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.