Abstract
The common shrimp disease, acute hepatopancreatic necrosis disease (AHPND), has caused extensive damage to the shrimp farming industry due to its rapid spread and high mortality rates. However, the alterations in gastrointestinal microbiota (GM) ecosystem in subadult shrimps (Litopenaeus vannamei) with AHPND occurrence are still unclear. This study identified AHPND according to clinical symptoms and the existence of the toxin gene pirAVP, analyzed the microbiome dynamics of healthy and diseased subadult shrimps, and built an ecological model for quantitative evaluation of the GM imbalance. The results showed that the GM community diversity in diseased shrimps was significantly lower than that in healthy ones. The structural composition, dysbiosis-related indices, and assembly processes of the GM community were also evidently changed in diseased shrimps. The different operational taxonomic units (OTUs) in GM of diseased shrimps were mainly composed of Vibrio spp. with a relative abundance >90%, the majority of these were neutrally distributed in the neutral model of AHPND occurrence. Of 39 biomarkers for predicting AHPND occurrence, nine belonging to Vibrio were overrepresented in diseased shrimps, whereas biomarkers such as Rhodobacteraceae OTU3427, Candiadatus aysiosphaera OTU1041, KD4-96 OTU4963, and Rhodobacter OTU3366 were enhanced in healthy shrimps. Functional prediction showed that the gene abundances of the NOD receptor signaling pathway (p = .04), Vibrio infection (p < .01), and Vibrio pathogenic cycle function (p < .01) were significantly increased in diseased compared with healthy shrimps. Disturbed GM was closely correlated with infectious diseases and pirA gene. In contrast, stable GM was maintained by multiple bacterial taxa, which may be benefit for shrimp health through regulating immune system and environmental adaptation. These results indicated that GM imbalance caused by AHPND with the characteristics of expanded variation of GM diversity, increased dysbiosis-related indices, higher abundance of potential pathogens, and lager loss of potential beneficial bacteria or ecological functions, might further accelerate the progression of AHPND outbreaks. This study may provide a basis for understanding the etiology of AHPND from a microecological perspective in subadult shrimp.
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