We investigated H2S attenuation by dissimilatory perchlorate-reducing bacteria (DPRB). All DPRB tested oxidized H2S coupled to (per)chlorate reduction without sustaining growth. H2S was preferentially utilized over organic electron donors resulting in an enriched (34S)-elemental sulfur product. Electron microscopy revealed elemental sulfur production in the cytoplasm and on the cell surface of the DPRB Azospira suillum. Based on our results, we propose a novel hybrid enzymatic-abiotic mechanism for H2S oxidation similar to that recently proposed for nitrate-dependent Fe(II) oxidation. The results of this study have implications for the control of biosouring and biocorrosion in a range of industrial environments.

Acute esophageal necrosis (AEN), also called black esophagus, is quite exceptional. Endoscopic findings show circumferential black discolouration of the esophagus with or without exudates. The etiology of AEN is presently unknown and is assumed to be multifactorial. Distal esophageal involvement with proximal extension ending sharply at the gastroesophageal junction is the most common presentation. The present case report describes the clinical and endoscopic evolution of black esophagus observed in a patient with significant peripheral vascular disease, who was presented to the intensive care unit at the Hopital Saint-Francois d'Assise (Quebec City, Quebec). Through an extensive review of the literature, common underlying clinical conditions of patients diagnosed with AEN have been identified.

The radiological and histological appearance of pulmonary hyalinizing granuloma (PHG) and its pathogenesis are described. The histological features bear a striking resemblance to fibrosing mediastinitis. Patients present clinically with nonspecific respiratory or general symptoms. Slowly growing solitary or, more often, multiple nodules are found on radiographs of the chest, suggesting neoplastic disease. Four patients with PHG are described. Four patients with PHG are described. One had lesions in the kidneys that were pathologically identical to those of PHG. There is no clear etiology for this disease, but from the cases reported here and those reported previously it is postulated that diverse etiologic factors might lead to a common immunological response. Inflammatory agents such as tubercle bacilli or fungal organisms (e.g., Histoplasma), or a collagen or autoimmune disease may act as trigger mechanisms for the induction of PHG.

Summary Hydrogen sulfide produced by sulfate‐reducing microorganisms (SRM) poses significant health and economic risks, particularly during oil recovery. Previous studies identified perchlorate as a specific inhibitor of SRM. However, constant inhibitor addition to natural systems results in new selective pressures. Consequently, we investigated the ability of Desulfovibrio alaskensis G20 to evolve perchlorate resistance. Serial transfers in increasing concentrations of perchlorate led to robust growth in the presence of 100 mM inhibitor. Isolated adapted strains demonstrated a threefold increase in perchlorate resistance compared to the wild‐type ancestor. Whole genome sequencing revealed a single base substitution in Dde_2265, the sulfate adenylyltransferase (sat). We purified and biochemically characterized the Sat from both wild‐type and adapted strains, and showed that the adapted Sat was approximately threefold more resistant to perchlorate inhibition, mirroring whole cell results. The ability of this mutation to confer resistance across other inhibitors of sulfidogenesis was also assayed. The generalizability of this mutation was confirmed in multiple evolving G20 cultures and in another SRM, D. vulgaris Hildenborough. This work demonstrates that a single nucleotide polymorphism in Sat can have a significant impact on developing perchlorate resistance and emphasizes the value of adaptive laboratory evolution for understanding microbial responses to environmental perturbations.