What is a chemotherapeutic agent
a drug that fights against diseases
What is an antimicrobial agent
a drug that treats infections
What is an Antibiotic
Antimicrobial agents produced by microorganisms that kill or inhibit the growth of other organisms
What is a semisynthetic agent
an agent whose parent compound was made by a microbe, but was then chemically modified.
which types of antibiotics work to inhibit cell wall synthesis
cephalosporins
penecillins
vancomycin
penems
Which types of antibiotics work to inhibit protein synthesis
Eyrthromycin clindamycin chloramphenicol tetracycline aminoglycosides
which types of antibiotics inhibit Nucleic Acid Synthesis
Quinolones (ciproflaxin) rifampin sulfa drugs metronidazole nucleoside analogs
Which types of antibiotics inhibit metabolic pathways
sulfa drugs
trimethoprim
amantadine
Which types of antibiotics alter cell membrane permeability
nystatin
amphotericin B
Polymixins
how do the Beta-Lactam rings inhibit cell wall synthesis
They bind to the enzymes that are responsible for cross linking NAM subunits of the bacterial cell wall. So when those enzymes are bound, the cell wall can’t be properly synthesized, they will be weak, and the bacteria will lyse
What are some important beta-lactam drugs
penicillin methicillin cephalosporins monobactams carbapenems
how does augmentin (beta-lactamase inhibitor) help the beta-lactam drugs to be more effective
it deactivates the bacterial beta-lactamase enzymes, so that the bacteria can’t fight back against the beta-lactams drugs. normally bacteria with beta-lactamase activity can resist beta-lactam drugs
What can be the problem with broad spectrum antimicrobials
they can kill off some of the normal flora, which can lead to the development of superinfections or secondary infections.
Which antimicrobial drugs interfere with particular alanine-alanine bridges that link NAM subunits in many gram positives
Vancomycin and Cycloserine
Which antimicrobial is topical only and blocks the secretion of NAG and NAM from the cytoplasm
bacitracin
which drugs disrupt formation of arabinogalactan-mycolic acid complexes in mycobacterial species
Isoniazid and ethambutol
what is the affect of cell wall inhibiting drugs on growing cells, mature cells, animal cells, and plant cells
They destroy growing cells, (don’t let peptidoglycan form properly)
They have no effect on mature cells (because they only prevent the peptidoglycan from forming, they don’t have any affect on the existing peptidoglycan)
They have no effect on plant or animal cells since those don’t have peptidoglycan.
Why can drugs that inhibit protein synthesis be harmful in large doses
because animals have mitochondrial ribosomes that are similar to the bacterial ribosomes that are the target of these drugs that inhibit protein synthesis
For what type of infection is amphotericin B used
fungal infections
what is the mechanism of action of amphotercin B against fungi
it attaches to ergosterol that is found in fungal membranes. This negatively affects the integrity of the fungal membrane by creating pores in the membrane
Why can humans be susceptible to Amphotericin B?
