Malaria is primarily transmitted by the bite of an infected female Anopheles mosquito to infect humans [1]. Diffuse interstitial edema, pulmonary edema, pleural effusion, and lobar consolidation are presented in severe falciparum malaria [2]. Sanklecha and colleagues reported three cases of childhood falciparum malaria in a family and revealed that two cases demonstrated bilaterally fluffy pulmonary infiltrates whereas the remaining case showed normal chest roentgenogram [3]. All reported patients with sickle cell anemia in their study demonstrated bilaterally pulmonary infiltrates [4]. Chest roentgenographic presentations are usually nonspecific, but they should be recognized in high endemic areas of malaria [4]. A patient with Plasmodium vivax malaria demonstrated diffuse bilateral alveolar opacities which indicated acute respiratory distress syndrome [5]. In India, three cases of ARDS with Plasmodium vivax malaria were also reported and demonstrated one case with bilateral parahilar infiltrates, one case with bilateral diffuse extensive opacities, and another case with bilateral basal ground glass opacities [6]. Pulmonary edema is an universal finding at autopsy [7]. The alveoli are filled parasite-red blood cells, non-parasited red blood cells, neutrophils and pigment-laden macrophages, and laminated periodic acid-schiff (PAS) positive membrane which finally destroys and incorporated the alveolar wall within it in many severe cases [7]. This is associated with abundant edematous fluid, pulmonary vasodilatation, and may have a marked inflammatory infiltrate [7]. Particularly in falciparum malaria, there is hyaline membrane formation in the alveoli that indicates leakage of proteinaceous fluid [7]. In the lungs of severe cases, the majority of blood vessels showed parasite-red blood cell sequestration in the septal capillaries and small blood vessels [8]. Mononuclear cell-pigment laden macrophage were seen admix with parasite-red blood cells in the microvessels of alveolar septa [8]. Platelet- activating- factor receptor activation was significant in the pathogenesis of pulmonary damage associated with Plasmodium berghei ANKA strain infection in a mice model, demonstrated in a recent study [9]. Approximately 60% of these infected mice had hypoxemia, dyspnea, pleural effusion, airway obstruction, pulmonary edema, and pulmonary hemorrhage [9]. There is little knowledge about the pathogenesis of malaria-associated acute lung injury and adult respiratory distress syndrome (ARDS) [10]. Increased endothelial permeability and inflammatory mediators may play a significant role, while parasite sequestration may take a minor role that supported by elevation of level of vascular endothelial growth factor found in mice model [10]. Plasmodium falciparum merozoite proteins could increase pulmonary endothelial permeability, while Plasmodium falciparum infected-red blood cells did not reveal the same properties indicating that the effects of the malaria parasites on the pulmonary endothelium are probably mediated the activity of Src-family kinases [10]. In infected mice lungs, increased water content was demonstrated, and contributed to the development of pulmonary edema [10]. DBA2 mice infected with Plasmodium berghei K173 showed proteins and inflammatory cells mainly CD4+ and CD8+ lymphocytes, monocytes and neutrophils accumulated in the lungs of infected mice [10]. Levels of cytokines and chemokines associated with ARDS were measured by Van den Steen   Read More

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