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本文引用的文献

1
Immune responses in hibernating little brown myotis () with white-nose syndrome.患有白鼻综合征的冬眠小棕蝠的免疫反应
Proc Biol Sci. 2017 Feb 8;284(1848). doi: 10.1098/rspb.2016.2232.
2
Vitamin B2 as a virulence factor in Pseudogymnoascus destructans skin infection.维生素 B2 作为毁灭拟茎点霉皮肤感染的毒力因子。
Sci Rep. 2016 Sep 13;6:33200. doi: 10.1038/srep33200.
3
The cutaneous lipid composition of bat wing and tail membranes: a case of convergent evolution with birds.蝙蝠翅膀和尾膜的皮肤脂质组成:与鸟类趋同进化的一个实例。
Proc Biol Sci. 2016 Jun 29;283(1833). doi: 10.1098/rspb.2016.0636.
4
Environment, host, and fungal traits predict continental-scale white-nose syndrome in bats.环境、宿主和真菌特征预测蝙蝠的白鼻综合征在大陆范围内的发生。
Sci Adv. 2016 Jan 29;2(1):e1500831. doi: 10.1126/sciadv.1500831. eCollection 2016 Jan.
5
White-Nose Syndrome Disease Severity and a Comparison of Diagnostic Methods.白鼻综合征疾病严重程度及诊断方法比较。
Ecohealth. 2016 Mar;13(1):60-71. doi: 10.1007/s10393-016-1107-y. Epub 2016 Mar 8.
6
The White-Nose Syndrome Transcriptome: Activation of Anti-fungal Host Responses in Wing Tissue of Hibernating Little Brown Myotis.白鼻综合征转录组:冬眠的小棕蝠翼组织中抗真菌宿主反应的激活
PLoS Pathog. 2015 Oct 1;11(10):e1005168. doi: 10.1371/journal.ppat.1005168. eCollection 2015 Oct.
7
Conservation Physiology and Conservation Pathogens: White-Nose Syndrome and Integrative Biology for Host-Pathogen Systems.保护生理学与保护病原体:白鼻综合征与宿主 - 病原体系统的整合生物学
Integr Comp Biol. 2015 Oct;55(4):631-41. doi: 10.1093/icb/icv099. Epub 2015 Aug 24.
8
Destructin-1 is a collagen-degrading endopeptidase secreted by Pseudogymnoascus destructans, the causative agent of white-nose syndrome.破坏素-1是一种由白鼻综合征病原体毁灭裸囊菌分泌的胶原蛋白降解内肽酶。
Proc Natl Acad Sci U S A. 2015 Jun 16;112(24):7478-83. doi: 10.1073/pnas.1507082112. Epub 2015 May 5.
9
Interruption to cutaneous gas exchange is not a likely mechanism of WNS-associated death in bats.皮肤气体交换中断不太可能是蝙蝠白鼻综合征相关死亡的机制。
J Exp Biol. 2015 Jul;218(Pt 13):1986-9. doi: 10.1242/jeb.118950. Epub 2015 May 5.
10
White-nose syndrome initiates a cascade of physiologic disturbances in the hibernating bat host.白鼻综合征会在冬眠的蝙蝠宿主中引发一系列生理紊乱。
BMC Physiol. 2014 Dec 9;14:10. doi: 10.1186/s12899-014-0010-4.

白鼻综合征会提高冬眠蝙蝠的蛰伏代谢率并增加其蒸发失水。

White-nose syndrome increases torpid metabolic rate and evaporative water loss in hibernating bats.

作者信息

McGuire Liam P, Mayberry Heather W, Willis Craig K R

机构信息

Department of Biology, University of Winnipeg, Winnipeg, Manitoba, Canada;

Department of Biological Sciences, Texas Tech University, Lubbock, Texas; and.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2017 Dec 1;313(6):R680-R686. doi: 10.1152/ajpregu.00058.2017. Epub 2017 Aug 23.

DOI:10.1152/ajpregu.00058.2017
PMID:28835446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5814698/
Abstract

Fungal diseases of wildlife typically manifest as superficial skin infections but can have devastating consequences for host physiology and survival. White-nose syndrome (WNS) is a fungal skin disease that has killed millions of hibernating bats in North America since 2007. Infection with the fungus causes bats to rewarm too often during hibernation, but the cause of increased arousal rates remains unknown. On the basis of data from studies of captive and free-living bats, two mechanistic models have been proposed to explain disease processes in WNS. Key predictions of both models are that WNS-affected bats will show ) higher metabolic rates during torpor (TMR) and ) higher rates of evaporative water loss (EWL). We collected bats from a WNS-negative hibernaculum, inoculated one group with , and sham-inoculated a second group as controls. After 4 mo of hibernation, TMR and EWL were measured using respirometry. Both predictions were supported, and our data suggest that infected bats were more affected by variation in ambient humidity than controls. Furthermore, disease severity, as indicated by the area of the wing with UV fluorescence, was positively correlated with EWL, but not TMR. Our results provide the first direct evidence that heightened energy expenditure during torpor and higher EWL independently contribute to WNS pathophysiology, with implications for the design of potential treatments for the disease.

摘要

野生动物的真菌病通常表现为浅表皮肤感染,但可能对宿主的生理机能和生存造成毁灭性后果。白鼻综合征(WNS)是一种真菌性皮肤病,自2007年以来已导致北美数百万只冬眠蝙蝠死亡。感染这种真菌会使蝙蝠在冬眠期间过于频繁地苏醒,但苏醒率增加的原因尚不清楚。基于对圈养和自由生活蝙蝠的研究数据,已经提出了两种机制模型来解释WNS的疾病过程。这两种模型的关键预测是,受WNS影响的蝙蝠在蛰伏期间将表现出)较高的代谢率(TMR)和)较高的蒸发失水率(EWL)。我们从一个没有白鼻综合征的冬眠洞穴中收集蝙蝠,给一组接种 ,另一组进行假接种作为对照。经过4个月的冬眠后,使用呼吸测定法测量TMR和EWL。这两个预测都得到了支持,我们的数据表明,受感染的蝙蝠比对照组更受环境湿度变化的影响。此外,如翅膀紫外线荧光区域所示的疾病严重程度与EWL呈正相关,但与TMR无关。我们的结果提供了第一个直接证据,即蛰伏期间能量消耗增加和较高的EWL独立地导致了白鼻综合征的病理生理过程,这对该疾病潜在治疗方法的设计具有启示意义。