Exam One Flashcards

1
Q

Sequence the Ames Test. What does it test for?

A

Tests for mutagenic substances.

rat liver extract, histidine-auxotroph salmonella, suspected mutagen cultured on a disk that does not contain histidine

mutation rate measured by the number of salmonella that survive without histidine

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2
Q

List some examples of bacteria that are virulent because of the introduction of toxin-encoding genes by phages

A

Vibrio cholerae – cholera toxin

E coli – shigalike toxin, causing hemorrhagic diarrhea

Clostridium botulinum – botulinum toxin

Corneybacterium diptherine – diptheria toxin

Streptococcus pyogenes – erythrogenic toxin – scarlet fever

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3
Q

What are aponenzymes and holoenzyme?

A

Aponenzyme – enzyme that needs a cofactor

Holoenzyme – enzyme coupled with cofactor

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4
Q

What is the rate of division in E coli, mycobacterium tuberculosis, M. leprae?

A

E coli - 20 min
Mycobacterium tuberculosis - 15-20h
M. leprae - 14 days

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5
Q

What are the four phases of bacterial growth called?

A

Lag, log, stationary, death

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6
Q

What % salt can halotolerant bacteria tolerate?

What % salt do halophilic bacteria prefer?

A

Halotolerant - 10%

Halophilic marine bacteria - 3%
Extreme halophiles - 9% +

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7
Q

What are microaerophiles?

A

Need some oxygen but not a whole load

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8
Q

What are the four temperature preference bacterial classes?

A

Psychrophiles - 0-20 celsius
Mesophiles - 15-40 celsius
Thermophiles - 40-80 celsius
Hyperthermophiles - 60+ celsius

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9
Q

Discuss the relationshiop of helicobacter pylori and vibrio cholerae to PH

A

H. Pylori - not acidophile but acid tolerant, and produces urease

V. Cholerae - survives up to PH 9!

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10
Q

Describe the structure of peptidoglycan

A

Two layers of glycan, made of alternating NAG / NAM subunits

Linked by 2x tetrapeptide chains and a peptide interbridge, built with transpeptidase

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11
Q

How do penicillin, cephalosoprin, lysozomes mess with peptidoglycan?

A

Cephalosporin, penicillin – inhibit transpeptidase

Lysozomes - cleave glycan backbone

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12
Q

Why are cephalosporin and penicillin less effective in gram negative bacteria?

A

Gram negative have less peptidoglycan

Also peptidoglycan hidden behind lipid bilayer outer membrane – inhibits access!

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13
Q

Discuss the cell wall of a gram +ve bacterium, outside in

A
  • Peptidoglycan and telchoic acid trees, in gel-like material (rigid)
  • Cytoplasmic membrane
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14
Q

Discuss the cell wall of a gram -ve bacterium, outside in

A
  • LPS
  • Outer membrane – lipid bilayer, with porins for small molecules
  • Thin layer of peptidoglycan in periplasm
  • Cytoplasm
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15
Q

How does LPS affect the body?

A

Presence triggers immune response

Lipid A = endotoxin – large release causes fever, sepsis

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16
Q

Discuss the structure of LPS, top down

A

O antigen – used to identify spp/strain
Core
Lipid A at bottom

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17
Q

What are the two classes of glycocalces? What are they composed of?

A

Capsule – distinct, gelatinous
Slime layer – diffuse, irregular

Both composed of glycolax and some proteins

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18
Q

What are the functions of glycocalces?

A
  • Protective against phagocytosis [unless opsonized]

- Allows adhesion and formation of biofilm on intert surfaces, e.g. rocks, dental plaque

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19
Q

What are the three classes of flagella?

A

Monotrichous - one flagellum
Lophotrichous – multiple flagella from one place
Petritrichous – many flagella from many places

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20
Q

What are axial filaments?

A

Flagella in periplasmic space. Found in spirochetes - causes corkscrew

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21
Q

Discuss different endospore locations

A

Central, swollen sporangium, terminal, subterminal

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22
Q

What are fimbriae?

A

hairlike bristles extending from surface, help in adhestion

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23
Q

What is an inclusion/granule?

A

Stored nutrients, deposited as crustals

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24
Q

Which bacterium does not have a cell wall?

