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The distribution and intensity of parasite sequestration in comatose Malawian children
Karl B Seydel1, Danny A Milner, Steve B Kamiza
1Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Insights
Severe malaria involves parasite sequestration in multiple organs, not just the brain. Higher parasite loads in organs like the brain, intestine, and skin were observed in fatal cerebral malaria cases.
Area of Science:
- Malariology
- Pathogenesis of Infectious Diseases
- Clinical Tropical Medicine
Background:
- Plasmodium falciparum sequestration in capillaries is key to severe malaria pathogenesis.
- Sequestration occurs in all infections, indicating other factors influence disease severity.
- Understanding sequestration's role in clinical syndromes is crucial for disease mechanism insights.
Purpose of the Study:
- To investigate the relationship between parasite sequestration and cerebral malaria.
- To determine if parasite sequestration shows a predilection for cerebral vasculature in fatal cases.
Main Methods:
- Measured parasite-derived lactate dehydrogenase (pLDH) concentration in autopsy tissue samples.
- Classified patients into presumed cerebral malaria or non-malarial death groups.
- Used ELISA to quantify parasite load in various organs.
Main Results:
- Higher parasite loads detected in the brain, intestine, and skin of patients with presumed cerebral malaria.
- Parasite load was significantly higher in these organs compared to those with identified non-malarial causes of death.
Conclusions:
- Sequestration in fatal cerebral malaria affects multiple organs.
- Parasite sequestration does not specifically target cerebral vasculature in severe malaria.
Background:
The sequestration of Plasmodium falciparum-infected erythrocytes in capillary beds is a characteristic feature of severe malaria and is believed to be central to disease pathogenesis. Sequestration occurs in all P. falciparum infections, including those in asymptomatic individuals. Therefore, sequestration cannot be the sole determinant of severe disease; the intensity or distribution of infected erythrocytes may also contribute. Discerning the relationship between sequestration and well-defined clinical syndromes may enhance understanding of disease mechanisms.
Methods:
We measured the concentration of parasite-derived lactate dehydrogenase (pLDH) in tissue samples obtained at autopsy from patients with clinically defined cerebral malaria. On the basis of the autopsy findings, patients were divided into 2 groups: those with an identifiable, nonmalarial cause of death and those without, who were presumed to have died of cerebral malaria. The concentration of pLDH, as determined by enzyme-linked immunosorbent assay, was used to estimate parasite load in different organs.
Results:
When pLDH could be detected, the parasite load was higher in patients with presumed cerebral malaria than in parasitemic patients with assumed cerebral malaria with a nonmalaria cause of death identified at autopsy (P<.05 for brain, intestine, and skin).
Conclusions:
These findings suggest that sequestration in patients with fatal cerebral malaria occurs in multiple organs and does not reflect a predilection in the parasite for the cerebral vasculature.
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