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Clinical Characteristics and Pathology (continued)

Children in Gambia (West Africa) who are under 5 years-old are reported as having a high rate of coincidence between levels of malaria parasites of 5,000/µl or over and abnormal chest radiographs. The explanation is undecided: Does malaria predispose to pulmonary complications, or is it the other way around?

In adults there is a spectrum of chest abnormalities, occurring in vivax as well as falciparum malaria. There is a poor correlation between the clinical illness and the extent of the radiological abnormalities or the severity of the parasitemia: pleural effusions, sometimes bilateral, septal thickening, and interstitial edema may be seen on a chest radiograph when the patient has few respiratory symptoms. There is clinical evidence that the lung lesions respond to antimalarial therapy and are usually much improved or entirely clear within 3 to 7 days. Experimental malaria in mice is known to cause pneumonia and responds to therapy in the same way.

Far more serious is the pulmonary edema which develops, usually in nonimmune adults, and which has been recognized for 70 years. It, like much else in malaria, is poorly understood. Clinically there may be dehydration and relative hypovolemia, followed by severe shock and renal failure. At the same time, the patient deteriorates and, if pulmonary edema develops, death can occur within a few hours, usually with severe cerebral dysfunction. This pulmonary edema does not respond to any type of treatment and has a greater than 50% mortality. It can develop even after the patient has been on antimalarial therapy for a few days and clinically seems to be improving: an increased respiratory rate may be the only indication that this grave complication is imminent.

Why the pulmonary edema should develop in malaria has not been explained. Cardiac decompensation has been blamed and at autopsy the heart may show epicardial and endocardial echymoses, interstitial edema, and fatty infiltration. Myocardial necrosis, however, has not been reported. Moreover, clinical evidence of cardiac decompensation is usually lacking. Although excessive administration of fluid may occur in patients who are admitted in circulatory collapse (algid malaria), or who have renal complications, this is not always the explanation. It is probable that there is damage to the microcirculation, with increased capillary permeability perhaps from adherence of parasitized red blood cells to pulmonary endothelial cells. This suggestion is confirmed by experimental malarial infections in hamsters. In addition to the partial occlusion of pulmonary veins, lymphatic vessels become thrombosed and pulmonary edema follows. Autopsy studies on children in Ghana have shown pulmonary abnormalities following death from cerebral malaria. As the authors of one publication suggest, "some caution is needed in assessing the likely significance" of many of these findings.

In malarial infections, lymph nodes throughout the body may become enlarged, congested, soft, and pigmented. During pregnancy malaria causes many problems and in some areas, e.g., Zambia, up to 75% of pregnant women have circulating malarial parasites: parasites in the placenta are a frequent cause of abortion and of maternal death following the 3rd month of pregnancy, but the parasites do not cross into the fetal circulation. Anemia is also a particular problem when there is malaria during pregnancy, and 20% of the babies born to malarial mothers will have low birth weights. Malaria may cause gastrointestinal symptoms, but these are often due to the drugs used for prophylaxis.

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Copyright: Palmer and Reeder