原发性阿米巴脑炎

阿米巴原虫可分为自由生活的阿米巴和溶组织阿米巴，某些自由生活的阿米巴可以引起具有致死性的原发性阿米巴脑炎。它分为两类：人格勒属阿米巴引起的原发性阿米巴脑膜脑炎和棘属阿米巴引起的肉芽肿性阿米巴脑炎。     

肉芽肿性阿米巴脑炎(附1例病例)

原发性阿米巴脑膜脑炎是由自由生活的阿米巴引起,多数为福勒尔一耐格里（Naegleriafowleri）原虫,少数由棘阿米已（Acantl。－。;n。0。、ba）原虫弓l起,故该病包括两类：一类为原发性阿米巴脑膜脑炎,多为福勒尔一耐格里原虫感染;另一类为肉芽肿性阿米巴脑炎,多由棘阿米巴原虫感染引起。这类阿米巴病不经过胃肠道感染阶段,起病急,症状严重,死亡率高,临床常易误诊或漏诊,必须引起广泛的注意。我院于1997年9月尸检一例,经病理检查证实为Acanth－amoeba所致的肉芽肿性阿木巴脑炎．为厂引起临床对本病的重视,复习文献．报告如下…     

慢性阿米巴性脑膜脑炎

原发性阿米巴性脑膜脑炎是由自由生活阿米巴所致罕见感染。该疾病以急性或亚急性起病,通常是致命的。作者报告一例以前未报告过的慢性阿米巴性脑膜脑炎。患者男性,30岁,嗜睡已有5年之久。夜晚睡眠长达12小时,白天在合适情况下均能入睡。病人情况尚好,神经系统无异常体征。脑脊液显示乳白色;发现脊液白细胞数,300/cumm,淋巴球占80％,     

狒狒巴拉姆希阿米巴合并人疱疹病毒6A脑炎一例

目的狒狒巴拉姆希阿米巴、人疱疹病毒6A脑炎临床少见,均可致死,两者合并感染更为少见。本文分析狒狒巴拉姆希阿米巴合并人疱疹病毒6A脑炎的临床特点。方法报道1例狒狒巴拉姆希阿米巴合并人疱疹病毒6A脑炎患者,并结合文献分析其临床特点和预后。结果患者老年男性,急性起病,主要临床表现为意识障碍、四肢活动障碍、癫痫发作,先后2次脑脊液二代测序均检测出狒狒巴拉姆希阿米巴及人类疱疹病毒6A,头颅MRI示中脑左侧份、脑桥左侧份、右侧基底核区、丘脑DWI弥散受限信号,予以抗细菌、抗病毒、抗真菌综合治疗后,患者症状稍有缓解,后逐渐加重,且出现全身多器官功能障碍、脓毒性休克,自动出院后死亡。结论狒狒巴拉姆希阿米巴感染及人疱疹病毒6A感染脑炎的临床表现均复杂多样,两者合并感染极为少见,且病情凶险,预后极差。早期诊断,多种药物(如喷他脒羟乙磺酸盐、米替福辛、氟康唑、氟胞嘧啶、磺胺嘧啶和大环内酯类抗生素抗狒狒巴拉姆希阿米巴感染;更昔洛韦、西多福韦及膦甲酸抗HHV-6感染)联合治疗至关重要。     

原发性阿米巴脑膜脑炎1例报告

原发性阿米巴脑膜脑炎极少见 ,现报告 1例如下。1　病例　男 ,33岁。因发热、头痛、呕吐 6天于 2 0 0 1年 8月16日入院。查体 :T 38.6℃ ,P 92次 /分 ,R 2 6次 /分 ,BP18.5 / 11k Pa。心肺正常 ,全身检查未见异常。意识清楚 ,表情淡漠 ,精神萎靡 ,颜面潮红。双眼底未见视乳头水肿 ,瞳孔等大等圆 ,对光反射存在 ,双眼外展露白 3mm,余颅神经正常。左侧上下肢肌力 3～ 4级 ,肌张力低 ;右上下肢肌力 5级 ,左上下肢腱反射减弱 ,左侧巴氏征 (+) ,腹壁及提睾反射 (- ) ;左半身痛觉减退 ,脑膜刺激征 (+)。实验室检查 :血白细胞4 .6× 10 9/ L ,中…     

