Satz N
Orthopädische Universitätsklinik Balgrist, Zürich.
Schweiz Med Wochenschr. 1992 Nov 21;122(47):1779-91.
Borrelia burgdorferi (B. burgdorferi), the etiologic agent of Lyme borreliosis, shows both a variety of outer surface proteins with molecular weights between 16 and 100 kiloDalton (kD) and a 41 kD flagellar protein, which induce the immunologic response. Lipopolysaccharides, another constituent of the bacterial capsule, are responsible for the inflammatory reaction, constitutional symptoms and for the Jarisch-Herxheimer reaction. First a vigorous T-cell immune response develops, followed later by a more slowly evolving humoral B-cell immune response. The delayed onset of the humoral immune response may explain why antibodies against B. burgdorferi could not be detected early in the course of the disease. But the antibody titers increase with duration of the illness. The humoral response shows the usual pattern of IgM appearing first, followed by IgG and IgA. The IgM titer normalizes after recovery while the IgG titer could persist over years or decades. It is hardly possible to detect B. burgdorferi microscopically or by cultivation from blood, joint or cerebrospinal fluid. For routine diagnosis the fluorescent antibody staining and the ELISA methods are available which detect IgM or IgG antibodies against B. burgdorferi. But the sensitivity and specificity of these tests are still unsatisfactory. Other methods such as the ELISA-capture method, complement binding reaction, passive hemagglutination or the polymerase chain reaction are not yet established for routine purposes. Western blot analysis did not yield an essential diagnostic advantage but may be helpful in long term observation or in special cases. The measurement of the cellular immune response by T-cell proliferation tests remains controversial. First of all Lyme borreliosis has to be diagnosed by clinical findings and by elimination through differential diagnosis. An elevated antibody titer or a positive T-cell proliferation test may confirm the diagnosis but cannot prove it. Without consistent clinical findings they are of no practical significance. Some general guidelines for interpretation of laboratory results are given.
莱姆病疏螺旋体(Borrelia burgdorferi,B. burgdorferi)是莱姆病的病原体,它具有多种分子量在16至100千道尔顿(kD)之间的外表面蛋白以及一种41 kD的鞭毛蛋白,这些蛋白可引发免疫反应。脂多糖是细菌荚膜的另一种成分,可引起炎症反应、全身症状以及雅里希-赫克斯海默反应。首先会产生强烈的T细胞免疫反应,随后是发展较为缓慢的体液B细胞免疫反应。体液免疫反应的延迟出现可能解释了为何在疾病早期无法检测到抗B. burgdorferi的抗体。但抗体滴度会随着病程的延长而升高。体液反应呈现出通常的模式,即首先出现IgM,随后是IgG和IgA。恢复后IgM滴度恢复正常,而IgG滴度可能会持续数年或数十年。通过显微镜检查或从血液、关节或脑脊液中培养很难检测到B. burgdorferi。对于常规诊断,可采用荧光抗体染色和ELISA方法来检测抗B. burgdorferi的IgM或IgG抗体。但这些检测方法的敏感性和特异性仍不尽人意。其他方法,如ELISA捕获法、补体结合反应、被动血凝反应或聚合酶链反应尚未用于常规诊断。蛋白质印迹分析并未产生实质性的诊断优势,但可能有助于长期观察或特殊情况。通过T细胞增殖试验来测量细胞免疫反应仍存在争议。首先,莱姆病必须通过临床症状以及鉴别诊断来排除其他疾病进行诊断。抗体滴度升高或T细胞增殖试验呈阳性可能会支持诊断,但不能确诊。没有一致的临床症状,这些结果就没有实际意义。文中给出了一些实验室结果解读的一般指导原则。