microbe nutrition + growth - post midterm

Question 1

chemotherapeutic agents

Answer 1

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

Question 2

what is selective toxicity

Answer 2

allows chemicals to target the microbe without harming the host

Question 3

most chemotherapeutic agents?

Answer 3

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

Question 4

Paul Ehrlich: discovered?

Answer 4

salvarsan

• organo-arsenic compound.
• treat syphilis, replaces mercury which was equally toxic

Question 5

gerhard Damagk discovered?

Answer 5

dyes against streptococcus

- prontosil was first of sulfa drugs

Question 6

alexander fleming discovereD?

Answer 6

penicillin

Question 7

selman waksman discovered?

Answer 7

streptomycin

Question 8

antibiotic use - human vs agriculture

Answer 8

huma = 36%
agriculture = 64%

Question 9

frequency of antibiotic type use

Answer 9

penicillin = 40%
cephalosporin = 24%
macrolides = 12%
quinolones = 11%

Question 10

what are dilution susceptibility tests

Answer 10

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

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

Question 11

target in bacterial cells?

Answer 11

cell wall, dna synthesis.

attack things diff from human

Question 12

what are sulfa drugs?

Answer 12

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

Question 13

growth factor analogs

Answer 13

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

Question 14

competitive inhibition

Answer 14

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

Question 15

what are quinolones

Answer 15

synthetic antibacterial compounds

• inhibit bacterial DNA gyrase, enzyme that supercoils DNA for packing into cell
• gram (-) effective
• B.anthracis effective

Question 16

RNA synthesis inhibitors

Answer 16

rifamycin + rifampin

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

Question 17

cell wall biosynthesis inhibitors

b-lactams

Answer 17

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

Question 18

b-lactamases and cell wall

Answer 18

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

Question 19

PG cross-linking in G-

Answer 19

no interbridge link. d-ala to DAP

Question 20

PG cross linking in G+

Answer 20

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

Question 21

peptide bond formation as target for penicillin

Answer 21

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

Question 22

new penicillins on g-

Answer 22

b-lactam dont work bc b-lactamases.

now, penicillin structures not hydrolyzed by b-lactamases.

Question 23

co-treatment of b-lactam drugs on g-

Answer 23

ampicillin + clavulanic acid

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

Question 24

cycloserine
bacitracin
vancomycin

Answer 24

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

Question 25

protein synthesis inhibitors
-aminoglycosides
macrolides
tetracyclines

Answer 25

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-

Question 26

daptomycin

Answer 26

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

Question 27

anti-fungal difficult why

Answer 27

biological similarity between host + pathogen

- limits point of attak

Question 28

what is targeted in anti-fungals?

Answer 28

sterols + chitin.

Question 29

anti-fungal name?

Answer 29

nyastatin

Question 30

what are superficial mycoses

Answer 30

fungal infection on outer surface of tissue.

- topical application of nystatin - don’t ingest can be toxic

Question 31

antiviral drugs

Answer 31

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

Question 32

trick with antiviral why?

Answer 32

diff than bacteria or euk bc not it’s own cell. have to target virus without killing host even tho host cell is used

Question 33

antibiotic resistance

Answer 33

• continues to build
• origin and transmission of antibiotic resistance involves chromosomal or plasmid genes for drug resistance
• plasmid transfer

Question 34

what are nocosomial infections?

Answer 34

hospital-acquired.

Question 35

4 mechanisms of resistance?

Answer 35

1.exclusion (efflux)
2enzymatic inactivation
3modification of antibiotic or target
4alternative pathway or increase target

Question 36

sources of resistance genes

Answer 36

1. bacterial chromosomes - spontaneous mutation
2. plasmids: transferred with HGT
3. mobile genetic elements

Question 37

mechanisms of transfer

Answer 37

transformation: lost + picked up
conudation: transfer from M->F
transduction: viral delivery

Question 38

preventing drug resistance

Answer 38

high concentrations

• 2+ drugs
• only when necessary
• develop new drugs + use bacteriophages (hard and inefficient, but less resistance)