Zhou Zhongjiang, Lu Jiaqi, Zhan Pingping, Xiong Jinbo
State Key Laboratory for the Quality and Safety of Agro-Products, School of Marine Sciences, Ningbo University, Ningbo 315211, China.
Key Laboratory of Aquacultural Biotechnology, Ministry of Education, School of Marine Sciences, Ningbo University, Ningbo 315211, China.
Microorganisms. 2025 Mar 24;13(4):720. doi: 10.3390/microorganisms13040720.
Postlarval shrimp frequently face threats from acute hepatopancreatic necrosis disease (AHPND). Although AHPND affects both postlarval and adult shrimp, abiotic and biotic factors are distinct between life stages, such as rearing water nutrient levels and host life stage-dependent microbiota. The response of postlarvae-associated microbiota to AHPND, however, remains largely unexplored compared with its effects on juvenile and adult shrimp. To address this knowledge gap, a comparative analysis of postlarvae-associated microbiota and the ecological processes underlying AHPND progression was performed by sequencing the bacterial V3-V4 hypervariable region of the 16S rRNA gene. AHPND infection was validated by high copies of genes (Toxin 1) in diseased shrimp hepatopancreas. Advanced AHPND significantly altered the structure of the postlarvae-associated microbiota, with significant enrichment of Bacilli and Bdellovibrionia species in healthy larvae compared with matched AHPND-infected cohorts, although gut microbiota recovery was observed at the late disease stage, corresponding with the cessation of postlarval mortality. AHPND infection explained 11.0% ( < 0.001) of the variance in community structures, whereas postlarvae days post hatching also significantly influenced bacterial communities (7.1% variance, < 0.001). AHPND-infected shrimp exhibited reduced homogeneous selection and increased dispersal limitation and drift governing their microbiota. These changes were primarily driven by specific microbial lineages, including enriched Bin36 Rhodobacteraceae and Bin11 Flavobacteriaceae, and suppressed Bin63 and Bin9 in AHPND-infected shrimp. After excluding shrimp age effect, 13 AHPND-discriminatory taxa were identified, accurately distinguishing infected shrimp from healthy individuals with 100% precision. Furthermore, AHPND outbreak weakened the network complexity and stability, which was driven by the suppressed keystone taxa that were positively associated with network robustness. Collectively, our findings deepen the understanding of the inextricable interplay between postlarval shrimp health, microbiota dynamics, and survival, as well as the underlying ecological mechanisms over AHPND progression.
幼虾后期常面临急性肝胰腺坏死病（AHPND）的威胁。尽管AHPND会影响幼虾后期和成年虾，但非生物和生物因素在不同生命阶段有所不同，如养殖水体营养水平和宿主生命阶段依赖性微生物群。然而，与AHPND对幼虾和成虾的影响相比，幼虾相关微生物群对AHPND的反应在很大程度上仍未得到探索。为了填补这一知识空白，通过对16S rRNA基因的细菌V3 - V4高变区进行测序，对幼虾相关微生物群以及AHPND进展背后的生态过程进行了比较分析。通过患病虾肝胰腺中高拷贝的 基因（毒素1）验证了AHPND感染。晚期AHPND显著改变了幼虾相关微生物群的结构，与匹配的AHPND感染组相比，健康幼虾中的芽孢杆菌属和蛭弧菌属物种显著富集，尽管在疾病后期观察到肠道微生物群恢复，这与幼虾后期死亡率的停止相对应。AHPND感染解释了群落结构变异的11.0%（<0.001），而孵化后幼虾的天数也显著影响细菌群落（变异7.1%，<0.001）。AHPND感染的虾表现出均匀选择减少，其微生物群的扩散限制和漂移增加。这些变化主要由特定的微生物谱系驱动，包括AHPND感染虾中富集的Bin36红杆菌科和Bin11黄杆菌科，以及被抑制的Bin63和Bin9。排除虾龄影响后，鉴定出13个AHPND鉴别分类群，能以100%的精度准确区分感染虾和健康个体。此外，AHPND爆发削弱了网络复杂性和稳定性，这是由与网络稳健性呈正相关的被抑制的关键分类群驱动的。总的来说，我们的研究结果加深了对幼虾健康、微生物群动态和生存之间不可分割的相互作用以及AHPND进展背后潜在生态机制的理解。
