Marine Biotoxins Program, National Oceanic and Atmospheric Administration/National Ocean Service, Charleston, South Carolina, USA.
PLoS One. 2012;7(8):e42974. doi: 10.1371/journal.pone.0042974. Epub 2012 Aug 15.
In the Florida Panhandle region, bottlenose dolphins (Tursiops truncatus) have been highly susceptible to large-scale unusual mortality events (UMEs) that may have been the result of exposure to blooms of the dinoflagellate Karenia brevis and its neurotoxin, brevetoxin (PbTx). Between 1999 and 2006, three bottlenose dolphin UMEs occurred in the Florida Panhandle region. The primary objective of this study was to determine if these mortality events were due to brevetoxicosis. Analysis of over 850 samples from 105 bottlenose dolphins and associated prey items were analyzed for algal toxins and have provided details on tissue distribution, pathways of trophic transfer, and spatial-temporal trends for each mortality event. In 1999/2000, 152 dolphins died following extensive K. brevis blooms and brevetoxin was detected in 52% of animals tested at concentrations up to 500 ng/g. In 2004, 105 bottlenose dolphins died in the absence of an identifiable K. brevis bloom; however, 100% of the tested animals were positive for brevetoxin at concentrations up to 29,126 ng/mL. Dolphin stomach contents frequently consisted of brevetoxin-contaminated menhaden. In addition, another potentially toxigenic algal species, Pseudo-nitzschia, was present and low levels of the neurotoxin domoic acid (DA) were detected in nearly all tested animals (89%). In 2005/2006, 90 bottlenose dolphins died that were initially coincident with high densities of K. brevis. Most (93%) of the tested animals were positive for brevetoxin at concentrations up to 2,724 ng/mL. No DA was detected in these animals despite the presence of an intense DA-producing Pseudo-nitzschia bloom. In contrast to the absence or very low levels of brevetoxins measured in live dolphins, and those stranding in the absence of a K. brevis bloom, these data, taken together with the absence of any other obvious pathology, provide strong evidence that brevetoxin was the causative agent involved in these bottlenose dolphin mortality events.
在佛罗里达狭长地带,宽吻海豚(Tursiops truncatus)极易受到大规模异常死亡事件(UME)的影响,这些事件可能是由于暴露在夜光藻(Karenia brevis)及其神经毒素——短裸甲藻毒素(PbTx)的大量繁殖中所致。1999 年至 2006 年,佛罗里达狭长地带发生了三起宽吻海豚 UME。本研究的主要目的是确定这些死亡事件是否是由于短裸甲藻中毒引起的。对 105 只宽吻海豚及其相关猎物的 850 多个样本进行了分析,以检测藻类毒素,并详细说明了组织分布、营养转移途径以及每个死亡事件的时空趋势。1999/2000 年,在广泛的夜光藻大量繁殖之后,有 152 只海豚死亡,在接受测试的 52%的动物中,检测到的短裸甲藻毒素浓度高达 500ng/g。2004 年,在没有可识别的夜光藻爆发的情况下,105 只宽吻海豚死亡;然而,在接受测试的 100%的动物中,短裸甲藻毒素的浓度高达 29,126ng/mL。海豚胃内容物中经常含有受短裸甲藻毒素污染的鲱鱼。此外,另一种潜在的产毒藻类物种——拟菱形藻也存在,并且几乎所有接受测试的动物体内都检测到低水平的神经毒素——软骨藻酸(DA)(89%)。2005/2006 年,90 只宽吻海豚死亡,最初与夜光藻高密度同时发生。在接受测试的动物中,大多数(93%)短裸甲藻毒素的浓度高达 2,724ng/mL。尽管存在密集的产生软骨藻酸的拟菱形藻藻华,但在这些动物中未检测到 DA。与活海豚或在没有夜光藻爆发的情况下搁浅的海豚中测量到的短裸甲藻毒素的缺乏或非常低水平相比,这些数据,加上没有任何其他明显的病理学证据,有力地证明了短裸甲藻毒素是导致这些宽吻海豚死亡事件的原因。