Topic 8 Flashcards

1
Q

Human microbiota

A

collection of microbes in/living on us

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2
Q

Human microbiome

A

microbiota and the environment(s) they live in

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3
Q

“Microbial flora”

A

basically used in the same sense as microbiota

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4
Q

Dysbiosis

A

used to describe an altered microbiota that is unhealthy for the host

  • out of balance
  • loss of important commensals
  • increase in microbes associated with disease
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5
Q

What alters the microbiome?

A

diet, exercise, antibiotics, etc.

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6
Q

T or F. Most members of human microbiota are not culturable

A

T, vast majority of out knowledge comes from DNA sequencing (16S, shot gun)

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7
Q

Animal models

A
  • germ-free animals then introduce microbes

- no model is perfect but we learn los from these!

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8
Q

Things we have learned lots about

A
  • Links between microbiota composition and health/disease
  • composition of microbiota – how it changes over time
  • factors influencing composition
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9
Q

Things we know very little about

A
  • community dynamics; how microbes interact
  • whether links b/w microbiota/disease CAUSAL or only correlative
  • potential mechanisms linking microbiota and disease
  • how to introduce a healthy microbiome to an individual with dysbiosis
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10
Q

Mucus

A

thick, slippery suspension that includes antimicrobial factors and mucin (gel-like glycoprotein substance, serves a barrier function)

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11
Q

Gram negative bacteria – masters of complex carbohydrate metabolism

A

Bacteriodetes

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12
Q

Very diverse phylum of gram positive bacteria

A

Firmcutes

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13
Q

Proteobacteria

A
  • generally facultative anaerobes
  • rapidly consume any O2 present
  • important for maintaining anaerobic environment
  • high proportions = dysbiosis?
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14
Q

IBS

A

high proportion of proteobacteria

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15
Q

Primary fermenter in gut microbiota

A
  • many species but especially Bacterioetes

- can ferment diverse carbs from food or mucin

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16
Q

Fermentation products in gut microbiota by primary fermenters

A

some absorbed by short chain fatty acids (host) or feed other microbes (syntrophy)

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17
Q

Probiotic

A

liv microorganisms that when administered, have beneficial effect on host; consuming “ good bacteria”

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18
Q

Prebiotic

A

a substance that when consumed, promotes the growth of beneficial microbes; can be simple and effective (eg: fibre in diet)

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19
Q

T or F. We have neutral/beneficial interactions with the vast majority of microbes we interact with

A

T! although rare, many different bacteria can cause disease (also eukaryotic microbial pathogens); no known archaeal pathogens

20
Q

Infection

A

invasion of body by a disease-causing organism; can be asymptomatic, or can result in different disease (NOT same thing as disease)

21
Q

Disease

A

damage or injury to host organism (overt symptoms); some bacteria cause disease without establishing an infection (TOXINS)

22
Q

Pathogen

A

an organism that causes disease

23
Q

Pathogenesis

A

mechanism that leads to disease

24
Q

Virulence

A

similar to pathogenicity, but often used to describe the severity of the disease (“highly virulent”)

25
Inflammation
body's immune response to infection or injury -- important part of how we clear infections
26
Symptoms of bacterial diseases
- can be from activities of pathgoens (toxins, tissue damage, etc.) - or caused by our immune response to the pathogen (fever, redness, swelling, etc)
27
Adherence: Colonization: Invasion: Spread
Adherence: binding; foothold Colonization: expanding population (planktonic or biofilm) Invasion: gain access to privileged sits ( penetrate mucus membranes) Spread: does not always occur; moving beyond initial site of infection
28
Uncontrolled systematic spread
via bloodstream; often results in very serious infections/disease
29
This is often key to establishing an infection
- adherence; microbes generally target specific cells or tissue types (adhered to specific receptors on cells -- glycoproteins or glycolipids)
30
Adherence factors
- pili, fimbriae, adhesins, surface proteins, capsules
31
Mucous membranes
tightly packed cell layers covered with a mucous layer; important protective layer
32
Invasion
ability of pathogen to enter host cells and/or tissues; penetrate beyond where microbes (microbiota) normally reside
33
Virulence factors
molecules | (typically proteins) produced by a pathogen that contributes to its ability to cause disease
34
Common types of virulence factors
- adhesion factors - nutrient acquisition (siderophores -- capture iron) - immune resistance (eg: resistance to reactive O2 species) - immune evasion/disruption (hides microbe from immune system or disrupts the function of immune system - extracellular enzymes, protein secretion systems/effectors, and toxins that damage host cells and/or manipulate host cell biology
35
DNA polymerase
required for bacteria to cause disease or LIVE so not considered a virulence factor
36
Virulence factors: Immune evasion
- hide inside cells (intracellular) - capsule: hide surface antigens; prevent detection; can be sugar or proteins - some hide pathogen associated molecular patterns (PAMPs) like LPS (triggers immune response)
37
Virulence factors: extracellular enzymes
secreted or surface enzyme that can promote virulence in different ways: - provide free up nutrients - damage host cells - inactivate immune cell mechanisms - disrupt barriers to enable pathogen invasion/spread
38
Streptokinase vs Coagulase
- both secreted enzyme virulence factors - --> Coagulase: induces clots to prevent immune detection (S. aureus) - --> Streptokinase: dissolves clots, enabling pathogen to spread (S. pyogenes)
39
Exotoxins
- similar to bacteriocins, but target host - among the most important virulence factors - we knew about some toxins as soon as we knew about bacteria causing disease - not all produce toxins; some produce multiple
40
Alpha toxin from S. aureus
- polymerize in host cell membrane to form a pore - can have a range of effects: cell lysis to signalling changes - major effect on virulence of S. aureus strains ; this isn't the disease though just less virulent without this
41
AB-type toxins
- target some aspect of biology inside cell; need to cross the host cell membrane - A subunit exerts biological effect; generally, modify or degrade specific molecules (typically host cell protein) - B subunit bind host cell receptor (usually glycolipid/glycoprotein) to mediate uptake - AB5 toxins: pertussis, cholera, O157:H7,
42
C. botulinum
- rarely infects adult humans; but grows/ produce toxins on food we consume - AB-type toxin - B subunit targets motor neurons - A subunit is a protease that cleaves specific NARE proteins that are required by cells to release Ach - absence of Ach --> muscle paralysis - one of the most deadly substances known (0.1 microgram can kill you) - VERY POTENT; game over even if one toxin gets in
43
Toxoids
inactivated toxins as vaccines
44
T or F. toxins can be used to treat non-bacterial disease
T, since they efficiently manipulate human biology in a targeted way ; ex: botox (migraines, cerebral palsy, etc); relaxes muscles
45
Effector proteins vs toxins
Toxins can be produced at a certain site of infection and can act elsewhere Whereas, secretion systems; bacteria has to be present to physically inject Toxins often more potent and ca lone, whereas effectors are part of a bigger biological program
46
Yersinia pestis
- plague - gram neg proteobactrium - rodents; caused by disease vector (fleas -- survives in fleas); humans are incidental or emergency host - person-to-person spread (lice?)
47
Types of plague
- bubonic: infection of lymph nodes - pneumonic: infection of lungs - septicemic plague: bloodstream (rare); bacterial spread ^^ all have high mortality rates is untreated; bubonic most common and pneumonic/septicemic death rates =100% if untreated