Microbiology Flashcards

1
Q

Define microbiome

A

complex mixture of microbes that live in gut

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2
Q

What’s normal flora?

A

on all our surfaces + gut

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3
Q

What’s resident flora?

A

for life, microbial melting pot

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4
Q

What’s transient flora?

A

colonise us but can temporarily be reduced, carried or changed according to factors eg environment

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5
Q

eg a change in transient flora?

A

-baby ->adult
-change from bifidobacter which likes breast milk
-other changes could be stress, hormones, age
-1st baby defacates (sterile meconium)
-change in stools as baby aquires microbial flora
-start with facultative anaerobes
(live anaerobically but can live in oxygen too)
-ends up being strictly anaerobic gut that live in colon
-bifidobacterium is strict anaerobe
-metabolise breast milk sugars that gives itself energy + produces nutrients
-as wean off breast milk
-get adult-like gut microbiota eg bacteroides, clostridia, eubacteria - gram -ve

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6
Q

Features of bifidobacterium?

A
  • Gram +ve
  • Produce lactic acid
  • Prevent growth of Gram -ve
  • Metabolise breast milk sugars
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7
Q

Are gut flora commensal?

A

No one species of gut flora is a commensal but together

flora are commensal (no harm to the host) due to extensive co-evolution.

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8
Q

Percentage of colon gut bacteria?

A

51% Firmicutes
Gram +ve phyla:
Bacillus, Listeria, Staphylococcus, Streptococcus, Enterococcus, Clostridium
48% Bacteriodetes

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9
Q

Why are there microbiome alterations + eg?

A

-Associated with disease states
-Generalised diversity changes + species differences
-Dysbiosis
Crohn’s disease
Inflammatory bowel disease – ulcerative colitis
Irritable bowel syndrome – IBS
Clostridium difficile
Colon Cancer
Allergy
Celiac disease (gluten)
Diabetes – type I and II
Obesity (↓Bacteroidetes/↑Firmicute ratios)
Mental health + depression

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10
Q

Why are there microbiome alterations + eg?

A

-Associated with disease states
-Generalised diversity changes + species differences
-Dysbiosis
Crohn’s disease
Inflammatory bowel disease – ulcerative colitis
IBS
Clostridium difficile
Colon Cancer
Allergy
Celiac disease
Diabetes – type I + II
Obesity (↓Bacteroidetes/↑Firmicute ratios)
Mental health + depression

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11
Q

eg of change in microbiome?

A
  • Faecal transplants
  • Gastric bands –> weight loss, microbiome changes, altered metabolism, bile acid profiles, ↑adipogenesis (heart disease)
  • Duodenal infusion of donor faeces resolves C.difficile infections
  • Weight loss due to ↑Bacteroidetes, ↓Firmicutes
  • Microbiome - age related, sex differences, partner selection + attraction
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12
Q

Defence mechanisms of gut?

A
  • Structural : seamless epithelium, tight junctions, sloughing/turnover
  • Mechanical : peristalsis, chewing, fluid movement
  • Biochemical : gastric acid, bile, mucous
  • Immunological : secretory IgA, intra-epithelial lymphocytes
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13
Q

Problems with defence mechanisms of gut?

A

Problems - Spread of infections to the body

damage of barriers, pH change, overgrowth, AIDS

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14
Q

Benefits of gut flora?

A
  • Colonisation resistance : blocks pathogens
  • Metabolites of benefit to host : Vit K2, B12, organic acids, enhanced utilisation of AA, butyrate for colonocytes – maintain anerobiasis
  • Development of immunity tolerance : antigenic stimulation, Tregs, IL17
  • Digestion : fermentation of sugars (10% of energy), gases H2 or methane, regulation of fat storage
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15
Q

Use of probiotics in medicine?

A
  • probiotic organisms produce lactic + organic acids
  • 10% absorbable energy from dietry fibre
  • ↑ diversity of polysaccharides for metabolism eg beans, Raffinose, Stachyose – non-absorbable
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16
Q

Role of probiotics + eg?

A

organisms we think will contribute to a healthy
biome - produce lactic acid + organic acids
eg Lactobacillus acidophilus, Bifidobacteria - B.longum, Bacterioides thetaiotamicron, Some Streptococci

17
Q

Role of prebiotics + eg?

