Antimicrobial chemotherapy Flashcards
what do anti-fungal drugs target
class 2 reactions
what do fungal cell membranes contain
ergosterol
instead of cholesterol
what do drugs that inhibit ergosterol synthesis do
impair fungal membrane function without affecting the host cell membrane
e.g. fluconazole
drugs targeting endoplasmic reticulum
allylamines
benzylamines
imidazoles
triazoles
drugs targeting cell wall
echinocandins
drugs targeting plasma membrane
polyenes (amphotericin B)
drugs targeting DNA synthesis
flucytosine
drugs targeting the mitotic spindle
griseofulvin
what is fungal synthesis of nucleic acid dependent on
folate mechanism
some anti-fungals are converted to anti-metabolites (false substrates) in fungi but not in host cells
what is flucytosine metabolised to in fungi
5-FU
which stages of the cell cycle to anti-viral drugs target
entry to host cells
nucleic acid replication
viral protein synthesis
exit from host cells
how do anti-viral drugs target the entry to host cells
drugs may inhibit fusion of virus with host cell membrane following binding to surface receptor
how do anti-viral drugs target nucleic acid replication
drugs may inhibit DNA/RNA polymerases e.g. aciclovir or retroviral reverse transcriptase (zidovudine)
how do anti-viral drugs target viral protein synthesis
may inhibit girl proteases involved in processing large poly proteins
how do anti-viral drugs target exit from host cells
may inhibit neuraminidase-catalysed cleavage (oseltamivir)
attachment and entry inhibitor anti-virals
maraviroc
enfuvirtide
ion channel blockers anti-virals
amantadine
rimantadine
polymerase inhibitors anti-virals
acyclovir
zidovudine
efavirenz
integrase inhibitors anti-virals
raltegravir
protease inhibitors anti-virals
saquinavir
ritonavir
neuraminidase inhibitors anti-virals
zanamivir
oseltamivir
remdesivir mechanism of action
RNA- dependent RNA polymerase inhibitor
ribavirin mechanism of action
RNA dependent RNA polymerase inhibitor
Lopinavir-ritonavir mechanism of action
3CL protease inhibitor
favipiravir mechanism of action
RNA dependent RNa polymerase inhibitor
chloroquine mechanism of action
viral entry inhibitor
hydroxychloroquine mechanism of action
viral entry inhibitor
oseltamivir mechanism of action
neuraminidase inhibitor
umifenovir mechanism of action
spike protein/ ACe2 membrane fusion inhibitor
examples of immunomodulatory agents
tocilizumab
interferons
examples of adjunctive agents
arithromycin
corticosteroids
tocilizumab mechanism of action
IL-6 inhibitor
interferon mechanism of action
activate interferon-stimulated genes
-interfere with viral replication
-immunomodulatory effects
azithromycin mechanism of action
antibacterial, used in combination with hydroxychloroquine for synergistic antiviral effect
corticosteroid mechanism of action
cytokine gene expression inhibitor
camostat mesylate mechanism of action
serine protease inhibitor
ACE inhibitor mechanism of action
Ace inhibitor; inhibitor the formation of angiotensin 11
ARB; angiotensin 11 receptor antagonist
how do bacteria transmit resistant
spontaneous mutation
gene transfer or transferred resistance
spontaneous mutations
happens when cells replicate
within a population there will be some bacteria with acquired resistance
drug eliminates the sensitive organisms and the resistant ones proliferate
gene transfer or transferred resistance
usually spread through conjugative transfer of R plasmid (may be virally mediated)
4 mechanisms responsible for resistance to antimicrobial drugs
- inactivating enzymes that destroy the drug (beta lactamases)
- decreased drug accumulation (tetracyclins, beta lactams)
- altering the binding sites ( aminoglycosides and erythromycin)
- development of alternative metabolic pathways (sulphonamides e.g. dihydropteroate synthease and trimethoprim e.g. dihydrofolate reductase)
increased elimination
drug enters cell but efflux pump ejects it
drug-inactivating enzyme
enzyme modifies drug
inactivates it
alteration in target
drug can’t bind to the target
decreased uptake
prone proteins prevent entry into the cell
4 ways to slow the emergence and spread of antimicrobial resistance
- understand the mechanisms
- use of combination therapies
- responsibilities of physicians: work to identify the microbe and prescribe suitable antimicrobials, educate patients
- responsibilities of patients: carefully follow instructions
in the absence of drug will a sensitive or resistant cell grow faster
the sensitive cell
resistant cells use more energy