儿童病毒性脑炎198例临床分析

病毒性脑炎（Viral encephalitis)是由各种病毒所致的原发性脑炎，也称病素性脑膜脑炎。随着病原学诊断方法是不断发展，一般采用病毒学命名，如单纯疱诊病毒（HSV-1 HSV-2）脑炎、柯萨奇病素（COXBV）脑炎、流行性腮腺炎病毒（PPMV）脑炎等。现将我院1998-08—2003-08收治的198例病毒性脑炎患儿的诊治分析如下。     

CT和MRI在中枢神经系统感染性疾病诊断中的应用

中枢神经系统感染也称颅内感染，是细菌、病毒、真菌、螺旋体、原虫和寄生虫等引起的炎性病变以及获得性免疫缺陷综合征等。感染途径包括血行播散、邻近病灶的浸润和沿周围神经蔓延。根据病变部位，可分为脑膜炎和脑炎。不少病变同时累及脑膜和脑实质，又称为脑膜脑炎。病理改变包括脓肿、肉芽肿、粘连、囊性炎、血管炎、脱髓鞘和脑积水等。近     

自身免疫性脑炎患者并发抑郁综合征的研究进展

自身免疫性脑炎泛指一类免疫反应介导的脑炎，由特殊抗体介导的为新型自身免疫性脑炎。精神障碍作为自身免疫性脑炎患者的主要表现之一，受到了广泛的关注，而抑郁综合征作为精神障碍的一种表现，临床中并不少见，但与其相关的诊断、治疗及预后等研究却较少。为丰富临床医师对自身免疫性脑炎患者抑郁综合征的认识，本文从抑郁综合征在自身免疫性脑炎中的患病率、发病机制、诊断、治疗及其预后方面进行综述。     

胶质瘤样的单纯疱疹病毒性脑炎 (附2例临床报道)

单纯疱疹病毒(HSV)性脑炎是由单纯疱疹病毒引起的急性坏死性脑炎,在散发坏死性脑炎中占20%～75%,病死率高达40%～70%,近10%的患者可恢复正常的生活能力.尽早诊断和治疗对该病尤为重要.现将我科收治的2例患者的临床与影像学特点进行分析,并结合文献报告如下.     

自身免疫性脑炎临床鉴别诊断及治疗研究

目的分析自身免疫性脑炎的鉴别诊断及治疗措施。方法选取2015-01—2016-02我院治疗的病毒性脑炎患者为病毒性脑炎组,自身免疫性脑炎患者为自身免疫性脑炎组,每组50例,进行相关鉴别诊断;同时将自身免疫性脑炎患者按随机数字表法分为观察组(25例)与对照组(25例),观察组给予免疫球蛋白、激素治疗,对照组仅给予激素治疗。观察并比较自身免疫性脑炎的鉴别诊断及效果。结果自身免疫性脑炎组脑脊液蛋白质含量正常率(74.00%)、亚急性发作率(52.00%)、脑脊液与血清中抗NMDA抗体(54.00%)均高于病毒性脑炎组,影像学累及颞叶率(12.00%)低于病毒性脑炎组;观察组总有效率(84.00%)优于对照组(56.00%),差异具有统计学意义(P0.05)。结论自身免疫性脑炎大多亚急性发作,其脑脊液蛋白质含量基本正常,自身免疫性脑炎患者在脑脊液与血清中均存在不同程度的自身免疫性抗体,同时免疫球蛋白联合激素有更好的治疗效果。     

Neuropathological and ultrastructural features of amebic encephalitis caused by Sappinia diploidea

