A good antibiotic kills or helps to kill pathogens without causing bad side effects in the patient who is under treatment. Antibiotics are used on both humans and animals. Before the antibiotic can attack the pathogens, it must reach them. In other words, the antibiotic must find transportation to the site of the pathogens, enter into them, achieve a sufficiently high internal concentration, and do all this without being degraded somewhere along the way. Once inside the pathogens, the antibiotic disrupts one or more of their vital processes.
However, these same vital processes which are targeted by the antibiotic may take place in other cells as well. Often these targeted processes are also found among other other kinds of prokaryotic cells, extending the effects of the antibiotic beyond pathogens to many other prokaryotic cells, such as microflora -- the numerous non-pathogenic microorganisms which compete with harmful bacteria for resources and thereby minimize the populations of many pathogens. Once the antibiotic has routed the microflora, the patient is susceptable to a second infection, since resources previously used by the microflora are free. Antibiotics which affect many kinds of prokaryotic cells are called broad spectrum antibiotics. While these antibiotics are useful for treating an unidentified infection, they can put the patient in danger of a more serious second infection.
Antibiotics can work in many different ways, but the mechanics of antibiotics fall into several major catagories. The first catagory is inhibition of cell wall (peptidoglycan) synthesis. A large class of antibiotics known as Beta-Lactam antibiotics fall into this catagory. These antibiotics include penicillin, cephalosporin, carbapenems, and monobactams. Normally, the cell wall is composed of many polymers of surgar molecules and amino acids, all bonded together in a mesh called peptidoglycan. The polymers are cross connected by transpeptide bonds, and the process by which these bonds are formed is called transpeptidation. Normally, this process is in a sort of an equilibrium with the action of autolysins, enzymes that degrade peptidoglycan (the cell wall). Thus, the cell wall is stable. The action of the autolysins, together with transpeptidation, allows the cell wall to change shape during cell growth and cell division.
The presence of Beta-Lactam antibiotics, however, disrupts this equilibrium. Beta-Lactam antibiotics bind to transpaptidase, the enzyme that catalyzes transpeptidation, and prevents transpeptidation from occurring. Instead of being a strong mesh, the newly-formed cell wall is just a spagetti of loose polymers. Furthermore, Beta-Lactam antibiotics apparently interfere with the feedback control of the autolysin (the peptidoglycan degrader), causing the pathogen to produce too much. The surge of autolysins descends on the peptidoglycan and degrades it, while binding of transpeptidase occurs and brings transpeptidation to a halt. Water rushes into the cell as the cytoplasmic membrane bulges out from osmotic pressure, and the pathogen lyses (i.e., spills its guts out). Glycopeptides, such as vancomycin and teichoplanin, are another type of peptoglycan synthesis inhibitors.
The second category of antibiotic mechanisms is protein synthesis inhibitors. Aminoglycosides, such as kanamycin and gentamicin, target bacterial ribosome. These antibiotics bind to the light ribosomal subunit. The subunit hops on the mRNA and accepts the first tRNA in the P site, but the subunit can go no further because the aminoglycoside bound to it prevents the heavy subunit from joining on. No protein is produced. Tetracyclines also inhibit protein synthesis by binding to the light subunit. These antibiotics distort the A site so that no tRNA can dock with the mRNA. No amino acids can be linked together into a protein. Macrolides and Lincosamides inhibit protein synthesis by binding to the heavy subunit. They inhibit the translation process, preventing proteins from elongating.
Finally, there is a class of antibiotics that inhibits DNA replication. Among these antibiotics are quinolones, rifampin, nitrofurantoins, nitroimidazoles. Quinolones bind to and inhibit the activity of an enzyme essential to DNA replication that allows supercoils to by relaxed and reformed. Other classes of antibiotics inhibit metabolism.
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