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Antimicrobial agents

Chapter 33

Selective toxicity The antimicrobial agents should act at a target site present in the infecting organism, but absent from host cells
Antibiotic Natural metabolic products of fungi, actinomycetes and bacteria that kill or inhibit the growth of micro-organisms
Antibacterial agents classification (3) 1. according to whether they are bactericidal or bacteriostatic 2. by their target site 3. by their chemical structure
Difference between bactericidal and bacteriostatic Bactericial agents kill the bacteria and is irreversible, while bacteriostatic agents inhibit bacteria growth and is a reversible process
5 main target sites for antibacterial action 1. cell wall synthesis 2. protein synthesis 3. nucleic acid synthesis 4. metabolic pathway 5. cell membrane function
Resistant organism An organism that will not be inhibited or killed by an antibacterial agent at concentrations of the drug achievable in the body after normal dosage
Inhibitors of cell wall syntesis antibacterial classes (2) Beta-lactams and Glycopeptides
Anti-bacterial mechanism of beta-lactams Inhibits cell wall synthesis by binding to PBPs and inhibiting the synthesis of the peptidoglycan layer of bacterial cell walls
Penicillin-binding proteins (PBPs) Membrane proteins capable of binding to penicillin and are responsible for the final stage of crosslinking of the bacterial cell wall structure
Result of inhibition of peptidoglycan layer syntheisis(3) Accumulation of precursor cell wall units, leading to activation of the cell's autolytic system and cell lysis
Bacterial species not susceptible to beta lactams + example(3) Species that lack a cell wall (mycoplasma), species with very impermeable cell wall (mycobacteria) or intracellular pathogens (chlamydia)
Five members of beta lactam family Penicillins (G+), cephalosporins (G+), Cephamycins (G+), Carbapenems (G-/+) and Monobactams (G-)
Mechanisms to become beta-lactam resistant (3) Alteration of PBP target site, altering the access to the PBP target site and production of beta-lactamases
Mechanism to alter PBP target site + bacterial species Staphyloccus Aureus has a mecA gene in his chromosome which encodes for PBP2a with lower affinity for beta-lactams
Mechanism to inhibit access to PBP target site + bacteria class Mutation in porin genes result in decrease in permeability of the outermembrane of gram-negative cells. No more diffusion of beta lactams through porins in outer membrane
Beta-lactamases + location Enzymes that catalyze the hydrolysis of the beta-lactam ring to generate inactive products. Found on chromosomes and on plasmids
Difference between beta lactamase in Gram + and - bacteria Beta lactamases of Gram + are released into the extracellular environment and beta lactamases of Gram - bacteria remain whithin the periplasm
Beta-lactamase inhibitors Molecules that contain a beta-lactam ring, and binds to beta-lactamases hereby preventing them from destroying beta-lactams
Glycopeptides Bactericidal compounds that interfere with cell wall synthesis by binding to terminal D-alanine-D-alanine at the end of pentapeptide chains which are part of the growing bacterial cell wall structure
Glycopeptide antibiotics + usage Vancomycin and Teicoplanin are active only against Gram + bacteria and are used to treat beta lactam resistant Gram + rods and coccus and patients allergic to beta lactam
Glycopeptide resistance genes + mechanisms vanA, vanB and vanD encode for a ligase that produces a pentapeptides that terminate in D-alanine-D-lactate
vanA characteristics and location VanA causes high inducible resistance to vancomycin and teicoplanin adn can be found on chromosomes and plasmids
vanB characteristics and location VanB causes high inducible resistance to vancomycin but NOT teicoplanin and is chromocal and plasmid linked
vanD characteristics and location vanD is chromocomal and non-transferable resulting in constitutice resitance to high levels of vancomycin but low levels of teicoplanin
Inhibitors of protein synthesis antibacterial classes (6) 1. Aminoglycosides 2. Tetracyclines 3. Chloramphenicol 4. Macrolides, lincosamides and Streptogramins 5. Oxazolidones 6. Fusidic acid
Aminoglycosides antibiotics (2) + treatment Gentamycin is important for the treatment of serious Gram - infection. Streptomycin is important for the treatment of mycobacterial infections
Aminoglycosides mechanism one Binds to specific proteins in the 30S ribosomal subunit, and interferes with the binding of fmet-tRNA to the ribosome, thereby preventing the formation of initiation complexes from which protein synthesis proceeds
Aminoglycosides mechanism two They cause misreading of mRNA codons and tend to break apart functional polysomes into non-functional monosomes
