Hematodinium sp. infection does not drive collateral disease contraction in a crustacean host.

Hematodinium sp. infection does not drive collateral disease contraction in a crustacean host.
复制标题

DOI:
10.7554/elife.70356
复制
发表时间:
2022-02-18
期刊:
影响因子:
7.7
通讯作者:
Coates CJ
Coates CJ
中科院分区:
生物学1区
文献类型:
--
作者:
Davies CE;Thomas JE;Malkin SH;Batista FM;Rowley AF;Coates CJ

文献摘要

被引文献

相似文献

宿主、病原体和环境是疾病三角的决定因素,后者是社区内疾病结果和持续性的关键驱动因素。血甲藻属(Hematodinium)对全球的甲壳类动物都是有害的,它被认为抑制了宿主的先天防御,使它们更容易受到共同感染。支持免疫抑制的证据主要是轶事和来源于妥协十足类的分散帐户。我们使用了人口的海岸蟹(Carcinus maenas),血甲藻属是地方性的,以确定在两个不同的环境(开放水域,半封闭码头)的附带感染的程度。使用多资源的方法(PCR,组织学,血液学,群体遗传学,eDNA),我们确定了162血甲藻阳性螃蟹和大小/性别匹配这些162血甲藻自由螃蟹1191分析。询问螃蟹已知的其他致病因子;单孢子虫、微孢子虫、微胞体、弧菌属,真菌、囊藻、吸虫和血淋巴细菌负荷。我们发现,在任何一个地点,血甲藻阳性和无血甲藻螃蟹之间的附带感染的发生率、严重程度或组成没有显著差异,但至关重要的是,我们记录了受地点限制的病原体混合物。我们没有发现在存在或不存在其他病原体的情况下宿主细胞对血吸虫的免疫反应性的大体迹象。我们认为血甲藻不是海岸中合并感染的近端驱动因素,这表明在这种环境塑料宿主中存在进化驱动力。
Host, pathogen, and environment are determinants of the disease triangle, the latter being a key driver of disease outcomes and persistence within a community. The dinoflagellate genus Hematodinium is detrimental to crustaceans globally – considered to suppress the innate defences of hosts, making them more susceptible to co-infections. Evidence supporting immune suppression is largely anecdotal and sourced from diffuse accounts of compromised decapods. We used a population of shore crabs (Carcinus maenas), where Hematodinium sp. is endemic, to determine the extent of collateral infections across two distinct environments (open-water, semi-closed dock). Using a multi-resource approach (PCR, histology, haematology, population genetics, eDNA), we identified 162 Hematodinium-positive crabs and size/sex-matched these to 162 Hematodinium-free crabs out of 1191 analysed. Crabs were interrogated for known additional disease-causing agents; haplosporidians, microsporidians, mikrocytids, Vibrio spp., fungi, Sacculina, trematodes, and haemolymph bacterial loads. We found no significant differences in occurrence, severity, or composition of collateral infections between Hematodinium-positive and Hematodinium-free crabs at either site, but crucially, we recorded site-restricted blends of pathogens. We found no gross signs of host cell immune reactivity towards Hematodinium in the presence or absence of other pathogens. We contend Hematodinium sp. is not the proximal driver of co-infections in shore crabs, which suggests an evolutionary drive towards latency in this environmentally plastic host.