To date, hepatopancreatic necrosis disease (HPND) in Eriocheir sinensis is causing huge financial losses to the aquaculture industry while the cause of HPND remains unclear. Our previous study has implied that HPND is probably relevant to the damages caused by insecticide residues. In this work, the comparative studies regarding histopathology and trends in immune‐related/detoxifying enzymes activities of the crabs were performed between exposed to the low concentration of insecticides (i.e. β‐cypermethrin 8.52 × 10−12 g/L and trichlorfon 5 × 10−5 g/L) in a long‐term (90‐days) and suffered from HPND. The concentration was obtained by a median‐lethal concentration (LC50) and a safe concentration (SC), and it was 10 times lower than the safe concentration in this experiment. This work's principal aim was to investigate the potential chronic effects of low concentrations of insecticides exposure on crabs and their relevance with HPND. As a result, crabs exposed to the low concentration of insecticides caused similar clinical symptoms and severity in hepatopancreas and other tissue damages like HPND. Meanwhile, catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), acid phosphatase (ACP), alkaline phosphatase (AKP), lysozyme (LZM) and carboxylesterase (CarE) enzymatic activity increased after exposure to the two insecticides and then decreased in the later stages, while the activity of glutathione S‐transferase (GSTs) has barely changed. Results of enzymatic activity indicated that the two insecticides induced oxidative damage to the hepatopancreas of E. sinensis. These evidence indicated that the chronic damage caused by the low concentration of insecticides, which is considered insecticide residue, might be part of the causes of HPND in crabs. The present work may enhance our understanding of the pathogenesis of HPND and provide a theoretical basis for the management of intensive crab aquaculture.

Each year from April to May, high mortality rates are reported in red swamp crayfish (Procambarus clarkii) cultured in Jiangsu and other regions, in China, and this phenomenon has come to be known as “Black May” disease (BMD). Therefore, in order to investigate the possible causes of this disease, this study gathered BMD-affected P. clarkii samples and performed transcriptome analysis on hepatopancreas, gill, and muscle tissues. A total of 19,995,164, 149,212,804, and 222,053,848 clean reads were respectively obtained from the gills, muscle, and hepatopancreas of BMD-affected P. clarkii, and 114,024 unigenes were identified. The number of differentially expressed genes (DEGs) in gill, muscle, and hepatopancreas was 1703, 964, and 476, respectively. GO and KEGG enrichment analyses of the DEGs were then conducted. Based on KEGG pathway enrichment analysis, the most significantly differentially expressed pathways were mainly those involved with metabolism, human disease, and cellular processes. Further analysis of the significantly DEGs revealed that they were mainly related to the mitochondrial-mediated apoptosis pathway and that the expression of these DEGs was mostly down-regulated. Moreover, the expression of genes related to immune and metabolism-related pathways was also significantly down-regulated, and these significantly-inhibited pathways were the likely causes of P. clarkii death. Therefore, our results provide a basis for the identification of BMD causes.

The peak period of morbidity and death in cultured Procambarus clarkii is around May each year and is called the “Black May” disease. The pathogen causing “Black May” disease is believed to be a white spot syndrome virus (WSSV). In 2018, a significant number of P. clarkii died in the pond culture of Xinglong Township, Xuyi County. Two sampling tests on the affected pond showed that, in addition to WSSV, a novel Dicistro‐like virus (PcDV) was present. Genomic sequence analysis indicated that this new virus belongs to the Dicistroviridae family, Picornaviridaes order. A high number of spherical particles were detected in gill tissues of P. clarkii with “Black May” disease by electron microscopy, a finding consistent with viruses from the Picornaviridaes order. From October 2018 to September 2019, we took monthly samples from Hubei, Jiangsu and Anhui provinces, and tested for the presence of PcDV and WSSV in P. clarkii. The detection rates of PcDV in P. clarkii peaked from April to June, consistent with the onset of the “Black May” disease. In conclusion, we believe that the discovery of PcDV will provide new research directions for investigating the pathogens causing “Black May” disease in P. clarkii.

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