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MICRB 265 > Topic 8 > Flashcards

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
Q

Inflammation

A

body’s immune response to infection or injury – important part of how we clear infections

26
Q

Symptoms of bacterial diseases

A
  • can be from activities of pathgoens (toxins, tissue damage, etc.)
  • or caused by our immune response to the pathogen (fever, redness, swelling, etc)
27
Q

Adherence:
Colonization:
Invasion:
Spread

A

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
Q

Uncontrolled systematic spread

A

via bloodstream; often results in very serious infections/disease

29
Q

This is often key to establishing an infection

A
  • adherence; microbes generally target specific cells or tissue types (adhered to specific receptors on cells – glycoproteins or glycolipids)
30
Q

Adherence factors

A
  • pili, fimbriae, adhesins, surface proteins, capsules
31
Q

Mucous membranes

A

tightly packed cell layers covered with a mucous layer; important protective layer

32
Q

Invasion

A

ability of pathogen to enter host cells and/or tissues; penetrate beyond where microbes (microbiota) normally reside

33
Q

Virulence factors

A

molecules

(typically proteins) produced by a pathogen that contributes to its ability to cause disease

34
Q

Common types of virulence factors

A
  • 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
Q

DNA polymerase

A

required for bacteria to cause disease or LIVE so not considered a virulence factor

36
Q

Virulence factors: Immune evasion

A
  • 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
Q

Virulence factors: extracellular enzymes

A

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
Q

Streptokinase vs Coagulase

A
  • both secreted enzyme virulence factors
  • –> Coagulase: induces clots to prevent immune detection (S. aureus)
  • –> Streptokinase: dissolves clots, enabling pathogen to spread (S. pyogenes)
39
Q

Exotoxins

A
  • 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
Q

Alpha toxin from S. aureus

A
  • 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
Q

AB-type toxins

A
  • 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
Q

C. botulinum

A
  • 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
Q

Toxoids

A

inactivated toxins as vaccines

44
Q

T or F. toxins can be used to treat non-bacterial disease

A

T, since they efficiently manipulate human biology in a targeted way ; ex: botox (migraines, cerebral palsy, etc); relaxes muscles

45
Q

Effector proteins vs toxins

A

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
Q

Yersinia pestis

A
  • 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
Q

Types of plague

A
  • 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

MICRB 265 (6 decks)

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