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Microbiology > Introduction > Flashcards

Introduction Flashcards

1
Q

How does the human microbiome protect against pathogens (name 3)?

A
  1. Competition for nutrients and colonization sites
  2. Production of antimicrobial molecules
  3. Intact microbiome is important for development of gut-associated immune system
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2
Q

What is the role of the microbiome in metaboilsm (name 4)?

A
  1. Degradation of complex carbohydrates
  2. Production of short-chain fatty acids
  3. Synthesis of Vit K and oflic acid
  4. Converison of bile acids
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3
Q

How is the human microbiome studied?

A

DNA extraction from stool sample.

  • 16S rRNA gene sequencing > bacterial genera
  • total DNA sequencing > bacterial species

Small molecule extration.
MS > metabolits

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4
Q

Where is most of the human microbiome localized?

A

99% in colon.

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5
Q

Which phlya are dominant in colon?

A

Bacteroidetes, Proteobacteria, Actinobacteria, Firmicutes

mostly obligate anaerobes

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6
Q

How does gut microbiome vary?

A

Correlations are found with: nutrition, body weight, age (diversity decreases in elderly), host lifestyle, host genotype, host immune system, geographic origin,…

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7
Q

How can gut communitties be classified?

A

Classification into several stable Enterotypes, associated with long-term diet.

  • Proteins/saturated FA > Bacteroides
  • Carbohydrates > Prevotella
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8
Q

What is dysbiosis? Consequence?

A

Microbial imbalance.
Ass. with diabetes/colon cancer/antibiotic treatment/etc.
» Pathogenic bacteria like Clostridium difficile can colonize the gut and cause disease

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9
Q

How can gut symbiosis be restored

A

Functional foods, fibers.

Fecal microbioate transplantation.

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10
Q

Define pathogenicity.

A

Potential of a pathogen to cause disease (binary term!)

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11
Q

Define virulence. How can it be quantified?

A

Quantitative term describing severity of disease (mortality rate: 1-100%) > varies

LD50, ID50

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12
Q

Define LD50.

A

Lethal dose of microbes that will kill 50% of experimentally inoculated test animals

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13
Q

Define ID50.

A

Infectious dose required to cause disease in 50% of inoculated test animals

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14
Q

What is an obligate pathogen?

A

High virulence. Capable of establishing disease in a previously healthy individual with intact immunological defence.
Normally not ass with host.

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15
Q

What is an opportunistic pathogen?

A

Low virulence. Cause disease only when defense is impaired (eg by disease/treatment)
Can be part of the microbiome.

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16
Q

How can virulence factors vary?

A

Virulence depends on the equipment with virulence factors (toxins, adhesions, capsule).
Virulence varies not only from species to species, but also between strains within one species.
Usually pathogens possess more than one virulence factor.
Different combinations of virulence factors can cause different types of diseases.

17
Q

What are pathogenomics?

A

Understanding of evolution and diversity of pathogens.

Also in smaller time scales.

18
Q

What 3 forces drive diversity in bacterial genomes?

A

gene gain, gene loss, gene change

19
Q

Core genome

A

Essential genes of a species that are shared by all strains within this species.
(dispensable: in some strains, unique: in only one strain)

20
Q

What do virulence factors enable bacteria to do (4)?

A

Colonization of the host.
Obtain nutrients from the host.
Evasion of host defenses.
Damage the host (ie by toxins).

21
Q

What are aspects of host colonization (4)?

A

adherence, changing location, adaptation, quorum sensing

22
Q

What are challenges of adherence?

A

Needed to avoid physical and immunological removal. Pathogens have to compete with normal flora for attachment sites.

23
Q

How do bacteria adhere? (where, with what)

A

Bacteria adhere to: cell surfaces and extrazellular matrix (eg in GI tract), solid surfaces (eg teeth), other bacteria (biofilm).

Bacteria adhere via: fimbriae (direct binding to host structures, molecular bridging via eg fibronectin), surface/outer membrane proteins, capsular slime (polysaccharides).

24
Q

Why do bacteria need to change location?

A

Finding the right ecological niche requires motility and ability to deal with barriers

25
Q

How do E. coli move?

A

Flagellar motility. Petrichous flagellar organization (multiple aorund cell).
Bundle formation > run phase
Bundle dissolved > tumbling phase

26
Q

How does bacterial chemotaxis work?

A

Gradient > modulation of run phase duration.

Ligand binds to chemoreceptor > conformation change > histidine kinase (CheA) becomes phosphorylated > CheA transfers phosphate to tranducer protein (CheY) > phosphorylated transducer interacts with flagellar motor

27
Q

How do bacteria deal with barriers (3 examples)?

A

Transmigration through epithelial cells (Shigella flecneri: M cell > DC > epith. cell).
Tolerating the low pH in stomach (Helicobacter pylori: cleaves urea into ammonia > secretion).
Secretion of destructive enzymes (hyaluronidases, collagenases, etc)

28
Q

Are virulence factors regulated? Why?

A

The expression of many virulence factors is regulated (to avoid immediate immune response) > timing is important

29
Q

What is quorum sensing?

A

Changing behavior in response to bacterial density > once threshold level is reached, changes in gene expression occur.
Bacteria use quorum sensing to coordinate processes as virulence, biofilm formation, antibiotic production, sporulation, competence.

30
Q

What is an example of nutrient acquisition from host?

A

Iron scavenging (most bacteria need iron).

31
Q

How do bacteria squire iron?

A

Siderophores chelate (bind) available iron and transport it into bacteria.

Iron can be scavenged direct from host iron-binding proteins eg by lactoferrin-binding proteins.

(Iron-abstinence: rare)

32
Q

How do bacteria evade innate immunity (3)?

A 
Survive stress (oxidative, heat).
Evade cationic antimicropbial peptides (CAMPs).
Phagocytosis resistance (capsule!).
33
Q

How do bacteria evade CAMPs?

A

CAMPs: positive net charge > attracted to negative bacterial cell wall.
Bacteria: introduce positive charges.
Gram-pos: D-Alanin into teichonic acids
Gram-neg: modification of Lipid A

34
Q

How do bacteria evade adaptive immunity (3)?

A 
Antigen mimicry (prevents IgG production).
Antigenic variation (sequential expression of antigenically different but functionally conserved molecules).
Protein A of S. aureus (prevents IgG binding).
35
Q

How do bacteria damage the host? (3 compounds)

A

Toxins,

hemolysins, superantigens

Microbiology (10 decks)

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