When bacteria overcome the cutaneous or mucosal barriers and penetrate body tissues, a bacterial infection is present. Frequently the body succeeds in removing the invaders, without outward signs of disease, by mounting an immune response. If bacteria multiply faster than the body's defenses can destroy them, infectious disease develops with inflammatory signs, e.g., purulent wound infection or urinary tract infection. Appropriate treatment employs substances that injure bacteria and thereby prevent their further multiplication, without harming cells of the host organism (1).
Apropos nomenclature: antibiotics are produced by microorganisms (fungi, bacteria) and are directed "against life" at any phylogenetic level (prokaryotes, eukaryotes). Chemotherapeutic agents originate from chemical synthesis. This distinction has been lost in current usage.
Specific damage to bacteria is particularly practicable when a substance interferes with a metabolic process that occurs in bacterial but not in host cells. Clearly this applies to inhibitors of cell wall synthesis, because human and animal cells lack a cell wall. The points of attack of antibacterial agents are schematically illustrated in a grossly simplified bacterial cell, as depicted in (2).
In the following sections, polymyx-ins and tyrothricin are not considered further. These polypeptide antibiotics enhance cell membrane permeability. Due to their poor tolerability, they are prescribed in humans only for topical use.
The effect of antibacterial drugs can be observed in vitro (3). Bacteria multiply in a growth medium under control conditions. If the medium contains an antibacterial drug, two results can be discerned: 1. bacteria are killed—bactericidal effect; 2. bacteria survive, but do not multiply—bacteriostatic effect. Although variations may occur under therapeutic conditions, different drugs Lüllmann, Color Atlas of Pharmacology © 2000 Thieme All rights reserved. Usage subject to terms and conditions of license.
can be classified according to their respective primary mode of action (color tone in 2 and 3).
When bacterial growth remains unaffected by an antibacterial drug, bacterial resistance is present. This may occur because of certain metabolic characteristics that confer a natural insensitiv-ity to the drug on a particular strain of bacteria (natural resistance). Depending on whether a drug affects only a few or numerous types of bacteria, the terms narrow-spectrum (e.g., penicillin G) or broad-spectrum (e.g., tetracyclines) antibiotic are applied. Naturally susceptible bacterial strains can be transformed under the influence of antibacterial drugs into resistant ones (acquired resistance), when a random genetic alteration (mutation) gives rise to a resistant bacterium. Under the influence of the drug, the susceptible bacteria die off, whereas the mutant multiplies unimpeded. The more frequently a given drug is applied, the more probable the emergence of resistant strains (e.g., hospital strains with multiple resistance)!
Resistance can also be acquired when DNA responsible for nonsuscepti-bility (so-called resistance plasmid) is passed on from other resistant bacteria by conjugation or transduction.
Was this article helpful?
Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...