| what are the different classes of antibiotics? | beta lacatams (target cell wall)
penicillins
cephalosporins, cephamycin
carbapenems
monobactams
target protein synthesis
aminoglycosides
macrolides
target nucleic acid synthesis
quinolones
antimetabolites |
| what is the differences between penicillins and cephalosporins? | the beta-lactam ring of cephalosporins is fused with a dihydrothiazine ring
cephalosporins have a wider spectrum than penicillins |
| how do quinolones work? | they target nucleic acid synthesis by inhibiting topoisomerase type II for gram-negative bacteria and topoisomerase type IV for gram-positive bacteria.
this prevents DNA replication, recombination and repair. |
| how do antimetabolites work? | they target nucleic acid synthesis by competing with the enzyme PABA, which is needed for the production of folic acid. because of this inhibition purines and pyrimidines cannot be made |
| how do aminoglycosides work? | they target protein synthesis by binding to the 30S subunit of the ribosome. this creates the wrong proteins causing cell death |
| how do macrolides work? | they target protein synthesis by binding to the 23S ribosomal RNA of the 50S ribosome. this blocks peptide elongation. this is a reversible mechanism |
| how do the beta-lactams work? | they target the cell wall synthesis by binding to the penicillin-binding proteins, which inhibits the assembly of peptidoglycan. this causes lysis and cell death |
| which antibiotics are bactericidal and which ones are bacteriostatic? | bactericidal: aminoglycosides, beta-lactams,
bacteriostatic: macrolides |
| what is the difference between penicillin G and V? | penicillin G is unstable in gastric acid and is thus administered intravenously
penicillin V is more resistant to gastric acid and is administered orally |
| why do penicillins work better on gram-positive than gram-negative bacteria? | the gram-negative bacteria have an outer membrane that the penicillins have to cross before they can do their job. this crossing depends on if the antibiotic fits through the pores of the bacteria.
the gram-positive bacteria do not have this membrane |
| what is the difference between cephalosporins and cephamycins? | cephalosporins contain sulfer in their dihydrothiazine ring, while cephamycins have oxygen located there |
| what do the different spectrums tell you about cephalosporins? | the narrow spectrum cephalosporins are the antibiotics that were first found and that are not that effective to a lot of bacteria.
the more you move up in spectrum (expanded, broad, extended) the more active the antibiotics are to other bacteria.
the antibiotics in the broad spectrum can pass the blood-brain barrier and the ones in the extended spectrum can pass the outer membrane more easily. |
| how is the peptidoglycan of the cell wall synthesized? | 1. the precursors are synthesised and activated in the cell
2. the acetylglucosamine and acetylmuramic acid are attached to bactoprenol
3. bactoprenol is transferred to the other side of the cell wall
4. peptidoglycan is extended; transpeptidases cross-link the peptidoglycan and D-carboxypeptidases remove unreacted D-alanines |
| what does LPS compose of and in what order? (from proximal to distal of the cell) | 1. lipid A
2. core polysaccharide
3. O antigen
the bacteria is recognized by its O antigen |
| how does bacterial resistance develop for each antibiotic? | beta-lactams: decreased concentration of antibiotic at the target, decreased binding to PBP, hydrolysis by beta-lactamases
aminoglycosides: modification of the antibiotic, mutation of the ribosome, decreased uptake of antibiotic in the cell, increased efflux
quinolones: chromosomal mutations, increased efflux, membrane permeability mutation
antimetabolites: changes to the cell membrane |
| what are the four general mechanisms for developing resistance against antibiotics for bacteria? | target modification
efflux
immunity (antibiotics bound to other proteins so they can't bind their target)
enzyme catalyze destruction (enzyme destroys the antibiotic) |
| what are the four classes of beta-lactamases? | class A: SHV-1, TEM-s and ESBLs
class B: zinc dependent metalloenzymes
class C: mainly cephalosporinases
class D: mainly penicillinases |
| what is the function of beta-lactamases? | they work against beta-lactam antibiotics by hydrolyzing them, meaning the addition of a water molecule. this causes the beta-lactam to fall apart in small pieces. |
| what types of ESBLs are there and how are they formed? | TEM: formed by point mutation (in TEM-1 or TEM-2)
SHV: formed by point mutation
CTX-M: formed by horizontal gene transfer |
| how is bacterial resistance tested? | disc diffusion test: bacteria are put on an agar plate, antibiotic is applied and discs are incubated, looked at the zone of inhibition
broth dilution: bacteria is mixed with media and compared to other tubes to determine the minimum inhibitory concentration (MIC) |
| what is the breakpoint and minimum inhibitory concentration? | breakpoint: chosen concentration of the antibiotic which defines whether the bacteria is susceptible or resistant to the antibiotic
minimum inhibitory concentration: lowest concentration of the antibiotic that inhibits the growth of the bacteria
bacteria is resistant when MIC is above the breakpoint
bacteria is susceptible when MIC is equal to or below the breakpoint |
