Literature frequently mentions increased nitrite concentrations along with its inhibitory effect towards bacteria and aquatic life. Nitrite accumulation has been studied for decades, and although numerous causal factors have already been commented on in literature, the mechanism of nitrite accumulation is not always clear. From the broad range of parameters and environmental factors reviewed in this paper, it is obvious that the causes and consequences of nitrite accumulation are not yet completely understood. Among others, pH, dissolved oxygen, volatile fatty acids, phosphate and reactor operation have been found to play a role in nitrite accumulation, which results from differential inhibition or disruption of the linkage of the different steps in both nitrification and denitrification. In the case of nitrification, this differential inhibition could lead to the displacement or unlinking of the ammonia oxidisers and nitrite oxidisers. In this paper, the idea is formulated that the nitrifier population forms a role model for the total microbial community. Increased nitrite concentrations would in this aspect not only signal a disruption of nitrifiers, but possibly also of the total configuration of the microbial community.Abbreviations: AMO -Ammonia mono-oxygenase; Anammox -Anaerobic ammonium oxidation; AOBAmmonia-oxidising bacteria; ATP -Adenosine triphosphate; COD -Chemical oxygen demand; DNRA -Dissimilatory nitrate reduction to ammonium; DO -Dissolved oxygen; EU -European union; FA -Free ammonia; F/M -Food to micro-organism ratio; FNA -Free nitrous acid; HAO -Hydroxylamine oxidoreductase; HRTHydraulic residence time; NDBEPR -Enhanced biological phosphate removal with nitrification and denitrification; NO -Nitric oxide; NOB -Nitrite-oxidising bacteria; NOR -Nitrite oxidoreductase; OLAND -Oxygen limited autotrophic nitrification denitrification; RBC -Rotating biological contactor; Sharon -Single reactor high activity ammonia removal over nitrite; SRT -Sludge residence time; TAN -Total ammoniacal nitrogen; TOC -Total organic carbon; VAS -Volatile attached solids

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BackgroundClostridium perfringens is an anaerobic toxin-producing bacterium that has long been associated with intestinal diseases, particularly in neonatal humans and animals. More recently, infant gut microbiome studies have suggested an important link between C. perfringens and the devastating preterm-associated disease Necrotising Enterocolitis (NEC), but in-depth studies on this pathogen (genomics and mechanistic) are lacking.Methods/MaterialsWe isolated and whole-genome sequenced 274 infant-associated C. perfringens isolates from 5 hospitals across the UK between 2011-2016 (including longitudinal samples from 31 individuals). We performed in-depth genomic analyses, phenotypically characterised pathogenic traits of 10 strains (including 4 C. perfringens from NEC patients) and established a novel oral-challenge C57BL/6 mouse infection model for microbe-host studies.ResultsPore-forming toxin encoding genes pfoA and cpb2 were enriched within hypervirulent lineages that exclusively consisted of C. perfringens-associated NEC (CPA-NEC) strains, in addition to overabundance of colonisation factors. Importantly, we identified a circulating C. perfringens variant, eventually linked to a fatal CPA-NEC case. The variant was detected consistently within 6 individuals in two sister hospitals across a 40-day window, demonstrating for the first time the intra- and inter-hospital dissemination of C. perfringens. CPA-NEC isolates were determined phenotypically to be more virulent (linked with overabundance of gene pfoA) than isolates obtained from non-NEC preterm babies. In addition, two pfoA-positive CPA-NEC C. perfringens strains were confirmed to induce clinical inflammatory tissue lesions in vivo.ConclusionsHypervirulent lineages are linked to CPA-NEC, potentially due to the production of pore-forming toxins, coupled with higher metabolic, transmission, and pathogenic capacities. These studies indicate C. perfringens is an important bacterial pathogen in preterm infants and highlights the requirement for further investigation into development of intervention and therapeutic strategies.