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This critical review outlines a roadmap for the conversion of chemical oxygen demand (COD) contained in sewage to commodities based on three-steps: capture COD as sludge, ferment it to volatile fatty acids (VFA), and upgrade VFA to products. The article analyzes the state-of-the-art of this three-step approach and discusses the bottlenecks and challenges. The potential of this approach is illustrated for the European Union's 28 member states (EU-28) through Monte Carlo simulations. High-rate contact stabilization captures the highest amount of COD (66-86 g COD person equivalent day in 60% of the iterations). Combined with thermal hydrolysis, this would lead to a VFA-yield of 23-44 g COD person equivalent day. Upgrading VFA generated by the EU-28 would allow, in 60% of the simulations, for a yearly production of 0.2-2.0 megatonnes of esters, 0.7-1.4 megatonnes of polyhydroxyalkanoates or 0.6-2.2 megatonnes of microbial protein substituting, respectively, 20-273%, 70-140% or 21-72% of their global counterparts (i.e., petrochemical-based esters, bioplastics or fishmeal). From these flows, we conclude that sewage has a strong potential as biorefinery feedstock, although research is needed to enhance capture, fermentation and upgrading efficiencies. These developments need to be supported by economic/environmental analyses and policies that incentivize a more sustainable management of our resources.

Urine contains the majority of nutrients in urban wastewaters and is an ideal nutrient recovery target. In this study, stabilization of real undiluted urine through nitrification and subsequent microalgae cultivation were explored as strategy for biological nutrient recovery. A nitrifying inoculum screening revealed a commercial aquaculture inoculum to have the highest halotolerance. This inoculum was compared with municipal activated sludge for the start-up of two nitrification membrane bioreactors. Complete nitrification of undiluted urine was achieved in both systems at a conductivity of 75mScm(-1) and loading rate above 450mgNL(-1)d(-1). The halotolerant inoculum shortened the start-up time with 54%. Nitrite oxidizers showed faster salt adaptation and Nitrobacter spp. became the dominant nitrite oxidizers. Nitrified urine as growth medium for Arthrospira platensis demonstrated superior growth compared to untreated urine and resulted in a high protein content of 62%. This two-stage strategy is therefore a promising approach for biological nutrient recovery.

White spot syndrome virus (WSSV) is an extremely destructive virus in shrimp farming which has caused a serious economic loss to global shrimp industry. Learning its infection routes is the basis for WSSV prevention and control. The digestive tract and gill were generally considered to be the target tissues for WSSV entry into shrimp. However, whether there is any other target tissue for WSSV entry into the shrimp is still not clear. In the present study, we firstly found that the transcripts of WSSV could be detected in the antennal gland of the Pacific white shrimp Litopenaeus vannamei cultured in the sea water without any signs of disease. Considering that the antennal gland is an important organ which functions in regulating the osmotic pressure and balance of ions in shrimp, we want to know whether it is also an entry for WSSV infection to shrimp. The spatial expressions of WSSV in shrimp tissues including antennal gland were firstly analyzed in shrimp naturally infected with WSSV, and the data showed that WSSV could be detected in antennal gland of shrimp at the early stages of WSSV infection, and intact virus particles were observed under transmission electronic microscope. Reverse perfusion of WSSV into antennal gland could cause the infection and lead to the death of shrimp. Incubation of WSSV with antennal gland tissues in vitro also led to the replication of WSSV in cultured antennal gland. These data indicated that antennal gland was an entry of WSSV into shrimp to cause the infection. The effect of salinity on WSSV infection was analyzed, and the data showed that salinity stress could induce faster WSSV replication in antennal gland, and accelerate the process of disease. Our study confirmed a new infection route of WSSV, and salinity stress could lead to the disease outbreak caused by WSSV. These data will provide useful information for the development of strategy for WSSV prevention and control.