antibiotics

Question 1

three modes of action of antibiotics

Answer 1

bacteriostatic, bactericidal, bacteriolytic

Question 2

bacteriostatic

Answer 2

agents that stops bacteria from reproducing, while not necessarily killing them otherwise

Question 3

bacteriocidal

Answer 3

bacteria killed directly

Question 4

bacteriolytic

Answer 4

dissolution or destruction of bacteria

Question 5

antibiotics which effect cell wall synthesis

Answer 5

cycloserine, vancomycin, bacitracin, penicillins, cephalosporins, monobactams, carbapenems

Question 6

DNA gyrate ( decoils DNA)

Answer 6

Nalidixic acid, ciprofloxacom.. novobiocin

Question 7

RNA eleongation

Answer 7

actinomycin

Question 8

DNA directed RNA polymerase

Answer 8

Rifampin, Streptovaricins

Question 9

Protein synthesis (50s inhibitor)

Answer 9

Erythromycin (macrocodes)
Chloramphenicol
Clindamycin
Lincomycin

Question 10

Proteinsynthesis (30s)

Answer 10

tetracyclines, spectinomycin, streptomycin, gentamicin, kanamycin, amikacin, nitrofurans

Question 11

protein synthesis (tRNA)

Answer 11

Mupirocin, puromycin

Question 12

Lipid biosynthesis

Answer 12

platensimycin

Question 13

Cytoplasmic membrane structure and function

Answer 13

Polymyxins, daptomycin

Question 14

folic acid production

Answer 14

trimethoprim, sulfonamides

Question 15

Macrolides

Answer 15

12-16 member macrolactone rings decorated with amino-sugars. Binding site is the large ribosomal subunit in the upper part of the nascent peptide exit tunnel

Question 16

nascent peptide exit tunnel of macrolides

Answer 16

allows easy passage of the newly made protein through the tunnel- crucial for protein synthesis

Question 17

How do macrocodes inhibit translation

Answer 17

binding of the macrolide in the tunnel impedes profession of the nascent peptide and results in a general inhibition of translation

Question 18

target of fluorquinolones

Answer 18

target DNA gyrate (topoisomerase II and IV)

Question 19

how to fluorquinolones enter bacteria

Answer 19

passive diffusion into gram +ve and via outer membrane prions in gram -ves

Question 20

newer fluoroquinonlines have a

Answer 20

broader spectrum and work best against gram +ve

Question 21

how common are fluoroquinolone

Answer 21

2nd most used

Question 22

how do fluoroquinolone work

Answer 22

topoisomerase IV carries out decatenation and relaxation of DNA, and assists the segregation of replicating chromosomes or plasmid in bacteria. Inhibition disrupts this process, contributing to bactericidal activity of fluoroquinolobnes.

Question 23

which bacteria have high levels of resistance to fluorquinolones

Answer 23

S pneumonia and staphylococcus aureus - have demonstrated that for ciprofloxacin-selected mutatantsm the first step involves a motion in parC- suggesting topoisomerase IV is the primary target in these bacteria.

Question 24

are fluorquinolones synthetic

Answer 24

yes

Question 25

name a broad spectrum, semi synthetic beta- lactic antibiotic

Answer 25

cephalosporins

Question 26

cephalosporins are derived from the

Answer 26

mould, cephalosporium

Question 27

cephalosporins are chemically related to

Answer 27

penicillins, same mechanism of action

Question 28

how do cephalosporins and penicillins cause cell damage

Answer 28

by interfering with bacterial cell wall synthesis

Question 29

new antibiotics are being discovered

Answer 29

semi- regularly, although not as frequently as in the past

Question 30

alternative phage stratagies

Answer 30

uses phage to deliver a protein that interferes with an essential bacterial process rendering the bacteria more susceptible to antibiotic- causing bacterial cell lysis- very specific, will only attach to the pathogen and not the animal cell

Question 31

anti-virulence strategies

Answer 31

inhibit specific mechanisms that promote infection and are essential to persistence in a pathogenic cascade and or cause of disease

Question 32

anti-virulence strategies offer

Answer 32

a reduced selection pressure for drug resistant mutations

Question 33

benefits of anti-virulence strategies

Answer 33

avoids undesirable dramatic alterations of the host microbiota that are associated with current antibiotics e.g. UPEC

Question 34

UPEC

Answer 34

chemical structures of anti-adhesive carbohydrate ligans- ligand for the FmH adhesion and (D) PapG adhesion. e.g. if the bacteria cannot get into the cell it can not cause damage e.g. e.coli

Question 35

anti-virulence strategies- inhibiting secretly systems

Answer 35

both type 3 and 6 secretory systems inject proteins (15-30). Many bacteria inject proteins which manipulates the actin cytoskeleton-herby forcing uptake. Gram negative bacteria have complex protein translocation mechanisms

Question 36

it is thought that genes found in faecal extracts inhibit

Answer 36

salmonella rowth

Question 37

faecal extracts inhibit the growth of salmoenlla

Answer 37

62 genes were unregulated during growth in the faecal extract, whereas 76 genes were downgrade. Of the 76 genes repressed by faecal extracts, 29 (38.2%) are involved in salmonella host invasion- demonstrating major effect of the gut micro biome in repression f invasion

Question 38

problems with antibiotic usage

Answer 38

synergistic drugs suppress drug susceptible subpopulation more than single drug therapy, however this eliminates competitors of the drug resistant cells wo grow more rapidly than the non resistant cells would have done at weaker synergies- thus greater singer can increase population densities.

Question 39

example of what new antimicrobial drugs are developing to beat B-lactam resistance

Answer 39

INACTIVATION OF B-LACTAMASE INHIBITORS

Question 40

some phages develop

Answer 40

specific enzymes degrading exopolysaccharide structures (capsule, slime), masking or covering a targeted receptor.

Question 41

phages as antimicrobials: advantages

Answer 41

specific and cheap

Question 42

phages as antimicrobials: disadvantages

Answer 42

narrow spectrum/ bacterial resistance

Question 43

phage as antimicrobials

Answer 43

where pages attach to certain active sites on the outside of human cells e.g. mannose receptors--> if an inhibitor is added that has a higher affinity to the phage, then they won't attach to the outside of the cell and inject their DNA- causing disease

Question 44

Stages of phage infection

Answer 44

- adsorption to specific receprot- phage attachment is highly specific - DNA injection, after peptidoglycan degradation and pore formation in the bacterial cell - redirection of host metabolism to phage DNA replication and phage protein synths - assembly and packaging of phage particles - bacterial cell lysis and phage progeny release - virions burst into the environment

Question 45

phages can be used to fight

Answer 45

bacterial infection