Lung Injury in Vivax Malaria: Pathophysiological Evidence for Pulmonary Vascular Sequestration and Posttreatment Alveolar‐Capillary Inflammation

International Health Program, Infectious Diseases Division, Menzies School of Health Research and Charles Darwin University, Darwin, NT 0811, Australia.
The Journal of Infectious Diseases (Impact Factor: 6). 03/2007; 195(4):589-96. DOI: 10.1086/510756
Source: PubMed


The mechanisms underlying lung injury in vivax malaria are not well understood. Inflammatory responses to Plasmodium falciparum and P. vivax, to our knowledge, have not previously been compared at an organ level.
Respiratory symptoms and physiological aspects were measured longitudinally in Indonesian adults with uncomplicated vivax (n=50) and falciparum (n=50) malaria. Normal values were derived from 109 control subjects. Gas transfer was partitioned into its alveolar-capillary membrane (D(M)) and pulmonary capillary vascular (V(C)) components, to characterize the site and timing of impaired gas transfer.
Mean baseline V(C) volume was significantly reduced in vivax and falciparum malaria, improving with treatment in each species. Baseline D(M) function was not impaired in either species. The progressive deterioration in D(M) function after treatment was statistically significant in vivax malaria but not in uncomplicated falciparum malaria. Oxygen saturation deteriorated after treatment in vivax but improved in falciparum malaria.
The baseline reduction in V(C) volume but not in D(M) function suggests encroachment on V(C) volume by parasitized erythrocytes and suggests that P. vivax-infected erythrocytes may sequester within the pulmonary microvasculature. Progressive alveolar-capillary dysfunction after treatment of vivax malaria is consistent with a greater inflammatory response to a given parasite burden in P. vivax relative to that in P. falciparum.

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    • "Patients with vivax or falciparum malaria have reduced gas exchange in pulmonary capillaries of similar intensities. However, after treating the infection, progressive alveolocapillary dysfunction was observed in patients with P. vivax, suggesting severe inflammatory response, probably due to the greater pulmonary vascular sequestration observed in the infection by that plasmodium species38. "
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    • "It is known to occur in P. falciparum malaria due to sequestration but not reported in P. vivax malaria very often. The recent studies have shown that organ specific sequestration, cytokines, and nitric oxide production are mainly responsible for this complication of P. vivax malaria [21, 22]. "
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    • "Interestingly, treatment of malaria reduced the respiratory distress substantially, which confirms the role of Plasmodium in increasing the previous pulmonary injury she presented at admission. The mechanism of vivax-induced respiratory distress is currently attributed to cytoadherence to the lung microvasculature [38] and increased permeability of the alveolar-capillary membrane caused by sequestration and inflammatory response to the Plasmodium and its treatment [39], which is supported by post-mortem findings in Brazil [40]. On the other hand, malaria can also impairs cardiac function. "
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