Ultrastructure of the Lung in Falciparum Malaria

Duarte, M. I. S.; Corbett, Carlos Eduardo Pereira; Boulos, Marcos; Neto, VT

doi:10.4269/ajtmh.1985.34.31

Cited by 74 publications

(42 citation statements)

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“…125 Endothelial cell involvement. Several investigators have described endothelial injury and endothelial cell swelling in association with PRBCs, 117,126 but since the post-mortem intervals were not stated, these may reflect a post-mortem artifact. They are not present in samples from studies with short post-mortem intervals.…”

Section: Pathophysiology Of Fatal Malariamentioning

confidence: 99%

Pathophysiology of fatal falciparum malaria in African children.

Newton¹,

Taylor²,

Whitten³

1998

Am J Trop Med Hyg

122

121

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Abstract. Children living in sub-Saharan Africa bear the brunt of the mortality from falciparum malaria, yet there is a dearth of relevant post-mortem data. Clinical studies from centers in Africa suggest that the pathophysiology of severe malaria is different in children and adults. Three overlapping clinical syndromes, metabolic acidosis manifesting as hyperpnea, cerebral malaria, and severe anemia, are responsible for nearly all the deaths in African children. Despite improvements in antimalarial treatment, there has not been a significant reduction in mortality. We review the pathology and pathophysiology of fatal falciparum malaria in African children. Many questions remain, the answers to which would facilitate the development and evaluation of new approaches to the management of this disease.Severe and complicated Plasmodium falciparum infections continue to threaten the survival of young children in sub-Saharan Africa: one in 15 children on the Kenyan coast will have experienced an episode of severe malaria before the age of five, 1 and 1% of Gambian children less than five years of age will die of malaria. 2 The annual death toll is estimated to be one million children across the continent; 90% of the annual worldwide malaria mortality. 3 Although most children die in the community, on the Kenyan coast it is estimated that more than 40% die in a hospital (Marsh K, unpublished data) and one-third of pediatric hospital admissions and one-third of pediatric hospital deaths in Malawi can be attributed to malaria. 4

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Section: Pathophysiology Of Fatal Malariamentioning

confidence: 99%

Pathophysiology of fatal falciparum malaria in African children.

Newton¹,

Taylor²,

Whitten³

1998

Am J Trop Med Hyg

122

121

View full text Add to dashboard Cite

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“…Alternatively, lower peripheral blood monocyte counts in patients with severe and complicated malaria might reflect monocyte sequestration or adherence to the activated vascular endothelium. Monocytes are activated in patients with malaria, and occasional case reports document sequestration of monocytes to the capillary or venular vessel wall (15,28). However, larger post mortem studies of human falciparum malaria have failed to demonstrate massive adherence of monocytes or macrophages, which would explain drastically lower peripheral monocyte counts in patients with severe and complicated disease than in patients with uncomplicated disease (25,27).…”

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confidence: 99%

High Levels of Inducible Nitric Oxide Synthase mRNA Are Associated with Increased Monocyte Counts in Blood and Have a Beneficial Role inPlasmodium falciparumMalaria

2000

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To date, there have been conflicting reports concerning the clinical significance of nitric oxide (NO) in Plasmodium falciparum malaria. Some authors have proposed that NO contributes to the development of severe and complicated malaria, while others have argued that NO has a protective role. To investigate these apparently contradictory reports, reverse transcription-coupled PCR was used to study inducible NO synthase (iNOS) in whole-blood RNA samples from patients with severe and complicated malaria or uncomplicated malaria and from healthy donors. This work produced three principal findings. First, samples of patients with severe and complicated malaria were variably positive, with weak to moderate intensity. Markedly higher iNOS RNA levels were observed in samples of patients with uncomplicated malaria than in patients with severe and complicated malaria. Samples of healthy donors were uniformly negative. Second, since we initially demonstrated iNOS expression in whole-blood RNA samples, we extended our investigations to individual blood cells such as monocytes, lymphocytes, neutrophils, and platelets to identify the cellular source of iNOS. We found that iNOS was expressed predominantly in monocytes. Third, retrospective statistical analysis of monocyte counts clearly demonstrated that patients with uncomplicated malaria had higher monocyte counts at the time of presentation than patients with severe and complicated malaria. Taken together, our findings give room to the interpretation that NO may have a beneficial rather than a deleterious role in falciparum malaria.

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“…3 In the context of P. falciparum-related ARDS, a role of the infected erythrocyte has been investigated. 4,5 This entity may bind to capillary endothelial cells, with the basis for respiratory distress being associated edema, leukocyte tropism, and capillary narrowing.…”

Section: Discussionmentioning

confidence: 99%