The Pathology of Acute Falciparum Malaria

Spitz, Sophie

doi:10.1093/milmed/99.5.555

Cited by 123 publications

(87 citation statements)

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“…These findings further emphasize the inter-and intrapatient variability that has been previously detailed in other clinicopathological studies of fatal malaria. [2][3][4][5] Recent literature has raised the possibility that hypoxia, 26 raised intracranial pressure, 26 -29 and hypoglycemia 30 can cause AI. We found no association between AI and intracranial pressure or hypoglycemia.…”

Section: Discussionmentioning

confidence: 99%

“…Histopathological studies reveal a variety of neurological abnormalities including chromatolysis, neuronophagia, and decreased glial cell numbers. [2][3][4][5] …”

mentioning

confidence: 99%

“…Histopathological studies reveal a variety of neurological abnormalities including chromatolysis, neuronophagia, and decreased glial cell numbers. [2][3][4][5] These changes may result from several coexisting pathological processes including hypoxia, hypoglycemia, cerebral swelling, hemorrhage, and inflammation. Despite these findings in patients who have died from CM, neurological recovery from CM is usually rapid and the majority of patients who survive make a complete recovery within several days.…”

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confidence: 99%

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Axonal Injury in Cerebral Malaria

Medana¹,

Day²,

Hien³

et al. 2002

The American Journal of Pathology

155

130

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Impairment of consciousness and other signs of cerebral dysfunction are common complications of severe Plasmodium falciparum malaria. Although the majority of patients make a complete recovery a significant minority, particularly children, have sequelae. The pathological process by which P. falciparum malaria induces severe but usually reversible neurological complications has not been elucidated. Impairment of transport within nerve fibers could induce neurological dysfunction and may have the potential either to resolve or to progress to irreversible damage. ␤-amyloid precursor protein (␤-APP) immunocytochemistry, quantified using digital image analysis, was used to detect defects in axonal transport in brain sections from 54 Vietnamese cases with P. falciparum malaria. The frequency and extent of ␤-APP staining were more severe in patients with cerebral malaria than in those with no clinical cerebral involvement. ␤-APP staining was often associated with hemorrhages and areas of demyelination, suggesting that multiple processes may be involved in neuronal injury. The age of focal axonal damage, as determined by the extent of the associated microglial response, varied considerably within tissue sections from individual patients. These findings suggest that axons are vulnerable to a broad range of cerebral insults that occur during P. falciparum malaria infection. Disruption in axonal transport may represent a final common pathway leading to neurological dysfunction in cerebral malaria. Cerebral malaria (CM) is a diffuse, potentially reversible, encephalopathy, caused by infection with the protozoan parasite Plasmodium falciparum. CM presents clinically with convulsions and coma, and carries 15 to 20% mortality. The malaria parasite invades and develops within erythrocytes that sequester in the cerebral microvasculature and other vital organs by adhesion to specific endothelial receptors. 1,2 The pathophysiological consequences of severe malaria infection have not been satisfactorily resolved. In particular it is not known how parasitized red blood cells, which remain within the vascular space, influence parenchymal brain function to induce coma and death. Histopathological studies reveal a variety of neurological abnormalities including chromatolysis, neuronophagia, and decreased glial cell numbers. [2][3][4][5]

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Section: Discussionmentioning

confidence: 99%

“…Histopathological studies reveal a variety of neurological abnormalities including chromatolysis, neuronophagia, and decreased glial cell numbers. [2][3][4][5] …”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Axonal Injury in Cerebral Malaria

Medana¹,

Day²,

Hien³

et al. 2002

The American Journal of Pathology

155

130

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“…Knobs are not present on erythrocytes infected with immature ring stage parasites, and only at this stage of parasite development do IRBC circulate freely (2)(3)(4). Knobpositive (K+) IRBC have been shown to bind in vitro to human endothelial cells (5), some melanoma cell lines (6,7), human monocytes (8,9), and phorbol ester-differentiated U937 histiocytic lymphoma cells (10).…”

Section: Introductionmentioning

confidence: 99%

“…Sequestration appears to contribute to parasite survival by allowing nondeformable IRBC to avoid the filtering action of the spleen (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14]. Sequestration may also contribute to host pathology.…”

Section: Introductionmentioning

confidence: 99%

Activation of monocytes and platelets by monoclonal antibodies or malaria-infected erythrocytes binding to the CD36 surface receptor in vitro.

Ockenhouse¹,

Magowan²,

Chulay³

1989

J. Clin. Invest.

128

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The CD36 leukocyte differentiation antigen, recognized by MAbs OKM5 and OKM8 and found on human monocytes and endothelial cells, has been implicated as a sequestration receptor for erythrocytes infected with the human malaria parasite Plasmodium falciparum (IRBC). CD36 is also expressed on platelets and appears to be identical to platelet glycoprotein IV. We investigated receptor activation of monocytes and platelets by anti-CD36 MAbs and by IRBC. Incubation of human monocytes with anti-CD36 MAbs or IRBC resulted in stimulation of the respiratory burst as measured by reduction of nitroblue tetrazolium and generation of chemiluminescence.Incubation of human platelets with anti-CD36 MAbs resulted in platelet activation as measured by aggregation or ATP secretion. Activation of monocytes and platelets required appropriate intracellular transmembrane signaling and was inhibited by calcium antagonists or by specific inhibitors of protein kinase C or guanine nucleotide binding proteins. Soluble CD36 inhibited binding of IRBC to both monocytes and platelets, suggesting that these interactions are mediated by the CD36 receptor. Using a cytochemical electron microscopic technique, the presence of reactive oxygen intermediates was identified at the interface between human monocytes and IRBC. These data provide support for the hypothesis that reactive oxygen intermediates produced by monocytes when IRBC ligands interact with cell surface receptors may play a role in the pathophysiology of falciparum malaria.

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