Vater Ashley, Byrne Barbara A, Marshman Blythe C, Ashlock Lauren W, Moore James D
Integrative Pathobiology Graduate Group, University of California, Davis, Davis, United States of America.
Pathology, Microbiology, Immunology, School of Veterinary Medicine, University of California, Davis, Davis, United States of America.
PeerJ. 2018 Jun 25;6:e5104. doi: 10.7717/peerj.5104. eCollection 2018.
The Rickettsiales-like prokaryote and causative agent of Withering Syndrome (WS)- Xenohaliotis californiensis ( Xc)-decimated black abalone populations along the Pacific coast of North America. White abalone--are also susceptible to WS and have become nearly extinct in the wild due to overfishing in the 1970s. Xenohaliotis californiensis proliferates within epithelial cells of the abalone gastrointestinal tract and causes clinical signs of starvation. In 2012, evidence of a putative bacteriophage associated with Xc in red abalone--was described. Recently, histologic examination of animals with Xc infection in California abalone populations universally appear to have the phage-containing inclusions. In this study, we investigated the current virulence of Xc in red abalone and white abalone at different environmental temperatures. Using a comparative experimental design, we observed differences over time between the two abalone species in mortality, body condition, and bacterial load by quantitative real time PCR (qPCR). By day 251, all white abalone exposed to the current variant of Xc held in the warm water (18.5 °C) treatment died, while red abalone exposed to the same conditions had a mortality rate of only 10%, despite a relatively heavy bacterial burden as determined by qPCR of posterior esophagus tissue and histological assessment at the termination of the experiment. These data support the current status of . Xc as less virulent in red abalone, and may provide correlative evidence of a protective phage interaction. However, white abalone appear to remain highly susceptible to this disease. These findings have important implications for implementation of a white abalone recovery program, particularly with respect to the thermal regimes of locations where captively-reared individuals will be outplanted.
类立克次氏体原核生物与枯萎综合征（WS）的病原体——加利福尼亚异鲍哈氏菌（Xc），致使北美太平洋沿岸的黑鲍种群数量锐减。白鲍也易感染WS，由于20世纪70年代的过度捕捞，它们在野外已几近灭绝。加利福尼亚异鲍哈氏菌在鲍鱼胃肠道的上皮细胞内增殖，并引发饥饿的临床症状。2012年，有报道称在红鲍中发现了一种与Xc相关的假定噬菌体。最近，对加利福尼亚鲍鱼种群中感染Xc的动物进行组织学检查，普遍发现含有噬菌体的包涵体。在本研究中，我们调查了不同环境温度下Xc对红鲍和白鲍的当前毒力。采用比较实验设计，通过定量实时PCR（qPCR）观察了两种鲍鱼在死亡率、身体状况和细菌载量方面随时间的差异。到第251天，暴露于温水（18.5°C）处理中当前Xc变体的所有白鲍均死亡，而暴露于相同条件下的红鲍死亡率仅为10%，尽管根据实验结束时后食道组织的qPCR和组织学评估确定细菌负荷相对较高。这些数据支持了Xc在红鲍中毒力较低的现状，并可能提供噬菌体保护性相互作用的相关证据。然而，白鲍似乎仍然对这种疾病高度易感。这些发现对实施白鲍恢复计划具有重要意义，特别是对于圈养个体放流地点的热状况而言。
