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Hannah Nichols
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Cards (39)
factors used to classify gram positive bacilli
endospore forming
- shape and
staining
- type of irregular shape or stain
why need acid fast stain for mycobacterium
no all bacteria stain well with gram stain, waxy
cell wall
doesn't allow stain to
penetrate
spores
highly
resistant
forms of
bacteria
that form when environmental conditions are adverse (non viable, non replicating)
bacillus anthracis
spore forming gram
positive
bacilli. causes
anthrax
disease (inhaled, ingested or contaminate food) = skin sores, vomitting, septic shock
bacillus cereus
spore forming gram
positive bacilli.
common cause of food poisoning, more serious in
immunocompromised
people
diphtheria
toxin mediated, membrane on
throat
and bullock,
vaccine
preventable
microbiome
microbial
community that occupies a well defined
habitat
dysbiosis
an imbalance in the
microbial
community associated with
disease
causes of dysbiosis
overgrowth of commensals,
loss
of commensals,
loss
of diversity
determinants
of
microbiota
environmental
parameters, interactions between microbes, rapid
evolution
, unpredictable forces
negative interaction between microbes
bacteria produce
antibiotics
that
inhibit
the growth of competing bacteria
positive
microbes interaction
crossfeeding
how measure microbiota
DNA,
RNA
production (activity),
proteins
(being produced by bacteria), metabolite
other factors influencing gut microbiome
genetics, exercise,
location
, mode of delivery, diet,
antibiotics
, age
role of gut microbiome -
positive
digestions
, helps immune system, pathogen clearance,
brain development
negative effects gut microbiome
allergy
and
metabolic
syndromes
diet high low high fibre
human enzymes can't break down
polysaccharides
, fermented by
gut bacteria
in colon= microbiota associated with metabolic health
untargeted microbiome interventions
exercise,
nutrition
,
faecal microbiota transplant
targeted microbiome interventions
prebiotics
, probiotics, synbiotics,
postbiotics
prebiotics
compound
metabolised
by and promotes healthy
gut
bacteria
probiotics
ingesting the bacteria themselves
postbiotics
taking
downstream
product of healthy
gut
microbiome
TB non infected people and death p.a
30%
worlds population infected with
latent
TB, 1.4 million deaths
risk for TB
poverty
,
overcrowding
- has killed more people than any other infection
acquisition of TB infection
has no animal or environment reservoir, direct human to human via
aerosol spread
TB
infectious
dose
very
low
1-10
bacteria
TB adhesion
small droplet
nuclei
enter terminal airspaces of
lung
, phagocytes by alveolar macrophages, live within them and spread around body
TB pathogenicity
largely due to host inflammatory reaction to the bacterium which causes
tissue destruction
(lungs -
abnormal immune response
as can't kill bacteria)
latent
TB
after initial immune control of bacteria - can stay contained, be eliminated or if exposed to immune insult 10% will reactive into active TB
primary TB infection
unable to control by innate or
adaptive
immune response = active TB in
macrophages
multidrug therapy
prevent emergence of
resistant strains
as a consequence of
chance mutations
in chromosome
therapeutic manipulation of microbiota
antibiotics
- kill some bacteria,
faecal oral
transplant helps to outcompete bad bacteria
where is clostridium difficile found
in faeces of neonates and 30% hospital patients, they have a
disrupted gut microbiome
and in
spores
in environment
why neonates risk of clostridium difficile infection
low density of
gut
bacteria, rapid colonised with it and dominates - if it has to compete with other bacteria can't colonised
gut
what do toxin producing strain of clostridium cause
antibiotic associated diarrhoea
(during/after use) can be mild to severe and most severe form is
colon ulcers
what is clostridium difficile disease a result of
disruption to
gut microbiome
treatment for clostridium difficile infection
first
antibiotics
to kill the bacteria, if severe faecal transplant to restore
gut
microbiome and outcompete
why asymptomatic c.difficile infection?
have
flora
competing with the bacteria,
bile acids
and IgA to inhibit its growth
why symptomatic c.difficile infection?
antibiotics killed flora,
proton pump
inhibits acid secretion, toxins break down
colon epithelium