Biological Sciences Research Group, University of Derby, Kedleston Road, Derby DE22 1GB, UK School of Biology, Molecular Health and Disease Laboratory, Newcastle University, Devonshire Building, Newcastle upon Tyne NE1 7RU, UK
Departamento de Estudios Ambientales, Universidad Simón Bolívar, Ap. 89000 Caracas, Venezuela.
Proc Biol Sci. 2014 Aug 7;281(1788):20140094. doi: 10.1098/rspb.2014.0094.
Coral diseases have been increasingly reported over the past few decades and are a major contributor to coral decline worldwide. The Caribbean, in particular, has been noted as a hotspot for coral disease, and the aptly named white syndromes have caused the decline of the dominant reef building corals throughout their range. White band disease (WBD) has been implicated in the dramatic loss of Acropora cervicornis and Acropora palmata since the 1970s, resulting in both species being listed as critically endangered on the International Union for Conservation of Nature Red list. The causal agent of WBD remains unknown, although recent studies based on challenge experiments with filtrate from infected hosts concluded that the disease is probably caused by bacteria. Here, we report an experiment using four different antibiotic treatments, targeting different members of the disease-associated microbial community. Two antibiotics, ampicillin and paromomycin, arrested the disease completely, and by comparing with community shifts brought about by treatments that did not arrest the disease, we have identified the likely candidate causal agent or agents of WBD. Our interpretation of the experimental treatments is that one or a combination of up to three specific bacterial types, detected consistently in diseased corals but not detectable in healthy corals, are likely causal agents of WBD. In addition, a histophagous ciliate (Philaster lucinda) identical to that found consistently in association with white syndrome in Indo-Pacific acroporas was also consistently detected in all WBD samples and absent in healthy coral. Treatment with metronidazole reduced it to below detection limits, but did not arrest the disease. However, the microscopic disease signs changed, suggesting a secondary role in disease causation for this ciliate. In future studies to identify a causal agent of WBD via tests of Henle-Koch's postulates, it will be vital to experimentally control for populations of the other potential pathogens identified in this study.
在过去几十年中,珊瑚疾病的报道越来越多,是全球珊瑚减少的主要原因之一。特别是加勒比地区,已被认为是珊瑚疾病的热点地区,而恰当地命名为“白色综合征”的疾病已经导致其范围内的优势造礁珊瑚的减少。自 20 世纪 70 年代以来,白色带病变(WBD)已导致棘冠柳珊瑚和扁脑珊瑚大量减少,这两种物种都被列入国际自然保护联盟濒危物种红色名录中的极危物种。尽管最近基于感染宿主滤液的挑战实验的研究得出结论,这种疾病可能是由细菌引起的,但 WBD 的病原体仍然未知。在这里,我们报告了一项使用四种不同抗生素处理的实验,针对与疾病相关的微生物群落的不同成员。两种抗生素,氨苄青霉素和帕罗霉素,完全阻止了疾病的发展,通过与未阻止疾病发展的处理方法所带来的群落变化进行比较,我们已经确定了 WBD 的可能候选病原体或病原体。我们对实验处理的解释是,一种或多达三种特定细菌类型,在患病珊瑚中始终被检测到,但在健康珊瑚中无法检测到,可能是 WBD 的病原体。此外,一种食腐性纤毛虫(Philaster lucinda)与在印度洋-太平洋地区的棘冠柳珊瑚中发现的白色综合征一致,也始终在所有 WBD 样本中被检测到,而在健康珊瑚中则未被检测到。用甲硝唑处理可将其降低到检测限以下,但不能阻止疾病的发展。然而,显微镜下的疾病迹象发生了变化,表明这种纤毛虫在疾病发病机制中起次要作用。在未来通过亨勒-科赫假设的检验来确定 WBD 的病原体的研究中,通过实验控制本研究中确定的其他潜在病原体的种群将是至关重要的。