Más P, Pelegrino J L, Guzmán M G, Comellas M M, Resik S, Alvarez M, Rodríguez R, Muné M, Capó V, Balmaseda A, Rodríguez L, Rodríguez M P, Handy J, Kourí G, Llop A
Institute of Tropical Medicine Pedro Kourí, Ministry of Public Health, Havana, Cuba.
Arch Pathol Lab Med. 1997 Aug;121(8):825-33.
To investigate the possibility of a viral agent in the central nervous system of patients with epidemic neuropathy.
Virus isolation attempts, in cell cultures and suckling mice, from cerebrospinal fluid (CSF) of neuropathy patients and controls undergoing lumbar puncture for unrelated reasons. Serologic studies in patients, contacts, and controls.
An epidemic of optic and peripheral neuropathy affected more than 50,000 people in Cuba in 1991 through 1993. Illness was associated with dietary limitations and increased physical demands accompanying the shortages of food and fuel experienced in Cuba since 1989. Most patients responded to parenteral vitamin therapy, and the epidemic began to subside when oral vitamin supplementation was begun for the entire Cuban population.
Coxsackievirus A9 (five isolates) and a similar, less cytopathic virus (100 isolates) were recovered from 105 (84%) of 125 CSF specimens from neuropathy patients. The strains with light cytopathic effect were antigenically related to Coxsackieviruses A9 and B4 by cross-neutralization and immunoblotting assays. Virus persisted in CSF of some patients for 1 to 12 months. Cerebrospinal fluid from patients and both types of virus from cell culture produced illness, including complete posterior flaccid paralysis, in newborn mice, and virus was reisolated from the mice. Mouse tissues and sural nerve biopsy specimens from patients were stained by immunoperoxidase and colloidal gold techniques using hyperimmune rabbit antisera against the virus with light cytopathic effect.
Coxsackievirus A9 or an antigenically related agent with a light cytopathic effect was present in CSF of 84% of 125 patients with epidemic neuropathy. The role of these agents, probably in combination with nutritional factors, in the pathophysiology of the disease requires further investigation.
研究流行性神经病患者中枢神经系统中存在病毒病原体的可能性。
尝试从因无关原因接受腰椎穿刺的神经病患者及对照者的脑脊液(CSF)中,在细胞培养物和乳鼠中分离病毒。对患者、接触者及对照者进行血清学研究。
1991年至1993年,古巴一场视神经和周围神经病疫情影响了超过5万人。该疾病与自1989年以来古巴经历的食物和燃料短缺所伴随的饮食限制及体力需求增加有关。大多数患者对肠外维生素疗法有反应,当对全体古巴人口开始口服维生素补充时,疫情开始缓解。
从125例神经病患者的105份(84%)脑脊液标本中分离出柯萨奇病毒A9(5株分离株)和一种类似的、细胞病变效应较轻的病毒(100株分离株)。通过交叉中和及免疫印迹分析,细胞病变效应较轻的毒株在抗原性上与柯萨奇病毒A9和B4相关。病毒在一些患者的脑脊液中持续存在1至12个月。患者的脑脊液及细胞培养的两种病毒均在新生小鼠中引发疾病,包括完全性弛缓性麻痹,且病毒可从小鼠中重新分离出来。使用针对细胞病变效应较轻的病毒的超免疫兔抗血清,通过免疫过氧化物酶和胶体金技术对患者的小鼠组织和腓肠神经活检标本进行染色。
125例流行性神经病患者中,84%的患者脑脊液中存在柯萨奇病毒A9或一种抗原性相关的、细胞病变效应较轻的病原体。这些病原体在该疾病病理生理学中的作用,可能与营养因素共同作用,需要进一步研究。