Miklossy Judith
International Alzheimer Research Center, Alzheimer Prevention Foundation, 1921 Martigny-Croix, Switzerland.
Open Neurol J. 2012;6:146-57. doi: 10.2174/1874205X01206010146. Epub 2012 Dec 28.
Whether spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was the subject of long-lasting debate. Detection of Treponema pallidum in the brains of patients with general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis. Today, the same question is in the center of debate with respect to Lyme disease. The goal of this review was to compare the established pathological features of neurosyphilis with those available for Lyme neuroborreliosis. If the main tertiary forms of neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi can be detected in brain lesions would indicate that the spirochete is responsible for the neuropsychiatric manifestations of late/chronic Lyme neuroborreliosis. The substantial amounts of data available in the literature show that the major forms of late/chronic Lyme neuroborreliosis (meningovascular and meningoencephalitis) are clinically and pathologically confirmed. Borrelia burgdorferi was detected in association with tertiary brain lesions and cultivated from the affected brain or cerebrospinal fluid. The accumulated data also indicate that Borrelia burgdorferi is able to evade from destruction by the host immune reactions, persist in host tissues and sustain chronic infection and inflammation. These observations represent evidences that Borrelia burgdorferi in an analogous way to Treponema pallidum is responsible for the chronic/late manifestations of Lyme neuroborreliosis.Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and both define tertiary neurosyphilis or tertiary Lyme neuroborreliosis. The use of chronic and late Lyme neuroborreliosis as different entities is inaccurate and can be confusing. Further pathological investigations and the detection of spirochetes in infected tissues and body fluids are strongly needed.
螺旋体是否在受感染的宿主组织中持续存在并导致神经梅毒的晚期/慢性表现一直是长期争论的主题。在全身麻痹患者的大脑中检测到梅毒螺旋体,确立了持续感染与神经梅毒三期表现之间的直接联系。如今,关于莱姆病也存在同样的争论焦点。这篇综述的目的是比较已明确的神经梅毒病理特征与莱姆病神经疏螺旋体病的病理特征。如果神经梅毒的主要三期形式也出现在莱姆病神经疏螺旋体病中,并且在脑损伤中能检测到伯氏疏螺旋体,这将表明螺旋体是莱姆病神经疏螺旋体病晚期/慢性神经精神表现的病因。文献中大量可用数据表明,莱姆病神经疏螺旋体病的主要晚期/慢性形式(脑膜血管型和脑膜脑炎型)在临床和病理上得到了证实。在三期脑损伤中检测到了伯氏疏螺旋体,并从受影响的大脑或脑脊液中培养出该菌。积累的数据还表明,伯氏疏螺旋体能够逃避宿主免疫反应的破坏,在宿主组织中持续存在并维持慢性感染和炎症。这些观察结果表明,伯氏疏螺旋体与梅毒螺旋体类似,是莱姆病神经疏螺旋体病慢性/晚期表现的病因。欧洲、美国和加拿大所有现行指南均认可晚期莱姆病神经疏螺旋体病。“慢性”和“晚期”这两个术语是同义词,都用于定义三期神经梅毒或三期莱姆病神经疏螺旋体病。将慢性和晚期莱姆病神经疏螺旋体病视为不同实体是不准确的,且可能造成混淆。迫切需要进一步的病理学研究以及在感染组织和体液中检测螺旋体。