what is selective toxicity?
if the drug targets a unique feature of the pathogen (not found in us), then the drug should only be harmful to the pathogen not the host
which group of microbes would be easy to develop drugs against?
why is it difficult to develop drugs against viruses?
they are very simple, non-living, and use our cell structures to replicate
why is it difficult to develop drugs against fungi, protozoans, and algae?
they are all eukaryotes and their basic cell structure is similar to ours
what are the four general features of antimicrobial drugs?
1. source of the drug
2. range and strength of action
3. the therapeutic index
4. actions of antimicrobial drugs
what are the 3 sources of drugs?
what is a natural drug?
drug is created by another living organism (penicillin created from mold)
what is a synthetic drug?
drug is created artificially in the lab (sulfa drugs)
what is a semi-synthetic drug?
drug is a combo of natural and synthetic
when are semi-synthetic drugs usually created?
when resistance occurs to the original, natural drug
what is the range of action?
broad and narow spectrum
what is the strength of action?
cidal or static
what is the therapeutic index?
measures/estimates selective toxicity
is a low or high therapeutic index preferrable?
if the TI is lower what will it cause more of?
what are the four actions of antimicrobial drugs?
1. target cell wall
2. target protein synthesis
3. target nucleic acid synthesis
4. act as a structural analogue
how does a drug target the cell wall?
it inhibits the synthesis of cell wall components or directly degrades pathogen cell wall
does targeting the cell wall have a high or low TI?
high because the cell wall is unique to pathogens
how does a drug target protein synthesis?
inhibits creation of proteins by altering or binding to ribosome
does trageting protein synthesis have a low or high TI?
low because ribosomes are not unique to pathogens and our cells have them
how does a drug target nucleic acid synthesis?
it inhibits transcription (creation of mRNA) or DNA replication before cell division
does targeting the nucelic acid syntheiss have a high or low TI?
low because many similarities in pathogen/enzymes in pathogen and our cell
how does a drug act as a structural analogue (antimetabolite) ?
the drug acts as a mimic to a natural substrate in a biosynthetic or metabolic pathway which is required for pathogen growth
what hapens when the drug mimic is used in the pathway instead of the natural substrate?
a non-functional end product is created and the functional end product is needed to grow, so no growth
how is the TI for a structural analogue?
it can be high or low depending on the pathway (if we have that pathway or not)
does the drug have to outnumber the normal substrate when it acts like a mimic?
what does resistance mean?
drug no longer kills of inhibits growth of pathogen
what is the greatest threat of microbial disease?
how does resistance evolve?
1. genetic change in pathogen
2. selection of resistant individuals
how does genetic change lead to resistance?
allows some individuals in the pathogen population to resist the drug
hwo does selection of resistant individuals cause resistance?
eliminates any non-resistant/ susceptible individuals and allows resistant individuals to survive and become the majority cell type on pathogen population
what are the four mechanisms of resistance?
1. block entry of drug
2. pump the drug back out
3. destroy/inactivate drug once it enters
4. alter the target structure/pathway of drug
how do microbes block entry of a drug?
they alter the carrier/pore used by the drug to enter
how does a microbe pump the drug out(efflux)?
use active transport
what is an exmaple of destroying or inactivating the drug once it enters?
what happens when the the microbe alters the target structure/pathway of the drug?
the target is no longer recognized