Here we present the neuropathological, ultrastructural, and radiological features of Sappinia diploidea, a newly recognized human pathogen. The patient was a 38-year-old man with visual disturbances, headache, and a seizure. Brain images showed a solitary mass in the posterior left temporal lobe. The mass was composed of necrotizing hemorrhagic inflammation that contained free-living amebae. Immunofluorescence microscopy showed that the organism was not a species of ameba previously known to cause encephalitis. Trophozoites had a highly distinctive double nucleus, and transmission electron microscopy confirmed that they contained 2 nuclei closely apposed along a flattened surface. The 2 nuclei were attached to each other by distinctive connecting perpendicular filaments. This and several other unique structural features led to the diagnosis of S. diploidea encephalitis. The patient was treated postoperatively with a sequential regimen of anti-amebic drugs (azithromycin, pentamidine, itraconazole, and flucytosine) and is alive after 5 years. Guidelines to recognize future cases of S. diploidea encephalitis are as follows. 1) It presented as a tumor-like cerebral mass without an abscess wall. 2) It had central necrotic and hemorrhagic inflammation that contained acute and chronic inflammatory cells without granulomas or eosinophils. 3) It contained trophozoites (40-70 microm diameter) that contained a distinctive double nucleus. 4) Cyst forms in the host were not excluded or definitely evident. 5) Trophozoites engulfed host blood cells and were stained brightly with Giemsa and periodic acid-Schiff. 6) Trophozoites often were present in viable brain parenchyma on the periphery of the mass without inflammatory response. 7) The prognosis after surgical excision and medical treatment was favorable in this instance.     

Granulomatous amebic encephalitis: a review and report of a spontaneous case from Venezuela

Granulomatous amebic encephalitis (GAE), or meningoencephalitis due to Acanthamoeba spp. and leptomyxid ameba are uncommon CNS infections that generally occur in immunocompromised hosts. We describe a case of GAE caused by Balamuthia mandrillaris previously designated as a leptomyxid ameba, in an apparently healthy 14-year-old Venezuelan boy. This case was characterized by sudden onset of seizures, focal neurologic signs and by a prolonged clinical course (from November 1992 to March 1993). Neuroimaging studies showed cerebral hypodense lesions in cerebral hemispheres, brain stem and cerebellum. Microscopically, we found a chronic granulomatous inflammatory reaction with necrotizing angiitis, large numbers of amebic trophozoites and few cysts in perivascular spaces and within necrotic CNS tissue. The amebas were identified as B. mandrillaris based on their immunofluorescence reactivity with the anti-B. mandrillaris serum. So far, 30 cases of GAE due to B. mandrillaris have been recognized in humans, two in AIDS patients. No visceral involvement by free-living amebas or any other significant abnormality was observed. This patient developed spontaneous GAE, but it remains possible that an undiagnosed abnormality in cell-mediated immunity or a deficient humoral immune response may explain the susceptibility of this patient to this opportunistic infection.Supported in part by the Pathology Education and Research Foundation (PERF) of the Department of Pathology, University of Pittsburgh     

Fatal granulomatous amoebic encephalitis due to free-living amoebae in two boys in two different hospitals in Lima,Perú

Granulomatous amoebic encephalitis caused by free-living amoebae is a rare condition that is difficult to diagnose and hard to treat, generally being fatal. Anti-amoebic treatment is often delayed because clinical signs and symptoms may hide the probable causing agent misleading the appropriate diagnostic test. There are four genera of free-living amoeba associated with human infection, Naegleria, Acanthamoeba sp., Balamuthia and Sappinia. Two boys were admitted with diagnosis of acute encephalitis. The history of having been in contact with swimming pools and rivers, supports the suspicion of an infection due to free-living amoebae. In both cases a brain biopsy was done, the histology confirmed granulomatous amoebic encephalitis with the presence of amoebic trophozoites.     

Amebic infections of the central nervous system

Journal of NeuroVirology - The report of death of a person from amebic meningoencephalitis, the proverbial “brain-eating ameba,” Naegleria fowleri, acquired in a state park lake in Iowa...     

Amoebae free-living. Report of the first Italian case of myelitis.

The AA. refer on the first Italian case of amoebae "Limax" primitive myelitis in a 25-year-old man. Microscopical observation showed amoebae free-living, but their cultivation and identification were not possible. The patient recovered because of the propriety of diagnosis and therapy with amphotericin B.     

Primary amebic meningoencephalitis: two new cases report from Venezuela

Primary amebic menigoencephalitis (PAM) is rare. Two cases of PAM in Venezuelan patients are described. Case 1, a 10 year-old male with headache, fever, vomiting. The patient swam in a water reservoir before the onset of his disease. He died during his third hospital day. Case 2, a 23 year-old male with a history of headache, fever, vomiting, drowsiness, and behavioral disturbances. The patient died on his second hospital day. The diagnosis in both cases was PAM due to Naegleria fowleri. Central nervous system infection by free-living amebas should be considered in meningoencephalitides with bacterial-free cerebro-spinal fluid.     

