Antimicrobials Flashcards
Antibiotics
substances produced by microbes that can destroy or inhibit growth of other microbes
Selective toxicity
-the ability to harm the microbial pathogen without causing significant harm to the host
Therapeutic index
-ratio of the toxic dose to the therapeutic dose
-toxic dose: the median dose at which the drug is lethal to the host
-therapeutic dose: the median dose to effectively treat an infection
true or false: the higher the therapeutic index the more specifically the drug harms the pathogen but not the host
True
inhibitors of cell wall
-penicillin and cephalosporin inhibit the enzyme that catalyzes the cross linking of the murrain
-inhibition of cell wall synthesis triggers the lysis of actively growing bacteria in hypotonic conditions
Drugs that disrupt cell membrane function
Polymyxins
Inhibitors of protein synthesis
tetracycline, streptomycin, erythromycin, chloramphenicol
Inhibitors of nucleic acid synthesis
-quinolones and rifampin
Antimetabolites
Sulfa drugs—> competitive inhibitors of a bacterial enzyme involved in folic acid synthesis
What happens if a patient does not finish a course of antibiotics?
-if a course of antibiotics is not finished then the bacteria that remain and multiply are the ones that are naturally more resistant to
what are two broad categories of genetic changes that confer resistance
-spontaneous chromosomal mutation: alters the target enzymes binding site for the drug
–>usually confers resistance to a single type of antibiotic
-extrachromosomal Resistance :
R plasmids or R factors carry 6 or 7 genes for resistance to different antibiotics
Outer membrane vesicles
-are derived from gram negative outer membranes
-can compete for binding antibiotics or phage
-can transfer antibiotic resistance genes or harbor enzymes that degrade antibiotics
Antifungal Drugs
-mode of action: many anti fungal drugs exploit differences between human and fungal cell membranes
What is the difference between a human cell membrane and fungal membrane?
-human cell membrane have cholesterol
-fungal cell membranes contain ergosterol
what are examples of antifungal drugs?
imidazole inhibit ergosterol synthesis
-nystatin binds to ergosterol in the cell membrane and disrupt the cell membrane
Antiviral Drugs
Mode of action: many antiviral are nucleotide analogs that inhibit viral nucleic acid synthesizing enzymes
what is the function of monoclonal antibodies?
-binds to the spike protein and prevent the virus from attaching to human cells and tag it for destruction
Modes of actions of chemical antimicrobial agents
-react with macromolecules of microbes or change the local environment around microbes to
–> denature and inactivate proteins
–> disrupt cell membrane
–>disrupt nucleic acids
Phenolics and alcohols
-denature proteins and disrupt membranes
CHEMICAL ANTIMICROBIAL AGENTS: HALOGENS, ALDEHYDES, AND HEAVY METALS
-halogens: react with proteins, membranes, and nucleic acids
-aldehydes: react with proteins and nucleic acids
-heavy metals: react with proteins
Name three antiviral drugs against SARS-CoV2 and describe their mode of action
- Molnupiravir: causes many mutations in the genome of SARS-CoV2
- Remdesivir: inhibits the RNA replicase of coronaviruses
3.AZT: inhibits reverse transcriptase
How is sterilization different than disinfection?
Sterilization decreases the number of microbes to levels that meet public health standards
-Disinfection–> is used to kill or inhibit microbes on objects
Bactericidal vs Bacteriostatic
-kills bacteria; minimum concentration of antibacterial needed to kill the bacteria
-inhibits bacterial growth; minimum concentration of antibacterial needed to inhibit bacterial growth
Ways in which bacteria become resistant to antibiotics
-spontaneous chromosomal mutation
(altering target enzyme’s ending site for the drug)
-extrachromosomal mutations
(R plasmid)
-mutation of the target enzyme or protein so antibiotic can no longer bind
(point mutation)
-inactivation of antibiotic by chemical modification (via point mutation)
–> ex: beta lactamase
-preventing antibiotic entry into the cell by decreasing cell permeability
(via point mutation)
-by passing the target enzyme
(need the acquisition of new genes)
-pumping the drug out of the cell immediately
(via point mutation)
