Thomas N J, Dubey J P, Lindsay D S, Cole R A, Meteyer C U
Department of the Interior, US Geological Survey, National Wildlife Health Center, Madison, WI, USA.
J Comp Pathol. 2007 Aug-Oct;137(2-3):102-21. doi: 10.1016/j.jcpa.2007.05.001. Epub 2007 Aug 10.
Protozoal meningoencephalitis is considered to be an important cause of mortality in the California sea otter (Enhydra lutris). Thirty nine of 344 (11.3%) California (CA) and Washington state (WA) sea otters examined from 1985 to 2004 had histopathological evidence of significant protozoal meningoencephalitis. The aetiological agents and histopathological changes associated with these protozoal infections are described. The morphology of the actively multiplicative life stages of the organisms (tachyzoites for Toxoplasma gondii and merozoites for Sarcocystis neurona) and immunohistochemical labelling were used to identify infection with S. neurona (n=22, 56.4%), T. gondii (n=5, 12.8%) or dual infection with both organisms (n=12, 30.8%). Active S. neurona was present in all dual infections, while most had only the latent form of T. gondii. In S. neurona meningoencephalitis, multifocal to diffuse gliosis was widespread in grey matter and consistently present in the molecular layer of the cerebellum. In T. gondii meningoencephalitis, discrete foci of gliosis and malacia were more widely separated, sometimes incorporated pigment-laden macrophages and mineral, and were found predominantly in the cerebral cortex. Quiescent tissue cysts of T. gondii were considered to be incidental and not a cause of clinical disease and mortality. Protozoal meningoencephalitis was diagnosed more frequently in the expanding population of WA sea otters (10 of 31, 32.3%) than in the declining CA population (29 of 313, 9.3%). Among sea otters with protozoal meningoencephalitis, those that had displayed neurological signs prior to death had active S. neurona encephalitis, supporting the conclusion that S. neurona is the most significant protozoal pathogen in the central nervous system of sea otters.
原生动物性脑膜脑炎被认为是加州海獭（Enhydra lutris）死亡的一个重要原因。1985年至2004年期间检查的344只加州（CA）和华盛顿州（WA）海獭中，有39只（11.3%）有显著原生动物性脑膜脑炎的组织病理学证据。描述了与这些原生动物感染相关的病原体和组织病理学变化。利用生物体活跃增殖生活阶段的形态（刚地弓形虫的速殖子和肉孢子虫的裂殖子）以及免疫组织化学标记来鉴定肉孢子虫（n = 22，56.4%）、刚地弓形虫（n = 5，12.8%）感染或两种生物体的双重感染（n = 12，30.8%）。在所有双重感染中均存在活跃的肉孢子虫，而大多数仅具有刚地弓形虫的潜伏形式。在肉孢子虫性脑膜脑炎中，多灶性至弥漫性胶质细胞增生在灰质中广泛存在，并始终存在于小脑分子层。在刚地弓形虫性脑膜脑炎中，离散的胶质细胞增生和软化灶分布更广泛，有时包含含色素巨噬细胞和矿物质，且主要见于大脑皮层。刚地弓形虫的静止组织囊肿被认为是偶然的，并非临床疾病和死亡的原因。在数量不断增加的华盛顿州海獭种群中，原生动物性脑膜脑炎的诊断更为频繁（31只中有10只，32.3%），而在数量不断减少的加州海獭种群中则较低（313只中有29只，9.3%）。在患有原生动物性脑膜脑炎的海獭中，那些在死亡前表现出神经症状的患有活跃的肉孢子虫脑炎，这支持了肉孢子虫是海獭中枢神经系统中最重要的原生动物病原体这一结论。
