Sluga E, Budka H, Pichler E
Wien Klin Wochenschr. 1975 Apr 4;87(7):248-51.
A child with acute infantile lymphoblastic leukaemia in remission after cytostatic therapy contracted apparently uncomplicated measles. 8 weeks later, an acute neurological syndrome developed, which led to death within 2 weeks. At autopsy, a peculiar type of inclusion body "encephalitis" almost without signs of inflammatory infiltration was found. Electron microscopic examination showed changes of paramyxovirus infection, which were attributable to slow measles virus disease of the CNS. There was evidence of disturbed nucleocapside synthesis, which is considered to be one of the basic defects in the development of slow-virus processes and their altered viral maturation. Possible pathogenetic factors are discussed in the light of our case.
一名接受细胞抑制疗法后处于缓解期的急性婴儿淋巴细胞白血病患儿感染了看似不复杂的麻疹。8周后,出现了一种急性神经综合征,在2周内导致死亡。尸检时,发现了一种特殊类型的包涵体“脑炎”,几乎没有炎症浸润的迹象。电子显微镜检查显示有副粘病毒感染的变化,这归因于中枢神经系统的慢麻疹病毒病。有证据表明核衣壳合成受到干扰,这被认为是慢病毒过程发展及其病毒成熟改变的基本缺陷之一。根据我们的病例讨论了可能的致病因素。