Enterococci are important human commensals and significant opportunistic pathogens. Biofilm-related enterococcal infections, such as endocarditis, urinary tract infections, wound and surgical site infections, and medical device-associated infections, often become chronic upon the formation of biofilm. The biofilm matrix establishes properties that distinguish this state from free-living bacterial cells and increase tolerance to antimicrobial interventions. The metabolic versatility of the enterococci is reflected in the diversity and complexity of environments and communities in which they thrive. Understanding metabolic factors governing colonization and persistence in different host niches can reveal factors influencing the transition to biofilm pathogenicity. Here, we report a form of iron-dependent metabolism for Enterococcus faecalis where, in the absence of heme, extracellular electron transfer (EET) and increased ATP production augment biofilm growth. We observe alterations in biofilm matrix depth and composition during iron-augmented biofilm growth. We show that the ldh gene encoding l-lactate dehydrogenase is required for iron-augmented energy production and biofilm formation and promotes EET.

A single Nitrospira sublineage I OTU was found to perform nitrite oxidation in full-scale domestic wastewater treatment plants (WWTPs) in the tropics. This taxon had an apparent oxygen affinity constant lower than that of the full-scale domestic activated sludge cohabitating ammonium oxidizing bacteria (AOB) (0.09 ± 0.02 g O2 m–3 versus 0.3 ± 0.03 g O2 m–3). Thus, nitrite oxidizing bacteria (NOB) may in fact thrive under conditions of low oxygen supply. Low dissolved oxygen (DO) conditions selected for and high aeration inhibited the NOB in a long-term lab-scale reactor. The relative abundance of Nitrospira sublineage I gradually decreased with increasing DO until it was washed out. Nitritation was sustained even after the DO was lowered subsequently. The morphologies of AOB and NOB microcolonies responded to DO levels in accordance with their oxygen affinities. NOB formed densely packed spherical clusters with a low surface area-to-volume ratio compared to the Nitrosomonas-like AOB clusters, which maintained a porous and nonspherical morphology. In conclusion, the effect of oxygen on AOB/NOB population dynamics depends on which OTU predominates given that oxygen affinities are species-specific, and this should be elucidated when devising operating strategies to achieve mainstream partial nitritation.

Sphingolipid metabolites are involved in the regulation of autophagy, a degradative recycling process that is required to prevent neuronal degeneration. Drosophila blue cheese mutants neurodegenerate due to perturbations in autophagic flux, and consequent accumulation of ubiquitinated aggregates. Here, we demonstrate that blue cheese mutant brains exhibit an elevation in total ceramide levels; surprisingly, however, degeneration is ameliorated when the pool of available ceramides is further increased, and exacerbated when ceramide levels are decreased by altering sphingolipid catabolism or blocking de novo synthesis. Exogenous ceramide is seen to accumulate in autophagosomes, which are fewer in number and show less efficient clearance in blue cheese mutant neurons. Sphingolipid metabolism is also shifted away from salvage toward de novo pathways, while pro-growth Akt and MAP pathways are down-regulated, and ER stress is increased. All these defects are reversed under genetic rescue conditions that increase ceramide generation from salvage pathways. This constellation of effects suggests a possible mechanism whereby the observed deficit in a potentially ceramide-releasing autophagic pathway impedes survival signaling and exacerbates neuronal death.