Antibiotics
Antibiotics are chemical compounds used to kill or inhibit the growth of
infectious organisms. Originally the term antibiotic referred only to organic
compounds, produced by bacteria or molds, that are toxic to other
microorganisms. The term is now used loosely to include synthetic and
semisynthetic organic compounds. Antibiotic refers generally to antibacterials;
however, because the term is loosely defined, it is preferable to specify
compounds as being antimalarials, antivirals, or antiprotozoals. All antibiotics
share the property of selective toxicity: They are more toxic to an invading
organism than they are to an animal or human host. Penicillin is the most
well-known antibiotic and has been used to fight many infectious diseases,
including syphilis, gonorrhea, tetanus, and scarlet fever. Another antibiotic,
streptomycin, has been used to combat tuberculosis. Antibiotics can be
classified in several ways. The most common method classifies them according to
their action against the infecting organism. Some antibiotics attack the cell
wall; some disrupt the cell membrane; and the majority inhibit the synthesis of
nucleic acids and proteins, the polymers that make up the bacterial cell.

Another method classifies antibiotics according to which bacterial strains they
affect: staphylococcus, streptococcus, or Escherichia coli, for example.

Antibiotics are also classified on the basis of chemical structure, as
penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, or
sulfonamides, among others. Most antibiotics act by selectively interfering with
the synthesis of one of the large-molecule constituents of the cell—the cell
wall or proteins or nucleic acids. Some, however, act by disrupting the cell
membrane . Some important and clinically useful drugs interfere with the
synthesis of peptidoglycan, the most important component of the cell wall. These
drugs include the B-lactam antibiotics, which are classified according to
chemical structure into penicillins, cephalosporins, and carbapenems. All these
antibiotics contain a B-lactam ring as a critical part of their chemical
structure, and they inhibit synthesis of peptidoglycan, an essential part of the
cell wall. They do not interfere with the synthesis of other intracellular
components. The continuing buildup of materials inside the cell exerts ever
greater pressure on the membrane, which is no longer properly supported by
peptidoglycan. The membrane gives way, the cell contents leak out, and the
bacterium dies. These antibiotics do not affect human cells because human cells
do not have cell walls. Many antibiotics operate by inhibiting the synthesis of
various intracellular bacterial molecules, including DNA, RNA, ribosomes, and
proteins. The synthetic sulfonamides are among the antibiotics that indirectly
interfere with nucleic acid synthesis. Nucleic-acid synthesis can also be
stopped by antibiotics that inhibit the enzymes that assemble these
polymers—for example, DNA polymerase or RNA polymerase. Examples of such
antibiotics are actinomycin, rifamicin, and rifampicin, the last two being
particularly valuable in the treatment of tuberculosis. The quinolone
antibiotics inhibit synthesis of an enzyme responsible for the coiling and
uncoiling of the chromosome, a process necessary for DNA replication and for
transcription to messenger RNA. Some antibacterials affect the assembly of
messenger RNA, thus causing its genetic message to be garbled. When these faulty
messages are translated, the protein products are nonfunctional. There are also
other mechanisms: The tetracyclines compete with incoming transfer-RNA
molecules; the aminoglycosides cause the genetic message to be misread and a
defective protein to be produced; chloramphenicol prevents the linking of amino
acids to the growing protein; and puromycin causes the protein chain to
terminate prematurely, releasing an incomplete protein.