Flashcards in Antibacterial Mechanisms Deck (15)
β-lactams (penicillins, cepalosporins)
Inhibit the final transpeptidation reaction in cross-linking of peptidoglycan. (Cell wall antimicrobials)
Inhibits utilization of lipid-linked intermediate at an intermediate step in peptidoglycan synsthesis, e.g., elongation of the peptidoglycan chain. (Cell wall antimicrobials)
Inhibits alanine racemase, preventing formation of muramyl pentapeptide, an early intermediate in peptidoglycan synthesis. (Cell wall antimicrobials)
Cationic surfactants that disrupt bacterial outer and cytoplasmic membranes. They are less active on mammalian cell membranes. (Outer and cytoplasmic membrane-active antimicrobials)
Aminoglycosides (including streptomycin, kanamycin, gentamicin, neomycin, tobramycin, amikacin, etc)
Bind to specific target proteins in the 30S ribosomal subunit and inhibit protein synthesis. (Inhibitors of protein synthesis at the ribosomal level)
Reversibly bind to the 30S ribosomal subunit and inhibit binding of aminoacyl tRNA. (Inhibitors of protein synthesis at the ribosomal level)
Binds reversibly to the 50S ribosomal subunit and inhibits peptidyl transferase and peptide bond formation. (Inhibitors of protein synthesis at the ribosomal level)
Macrolides (such as erythromycin)
bind to the 23S ribosomal RNA of the 50S subunit and inhibit peptidyl transferase. (Inhibitors of protein synthesis at the ribosomal level)
Lincomycins (such as lincomycin and clindamycin)
Bind to the 23S ribosomal RNA of the 50S subunit and inhibit peptidyl transferase. (Inhibitors of protein synthesis at the ribosomal level)
Inhibit DNA gyrase and topoisomerase and therefore interfere with DNA replication. (Inhibitors of nucleic acid synthesis)
Inhibits RNA polymerase and interferes with the initiation of transcription. (Inhibitors of nucleic acid synthesis)
Structural analogs of p-aminobenzoic acid (PABA), which is a component of folic acid. Enzymes that use folic acid derivatives as coenzymes are needed for one-carbon transfer reactions in the synthesis of many compounds, including thymidine and purines. Sulfonamides inhibit the formation of folic acid by competing with PABA, and this in turn prevents nucleic acid synthesis. The inhibition is selective because only bacteria, and not the host, possess enzymes for making folic acid (we get ours from the bacteria), whereas bacteria, in contrast to human cells, cannot utilize pre-formed folic acid.
Interferes with folate metabolism by inhibiting the enzyme dihydrofolate reductase. Since both bacterial and host cells both possess this
enzyme, the basis of selective toxicity lies in the 50,000-fold greater sensitivity of the bacterial enzyme to this drug.
Inhibits lipid synthesis (probably mycolic acid synthesis) in susceptible Mycobacteria.