A

Mycoplasma

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25
Q

CC peptidoglycan in gram+, gram-, acid fast bacteria cell walls

A

Gram+ = thick
Gram- = thin
Acid fast = small amount

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26
Q

CC teichoic acid in gram+, gram-, acid fast bacteria cell walls

A

gram+ = often
gram- = none
acid fast = none

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27
Q

CC lipids in gram+, gram-, acid fast bacteria cell walls

A

gram+ = v. little
gram- = LPS
acid fast = mycolic acid, waxes, glycolipids

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28
Q

CC outer membrane presence in gram+, gram-, acid fast bacteria cell walls

A

Only present in gram- bacteria

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29
Q

CC periplasmic space presence in gram+, gram-, acid fast bacteria cell walls

A

Only present in gram- bacteria

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30
Q

CC cell shape in gram+, gram-, acid fast bacteria cell walls

A

Gram+ is always rigid, others rigid or flexible

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31
Q

CC result of digestion in gram+, gram-, acid fast bacteria cell walls

A

gram+ = protoplast
gram- = spheroplast
acid fast = hard to digest

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32
Q

CC antibiotic sensitivity in gram+, gram-, acid fast bacteria cell walls

A

gram+ = most
gram- = some
acid fast = least

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33
Q

List six key bacterial shapes

A
Coccus - sphere
Bacillus = rod
coccobacillus = oval
Vibria = bean
Spirillum = rigid spiral
Spirochete = non rigid spiral
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34
Q

What do strepto- and staphylo-

A
Strepto- = strip
Staphylo- = cluster
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35
Q

What does the cholera toxin do?

A

Activates adenallyl cyclase in intestinal cells

  • > increased cAMP, fluid, electrolyte secretion
  • > diarrhea
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36
Q

What does the tetanus toxin do?

A

Inhibits release of inhibatory neurotransmitters in CNS => spastic paralysis

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37
Q

What does the botulism toxin do?

A

Inhibits release of acetylcholine from neurons => flaccid paralysis

38
Q

What does the diptheria toxin do?

A

Inhibition of protein synthesis => cell death

39
Q

What does streptolysin toxin from streptococcus pyogenes do?

A

Creates protein that blocks cell membrane pores -> cell death

40
Q

What does the pneumolysin txin from streptococcus pneumoniae do?

A

Creates protein that blocks cell membrane pores -> cell death

41
Q

What does alpha toxin from staphylococcus aureus do?

A

Creates protein that blocks cell membrane pores -> cell death

42
Q

What does beta toxin from staphylococcus aureus do?

A

Phospholipase - degrades cell membranes

43
Q

What does phospholipase C from pseudomonas aeruginosa do?

A

Phospholipase - degrades cell membranes

44
Q

What does alpha toxin from clostridium perfringens do?

A

Phospholipase - degrades cell membranes

45
Q

Which bacterium causes toxic shock syndrome?

A

Staphylococcus aureus

46
Q

Which bacterial toxins cause excessive cytokine stimulation?

A

Streptococcal mitogenic exotoxin and streptococcal pyrogenic exotoxin, both from streptococcus pyogenes

47
Q

What virulence factors aid adhesion?

A

Adhesins on pili/fibrae, e.g. in neisseria gonorrhaeae

Glycocalyx layers

48
Q

What virulence factors aid invasion?

A

Degrading extracellular matric, through hyaluronidase / collagenase

Modulating blood clotting in host - coagulase accelerates clotting, streptokinase dissolves clots

49
Q

What virulence factors aid bacterial defense?

A

Capsules

Proteases to degrade IgA, IgG

Antigenic variation

50
Q

What adaptations enable intracellular bacterial growth?

A

Inhibition of fusion with lysosome; inhibition of acidification of phagosome [mycobacterium legionella]

Escape from phagosome into cytoplasm [listeria]

51
Q

What is toxemia?

A

Presence of toxins in blood

52
Q

What are the differences between endotoxins and exotoxins?

A

Endotoxins – heat stable, systemic effect, high LD50

Exotoxins – not heat stable, specific and receptor mediated, low LD50

53
Q

What are the fie stages of infection?

A
Incubation
Prodromal
Illness
Decline
Convalescence
54
Q

What are the most common healthcare associated infection sites?

A

Urinary tract - 40%
Surgical wounds - 20%
Respiratory - 15%

55
Q

What is the difference between bacteremia, septicaemia, septic shock?

A

Bacteraemia - bacteria in blood
Septicaemia - in blood and multiplying
Septic shock – systolic pressure <90mmHg

56
Q

What is the difference between ID50 and LD50

A
ID50 = median infectious dose
LD50 = median lethal dose
57
Q

What are Koch’s postulates, 1884?

A

Agent present in diseased organism but not in healthy

Must be isolatable

When inoculated into healthy individual, must cause same disease

Must then be reisolatable

58
Q

What are nosocomial infections?

A

Healthcare related infections

59
Q

SEQ gram staining

A

1) Crystal violet added, stains +/- purple
2) Iodine added, makes stain adhere to cell walls
3) Alcohol added, stain washes off -ve
4) Safranin applied, -ve stained pink

60
Q

SEQ acid staining

A

1) Basic fuschin added, all stained pink

2) Acid-alcohol added, non-acid fast stained blue

61
Q

What types of staining other than gram / acid staining exist?

