Antimicrobials can be bactericidal (kill the microorganism directly) or bacteriostatic (prevent the microbe growth). In the case of bacteriostatic drugs, host defenses such as phagocytosis and antibody production usually destroy the microorganism. With the suspension of the second type of drug, bacteria can grow back. For bacteriostatic and bactericidal actions are apparent it is necessary to determine the MIC (Minimum Inhibitory Concentration) and MBC (minimum bactericidal concentration). As the therapeutic activity of antibiotics depends, among other factors, on their concentrations in body fluids, MICs and CBMs are essential determinations, since the establishment of the antibiotic regimen depends on them. The MIC and MBC are estimated in vitro, but used to determine bacteriostatic and bactericidal concentrations of antibiotics in body fluids (Maillard, 2002).
In Biofilms, MIC and MBC of antimicrobial agents usually must be greater than those required for plancttonic cells, due to its greater resistance to these drugs. In addition, optimal antimicrobials indicated for diseases that have bacteria organized in biofilms as etiological agent, must have good distribution in these structures. The main mechanisms of action of antimicrobials include: inhibition of cell wall synthesis, inhibition of protein synthesis, plasma membrane damage, inhibition of the synthesis of nucleic acids and inhibition of the synthesis of essential metabolites (Maillard, 2002).
Cell Wall Inhibition. The bacterium's cell wall consists of a network of macromolecules called peptidoglycan, which is found exclusively in bacteria's cell wall. Penicillin and other antibiotics prevent complete synthesis of peptidoglycan, consequently, the cell wall becomes fragile and cell undergoes lysis. As penicillin targets the synthesis process, only cells in active growth will be affected by this antibiotic. And as human cells do not have peptidoglycan, penicillin has low cytotoxicity to the host cell (Broadley et al. 1995).
Inhibition of Protein Synthesis. Protein synthesis is a characteristic common to all cells, both prokaryotes and eukaryotes, not presenting therefore a suitable target for selective toxicity. Eukaryotic cells have 80S ribosomes and prokaryotic cells have 70S ribosomes. The difference in the ribosome structure is responsible for selective toxicity to antibiotics that affect protein synthesis. However, the mitochondria (important cytoplasmic organelles) also has the 70S ribosomal unit similar to bacteria units. Antibiotics that act on the 70S ribosome may therefore have adverse effects on host cells. Among the antibiotics that interfere are the clorofenicol, erythromycin, streptomycin, and tetracycline (Nakamura & Tamaoki, 1968).
Damage to the plasma membrane. Certain antibiotics, especially polypeptide antibiotics, promote changes in the permeability of plasma membrane. These changes result in the loss of major metabolites of the microbial cell. For example, polymyxin B disrupts the plasma membrane by binding to membrane phospholipids (Lambert & Hammond, 1973). Likewise, planktonic cells, when exposed to higher concentrations of the chlorhexidine (CHX), suffer membrane rupture (Figure 2). This observation can be explained by the fact that CHX, which is positively charged, binds tightly to negatively charged bacteria membrane, causing its disruption (Gilbert & Moore, 2005).
Inhibition of nucleic acids synthesis. Some antibiotics interfere with the processes of DNA transcription and replication of microorganisms. Some drugs with this mode of action have limited use due to interference with DNA and RNA of mammals. Others, such as rifampin and quinolones, are more widely used in chemotherapy by having a higher degree of selective toxicity (Silver, 1967).
Inhibition of Synthesis of Essential Metabolites. The enzymatic activity of a specific microorganism can be competitively inhibited by a substance (antimetabolites) that closely resembles enzyme's normal substrate (Russell and Hugo, 1994).
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