Chapter 10: Controlling Microbial Growth in the Body: Antimicrobial Drugs (Vocabulary Flashcards)

Vocabulary flashcards covering key terms and concepts from the antimicrobial drugs lecture notes.

Arsenic compounds

Early antimicrobial agents that killed microbes but were toxic to humans.

Semisynthetic antibiotics

Chemically modified antibiotics with improved stability, absorption, or spectrum.

Synthetic antibiotics

Antimicrobials completely synthesized in the laboratory.

Selective toxicity

Property of an antimicrobial agent to be toxic to pathogen but not to the host.

Antibacterial

Drugs that act against bacteria; broad or narrow spectrum.

Beta-lactam

Antibiotics containing a beta-lactam ring that inhibit cell wall synthesis by blocking cross-linking enzymes.

Penicillin-binding protein (PBP)

Bacterial enzymes (transpeptidases) that cross-link NAM subunits; targeted by beta-lactams.

Peptidoglycan

Bacterial cell wall polymer made of sugars cross-linked by peptides.

NAM

N-acetylmuramic acid; a repeating subunit of peptidoglycan.

NAM-NAM cross-links

Peptide bridges linking NAM subunits; cross-linking is inhibited by certain antibiotics.

Vancomycin

Glycopeptide antibiotic that inhibits cross-linking by binding D-Ala-D-Ala termini.

Cephalosporin

Beta-lactam antibiotic related to penicillin with broad spectrum activity.

Bacitracin

Inhibits export of NAG and NAM from the cytoplasm; used topically.

Isoniazid

Antitubercular drug that disrupts mycolic acid synthesis.

Ethambutol

Antitubercular drug that disrupts mycobacterial cell wall formation.

Amphotericin B

Polyene antifungal that binds ergosterol to form membrane pores.

Ergosterol

Fungal membrane sterol targeted by many antifungals.

Azoles

Antifungal drugs that inhibit ergosterol synthesis (e.g., fluconazole).

Allylamines

Antifungal drugs that inhibit ergosterol synthesis (e.g., terbinafine).

Pyrazinamide

Antitubercular drug that disrupts membrane metabolism in M. tuberculosis.

70S ribosome

Prokaryotic ribosome (30S + 50S) targeted by specific antibiotics.

80S ribosome

Eukaryotic cytoplasmic ribosome; less commonly targeted by antibiotics.

30S subunit

Small subunit of the 70S ribosome; target of aminoglycosides and tetracyclines.

50S subunit

Large subunit of the ribosome; target of chloramphenicol, macrolides, and lincosamides.

Aminoglycosides

Antibiotics that bind the 30S subunit and cause mRNA misreading (e.g., streptomycin, gentamicin).

Streptomycin

Aminoglycoside antibiotic that binds 30S and inhibits protein synthesis.

Gentamicin

Aminoglycoside antibiotic used against Gram-negative bacteria; targets 30S.

Tetracyclines

Antibiotics that block the A site on the 30S ribosome, inhibiting tRNA docking.

Chloramphenicol

50S ribosome inhibitor that blocks peptidyl transferase.

Macrolides

50S ribosome inhibitors that block translocation and movement of the peptidyl chain.

Mupirocin

Antibiotic that inhibits isoleucyl-tRNA synthetase, halting protein synthesis.

Oxazolidinones

Antibiotics (e.g., linezolid) that block initiation of translation; effective against resistant Gram-positive bacteria.

Initiation of translation

First stage of protein synthesis; inhibited by oxazolidinones.

Sulfonamides

Antimetabolic agents; structural analogs of PABA that inhibit folic acid synthesis.

Folic acid

Active folate cofactors that are essential for one-carbon metabolism.

What is PABA

Crucial in the synthesis of nucleotides

Trimethoprim

Antimetabolic drug that inhibits dihydrofolate reductase, blocking THF synthesis.

Quinolones

Antibiotics that inhibit DNA gyrase, blocking bacterial DNA replication.

Why are Reverse transcriptase inhibitors beneficial

Act against an enzyme HIV uses in its replication cycle and does not harm humans because we lack reverse transcriptase.

Pleconaril

Attachment antagonist that blocks viral attachment for certain polioviruses and cold viruses.

Kirby-Bauer

Diffusion susceptibility test showing zones of inhibition around antibiotic disks.

MIC

Minimum Inhibitory Concentration—the lowest concentration that prevents growth.

MBC

Minimum Bactericidal Concentration—the lowest concentration that kills the organism.

Superinfection

Secondary infection that arises after normal flora are disrupted.

MRSA

Methicillin-resistant Staphylococcus aureus; resistant to many beta-lactams.

Beta-lactamase

Enzyme that destroys the beta-lactam ring, inactivating penicillins.

R-plasmids

Plasmids that carry antibiotic resistance genes and spread them via horizontal transfer.

Synergism

Combination of drugs producing a greater effect than either alone.

Biofilms

Slime layers that protect microbes and slow diffusion of drugs, promoting resistance.

MfpA

Protein in Mycobacterium tuberculosis contributing to quinolone resistance.

Gerhard Domagk

Discovered sulfanilamide

Selman Waksman

Isolated and characterized antibiotics

Mechanisms of antimicrobial action (6)

1-Inhibition of cell wall synthesis, 2-inhibition protein synthesis, 3-inhibition of DNA or RNA synthesis, 4-disruption or alteration of the cytoplasmic membrane, 5-inhibition of general metabolic pathway, 6-inhibition of pathogen attachment to or recognition of host.

Inhibition of cell wall synthesis

Prevent bacteria from increasing peptidoglycan; existing peptidoglycan remains.

Inhibition of cytoplasmic membranes

Some drugs form channels through cytoplasmic membranes and disrupt integrity

Inhibition of protein synthesis

Drugs can selectively target bacterial translation without harming host ribosomes.

Inhibition of metabolic pathways

Antimetabolic agents effective when pathogen and host metabolic process differ.

Inhibition of nucleic acid synthesis

Several drugs block DNA replication or mRNA transcription.

Preventions of virus attachment (4)

1-Attachment antagonist block viral attachment or receptor proteins, 2-blocked by peptide and sugar analogs of attachment or receptor proteins, 3-blocked viruses cannot attach or enter host cells, 4-new area of antimicrobial drug development.

Retarding resistance

Strategies to slow resistance development.

What’s drugs interfere with acid fast bacteria

Isoniazid and ethambutol

What are the concerns for humans dealing with Amphotericin B

Susceptible because cholesterol is similar to ergosterol

Why is terbinafine a better choice over amphotericin B

It inhibits the synthesis of ergosterol. While amphotericin attaches to ergosterol

How do microbial inhibit nucleic acid synthesis

By inhibiting DNA/RNA synthesis, interfering with DNA supercoiling enzymes, or directly damaging DNA. Which is a typical way to treat fungle/viral infections.

How do microbial work with viruses

They are constantly interacting which is important for nature and our own health.

How would you determine if an antibiotic is effective

Through MBI, MBC, and diffusion susceptibility test.

What is the zone of inhibition

The area where the growth of a tested microorganism is visibly prevented or inhibited.

How do microbes develop a mechanism of resistance (4)

1-Produce enzyme that destroy or deactivates drug,2- slow or prevent entry of drug into cell, 3-alter their metabolic chemistry, 4-alter target of drug so it binds less effectively.

How do we deal with microbial resistance mechanisms (4)

1-Maintain high concentration of drug in patient, 2-use antimicrobial agents in combination, 3-develop new variations of existing drugs, 4-search for new drugs