Unit IV: Bacteria Flashcards

1
Q

Structural Features of Bacteria (5)

A

Cell Wall (peptidoglycan)
Capsule (polysaccharides, increased virulence)
Glycocalyx (biofilms for adherence, protection)
Flagella (H antigens)
Pili

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2
Q

Different Membrane Compositions

A

Gram Positive: thicker peptidoglycan layer without a second cell wall, teichoic and lipoteichoic acids

Gram Negative: thin peptidoglycan w/ second lipid bilayer including lipopolysaccharides

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3
Q

Peptidoglycan

A

n-acetylglucosamine and n-acteylmuramic acid subunits w/ varying sidechains
Can be cross-linked or covalently linked to phospholipids

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4
Q

Lipopolysaccharides

A

Lipid A, core polysaccharide, O side chian

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5
Q

Teichoic Acid

A

covalently linked to peptidoglycan and extend beyond layer, involved in adherence

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6
Q

4 phases of bacterial growth phase

A

Lagging Phase: adjustment phase of new enzyme production.
Exponential phase: maximal cell division for resources available, growth proportional to # of cells (constant doubling time
Stationary Phase: essential nutrients consumed, toxic metabolites produced, growth slows
Death Phase: number of viable bacteria decreases via autolysis

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7
Q

5 Classifications of Bacteria

A

Aerobes: require oxygen, cannot ferment
Anaerobes: ferment and are killed in oxygen
Indifferent: ferment w/ or w/o oxygen
Facultative: respires w/ O2, ferments w/o
Microaerobic: grow best at low O2, but can grow w/o

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8
Q

Heterotrphic vs autotrophic

A

Heterotrophs require any form of carbon, Autotrophs require CO2 as source of carbon

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9
Q

Fermentation

A

use organic compounds as electron donors and acceptors with no net oxidation of substrates in both aerobic and anaerobic conditions

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10
Q

Respiration

A

ATP generated through electron transport with O2 as final electron acceptor.

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11
Q

Energy currencies

A

Higher cells generate energy currency in the form of ATP and electrochemical gradients.
Currency can also include electron holders (NADPH)

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12
Q

Antimicrobial targets (4)

A

Cell wall, inner and outer plasma membranes, protein synthesis, nucelic acid synthesis

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13
Q

3 Sources of Bacterial Genetic Diversity

A

Spontaneous Mutation
Recombination
Acquisition of New DNA

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14
Q

Spontaneous Mutation

A

PMs, insertions, or deletions
Very rare but can give growth advantage
(ABX resistance Pseudomonas/Myco and Strep Pyogenes invasiveness)

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15
Q

Recombination

A

site-specific or homologous recombination
occurs w/in an organism or between organisms
Includes phase variation through promoter changes

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16
Q

Acquisition of New DNA

A

Incorporation of free DNA into chromosome or plasmid

Transposons, bacteriophage, plasmid acquisition, pathogenicity islands

17
Q

Transformation

A

Naked DNA from lysing cells taken up by bacteria in correct growth phase in correct environment
Most common between similar species

18
Q

Tranduction

A

gene transfer via bacteriophage, bacterial DNA taken up by bacteriophage and injected into new bacterium

19
Q

Conjugation

A

F plasmid contains information for conjugation (replication, sex pilus, conjugative transfer, integration), DNA replicated into recipient cell and then incorporated into plasmid or genome

20
Q

Temperate Phage

A

Cause lysogenic response in addition to lytic response. Creates prophage that suppresses viral gene expression via repressor protein until it experiences stress.

21
Q

Lysogenic Conversion

A

Prophage in lysogenic phase obtains new phenotype

22
Q

Microbial Toxins

A

macromolecular products that alter cell structure or function. Manifest as symptoms of disease or contribute to pathogenesis w/o specific signs
Include bacterial proteins and LPS of gram negatives

23
Q

Steps to determine toxin is pathogenic

A

Toxin causes same symptoms as bacteria
Antitoxin prevents symptoms
Virulence corresponds to amount of toxin
Nontoxigenic mutants are a-virulent

24
Q

Mechanisms of action for microbial toxins (5)

A
Facilitating Spread of Microbes
Damage Cellular Membrane
Stimulating Cytokine Production
Inhibiting Protein Synthesis
Modifying Intracellular Signaling
25
Q

Facilitating Spread

A

toxic enzymes break down ECM (hyaluronidase/collagenase/etc.)

26
Q

Damaging Membranes

A

called hemolysins, actually cytolysins
toxins insert in membrane via recognized marker and form pore to lyse cell
Lecithinases degrade membrane components

27
Q

Stimulating Cytokine Production

A

Superantigens are potent T cell activators that bind MHC II to TCR outside of antigen pocket indiscriminantly of epitope presence. Also pyrogenic exotoxins.
Causes secretion of cytokines

28
Q

Inhibiting Protein Synthesis

A
Exotoxin A (pseudomonas/diphtheria): ribyltransferases inactivate EF2
Shiga/Ricin: RNA N-glycosidases that inactivate 60s ribosome
29
Q

Heat-Labile Enterotoxin

A

Vibrio Cholerae and E Coli

ADP Ribyltransferases increase cAMP by adding to the Gs protein. Active chloride secretion, diarrhea

30
Q

Pertussis Toxin

A

ADP ribyltransferase increase AC activity by inactivating Gi protein, increases cAMP

31
Q

Heat-Stable Enterotoxin

A

E Coli

Activates GC, increases cGMP

32
Q

Anthrax Edema Factor

A

Increase cAMP but requries calmodulin and calcium

33
Q

Anthrax Lethal Factor

A

Endopeptidase that cleaves Map Kinase Kinase and inactivates them.

34
Q

Clostridium Difficile Toxins A and B

A

Glucosyl transferaes alter actin cytoskeleton by transferring glucose from UDP-glucose to several Rho GTPases and inactivating them

35
Q

Inhibitors of NT release (2)

A

Botulinum toxin: flaccid peralysis via ACh

Tetanus: zinc-dependent, SNARE inactivator, stops inhibitory neurons

36
Q

2 Types of Microbial Toxins

A

Extracellular and Intracellular

37
Q

Extracellular Toxins

A

Act on PMs w/ wide variety of structure and function, specificity is only determined by target

38
Q

Intracellular Toxins

A

Must cross plasma membrane

  • bifunctional: activity and binding domains
  • use typical membrane markers as receptors (proteins or glycolipids)
  • Enter by endocytosis then enter cytosol (translocation domain)