Penicillin
Penicillin, the most famous of all antibiotics, is a group of antibiotics derived from the fungal mold Penicillium notatum (Adams, 2014) . Penicillin antibiotics are the most significant in history, for they were the first ones to prove effective against many diseases and infections which were previously seriously (Smith, 2014).
Penicillins exert their effects by interfering with the process of cell wall synthesis in the bacteria. Human cells lack a cell wall (Mobley 2018), making penicillin antibiotics highly selective on the bacteria while sparing human cells. Specifically, penicillins inhibit transpeptidation, the final process in cell wall synthesis. Transpeptidation refers to the cross-linkage of peptide chains leading to the synthesis of the peptidoglycan layer of the bacterial cell wall. Peptidoglycan is an important rigid component of the cell wall and serves to protect the cell wall from destruction (lysis).
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The resulting cell wall is weak and incapable of withstanding the osmotic gradient between the bacteria’s internal and external environments. As a result, excess water enters the bacterial cell, making it swell and explode, leading to the destruction of the bacteria.
The active portion of penicillins is the beta-lactam ring in its molecular structure (Adams, 2014). Most bacteria have a penicillin-binding protein on their cell walls that serves as the receptor for penicillin antibiotics (Adams, 2014). Since penicillins inhibit transpeptidation, bacterial cells must be actively dividing for penicillin to be effective, since resting bacteria do not synthesize new cell walls.
Tetracycline
Tetracyclines are bacteriostatic and act primarily by arresting bacterial growth, leaving their elimination to a person’s immunity. Tetracyclines enter microorganisms through passive diffusion and active transport. While in the cell, tetracyclines reversibly bind to the 30S subunit of the bacterial ribosome (Smith, 2014). The 30S subunit interprets genetic information. By interfering with it, new amino acids cannot be added to the growing peptide, thus interfering with protein synthesis, arresting the growth of the bacteria.
Tetracycline can accumulate and concentrate in susceptible bacterial cells. However, tetracyclines do not accumulate sufficiently to stop protein synthesis in human cells, giving the antibiotics a high selectivity (Mobley 2018).
Chloramphenicol
Chloramphenicol is a potent, selective inhibitor of protein synthesis in bacteria and exerts its effects by reversibly binding to the 50S subunit of the ribosome (Smith, 2014). The 50S unit is responsible for ordering the organization of peptide chains. By interfering with it, the synthesis of proteins is inhibited. Chloramphenicol is bacteriostatic, and like tetracyclines, it cannot accumulate in sufficient amounts in human cells to stop protein synthesis. This makes it a selective inhibitor.
Sulfonamides
Sulfonamides inhibit the synthesis of folic acid. Folic acid is essential in the synthesis of purines that synthesize nucleic acids (DNA and RNA). Human beings cannot synthesize folic acid and must use preformed folic acid found in the diet (Mobley 2018). On the other hand, susceptible organisms must synthesize folic acid from p-aminobenzoic acid (PABA). The selective toxicity of sulfonamides thus results from the mammalian inability to synthesize folic acid.
Sulfonamides interfere with the enzyme dihydropteroate synthetase (Smith, 2014). The enzyme is useful in the first step of folic acid synthesis, which is the formation of dihydropteroic acid from PABA and pteridine. Sulfonamides resemble PABA and are mistakenly used by the bacteria, thus acting either as a competitive inhibitor of dihydropteroate synthetase or as a substrate that results in nonfunctional folic acid formation.
Vancomycin
Vancomycin interferes with peptidoglycan formation and cross-linking, thus inhibiting cell wall synthesis (Smith, 2014). The peptidoglycan formed is hence weak, altering the permeability of the bacterial membrane, exposing it to lysis. Human cells neither have a cell wall, nor do they need or make peptidoglycan (Mobley 2018). This gives vancomycin its selective toxicity on susceptible microorganisms.
Antibiotics and Viruses
Antibiotics are generally ineffective against viruses. Viruses lack cellular components that are targeted by antibiotics. Viruses lack ribosomes, cell walls, plasma membrane, and cytoplasm (Aryal, 2015). Lacking these cellular components, antibiotics would, therefore, have no targets to attack. Furthermore, bacteria are extracellular as opposed to viruses that are obligate intracellular parasites. This means that bacterial infections are localized and can be easily targeted. On the contrary, viral infections are systemic (Aryal, 2015). Antibiotic can thus target bacteria without necessarily penetrating and harming human cells.
References
Adams, M. P. (2014). Pharmacology for Nurses: a Pathophysiologic Approach Fourth Edition . Pearson.
Aryal, S. (2015). Differences between bacteria and viruses. Retrieved from: https://microbiologyinfo.com/differences-between-bacteria-and-viruses/
Mobley, H. (2018). How do antibiotics kill bacterial cells but not human cells? Retrieved from: https://www.scientificamerican.com/article/how-do-antibiotics-kill-b/
Smith, B. T. (2014). Pharmacology for nurses . Jones & Bartlett Publishers.
