Organic acids antibacterial action

Bacteria are known to react differently to antibacterial agents. This is due either to inherent differences, which may be their unique cell envelope composition or proteins not being susceptible or as a result of resistance development, by adaptation exchange of genetic information. For organic acids to be effective as an antibacterial, they must be able to penetrate the cell envelope and attain a sufficiently high concentration at the target site where they will exert antibacterial action (Cloete, 2003). 

The snlfonamides are structurally related to p-aminoben-zoic acid. The presence of a free p-amino gronp is essential for the antibacterial action. Succinylsulfathiazole (sulfasuxi-dine) and phthalysnlfathiazole (sulfathalidine) are agents with a snbstitnted p-amino group. These intestinal antiseptics are slowly hydrolyzed in the intestine, releasing sulfathiazole, which exerts antiseptic effects against the coliform and clostridial organisms. 

The antibacterial action of acetic acid in these preparations is due to a specific effect of acetic acid as well as the lowering of the pH. There are two benefits, namely that acetic acid is bactericidal to Pseudomonas aeruginosa, the major pathogen isolated from otorrhoea, and that it also suppresses several fungi [3-5]. In chronic suppurative otitis media (CSOM), the most common organism is P. aeruginosa, followed by Staphylococcus aureus. 

The mechanisms by which probiotics (and prebiotics) produce beneficial effects on the gut have not yet been fully elucidated. However, at least three mechanisms of action have been proposed (i) antibacterial agents produced by probiotic organisms may have an inhibitory effect on pathogenic microbes (ii) immune responses may be enhanced to suppress potential pathogens and (iii) competition in the gut epithelium may allow lactic acid bacteria and bifidobacteria to supplant pathogenic organisms. 

Early workers [29] found that, like benzylpenicillin, vancomycin, ristocetin and bacitracin, novobiocin caused an excessive accumulation of cell wall precursor, uridine diphosphate-7V-acetylmuramic acid-L-alanine-D-glutamic acid-L-lysine-D-alanine-D-alanine (UDP-MurNAc-L-ala-D-glu-L-lys-D-ala-D-ala) in Staph, aureus and it was thus considered that novobiocin was a specific inhibitor of peptidoglycan synthesis with an effect similar to that of penicillin. However, subsequent studies led to the withdrawal of this hypothesis [26], since novobiocin caused the accumulation of other precursor-type compounds and also strongly inhibited both nucleic acid and protein synthesis in this organism. Thus, accumulation of particular precursors does not necessarily reflect the site of action of an antibacterial agent [30]. 

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