antibiotics Flashcards
what is the difference between a bacteriacidal vs a bacteriostatic drug
a bacteriocidal drug kills the bacteria bacteriostatic inhibits growth
when would you se a bacteriocidal drug
when you have an invasive infection such as bacteremia, menigitis, and bacterial endocarditis
when would you use a bacteriostatic drug
when the host defenses can be counted on to eliminate the bacteria
what are the four main methods of actions of antibiotics
cell wall inhibitors, protein synthsis inhibitors, nucleic acid synthesis, anti metabolites…folic acid inhibitors.
what type of bacteria would be most effected against the cell wall synthesis drugs
gram positive bacteria because they build more cell wall or peptioglycan.
what type of antibiotic is penicillian and how does it work
it is a cell wall inhibitor and it binds to the serine in the binding site of the PBP with its beta lactam ring and irreversibly blocks the active site so no cell wall cross linking can occure.
How does vancomycin work and how can cells be resistant
cell wall inhibitor, last line of defense bind to the two terminal d alanines of the penta peptide chain on NAM but resistive bacteria will replace the terminal d alanine with D lactate.
Name two protein synthesis inhibitors and how they work
chloramphenicol blocks the formation fo the peptide bond between the amino acids and erythromycin block translocation of tRNA from acceptor site to donor site.
how does rafampin work
nucleic acid synthesis inhibitor, inhibits RNA polymerase preventing RNA synthesis
how does metronidazole work
nucleic acid synthesis inhibitor, inhibit DNA topoisomerase to prevent supercoiling of DNA to properly fit inside of the bacterial cell
how does quinolones work
nucleic acid synthesis inhibitor causes breaks in bacterial DNA
what do sulfonamides and trimethoprim do
they both are antimetabolites that inhibit the production of folic acid needed for purine rings needed for DNA synthesis.
what are the advantages/disadvantages of narrow spectrum
avoids some of te destruction of the normal flora, but pathogen must e idintified for correct antibiotic.
what are the advantages/disadvantages of broad spectrum
high likelihood of effectiveness against an unidentified pathogen but may result in destruction of normal flora can cause C. diff or clostridium difficile colitis
what type of penicillin is broad spectrum
aminopenicillins active against gram positive as usual but also agasint some gram negative
what is the spectrum of cephalosporins and cephamycins
narrow to extended
what is the spectrum of carbapenems
broad
what is the spectrum of tetrycyclines and macrolides
both broad and both protein synthesis inhibitors
what is the spectrum of quinolones
narrow broad and extended
what is the mechanism of resistance for penicillins and sephalosporins
beta lactamase cleavage of the B lactam ring
what is the mechanism of resistance for aminoglycosides
modification by acetylation, adenylation, or phosphorylation
what is the mechanism of resistance for chloramphinicol
modification by acetlyation
what is the mechanism of resistance for erythromycin
change in receptor by methylation of rRNA
what is the mechanism of resistance for tatracyline
reduce uptake or increased export
what is the mechanism of resistance for sulfonamides
active export out of the cell and reduced affinity of enzyme
how does use of antibiotics contribute to antibiotic resistance
it selects for those that are naturally resistant and allowing those to survive.
what is the clinical importance of enterococcus faecalis and faecium
they carry a multi drug resistant conjugatve plasmid for vancomycin
what is the clinical importance of staphylococcus aureus
it has aquired genes for resistance from E. faecalis through transposones on a multi drug resistant plasmid making it a super multidrug resistant plasmid
what is the clinical importance of gram negative bacilli
they exchange drug resistance via a plasmid passed by conjugation
what is the clinical importance of neisseria gonorrhoeae
has its resistance on a non conjugated plasmid , has an oriT but not a tra operon,. A seperate plasmid can initiate conjugation and the non conjugated plasmid can be transferred to the new bacterium. This is called mobilization
how do we limit development of antibiotic resistance
only use them when necessary, have patients take all the presciption for the recommened period of time, antibiotics can be combined to lessen the chance that a dual resistance will occur
what is chemoprophylaxis and when should it be used
is when antibiotics are used to prevent disease rather than treat disease for people that have been exposed to certain pathogens like meningitidis and for the immunocomprimised and surgical patients.
what is the kirby bauer test
patient bacteria isolated on solid medium plate, then antibiotic disks placed on medium plate so the drugs can diffuse into the medium then the zones of inhibition are measured and compared to the standard to determine sensitive intermediate or resistant, results are qualitative, its cheap easy and does several antibiotics at once.
what is the mic and MBC
is used to determine the lowest concentration of drug that inhibits growth in the MIC, in the MBC is used to determine what level will make it so that it will kill the bacteria usually a same or higher concentration.
