Bacterial pyrite oxidation III. Adsorption of Thiobacillus ferrooxidans cells on solid surfaces and its effect on iron release from pyrite.

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Abstract
T. ferrooxidans cells were rapidly adsorbed on the solid surfaces of an agitated flask containing 1% pulp density of pyrite particles. More than 99% of the inoculated cells were adsorbed. Considerably fewer cells were adsorbed on pyrite particles than on the glass wall of the flask. Scanning electron microscopy revealed that T. ferrooxidans cells were adsorbed aggregatively on restricted areas of the pyrite particles. The surfaces of the pyrite particles were characteristically eroded to show etched polyhedral pits, but without prominent cell adsorption of the extensively eroded surfaces during markedly enhanced leaching. When T. ferrooxidans cells were adsorbed on the solid surfaces, the Fe-oxidizing activity was strongly inhibited, resulting in a failure to enhance pyrite oxidation. Adsorbed cells did not proliferate on the solid surfaces. When the adsorbed cells were released into an aqueous phase by the addition of the surface active agent Tween 20, the Fe-oxidizing activity inhibited by adsorption was recovered and pyrite oxidation was markedly promoted. Significant enhancement of pyrite oxidation by T. ferrooxidans was ascribed to the development and Fe-oxidizing activity of the freely dispersed cells in an aqueous phase. The surface active agent prevents tenacious adsorption of the bacterial cells to solid surfaces; organic substances, such as protein, nucleic acid, yeast extract, peptone and cell-free extracts, operate in the same way as the surface active agent. The enhancement of pyrite oxidation by intact cells of T. thiooxidans may be attributable to organic substances excreted from T. thiooxidans cells and/or to the exchange adsorption of cells. Apparently, the bacterial concentration in an aqueous phase rather than on pyrite particles plays a major role in the enhanced oxidation of pyrite by T. ferrooxidans and the bacteria contribute indirectly to pyrite oxidation through the regeneration of Fe3+.