A

prebiotic nutrients alter gut ecosystem
eg breast milk - ‘bifidus factor’
certain oligosaccharides eg fructo-oligosacchs
fermented in colon by probiotic organisms promotes growth of probiotes

18
Q

Role of microbial antagonism?

A
  • Maintains flora by complex interactions
  • Competition between flora
  • Limits growth of competitors + PATHOGENS
19
Q

Describe how microbial antagonism works

A

Bacteriocins

  • reduced numbers of available epithelial receptors
  • keeps pH low
  • controls oxidative potential (anaerobic growth)
  • limits pathogen growth
  • occupy all niches
  • high numbers
  • waste products
20
Q

What happens if there’s loss of flora?

A

Bacterial or pathogen overgrowth

21
Q

Effect of certain antibiotics eg ciprofloxacin on gut?

A
  • ciprofloxacin antibiotic disrupt microbiome
  • antibiotic associated colitis (inflammation of colon caused by introduction of antibiotics)
  • reduced gut flora + changed it (returns normal in 1 month)
  • overgrowth of clostridium difficile
  • pseudomembranous colitis
22
Q

Effect of clostridium difficile?

A
  • Cytotoxins
  • Ulcerations – inflammation to produce fibrinous coating
  • Severe diarrhoea
  • Serious hospital cross-infection risks (carriage rate up to 70%)
  • Treatable with antibiotics
23
Q

Define diarrhoea

A

watery or liquid stools with an increase in stool weight above 200g daily, increase in daily stool freq, sense of urgency

24
Q

Clinical consequence of diarrhoea?

A
-Severe dehydration :
excessive fluid and electrolyte loss
hypovolaemia; hypokalaemia; 
organ failure
-Long-term morbidity + reduced growth
25
Q

What’s dysentery?

A

Inflammatory disorder of GI tract – large intestine, associated with blood, pus, pain, fever, abdominal cramps

26
Q

Impact of diarrhoeal diseases?

A
  • 3 billion episodes / year
  • 760,000 deaths / year - due to dehydration
  • Under-5’s ; 6–8 episodes / year - global health burden
  • Preventable
27
Q

How do diarrhoeal diseases occur?

A

Infectious : microorganisms, bacteria, viruses, parasites – protozoal + worms
Shed in faeces – transmission to new hosts
Faecal – oral route

28
Q

Pattern of dysentery?

A

Acute or chronic diarrhoea + blood + Pus

29
Q

Pattern of poor fat adsorption?

A

Chronic diarrhoea + or malabsorption

30
Q

Pattern of ano-rectal STIs?

A

Infective proctitis

31
Q

Pattern of ulcers Helicobacter pylori?

A

Dyspepsia (indigestion)

32
Q

Pattern of oesophagus and Candida?

A

dysphagia

33
Q

Damage resulting from GIT infection + eg?

A
  • Pharmacological action of bacterial toxins which have local or distant effects to site of infection eg Cholera
  • Local inflammation from superficial microbial invasion eg shigella dysentery or campylobacter food poisoning
  • Deep invasion to blood, lymphatics, dissemination of organism to other body sites (enetric feevrs) eg typhoid fever, Hep A
  • Perforation/Ulceration of mucosal epithelium, peritonitis, intra-abdominal abscess eg Entamoeba
34
Q

Mechanisms of diarrhoea?

A

-Bacterial toxins : enterotoxins are toxins that affect gut
Exotoxins effect fluid/electrolyte transport by ↑/↓ cAMP
Cytotoxins produce direct cell damage
-Adherence : damage to epithelium eg E.coli EPEC enteropathogenic
-Penetration + invasion : disruption of tissue architecture, function, inflammation

35
Q

Properties of intestinal physiology effected by microbiome?

A
  • Energy balance regulation + pathophysiology of obesity
  • Modulates digestion + absorption ↑ energy harvesting
  • Microbiome influenced by diet, antibiotics, surgery, genes
  • Microbiome contributes to host metabolism +energy homeostasis beyond nutritional processing eg endocrine function + inflammatory signals
36
Q

Features of gut viruses?

A
Astrovirus (star)
Calicivirus (Star of David)
Norwalk (SRSVs)/ Norovirus (ill-defined lacelike)
Poliovirus (featureless)
Rotavirus  (wheel)
37
Q

Effect of enteropathogenic E.coli?

A

Attaching + effacing lesion
Microvillus elongation
Effacement of apical membrane
Pedestal formation