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Susceptibility to antibiotics/ antiviral or antifungals. Describe the class of antimicrobial drug, and why they are effective in destroying these microbes and why is this particular drug more effective based on their structure. What is the mode of action for viral or eukaryotic infection? Antibiotic resistance can also be described here, if applicable to the organism. Include how it relates to the information covered in class- which chap number and what was taught
Generally, there are two main classes of antimicrobial drugs -
Some are obtained from natural sources and also known as beta-lactam antibiotics because of their 4 member ring structure. They are basically cyclic amide and in their structure, the nitrogen atom is attached to the β-carbon relative to the carbonyl. Examples are penicillins and cephalosporins.
Then there are protein synthesis inhibitors and other synthetic agents which basically inhibits or reduces the proliferation of cells by disrupting the generating processes of new proteins. Examples are aminoglycosides, macrolides, tetracyclines, chloramphenicol, and polypeptides
Bacterial cells are surrounded by cell walls made of peptidoglycan. The antibiotic that affect cell wall act at different stages of peptidoglycan synthesis and cell wall assembly. Because mammalian cell do not have cell wall, this class of antibiotic is highly selective. They target bacteria and have a minimum effect on the mammalian hosts. Some antibiotics disrupt the intigrity of cell membrane by binding to membrane phospholipid. Because cell membranes are also found in a mammalian cell, these antibiotics are also toxic to host cells if administered systematicaly. Antibiotics that inhibit with bacterial protein synthesis may act at different stages of this process starting from the formation of 30s initiation complex, assembly of the 50s ribosome subunit, the formation of 70s ribosome form 30s and 50s complexes and elongation process.
Some of these antibiotics also inhibit the eukaryotic mammalian counterparts but their effect on bacterial ribosomes is significantly greater. Some antibiotics interfere with DNA synthesis by binding to bacterial topoisomerase II- the enzyme that relaxes the supercoil DNA before its replication. Some other interfere with the RNA synthesis by inhibiting the RNA polymerase. Some antibiotics of this class are selective and do not interact with mammalian counterparts of these enzymes while other do affect the mammalian host cell. The latter is used for cancer treatment because cancer cell grows faster than normal cells they are more affected by the action of these agents.
Bacteria synthesize their own folic acids, unlike humans who get vitamins form food. Because of this antibiotic that inhibit enzymes involved in folic acid synthesis only harm bacterial cells and not human cells,