One of the first targets of attack of the bacteriostatic strategy is the cell wall of the pathogen. The objective is to weaken the cell wall, causing the cell to undergo lysis. The key to this attack is the structure of the cell wall itself. Bacteria cell walls are comprised of a network of marcromolecules called peptidoglycan. Certain antibiotics inhibit the making of peptidoglycan (synthesis), thus weakening the cell wall. Antibiotics that affect the synthesis of the cell wall of bacteria are bacitracin, vancomycin, penicillin, and cephalosporins.
Another target of attack of the bacteriostatic strategy is the pathogen's capability to make protein. Protein is necessary for both eukaryotic and prokaryotic cells. If the antibiotic can inhibit protein synthesis, then the cell dies. The problem is for the antibiotic to identify only prokaryotic cells (bacteria) and not eukaryotic, which includes human cells.
The solution lies within the structure of ribosomes in eukaryotic and prokary-toic cells. Ribosomes are the sites of protein synthesis.
Eucaryotic cells have 80S ribosomes and procaryotic cells have 70S. The numbers are Svedberg units and indicate the relative sedimentation rates during centrifugation. Prokaryotic ribosomes consist of a small subunit referred to as 30S and a large subunit called 50S. The 30S subunit contains one molecule of rRNA and the 50S subunit contains two molecules of rRNA.
Antibiotics use the differences in ribosomes to identify the prokarytoic cell from the eukaryotic cell, thereby interfering with protein synthesis only for the prokarytoic cells. Some antibiotics interfere with the 50S subunit while other antibiotics attack the 30S subunit. These antibiotics include chloramphenicol, erythromycin, streptomycin, and tetracycline.
Chloramphenicol interferes with the 50S subunit by preventing peptide bonds from forming. Erythromycin is a narrow-spectrum antibiotic that also interferes with the 50S subunit but only for gram-positive bacteria. Tetracycline interferes with the 30S subunit and prevents the tRNA from carrying amino acids and prevents amino acids from attaching to the polypeptide chain. Streptomycin interferes with the 30S subunit by changing its shape, causing an incorrect reading of the genetic code on the mRNA. Streptomycin is an example of what is called an aminoglycoside antibiotic. (An aminoglycoside is made up of amino carbohydrates and an aminocyclitol ring).
Still another target of attack of antibiotics is the pathogen's plasma membrane. The plasma membrane is permeable, allowing substances in and out of the cell as part of normal cell metabolism.
Some antibiotics change the permeability of the plasma membrane, thereby disrupting the metabolism of the pathogen. One such antibiotic is polymyxin B, which attaches to the phospholipids of the plasma membrane, inhibiting permeability of the membrane.
Antifungal drugs also destroy fungus using a similar technique the cell membranes of fungi are made predominately of erogosterol. The plasma membrane of fungi have ergosterol. Antifungal drugs combine with sterols to inhibit the permeability of the membrane. Popular antifungal drugs include amphotericin B, ketoconazole, and miconazole.
Nucleic acids are blueprints for the reproduction of every cell; these are DNA and RNA. A commonly used bacteriostatic strategy is to interfere with the making of nucleic acid by using rifampin, quinolones, and other similar antibiotics.
Although disrupting the formation of nucleic acid results in the destruction of the pathogen, scientists are careful when choosing the antibiotic for this purpose because the antibiotic might interfere with the host's DNA and RNA.
A metabolite is a substance (such as an enzyme) that is necessary for cell metabolism. The bacteriostatic strategy interferes with a metabolite and prevents the growth of the pathogenic organism.
For example, pathogens require the substrate para-aminobenzoic acid (PABA) in order to synthesize folic acid. Folic acid is a coenzyme that is involved in the synthesis of purine and pyrimidine nucleic acid bases and many amino acids.
The antimetabolite called sulfanilamide, which is a sulfa drug, resembles PABA. When sulfanilamide is introduced into the pathogenic microorganism, the enzyme used in making folic acid combines with sulfanilamide instead of PABA. This then disrupts the formation of folic acid and eventually prevents the pathogenic microorganism from synthesizing purine and pyrimidine.
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