Garbe C
Universitäts-Hautklinik und Poliklinik, Klinikum Steglitz Freien Universität Berlin.
Hautarzt. 1991 Jun;42(6):356-65.
The description of Lyme disease in 1976 and the detection of its causative agent, the spirochete Borrelia burgdorferi (B. burgdorferi), in 1982 led to an increase in our knowledge of the course of B. burgdorferi infection and its clinical manifestations. The classic tick-borne dermatoses erythema chronicum migrans (ECM), lymphadenosis benigna cutis (LABC) and acrodermatitis chronica atrophicans (ACA) were proven by isolation of the spirochete from skin lesions to be caused by B. burgdorferi infection. In early disease (less than 1 year) ECM and LABC can develop locally at the site of infection (stage I), but both these skin manifestations can also occur together with multiple lesions after dissemination of the causative organism (stage II). ACA is typical for late infection (greater than 1 year, stage III). High titres of B. burgdorferi antibodies have been found in patients with localized sclerodermalike lesions (circumscribed scleroderma, lichen sclerosus et atrophicus, anetoderma), and frequent simultaneous occurrence of ACA suggests an association with late B. burgdorferi infection. Similarly, we found four cases of cutaneous B-cell lymphoma possibly arising from LABC in association with the same markers of late B. burgdorferi infection. Additionally, some cases of Schönlein-Henoch purpura and of Shulman syndrome may be associated with Lyme borreliosis. The disease is endemic in central Europe, and almost exclusively ticks of the Ixodes ricinus complex seem to transmit B. burgdorferi to humans, whereas the reservoir of infection seem to be rodents, especially mice. The main diagnostic tool is serological examination for B. burgdorferi antibodies, which will become detectable 3-6 weeks after infection. Enzyme-linked immunosorbent assay (ELISA) and the indirect immunofluorescence test (IFT) revealed similar sensitivity. In early disease, sensitivity for antibody detection could be improved by immunoblot technique and by flagellum-ELISA, which is specific for this early sensitizing B. burgdorferi antigen. For treatments, penicillin is no longer recommended as the drug of first choice, because low sensitivity of B. burgdorferi has been observed in vitro and in vivo. Tetracycline, doxycycline and amoxicillin p.o. are now preferred for the treatment of Lyme borreliosis, and in neurologic and cardiac abnormalities ceftriaxone i.v. is recommended. Treatment duration should be 14 days in early disease and 30 days in late disease.
1976年对莱姆病的描述以及1982年对其病原体——螺旋体伯氏疏螺旋体(B. burgdorferi)的检测,使我们对B. burgdorferi感染的病程及其临床表现的认识有所增加。经典的蜱传皮肤病慢性游走性红斑(ECM)、皮肤良性淋巴腺病(LABC)和萎缩性慢性肢端皮炎(ACA),通过从皮肤病变中分离出螺旋体,被证实是由B. burgdorferi感染引起的。在早期疾病(不到1年)中,ECM和LABC可在感染部位局部发生(I期),但这两种皮肤表现也可在病原体播散后出现多个病变时同时发生(II期)。ACA是晚期感染(大于1年,III期)的典型表现。在局限性硬皮病样病变(局限性硬皮病、硬化萎缩性苔藓、皮肤松弛症)患者中发现了高滴度的B. burgdorferi抗体,并且ACA的频繁同时出现提示与晚期B. burgdorferi感染有关。同样,我们发现4例皮肤B细胞淋巴瘤可能起源于LABC,并伴有相同的晚期B. burgdorferi感染标志物。此外,一些过敏性紫癜和舒尔曼综合征病例可能与莱姆疏螺旋体病有关。该病在中欧为地方病,几乎只有蓖麻硬蜱属的蜱似乎能将B. burgdorferi传播给人类,而感染源似乎是啮齿动物,尤其是小鼠。主要的诊断工具是检测B. burgdorferi抗体的血清学检查,感染后3 - 6周可检测到。酶联免疫吸附测定(ELISA)和间接免疫荧光试验(IFT)显示出相似的敏感性。在早期疾病中,免疫印迹技术和鞭毛ELISA可提高抗体检测的敏感性,鞭毛ELISA对这种早期致敏的B. burgdorferi抗原具有特异性。对于治疗,不再推荐青霉素作为首选药物,因为在体外和体内均观察到B. burgdorferi对其敏感性较低。四环素、强力霉素和阿莫西林口服现在是治疗莱姆疏螺旋体病的首选药物,对于神经和心脏异常,推荐静脉注射头孢曲松。早期疾病的治疗疗程应为14天,晚期疾病为30天。