Control of Microbial Population 2 Flashcards
type of microbial drug that is effect on both protozoa and fungi
azoles
why are sulfonamides so important
they can be used to treat both prokaryotes and eukaryotes
what are aminoglycosides not effective against and why
not effective against anaerobes because of absent oxidative phosphorylation due to lack of oxygen
what are glycopeptides not effective against and why
gram negative bacteria because they are too large and can’t penetrate through outer membrane
what are nitroimidazoles not effective against and why
aerobes because they require activation by flavodoxin which is found only in anaerobes
what are penicillins and cephalosporins not effective against and why
these things target particular structure which is the cell wall
mycoplasma because it lacks cell wall
mycobacteria because cell wall impenetrable
what are some challenges with fungi infections?
harder to treat, usually chronic, longer tx time, recurrence is common, eukaryotes so similar to humans
what was the first antifungal and are there many antifungals
azoles
not many because of challenge when it comes to treating fungi infections
what are some sites of target for antifungal agents
nucleic acid synthesis (flucytosine)
cell membrane
direct membrane
what do antifungal agents that target nucleic acids do
inhibits synthesis of DNA, RNA, and proteins
what antifungal targets nucleic acid and what is its mechanism?
cytosine analogue 5-fluorocytosine (uses fungal enzyme) –> 5-fluorouracil –> 5-fluorouridyllic acid –> blocks synthesis of p nucleic acids that the fungi is going to need to replicate
what is the difference between narrow and broad spectrum compounds
narrow - only treat one type of bacteria or fungi or virus
broad - treat several types of bacteria, fungi, or virus or even some cross over and treat both prokaryotes and eukaryotes
name of antifungal that targets cell membrane
polyenes e.g. amphotericin B
specifically ergosterol
what is the mechanism of polyenes (amphotericin B)
lipid loving compound that binds to ergosterol that create pores in the membrane causing leakage of ions out of the fungi –> cell lysis
which antifungal compound is fungicidal
polyenes (amphotericin B) because it actually kills the fungi
how does allylamines work
they are antifungals that interrupt the formation of ergosterol which is needed for cell membrane
it targets squalene epoxidase which turns squalene to lanesterol
example of allylamines
terbinafine
how do azoles work
they are antifungals that interrupt the formation of ergosterol which needed for cell membrane
it targets 14 alpha demethylase which turns lanesterol to ergosterol
example of azoles
fluconazole (triazole)
what are the two groups of azoles
imidazoles (two nitrogens)
triazoles (three nitrogens)
effects of azoles on fungal growth
fungistatic and fungicidal depending on species and specific compound
advantage of azoles
250 fold more effective against fungi sterols than against mammalian sterols
what antifungal targets cell wall
echinocandins eg caspofungin
mechanism of caspofungin
blocks (1,3) -beta-D-glucan synthetase –> prevents formation of chitin for cell wall
what antibiotics target metabolism
sulfonamides (inhibitors of metabolism or nucleic acid synthesis)
sulfonamides are derived from
prontosil
mechanism of sulfonamides
blocks folic acid synthesis
since bacteria synthesize their own antibiotics using PABA, sulfonamides are analogues of PABA so if taken up halts the production of folic acid
what two drugs synergistically inhibit the synthesis of folic acid in fungi
sulfamethoxazole and trimethoprim
TMP-SMX/SMZ
which antibiotics target protein synthesis in bacteria
tetracyclines, streptomycin, erythromycin, chloramphenicol
what antibiotics target cell wall of bacteria
beta lactams
what drugs fall under beta lactam and why? also how do these drugs work
penicillin, cephalosporins, monobactams, carbapenems – all have beta lactam ring
active only on growing cells
what drugs inhibit the formation of cell wall of bacteria by attacking cytoplasm and cytoplasmic membrane respectively
cytoplasm - cycloserine
cytoplasmic membrane - bacitracin glycopeptides
cross linking of NAM molecules in peptidoglycan is carried out by and this process is interfered with by what?
transpeptidases aka penicillin binding proteins
beta lactams
what happens to cell wall when beta lactams comes in and interferes with the cross linking of NAM molecules
they continue to grow (though they do not have the cement) but will eventually lyse since nothing is keeping it together
mechanisms in which bacterias use to resist against antibiotics
altered uptake - decrease/block uptake of antibiotic or as soon as antibiotic gets into the bacteria is as soon as bacteria pumps it back out
altered target - change in receptor affinity through mutation
drug inactivation: beta lactamases, chloramphenicol, acetyltransferases
most commonly used antifungal
azoles
which drug is susceptible to all resistance mechanism of bacteria: altered target, altered uptake, drug inactivation
beta lactam
which resistance mechanism by bacteria is mostly used against antibiotics
drug inactivation
sources of resistance by bacteria
chromosomal mutation
genes on transmissible plasmids
genes on transposable elements (transposons)
how does beta lactamase inactivate beta lactams
it cleaves the antibiotic at the beta lactam ring hence inactivating it
most common beta lactamase
TEM beta lactamase
confers resistance to all beta lactam anitibiotics and many other classes of antibiotics like aminoglycosides and fluoroquinolones
extended spectrum beta lactamases (ESBL)
exception to ESBL
cephamycin (cefoxitin and cefotetan), carbapenems
main producers of ESBL (extended spectrum beta lactamases) and KPC
enterobacteriacae particularly e. coli and klebsiella species
KPC (klebsiella pneumoniae carbapenemases) are resistant to what
all beta lactams, fluoroquinolones, aminoglycosides
associated with high therapeutic failure and high mortality rate
Actions YOU as a healthcare practitioner can take to help limit the spread of resistance and selection of resistant strains
- Wash your hands thoroughly between patient visits.
- Do not give in to patients’ demands for unneeded antibiotics.
- When possible, prescribe antibiotics that target only a narrow range of bacteria.
– Sensitivity testing - Isolate hospital patients with multi drug‐resistant infections.
- Familiarize yourself with local data on antibiotic resistance.
