microbe nutrition + growth - post midterm Flashcards

1
Q

chemotherapeutic agents

A

chemicals taken internally to kill or inhibit growth of microbes within host cell
= antibiotics: kill bacteria
= antifungals:
=antivirals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is selective toxicity

A

allows chemicals to target the microbe without harming the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

most chemotherapeutic agents?

A

antibiotics - chemicals synthesized by microbes that are effective in controlling the growth of bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Paul Ehrlich: discovered?

A

salvarsan

  • organo-arsenic compound.
  • treat syphilis, replaces mercury which was equally toxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

gerhard Damagk discovered?

A

dyes against streptococcus

- prontosil was first of sulfa drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

alexander fleming discovereD?

A

penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

selman waksman discovered?

A

streptomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

antibiotic use - human vs agriculture

A
huma = 36%
agriculture = 64%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

frequency of antibiotic type use

A
penicillin = 40%
cephalosporin = 24%
macrolides = 12%
quinolones = 11%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are dilution susceptibility tests

A

Minimum inhibitory concentration (MIC): lowest dose that prevents growth

Minimum lethal dose (MLD): lowest dose that kills pathogen. add antibiotic after growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

target in bacterial cells?

A

cell wall, dna synthesis.

attack things diff from human

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are sulfa drugs?

A

used as antibacterial.
more toxic to bacteria than host.
- sulfanilamide competitive inhibitor to PABA, PABA is substrate for folic acid synthesis. bacteria use folic acid to make nucleic acids - sulfa drug doesnt allow this

  • bio-mimic molecule. bind to same binding site as molecule it binds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

growth factor analogs

A

toxic to fast growing cells
- microbes, cancer cells
= halogenate = toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

competitive inhibition

A

folic acid biosynthesis is reduced in presence of sulfa drug inhibitor. need more concentration of PABA to out-compete sulfa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are quinolones

A

synthetic antibacterial compounds

  • inhibit bacterial DNA gyrase, enzyme that supercoils DNA for packing into cell
  • gram (-) effective
  • B.anthracis effective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

RNA synthesis inhibitors

A

rifamycin + rifampin

  • bind RNA polymerase + block transcription
  • not as selective bc prok and euk = not used as chemo agent
17
Q

cell wall biosynthesis inhibitors

b-lactams

A

cyclic peptides.
penicillin (5), cephalosporin (6)

bind to transpeptidases: enyme cross-link peptidoglycan monomers, cause weakening of cell wall
some bacteria have b-lactamases break b-lactam rings - leads to antibiotic resistance

18
Q

b-lactamases and cell wall

A

gram(-) : outer membrane impermebable to penicillin. b-lactamases in peiplasmic space
g+ more sensitive because no peri-plasmic space.

19
Q

PG cross-linking in G-

A

no interbridge link. d-ala to DAP

20
Q

PG cross linking in G+

A

peptide interbridge (5-glycine_ because d-ala to l-lys. not facing same direction

21
Q

peptide bond formation as target for penicillin

A

transpeptidation by transpeptidase. transpeptidaes is penicillin binding protein = activtiy is blocked. Penicillin-PBP complex = autolysin release to prevent formation of peptide bond.

22
Q

new penicillins on g-

A

b-lactam dont work bc b-lactamases.

now, penicillin structures not hydrolyzed by b-lactamases.

23
Q

co-treatment of b-lactam drugs on g-

A

ampicillin + clavulanic acid

- b-lactamase binds to vlaculanic acid + ampicillin attacks b-lactamase

24
Q

cycloserine
bacitracin
vancomycin

A

cell wall biosynthesis inhibitors
c: blocks d-ala peptidization
B: block dephosphorylation of bactoprenol phosphate (carries Nag/NAM across to PG)
v: block transpeptidation by binding d-ala

25
protein synthesis inhibitors -aminoglycosides macrolides tetracyclines
A: inhibit protein synthesis by small subunit. hit g- M: bind to large subunit of ribosome T: broad-spectrum antibiotic - inhibit tRNA attachement. g+ and g-
26
daptomycin
cyclic lipopeptide - insert into cytoplasmic membrane, makes pore - target g+ (bc no outer membrane, g- outer membrane protects leakage) resistance from changes in cell membrane structure
27
anti-fungal difficult why
biological similarity between host + pathogen | - limits point of attak
28
what is targeted in anti-fungals?
sterols + chitin.
29
anti-fungal name?
nyastatin
30
what are superficial mycoses
fungal infection on outer surface of tissue. | - topical application of nystatin - don't ingest can be toxic
31
antiviral drugs
developing - disrupt RNA or DNA synthesis of viral pathogen. interfere with replication of viral genome - selectively problematic - protease inhibitors against virus-specific enzymes interferons: stimulate production of host anti-viral proteins
32
trick with antiviral why?
diff than bacteria or euk bc not it's own cell. have to target virus without killing host even tho host cell is used
33
antibiotic resistance
- continues to build - origin and transmission of antibiotic resistance involves chromosomal or plasmid genes for drug resistance - plasmid transfer
34
what are nocosomial infections?
hospital-acquired.
35
4 mechanisms of resistance?
1.exclusion (efflux) 2enzymatic inactivation 3modification of antibiotic or target 4alternative pathway or increase target
36
sources of resistance genes
1. bacterial chromosomes - spontaneous mutation 2. plasmids: transferred with HGT 3. mobile genetic elements
37
mechanisms of transfer
transformation: lost + picked up conudation: transfer from M->F transduction: viral delivery
38
preventing drug resistance
high concentrations - 2+ drugs - only when necessary - develop new drugs + use bacteriophages (hard and inefficient, but less resistance)