A

Endospore, capsule, flagella

62
Q

What are the pros and cons of identifying an organism through culture and visual / metabolic identification?

A

+ : sensitive, inexpensive

- : can be slow

63
Q

SEQ the streak method for isolating pure colonies

A

Sterilize wand, make one streak from last sample

x 4 until pure colonies are apparent

64
Q

What are the pros and cons of molecular methods of microbial detection?

A

+ : no culturing required, good for fastidious or uncultivable bacteria, no need for sample purity, specific, sensitive, rapid, accurate
- : needs trained personnel, expensive

65
Q

How is bacterial genomic sequencing undertaken?

A

Gold standard = sequencing of 16S rRNA subunit.

66
Q

What does MALDI-TOF MS stand for?

A

Matric-assisted laster desorption ionisation time of mass-spectrometry

67
Q

What are the pros and cons of MALDI-TOF MS

A

Pros: rapid, fast, sensitive, less expensive than molecular identification methods, does not need trained lab personnel

Cons: identification only possible if species/strain present if database has peptide mass fingerprints of specific strains

68
Q

What is the major disadvantage of PCR amplification for diagnostic microbiology?

A

At least some sequence must be known to synthesize appropriate primers

69
Q

What is precipitin?

A

An insoluble complex formed when antigens and antibodies are present in appropriate ratio

70
Q

What are the pros and cons of serologic tests?

A

Pros: fast

Cons: less sensitive, accurate than nucleic acid methods; limited by availability of appropriate antibodies/antigens

71
Q

What are the pros and cons of serologic tests?

A

Pros: fast

Cons: less sensitive, accurate than nucleic acid methods; limited by availability of appropriate antibodies/antigens

72
Q

What is selective toxicity?

A

The ability to harm pathogens but not host

73
Q

What is the measure of toxicity?

A

Therapeutic index

74
Q

What is the difference between bacteriostatic and bacteriocidal drugs?

A
Bacteriostatic = inhibits growth
Bacteriocidal = kills them
75
Q

What is a superinfection? Give examples

A

Large population of drug-resistant bacteria after even normal flora have been killed off by antibiotics

E.g. candiasis after UTI treatment; Pseudomembranous colitis caused by C diff

76
Q

What are good selectively toxic bacterial targets?

A

Cell wall
Plasma membrane
Ribosomes – 30S subunit and 50S subunit
Metabolic pathways – esp. folic acid synthesis and mycolic acid synthesis

77
Q

What are good selectively toxic bacterial targets?

A
Cell wall 
Plasma membrane
Ribosomes -- 30S subunit and 50S subunit
Metabolic pathways -- esp. folic acid synthesis and mycolic acid synthesis
DNA/RNA synthesis
Mycobacterial ATP synthesis
78
Q

What are some key anti-drug bacterial adaptations?

A
Efflux pump
Blocked penetration
Enzyme inactivation
Target modification
Target overproduction
Target mimicry
Enzymatic bypass
79
Q

Describe penicillin

A

Contains beta-lactam ring – types differentiated by side chains on ring

Prevents crosslinking of peptidoglycans

80
Q

How are cephalosporins different from penicillin?

A

Different beta-lactam ring

Classed according to generation of development

81
Q

Give an example of intrinsic drug resistance in bacteria

A

Mycoplasma lack cell wall => do not respond to penicillin or cephalosporins

82
Q

Give an example of intrinsic drug resistance in bacteria

A

Mycoplasma lack cell wall => do not respond to penicillin or cephalosporins

83
Q

What does the Kirby-Bauer test test?

A

Sensitivity of particular bacterium to antibiotic

84
Q

SEQ the Kirby-Bauer test

A

Culture bacteria on plate
Add antibiotic drops
Measure radius of killed bacteria

85
Q

What are the limitations of the Kirby-Bauer test?

A

Qualitative not quantitative
Does not provide bactericidal v. bacteriostatic info
Not good for tricky/slow/anaerobic bacteria
Biofilm bacteria may be affected differently

86
Q

In the dilution test what is MBC and what is MIC?

A
MIC = minimum inhibitory concentration
MBC = minimum bactericidal concentration
87
Q

How is MBC measured in the dilution test?

A

Take some drops from each clear flask, place on petri dish, see if bacteria grow

88
Q

What is a biofilm?

A

Complex community of one or more microbe spp
Forms slimy coating
Attaches to inert or organic substances through secretin of EPS [extrapolymeric substance]

89
Q

What challenges to biofilms present?

A

Hard to observe – thick!

Resistant to antibiotics and immune system

Can form on medical devices

Hard to dehydrate b/c hold water like sponge

90
Q

What are the stages of biofilm development?

A

Initial attachment of planktonic cells to surface
Irreversible attachment [become sessile – attached to surface]
Maturation I - growth
Maturation II - EPS production
Dispersion