Microbially-Induced Corrosion of Cobalt by Pseudomonas chlororaphis subspecies aureofaciens Is Driven by the Complex...

Microbially-induced corrosion (MIC) driven by redox-active metabolites has been well studied for iron-bearing infrastructure, but whether such pathways solubilise economically critical cobalt is poorly understood. This study uses the model bacterium Pseudomonas chlororaphis subspecies aureofaciens to test if redox-active phenazines corrode elemental cobalt. Mutants incapable of phenazine production corroded as much cobalt as wild-type cells after one-week incubations with Co(0) wires, and phenazines alone did not induce corrosion. Anoxic corrosion assays with cell-free spent medium showed that phenazines can maintain Co(0) oxidation in the absence of oxidants like oxygen, but that oxygen and live cells strongly favour corrosion. Constraining metabolic pathways contributing to corrosion by creating a ∆phz∆hcn mutant led to twice as much cobalt being solubilised compared to the wild type due to metabolic rerouting that could affect the production of putative metallophores. Geochemical and electrochemical analyses suggested these metal-binding metabolites keep cobalt in solution and prevent the formation of a passivation layer that inhibits MIC. This study shows that complex interactions between abiotic and biotic pathways that control the solubility and bioavailability of cobalt govern MIC. Understanding these mechanisms is critical to mitigating concerns related to MIC damaging infrastructure and optimising sustainable cobalt recovery strategies for solid waste.