Aminoglycosides resistance mechanisms (4) 1. alteration of the 30S ribosomal target protein 2. alteration in cell wall permeability 3. alteration in the energy-dependent transport accross the cytoplasmic membrane 4. production of resistant enzymes
Aminoglycoside resistant enzymes (3) + mechanism and location Acetylase, adenylylase and phosphorylase alter the structure of the aminoglycoside molecule and inactivates the drug. They are often plasmid-mediated
Tetracycline + mechanism Bacteriostatic compound that inhibit protein synthesis by binding to the small ribosomal subunit in a manner that prevents aminoacyl tranfer RNA from entering the acceptor sites on the ribosome
Tetracyclines treatment Tetracyclines are used in the treatment of infections caused by mycoplasmas, chlamydiae and rickettsiae
Tetracycline resistant genes + mechanisms and location Resistance genes are carried on a transposon and cause the synthesization of new cytoplasmic proteins in the presence of tetracycline. The tetracyclin is then positively pumped out of resistant cells (efflux mechanism)
Chloramphenicol + mechanisms This compound binds to the 50S ribosomal subunit and blocks the action of peptidyl transferase and hereby prevents peptide bond synthesis
Chloramphenicol treatment It is used in the treatment of bacterial meningitis, aerobes and anaerobes, including intracellular organisms
Chloramphenical resistance genes Chloramphenicol acetyl transferases are intracellular, but are capable of inactivating all chloramphenicol in the immediate environment of the cell. Acetylated chloramphenicol fails to bind to the ribosomal target.
Macrolides, lincosamides and streptogramins form a group They share overlapping binding sites on ribosomes, and resistance to macrolides confers resistance to the other two classes
Macrolides, lincosamides and streptogramins mechanism They bind to the 50S ribosomal subunit (23S rRNA) and block the translocation step in protein synthesis, thereby preventing the releasing of tRNA after peptide bond formation
Oxazolidinones + mechanisms Oxazolidinones are active against Gram + bacteria and inhibit the initiation of protein synthesis by targeting 23S rRNA in the 50S subunit in a manner which prevents formation of a functional 70S complex
Fusidic acid + mechanisms Bacteriostatic agent that inhbits the protein synthesis by forming a stable complex with elongation factor G (EF-G), guanosine diphosphate and the ribosome
Inhibitors of nucleic acid antibacterial classes (4) 1. Quinolones 2. Rifamycins 3. Sulphonamides 4. Trimethoprim
Quinolones + mechanisms Bactericidal synthetic agents that inhibit the activity of bacterial DNA gyrase and topoisomerase
DNA gyrase DNA gyrase produces and removes supercoils in DNA ahead of the replication fork to maintain the proper tension required for efficient DNA duplication
Topoisomerase Topoisomerase acts to remove supercoils and to seperate newly formed DNA daugther strands after replication
Quinolones chromosomal mediated resistance (3) 1. mutations that alter the target enzyemes 2. alteration in cell wall permeability 3. efflux
Quinolones plasmid-mediated resistance (1) Production of a protein that protects the target DNA from quinolone binding
Rifamycins + mechanisms Bactericidal molecules that binds to the DNA-dependent RNA polymerase and blocks the synthesis of mRNA
Rifamycins resistance Chromosomal mutation that alter the RNA polymerase target, which then has lower affinity for the Rifamycin and escapes inhibition
Sulphonamides + mechanisms Bacteriostatic compounds that act in competition with PABA, for the active site of dihydropteroate synthetase, an enzyme that catalyses an essential reaction in the synthetic pathway of THFA
THFA THFA is required for the synthesis of purines and pyrimidines
Sulphonamide resistance Plasmid-mediated genes encode for an altered dihydropteroate synthetase. This is essentially unchanged in its affinity for PABA, but has a greatly decreased affinity for the sulphonamide
Trimethoprim + mechanism Trimethoprim prevents THFA synthesis by inhibiting dihydrofolate reductase
Trimethoprim resistance Plasmid-encoded dihydrofolate reductases with altered affinity for trimethoprim
Inhibitors of cytoplasmic mebrane functions antibacterial classes (2) Lipopeptides and Polymexins
Lipopeptides Lipopeptides acts in a calcium-dependent matter to insert and depolarize the bacterial cytoplasmic membrane. This then causes inability to synthesize ATP and interference in the uptake of nutrients
Polymexins Polymexins are bactericidal cyclic polypeptides. The free amino groups act as cationic detergents, disruption the phospholipid structure of the cell membrane.
Polymexins resistance Chromosomally-mediated alterations in membrane structure or antibiotic uptake
Created by: Beantha