Effects of exercise and steroid on skeletal muscle apoptosis in the mdx mouse

Reports concerning the influence of exercise loading and steroid administration on dystrophinopathy are inconsistent. To investigate the effect of muscle exercise in Duchenne muscular dystrophy (DMD), 15 control and 15 mdx mice, an animal model of DMD, were divided into free-living (n = 6), exercise (n = 6), and immobilization (n = 3) groups. Free-living and exercise groups were further divided into steroid-treated and sham-treated groups to evaluate the effect of steroid administration. We measured apoptotic changes by in situ DNA nick-end labeling (TUNEL), DNA fragmentation assay, and Western blotting for Bcl-2 and BAX. Apoptosis was most prominent in the sham-treated exercise group, and it was significantly reduced in the steroid-treated exercise group. The steroid-treated free-living group showed a higher rate of apoptotic change than the sham-treated free-living group. Apoptosis was minimized in the free-living condition, whereas exercise loading and immobilization caused apoptotic change in this muscular dystrophy animal model. Steroid administration induced apoptosis in muscle of free-living mice, but alleviated the apoptotic damage caused by exercise loading in mdx mice. These findings suggest that steroid administration may be effective in preventing a postexercise deterioration of skeletal muscle in animal models of DMD.     

Free-living amebic meningoencephalitis

The health problems associated with pathogenic free-living amebas are just beginning to be recognized. Little is known about the organisms themselves and even less about the selective pressures concerning their ecologic niche. Therapy is virtually non-existent, and the spectrum of organisms responsible for such infections has not been defined. In this article Richard Duma provides a summary of recent research in this area.     

An autopsy case of amebic meningoencephalitis. The first Japanese case caused by Balamuthia mandrillaris

We report here the first case of amebic meningoencephalitis caused by Balamuthia mandrillaris in a 78‐year‐old Japanese woman with Sjögren's syndrome. Fourteen days before her death, she presented with high fever and lost consciousness and later developed neck stiffness and abducens palsy. Computed tomography scans of the brain demonstrated multiple low‐density areas throughout the brain. Neuropathologically, hemorrhagic and necrotic lesions with many amebic trophozoites were scattered in the brain and spinal cord. Granulomatous lesions were only rarely found. The amebas were identified as Balamuthia mandrillaris based on immunofluorescence assay. Clinicopathologically, our case was thought to be an intermediate between primary amebic meningoencephalitis due to Negleria fowleri and granulomatous amebic encephalitis due to Acanthameba species. Essentially, the case was one of an elderly person with suspected immunodeficiency with fulminant necrotic meningoencephalitis and scanty granulomatous lesions of 14 days course.     

Increased Catabolic State in Spinocerebellar Ataxia Type 1 Patients

Autosomal dominant spinocerebellar ataxia type 1 (SCA1) is a genetic movement disorder with neuronal loss in the cerebellum, brainstem, and other cerebral regions. The course of SCA1 is accompanied with progressive weight loss and amyotrophia—the causes for that remain, however, unclear. We tested the hypothesis that an imbalance between energy intake and expenditure contributes to weight loss in SCA1 patients. Anthropometric measures, energy intake (food records), and resting (calorimetry) and free-living (accelerometry) energy expenditure were determined in 10 patients with genetically proven SCA1 and 10 healthy controls closely matched for age, sex, and body composition. At rest, energy expenditure per kilogram fat-free mass was 22 % and fat oxidation rate 28 % higher in patients vs. controls indicating an increased catabolic state. Under free-living conditions, total energy expenditure and daily step counts were significantly lower in patients vs. controls. However, most patients were able to maintain energy intake and expenditure in a balanced state. Resting energy expenditure, fat oxidation, and activity energy expenditure per step count are higher, whereas 24-h total energy expenditure is lower in SCA1 patients vs. healthy controls. An altered autonomic nervous system activity, gait ataxia, and a decreased physical activity might contribute to this outcome.