Mononeuropathy multiplex in rhesus monkeys with chronic Lyme disease
Mononeuropathy multiplex in rhesus monkeys with chronic Lyme disease
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DOI：
10.1002/ana.410410313
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发表时间：
1997-03-01
影响因子：
11.2
通讯作者：
Philipp, MT
中科院分区：
文献类型：
--
作者：
England, JD;Bohm, RP;Philipp, MT
周围神经病变是一种公认的，但知之甚少的表现莱姆病。我们进行了一系列的电生理研究8恒河猴慢性感染伯氏疏螺旋体JD1株，并与10个未感染的对照猴的类似研究的结果进行了比较。4只感染动物和2只未感染动物进行腓肠神经活检。5只感染动物和1只未感染动物还进行了死后神经病理学检查。总之，5只感染猴表现出主要的轴突损失多样性多灶性神经病变。只有一个神经病变表现出符合脱髓鞘的结果。病理学上，周围神经标本显示多灶性轴突变性和再生，偶见血管周围炎性细胞浸润，无血管壁坏死。未观察到游离螺旋体结构，但几个巨噬细胞表现出高度特异性抗B的阳性免疫染色。7.5kD脂蛋白单克隆抗体。在感染动物中，连续分析血清中抗B抗体。莱姆病表现出越来越多的IgG特异性和新的IgM特异性，表明持续感染。因此，在慢性感染B的恒河猴中，多发性单神经病形式的周围神经病变频繁发生。burgdorferi。这些神经病变的发病机制尚不清楚，但我们的研究表明，免疫介导的过程可能是由持续感染B。burgdorferi。
Peripheral neuropathy is a recognized but poorly understood manifestation of Lyme disease. We performed serial electrophysiological studies on 8 rhesus monkeys chronically infected with the JD1 strain of Borrelia burgdorferi and compared the results with those of similar studies on 10 uninfected control monkeys. Four infected and 2 uninfected animals underwent sural nerve biopsy. Five of the infected and 1 of the uninfected animals also had postmortem neuropathological examinations. Altogether, 5 of the infected monkeys demonstrated primarily axonal-loss-variety multifocal neuropathies. Only one nerve lesion exhibited findings compatible with demyelination. Pathologically, peripheral nerve specimens showed multifocal axonal degeneration and regeneration and occasional perivascular inflammatory cellular infiltrates without vessel wall necrosis. Free spirochetal structures were not seen, but several macrophages exhibited positive immunostaining with a highly specific anti-B. burgdorferi, 7.5-kd lipoprotein monoclonal antibody. In the infected animals, serial analysis of serum antibodies to B. burgdorferi showed increasing numbers of IgG specificities and new IgM specificities, suggesting persistent infection. Thus, peripheral neuropathy in the form of a mononeuropathy multiplex develops frequently in rhesus monkeys chronically infected with B. burgdorferi. The pathogenesis of these nerve lesions is not yet known, but our studies suggest an immune-mediated process perhaps driven by persistent infection with B. burgdorferi.