Pathophysiology of severe falciparum malaria in man.

Journal article

In humans, severe falciparum malaria disturbs the function of many tissues and organs. It is unlikely that a single pathophysiological process is responsible for the diverse effects of the infection. However, there is increasing evidence that impairment of local blood flow resulting from sticking of parasitized erythrocytes to the venular endothelium may be the initiating cause of cerebral, retinal, renal, gastrointestinal and bone-marrow abnormalities. The harmful effects of malaria are immediately and rapidly reversible in those who survive. This implies that the mechanism of symptoms such as coma must be a subtle metabolic derangement rather than a gross mechanical one such as thrombosis or infarction. Malarial pulmonary oedema closely resembles adult respiratory distress syndrome. In this case the adherent leucocytes may be responsible for capillary damage. The roles of various humoral mediator systems involved in the pathogenesis of fever, inflammation, haemostasis and the immune response remain to be worked out. Since the mortality of severe falciparum malaria remains very high, there is an urgent need to discover pathophysiological mechanisms and so improve treatment.

Authors: Warrell, D

• Publication status: Published
• Journal: Parasitology
• Volume: 94 Suppl
• Issue: SUPPL.
• Pages: S53-S76
• Publication date: 1987-01-01
• EISSN: 1469-8161
• ISSN: 0031-1820
• Language: English
• Keywords: Pulmonary Edema; Humans; Pregnancy; Anemia; Female; Liver Diseases, Parasitic; Kidney Failure, Chronic; Erythrocytes; Plasmodium falciparum; Blackwater Fever; Hypoglycemia; Malaria; Brain Diseases; Intestinal Diseases, Parasitic; Pregnancy Complications, Infectious