy - invasive
urea breath test
antigen in stools
treatment of h.pylori
antibiotics
rice water diarhhoea is a sign of
vibrio cholerae
how is v.cholerae transmitted
contaminated water or seafood
where does v.cholerae live
small intestine
v.cholerae virulence factors
pili to adhere to mucosa
toxin secretion
clinical features of v.cholerae
secretory watery diarrhoea (rice water stools)
severe dehydration
how is v.cholerae diagnosed
clinical picture and stool culture
treatment of v.cholerae
rehydration (IV if possible)
sometime antibiotics
where does shigella spp live
large intestine
how is shigella transmitted
contaminated water or food
which has a higher infectious load - cholerae or shigella
cholerae - very high
shigella - very low
main species of shigella is
s.dysenteriae
what effect does shigella have on gut
it is invasive so causes lots of inflammation of the epithelium
clinical features of shigella
bacterial dystentery
bloody diarhhoea
abdominal cramps
fever
diagnosis of shigella
stool culture
treatment of shigella
supportive
antibiotics
how is c.difficile transmitted
spores - often in healthcare settings
c.difficile virulence factors
toxin production
clinical features of c.difficile
a spectrum of
- asymptomatic carriage
- diarrhoea
- simple colitis (inflammation)
- pseudomembranouse colits
- fulminant colitis
- explosive (inflammatory) diarrhoea
diagnosis of c.difficile
clinical picture and
stool analysis (toxin, bacteria and culture)
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
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
