Human malaria is caused by one of four species of Plasmodium. The majority of cases of malaria worldwide are caused by P. falciparum, and P. falciparum is the only species that causes cerebral malaria. Malaria is transmitted to healthy individuals through the bite of an infected mosquito. The World Health Organization defines cerebral malaria as "unarousable coma not attributed to any other cause in a patient with P. falciparum malaria."^ Malaria can be transmitted by the bite of an Anopheles mosquito, through blood transfusions, and by intravenous injections with blood-contaminated needles. The incidence of cerebral malaria in a population is determined by the population's immunity. In holoendemic areas, which are areas of the world where significant transmission of malaria occurs annually with little change from year to year, native adults rarely develop cerebral malaria. Persons at risk for severe malaria in these areas are children from 1 to 4 years of age, new residents from nonendemic areas, returning residents that have lived abroad for years, residents who were maintained on chemoprophylaxis but have stopped, and pregnant women. Travelers to endemic areas are at high risk for infection. Infected mosquitoes can be transported from endemic areas via airplane, and travelers may acquire malaria during brief stopovers without disembarking from the airplane. P. falciparum malaria requires a minimum of 8 days for incubation, and 95 percent of all infections present within 4 weeks of the last mosquito exposure.
Systemic signs of malaria include jaundice, retinal hemorrhage, hepatosplenomegaly, fatigue, diarrhea, vomiting, abdominal pain, chest pain, cough, myalgia, and arthralgia. The majority of patients are febrile. Cerebral malaria presents with headache followed by an altered level of consciousness, and convulsions. On neurological examination, upper motor neuron signs are common as is decerebrate or decorticate posturing, delirium, hallucinations, delusions, and disorders of dysconjugate gaze. Coma is often associated with shock, acidosis, noncardiogenic pulmonary edema, hemolysis, anemia, renal insufficiency, and hypoglycemia. These are all potentially treatable complications. W Diagnosis is made by examining a blood smear for parasites. Blood smear should be examined every 12 to 24 hours for a period of 2 to 3 days, and the number of intraerythrocytic parasites should be counted.
In the United States, parenteral quinidine is the drug of choice for the treatment of cerebral malaria. Cerebral malaria is treated with a loading dose of 10 mg/kg of intravenous quinidine gluconate over a period of 1 to 2 hours followed by continuous infusion of 0.02 mg/kg/min. Loading doses of quinidine are not recommended for patients who have received mefloquine, quinine, or quinidine in the 24 hours before initiation of therapy. When the patient is able to take oral medication, therapy can be changed to one of the oral antimalarial agents to complete a total of 7 days of treatment from the initiation of intravenous therapy. [1251 Quinidine is cardiotoxic, and patients receiving parenteral forms of this agent should be monitored for arrhythmias, prolongation of the QT interval, and widening of the QRS complex. Recommendations for malaria chemoprophylaxis depend on the area to which the individual plans to travel. In the few areas where the parasite remains sensitive to chloroquine, this antimalarial agent should be taken in a weekly dose of 300 mg base. Chemoprophylaxis should begin 2 weeks before departure and should continue for 6 weeks after return. In areas where the parasite is resistant to chloroquine, mefloquine is recommended at a once per week oral dose of 250 mg beginning 2 weeks before departure and continued for 4 weeks after return. ye1
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