Microbial mechanisms.

In: Microbially Influenced Corrosion of Materials, (1996), S. 15-25
Zeitschriftenaufsatz / Fach: Chemie
Abstract:
A review with 51 refs. Generally, all kinds of microorganisms including bacteria, cyanobacteria, algae, fungi, and lichens are able to attack and degrade materials. The deterioration is caused by the excretion of metabolic intermediates and/or end products as well as exoenzymes. A discoloration of a resin or a total destruction of the material may be the result of a serious microbiol. influenced corrosion damage. Although many microorganisms are known to participate in these processes, the ways of action may be summarized by eight main categories: (a) attack by mineral acids like sulfuric, nitric, or carbonic acid leading to hydrolysis of materials; (b) attach by org. acids like acetic, citric, oxalic, gluconic, or other acids resulting in hydrolysis of materials and chelation of cations; (c) salt stress because of reaction products of (a) and (b) and water retention in porous materials causes increased susceptibility to freeze-thaw attract and favors crystn. leading to a swelling attack; (d) org. compds. may be transformed anaerobically into other org. solvents like alcs. or acids able to attack org. materials; (e) prodn. of noxious compds. like hydrogen sulfide or nitrogen oxides leading to prodn. of mineral acids or pptn. of metal sulfides; (f) biofilm effect where exopolymers cause localized corrosion as well as water retention in porous materials; in addn., hydrophobic effects on surfaces; (g) attack by exoenzymes resulting in cleavage of insol. org. compds. into small, water sol. mols.; and (h) prodn. of wetting agents favoring increased soly. of hydrophobic substances. Usually, the deterioration of a material is caused by a combined action of these factors. However, chem. methods often fail to detect the mechanisms properly because some compds. may be subject to metabolic turnover (org. acids, nitrogen compds. etc.). Microbiol. analyses are necessary for clearing up the mechanism of attack.