Gjeltema Jenessa L, Troan Brigid, Muehlenbachs Atis, Liu Lindy, Da Silva Alexandre J, Qvarnstrom Yvonne, Tobias Jeremy R, Loomis Michael R, De Voe Ryan S
J Am Vet Med Assoc. 2016 Feb 1;248(3):315-21. doi: 10.2460/javma.248.3.315.
CASE DESCRIPTION A 22-year-old male gorilla (Gorilla gorilla gorilla) housed in a zoo was evaluated for signs of lethargy, head-holding, and cervical stiffness followed by development of neurologic abnormalities including signs of depression, lip droop, and tremors. CLINICAL FINDINGS Physical examination under general anesthesia revealed a tooth root abscess and suboptimal body condition. A CBC and serum biochemical analysis revealed mild anemia, neutrophilia and eosinopenia consistent with a stress leukogram, and signs consistent with dehydration. Subsequent CSF analysis revealed lymphocytic pleocytosis and markedly increased total protein concentration. TREATMENT AND OUTCOME Despite treatment with antimicrobials, steroids, and additional supportive care measures, the gorilla's condition progressed to an obtunded mentation with grand mal seizures over the course of 10 days. Therefore, the animal was euthanized and necropsy was performed. Multifocal areas of malacia and hemorrhage were scattered throughout the brain; on histologic examination, these areas consisted of necrosis and hemorrhage associated with mixed inflammation, vascular necrosis, and intralesional amoebic trophozoites. Tan foci were also present in the kidneys and pancreas. Immunohistochemical testing positively labeled free-living amoebae within the brain, kidneys, eyes, pancreas, heart, and pulmonary capillaries. Subsequent PCR assay of CSF and frozen kidney samples identified the organism as Balamuthia mandrillaris, confirming a diagnosis of amoebic meningoencephalitis. CLINICAL RELEVANCE Infection with B mandrillaris has been reported to account for 2.8% of captive gorilla deaths in North America over the past 19 years. Clinicians working with gorillas should have a high index of suspicion for this diagnosis when evaluating and treating animals with signs of centrally localized neurologic disease.
病例描述 一只饲养在动物园的22岁雄性大猩猩（西部低地大猩猩）出现嗜睡、头部低垂和颈部僵硬症状，随后发展为神经功能异常，包括抑郁、嘴角下垂和震颤。临床发现 全身麻醉下的体格检查发现牙根脓肿和身体状况欠佳。全血细胞计数和血清生化分析显示轻度贫血、中性粒细胞增多和嗜酸性粒细胞减少，符合应激性白细胞象，并有脱水迹象。随后的脑脊液分析显示淋巴细胞增多和总蛋白浓度显著升高。治疗与结果 尽管使用了抗菌药物、类固醇和其他支持性护理措施，大猩猩的病情在10天内进展为昏迷并伴有癫痫大发作。因此，对该动物实施了安乐死并进行了尸检。大脑中散在多灶性软化和出血区域；组织学检查显示，这些区域由坏死和出血组成，伴有混合性炎症、血管坏死和病灶内阿米巴滋养体。肾脏和胰腺也有黄褐色病灶。免疫组织化学检测在大脑、肾脏、眼睛、胰腺、心脏和肺毛细血管内阳性标记了自由生活的阿米巴。随后对脑脊液和冷冻肾脏样本进行的聚合酶链反应检测确定该病原体为曼氏巴贝斯虫，确诊为阿米巴脑膜脑炎。临床意义 据报道，在过去19年中，北美圈养大猩猩死亡病例中有2.8%是由曼氏巴贝斯虫感染所致。在评估和治疗有中枢性局部神经疾病症状的大猩猩时，临床医生应对此诊断保持高度怀疑。
