Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team.

Ebola haemorrhagic fever in Sudan, 1976. Report of a WHO/International Study Team.
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苏丹埃博拉出血热,1976 年。世界卫生组织/国际研究小组的报告。

DOI:
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发表时间:
1978
影响因子:
11.1
通讯作者:
Jansá Jm
Jansá Jm
中科院分区:
医学2区
文献类型:
--
作者:
M. Lópaz;C. Amela;M. Ordobás;M. Domínguez;C. Álvarez;M. Martinez;M. Sierra;F. Simón;J. Jansá;D. Plachouras;J. Astray;Lópaz Ma;Amela C;Ordobas M;Domínguez;Á. C;M. M;S. Mj;Simon F;Jansá Jm

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1976年6月至11月,苏丹南部爆发大规模出血热(后命名为埃博拉出血热),共有284例病例;来源地恩扎拉有 67 例,迈里迪有 213 例,坦布拉有 3 例,朱巴有 1 例。恩扎拉的疫情似乎起源于一家棉花厂的工人。马里迪的疫情因在一家大型、活跃的医院中传播而扩大。该疾病的传播需要与急性病例密切接触,并且通常与护理患者的行为有关。潜伏期为7至14天。尽管这种联系尚未明确,但恩扎拉似乎可能是扎伊尔邦巴区类似疫情的感染源。 在这次疫情中,埃博拉出血热是一种独特的临床疾病,死亡率很高(总体为 53%),幸存者的恢复期也很长。该疾病以流感样综合征开始,包括发烧、头痛、关节和肌肉疼痛,很快引起腹泻(81%)、呕吐(59%)、胸痛(83%)、喉咙疼痛和干燥(63%)以及皮疹(52%)。出血表现很常见(71%),出现在半数康复病例和几乎所有死亡病例中。1976 年 11 月对患者进行了两次尸检。组织病理学结果类似于急性病毒感染,尽管特征具有特征性,但它们并不完全具有诊断意义。它们与马尔堡病毒感染中描述的特征非常相似,即肝脏中出现局灶性嗜酸性粒细胞坏死,淋巴细胞被破坏并被浆细胞取代。 1例病例有肾小管坏死的证据。1976年11月调查时,从马里迪医院急症患者的急性期血清中分离出两株埃博拉病毒。马里迪临床诊断的48名患者中,有42名患者通过免疫荧光法检测到埃博拉病毒抗体,而恩扎拉的31名患者中只有6例检测到埃博拉病毒抗体。讨论了间接免疫荧光检测不够灵敏的可能性。 在医院和当地社区的马里迪病例接触者中,19% 具有抗体。他们中很少有人给出任何患病史,这表明埃博拉病毒可以引起轻度甚至亚临床感染。恩扎拉棉厂的布房工人中有 37% 似乎已被感染,这表明该工厂可能是主要的感染源。
A large outbreak of haemorrhagic fever (subsequently named Ebola haemorrhagic fever) occurred in southern Sudan between June and November 1976. There was a total of 284 cases; 67 in the source town of Nzara, 213 in Maridi, 3 in Tembura, and 1 in Juba. The outbreak in Nzara appears to have originated in the workers of a cotton factory. The disease in Maridi was amplified by transmission in a large, active hospital. Transmission of the disease required close contact with an acute case and was usually associated with the act of nursing a patient. The incubation period was between 7 and 14 days. Although the link was not well established, it appears that Nzara could have been the source of infection for a similar outbreak in the Bumba Zone of Zaire.In this outbreak Ebola haemorrhagic fever was a unique clinical disease with a high mortality rate (53% overall) and a prolonged recovery period in those who survived. Beginning with an influenza-like syndrome, including fever, headache, and joint and muscle pains, the disease soon caused diarrhoea (81%), vomiting (59%), chest pain (83%), pain and dryness of the throat (63%), and rash (52%). Haemorrhagic manifestations were common (71%), being present in half of the recovered cases and in almost all the fatal cases.Two post mortems were carried out on patients in November 1976. The histopathological findings resembled those of an acute viral infection and although the features were characteristic they were not exclusively diagnostic. They closely resembled the features described in Marburg virus infection, with focal eosinophilic necrosis in the liver and destruction of lymphocytes and their replacement by plasma cells. One case had evidence of renal tubular necrosis.Two strains of Ebola virus were isolated from acute phase sera collected from acutely ill patients in Maridi hospital during the investigation in November 1976. Antibodies to Ebola virus were detected by immunofluorescence in 42 of 48 patients in Maridi who had been diagnosed clinically, but in only 6 of 31 patients in Nzara. The possibility of the indirect immunofluorescent test not being sufficiently sensitive is discussed.Of Maridi case contacts, in hospital and in the local community, 19% had antibodies. Very few of them gave any history of illness, indicating that Ebola virus can cause mild or even subclinical infections. Of the cloth room workers in the Nzara cotton factory, 37% appeared to have been infected, suggesting that the factory may have been the prime source of infection.