Knowlesi malaria: Human risk factors, clinical spectrum, and pathophysiology.

Knowlesi malaria: Human risk factors, clinical spectrum, and pathophysiology.
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Knowlesi疟疾:人类风险因素,临床谱和病理生理学。

DOI:
10.1016/bs.apar.2021.08.001
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发表时间:
2021
影响因子:
--
通讯作者:
Barber, Bridget E.
Barber, Bridget E.
中科院分区:
医学3区
文献类型:
--
作者:
Anstey, Nicholas M.;Grigg, Matthew J.;Rajahram, Giri S.;Cooper, Daniel J.;William, Timothy;Kho, Steven;Barber, Bridget E.

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诺氏疟原虫在东南亚流行,是人畜共患疟疾的最常见原因。诺氏疟原虫感染的临床疾病范围从无症状感染到严重疟疾和死亡。超过90%的临床疾病发生在成年人中,大多生活在正在经历密集土地利用变化的林缘地区。在人类的24小时无性生命周期中,可能会出现高寄生虫数量,但大多数诺氏疟疾临床病例并不合并低寄生虫血症。在共同流行地区,诺氏疟疾的中位寄生虫血症低于间日疟和恶性疟疾,这表明发烧阈值较低。有症状的成年人中有6%-9%会发生严重疟疾。诺氏疟原虫引起的严重疟疾的表现与恶性疟疾相似,但明显没有昏迷。年龄、寄生虫血症、心血管合并症和延迟诊断是严重疾病和死亡的风险因素,只有成年人才会出现这种情况。血小板减少症在成年人中几乎是普遍的,可能与血小板与红细胞的结合和清除有关。在非自然灵长类宿主的致命疾病中看到的微血管淤泥和在致命的人类疾病中寄生虫的微血管聚集的潜在机制尚不清楚。在人类和其他非自然灵长类宿主中,感染和未感染的红细胞变形性的显著降低与疾病的严重程度有关,可能导致微血管灌流受损和器官功能障碍。内皮激活、内皮功能障碍、糖基化降解和溶血也与严重疾病和器官功能障碍,特别是急性肾损伤有关,并可能导致这些疾病和器官功能障碍。
Plasmodium knowlesi is endemic across Southeast Asia, and is the commonest cause of zoonotic malaria. The spectrum of clinical disease from P. knowlesi infection ranges from asymptomatic infection, through to severe malaria and death. Over 90% of clinical disease occurs in adults, mostly living in forest edge areas undergoing intensive land use change. With a 24-h asexual life cycle in humans, high parasite counts are possible, but most clinical cases of knowlesi malaria are uncomplicated with low parasitaemia. In co-endemic areas, median parasitaemia in knowlesi malaria is lower than that seen in vivax and falciparum malaria, suggesting a lower fever threshold. Severe malaria occurs in 6–9% of symptomatic adults. Manifestations of severe malaria from P. knowlesi are similar to those seen with falciparum malaria, with the notable absence of coma. Age, parasitaemia, cardiovascular comorbidities and delayed diagnosis are risk factors for severe disease and death, which are only seen in adults. Thrombocytopenia is near-universal in adults, likely related to platelet-red cell binding and clearance. Mechanisms underlying the microvascular sludging seen in fatal disease in non-natural primate hosts and the microvascular accumulation of parasites in fatal human disease are not clear. Marked reductions in deformability of both infected and uninfected red blood cells are associated with disease severity in both humans and other non-natural primate hosts, likely contributing to impaired microvascular perfusion and organ dysfunction. Endothelial activation, endothelial dysfunction, glycocalyx degradation and haemolysis are also associated with, and likely contribute to, severe disease and organ dysfunction, particularly acute kidney injury.
DOI: 10.4269/ajtmh.1968.17.355
发表时间: 1968-01-01
影响因子: 3.3
作者:
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影响因子: 3
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发表时间: 1965-01-01
期刊: SCIENCE
影响因子: 56.9
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