Aroch Itamar, Baneth Gad, Salant Harold, Nachum-Biala Yaarit, Berkowitz Asaf, Shamir Merav, Chai Orit
Koret School of Veterinary Medicine, The Hebrew University of Jerusalem, Rehovot, Israel.
Department of Microbiology and Molecular Genetics, The Kuvin Center for the Study of Infectious and Tropical Diseases, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Vet Clin Pathol. 2018 Jun;47(2):289-293. doi: 10.1111/vcp.12582. Epub 2018 Feb 6.
An 8-year-old mixed-breed dog was presented for acute, progressive weakness and ataxia, inappetence, and weight loss. The patient was mentally normal, but nonambulatory, with a right head tilt, right positional ventral strabismus, and slight head tremors. A neurologic lesion was localized to the cerebellum and right brainstem. Cerebrospinal fluid (CSF) analysis showed a markedly increased protein concentration and mixed pleocytosis, with eosinophil predominance (44%), intracytoplasmic inclusions within eosinophils, consistent with Ehrlichia canis (E canis) morulae, and Toxoplasma gondii (T gondii) or Neospora caninum (N caninum) tachyzoites within eosinophils and monocytes. A serum indirect immunofluorescent antibody test was positive for N caninum (titer 1:12 800) and negative for T gondii. Both blood and CSF PCR results were N caninum- and E canis-positive and T gondii- and Anaplasma phagocytophilum-negative, and blood PCR, but not CSF PCR, was Hepatozoon canis-positive. The dog was treated for 30 days with clindamycin, sulfamethoxazole-trimethoprim, doxycycline, prednisone, and cephalosporin, but did not improve neurologically, and was euthanized. Brain histopathology showed moderate multifocal, subacute meningoencephalitis with necrosis and gliosis. The neurologic disease was mostly attributed to central nervous system (CNS) neosporosis, with the possible contribution of ehrlichiosis, which was likely a manifestation of blood-brain barrier disruption. Hepatozoonosis was probably a result or cause of underlying immunosuppression. To our knowledge, this is the first report of CNSN caninum and E canis co-infection detected by both CSF PCR and cytology and E canis morulae identified within CSF eosinophils.
一只8岁的混血犬因急性进行性虚弱、共济失调、食欲不振和体重减轻前来就诊。该犬精神正常，但无法行走，有右侧头部倾斜、右侧位置性腹侧斜视和轻微头部震颤。神经系统病变定位于小脑和右侧脑干。脑脊液（CSF）分析显示蛋白浓度显著升高且有混合性细胞增多，以嗜酸性粒细胞为主（44%），嗜酸性粒细胞内有胞质内包涵体，符合犬埃立克体（E canis）桑葚体，嗜酸性粒细胞和单核细胞内有刚地弓形虫（T gondii）或犬新孢子虫（N caninum）速殖子。血清间接免疫荧光抗体检测犬新孢子虫呈阳性（滴度1:12 800），弓形虫呈阴性。血液和脑脊液PCR结果犬新孢子虫和犬埃立克体均为阳性，弓形虫和嗜吞噬细胞无形体均为阴性，血液PCR犬肝簇虫呈阳性，但脑脊液PCR阴性。该犬用克林霉素、磺胺甲恶唑-甲氧苄啶、强力霉素、泼尼松和头孢菌素治疗30天，但神经功能未改善，最终实施安乐死。脑病理组织学检查显示中度多灶性亚急性脑膜脑炎伴坏死和胶质增生。神经系统疾病主要归因于中枢神经系统（CNS）新孢子虫病，可能还有埃立克体病的作用，后者可能是血脑屏障破坏的一种表现。肝簇虫病可能是潜在免疫抑制的结果或原因。据我们所知，这是首例通过脑脊液PCR和细胞学检测到中枢神经系统犬新孢子虫和犬埃立克体共感染以及在脑脊液嗜酸性粒细胞内鉴定出犬埃立克体桑葚体的报告。