because the ergosterol of fungi is similar to the choleterol in humans
What is the target of the antibacterial Polymixin
it binds to LPS and disrupts both of the gram negative membranes
why are polymixins usually used as a last resort
because they are relatively neurotoxic and nephrotoxic
How do the drugs that inhibit metabolic pathways of bacteria work
the drugs are structural analogs that bind to necessary metabolic enzymes and block them from performing their normal function
can antimetabolic drugs have an impact on viruses and parasitic worms
yes, they can paralyze the worms, and they can block viral activation
Why are sulfa drugs (sulfonamides) and trimethoprim used together (they are combined in bactrim and septra)
they both inhibit bacterial metabolic pathways, but they do it by inactivating different enzymes. so it is more effective when blocking both enzymes
What are the drugs that inhibit the metabolism of viruses
amantadine and rimantadine
what is the main problem with drugs that are used to inhibit nucleic acid synthesis
there are only a few slight differences between prokaryotic and eukaryotic
What are the mechanisms by which drugs that inhibit nucleic acid synthesis work
- they are nucleoside analogs, so they are inserted into nucleic acids instead of the actual nucleosides
- or they inhibit necessary enzymes in nucleic acid synthesis
What are drugs that inhibit nucleic acid synthesis usually used against
viruses and rapidly dividing cancer cells
What are the three most common nucleoside analogs
ribvarin
acyclovir
azidothymine
how do quinolones and fluoroquinolones work to inhibit nucleic acid synthesis
they act against prokaryotic DNA gyrase
how does rifampin work to inhibit nucleic acid synthesis
it binds to and inhibits RNA polymerase during transcription
can prevention of viral attachment be a plausible target of antiviral drugs
yes, there are drugs that do just that
name the common antifungal drug groups
polyenes (nystatin, amphotercin)
Azoles (miconazole, ketoconazole, fluconazole)
DNA analogues (Flucytosine)
What do the antifungal Azoles do to fight fungi
they inhibit the synthesis of ergosterol
What do the antifungal polyenes do to fight fungi
bind to the sterols in the cell membrane, causing leakage and death
What are the 6 characteristics of an ideal antimicrobial agent
- Readily available
- inexpensive
- chemically stable
- easily administered
- non-toxic, non-allergenic
- selectively toxic against many pathogens
What are the three ways to test the efficacy of antimicrobials
Diffusion susceptibility tests
minimum inhibitory concentration tests
minimum bactericidal concentration tests
how is a diffusion susceptibility test performed
you have a plate with growing colonies of your selected microbial, then you put little dabs of different antimicrobials on the plate, and observe which anti-microbials kill the microbial, and how drastically they do so
What does the minimum inhibitory concentration test show
it shows the lowest concentration at which an antimicrobial drug will leave no visible bacterial colonies after a night of incubation
what does the minimum bactericidal concentration test show
it shows the lowest concentration at which no bacterial colonies grow
What is topical administration
external application, applied directly to the infected area
What are the four maint types of drug administration
Topical
Oral
Intramuscular
Intravenous
What is the difference in relative concentration of the drug over time when given orally, intramuscular, and intravenously
Orally, slow increase, and decrease of a small amount of Drug
Intramuscular. a failry quick increase, of a moderate amount of Drug, followed by a fairly quick decline
Intravenous, Very quick rise or a high concentration of Drug
What are the three main side effects of anti-microbials
toxicity
allergies
disruption of normal microbiota
Are Drugs fine to take after they expire, why or why not
no, because some can become toxic after expiration
how common are allergies caused by anti-microbials
they are rare
what are the problems associated with anti-microbials that disrupt the normal microbiota?
- they can create secondary infections (too much open space for bacteria)
- they can lead to an overgrowth of normal flora (superinfection)
What are the two ways in which bacteria acquire drug resistance
- New mutations of chromosomal genes
2. Acquisition of R-plasmids from other bacteria
What are the four main ways in which microbes resist antibiotics
- inactivation of the drug
- altered uptake of the drug
- modification of the structural target of the drug
- altered metabolic pathway
What are mechanisms by which a microbe can inactivate a drug
cleavage of the drug
phosphorylation, adenylation, methylation
What ways does a bacteria alter its uptake up a antibiotic
alters its permeability
uses efflux pumps (after the drug gets in, the bacteria pumps it out)
Are resistances to antibiotics passed from one bacteria to another through plasmids
yes
How do populations of resistant organisms develop
you start with a population of organisms with only a few resistant organisms. then there is exposure to a drug which kills most of the non-resistant organisms. the few remaining organisms reproduce, leaving a population of mostly drug resistant organisms
can a single pathogen be resistant to multiple drugs
yes
Where do many of the organisms that are resistant to multiple drugs, or have acquired cross-resistance
in hospitals
What is cross-resistance in bacteria
cross-resistance is resistance acquired when a bacteria comes in contact with a substance similar to an antibiotic, and creates a resistance to it, and thus to the antibiotic
How do you prevent resistance to antibiotics
- use high concentrations of a drug, for long periods of time ]
- take advantage of synergism
- limit antimicrobials to necesssary cases
- Develop new drugs
what is synergism between antimicrobials
when two drugs used together work better than either of them do on their own.
What are CRE’s
carbapenem-resistant enterobacteriaceae
What’s the scary thing about CRE’s
these infections are very hard to treat, and have high mortality rates
