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Penicillins and cephalosporins are the major antibiotics that inhibit bacterial cell wall synthesis. They are called beta-lactams because of the unusual 4-member ring that is common to all their members. The beta-lactams include some of the most effective, widely used, and well-tolerated agents available for the treatment of microbial infections. Vancomycin, fosfomycin, and bacitracin also inhibit cell wall synthesis but are not nearly as important as the beta-lactam drugs.
The selective toxicity of the drugs discussed in this chapter is mainly due to specific actions on the synthesis of a cellular structure that is unique to the microorganism. More than 50 antibiotics that act as cell wall synthesis inhibitors are currently available, with individual spectra of activity that afford a wide range of clinical applications.
All penicillins are derivatives of 6-aminopenicillanic acid and contain a beta-lactam ring structure that is essential for antibacterial activity. Penicillin subclasses have additional chemical substituents that confer differences in antimicrobial activity, susceptibility to acid and enzymatic hydrolysis, and biodisposition. Penicillins vary in their resistance to gastric acid and therefore vary in their oral bioavailability. Parenteral formulations of ampicillin, piperacillin, and ticarcillin are available for injection.
Penicillins are polar compounds and are not metabolized extensively. They are usually excreted unchanged in the urine via glomerular filtration and tubular secretion; the latter process is inhibited by probenecid. Nafcillin is excreted mainly in the bile and ampicillin undergoes enterohepatic cycling. The plasma half-lives of most penicillins vary from 30 min to 1 h.
Procaine and benzathine forms of penicillin G are administered intramuscularly and have long plasma half-lives because the active drug is released very slowly into the bloodstream.
Most penicillins cross the blood-brain barrier only when the meninges are inflamed. Presently there is no proof that the former is the cause of the latter or vice versa. Penicillin by inhibiting cell wall synthesis would inhibit both growth and multiplication. Since the antibiotic is bactericidal to rapidly multiplying cells, its effect on cell wall would interfere with its bactericidal action.
There are several types of antimicrobial drugs that function by disrupting or injuring the plasma membrane. One example is daptomycin, a lipopeptide which has a distinct mechanism of action, disrupting multiple aspects of bacterial cell membrane function. It appears to bind to the membrane causes rapid depolarization, resulting in a loss of membrane potential leading to inhibition of protein, DNA and RNA synthesis, which results in bacterial cell death.
Another example is polymyxins antibiotics which have a general structure consisting of a cyclic peptide with a long hydrophobic tail. They disrupt the structure of the bacterial cell membrane by interacting with its phospholipids. Antimicrobial drugs inhibit nucleic acid synthesis through differences in prokaryotic and eukaryotic enzymes. The magnesium ion yellow is located at the enzyme active site.
The antimicrobial actions of these agents are a result of differences in prokaryotic and eukaryotic enzymes involved in nucleic acid synthesis.
Prokaryotic transcription is the process in which messenger RNA transcripts of genetic material are produced for later translation into proteins.
The transcription process includes the following steps: initiation, elongation and termination. Antimicrobial drugs have been developed to target each of these steps. Other antimicrobial drugs interfere with DNA replication, the biological process that occurs in all living organisms and copies their DNA and is the basis for biological inheritance. The process starts when one double-stranded DNA molecule produces two identical copies of the molecule.
In addition to DNA polymerase, the enzyme that synthesizes the new DNA by adding nucleotides matched to the template strand, a number of other proteins are associated with the fork and assist in the initiation and continuation of DNA synthesis. DNA replication, like all biological polymerization processes, proceeds in three enzymatically catalyzed and coordinated steps: initiation, elongation and termination.
Any of the steps in the process of DNA replication can be targeted by antimicrobial drugs. DNA Replication : The double helix is unwound and each strand acts as a template for the next strand.
Bases are matched to synthesize the new partner strands. Protein synthesis inhibitors are substances that disrupt the processes that lead directly to the generation of new proteins in cells. A protein synthesis inhibitor is a substance that stops or slows the growth or proliferation of cells by disrupting the processes that lead directly to the generation of new proteins.
It usually refers to substances, such as antimicrobial drugs, that act at the ribosome level. The substances take advantage of the major differences between prokaryotic and eukaryotic ribosome structures which differ in their size, sequence, structure, and the ratio of protein to RNA.
The differences in structure allow some antibiotics to kill bacteria by inhibiting their ribosomes, while leaving human ribosomes unaffected.
The ribosome has three sites: the A site, the P site, and the E site not shown in. The A site is the point of entry for the aminoacyl tRNA.
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