A review. Bioleaching of metal sulfides is caused by astonishingly diverse groups of bacteria. Today, at least 11 putative prokaryotic divisions can be related to this phenomenon. In contrast, the dissoln. (bio)chem. of metal sulfides follows only two pathways, which are detd. by the acid-soly. of the sulfides: the thiosulfate and the polysulfide pathway. The bacterial cell can effect this sulfide dissoln. by \"contact\" and \"non-contact\" mechanisms. The non-contact mechanism assumes that the bacteria oxidize only dissolved iron(II) ions to iron(III) ions. The latter can then attack metal sulfides and be reduced to iron(II) ions. The contact mechanism requires attachment of bacteria to the sulfide surface. The primary mechanism for attachment to pyrite is electrostatic in nature. In the case of Acidithiobacillus ferrooxidans, bacterial exopolymers contain iron(III) ions, each complexed by two uronic acid residues. The resulting pos. charge allows attachment to the neg. charged pyrite. Thus, the first function of complexed iron(III) ions in the contact mechanism is mediation of cell attachment, while their second function is oxidative dissoln. of the metal sulfide, similar to the role of free iron(III) ions in the non-contact mechanism. In both cases, the electrons extd. from the metal sulfide reduce mol. oxygen via a complex redox chain located below the outer membrane, the periplasmic space, and the cytoplasmic membrane of leaching bacteria. The dominance of either At. ferrooxidans or Leptospirillum ferrooxidans in mesophilic leaching habitats is highly likely to result from differences in their biochem. iron(II) oxidn. pathways, esp. the involvement of rusticyanin.