The treatment options for malaria vary according to the region where the traveler was likely to have acquired the infection. This is based on the local prevalence and antimalarial drug susceptibility of particular Plasmodium species. Chloroquine is the treatment of choice for patients infected with P vivax, P ovale, and P malariae.
Patients infected with either P vivax or P ovale must also take primaquine, because these species may lie dormant within the liver and are not eradicated by chloroquine alone. Failure to treat P vivax and P ovale with both agents frequently leads to recrudescence of the disease.
If P falciparum has been eliminated as the causative agent, patients may be treated in the ambulatory setting. When P falciparum infection is suspected, treatment should be initiated as soon as possible, because severe illness or death can occur in as little as 1-2 days after presentation. The Centers for Disease Control and Prevention recommends hospitalization in order to ensure that patients are able to tolerate oral therapy and have an appropriate response to treatment.
For patients returning from areas where Plasmodium species have known chloroquine resistance, such as southern Asia, sub-Saharan Africa, and Oceania, four treatment options are available: (1) oral quinine along with tetracycline, doxycycline, or clindamycin; (2) atovaquone/proguanil; (3) mefloquine along with doxycycline; or (4) artemether-lumefantrine. Due to toxicity issues and difficulty in obtaining quinine, atovaquone/proguanil or artemether-lumefantrine may be preferred. Depending on the severity of the disease and the region where the parasite was acquired, different lengths of treatment are recommended; these vary from 3 to 7 days of quinine therapy and 7 days of antibiotics.
For patients with severe malaria, an initial course of doxycycline with quinidine, an intravenous isomer of quinine, is recommended until the parasite burden is less than 1%, at which point oral therapy should be initiated. Unfortunately, quinine and quinidine have several side effects, and patients must be closely monitored for cardiac dysrhythmias caused by prolongation of the QTc, profound asymptomatic hypoglycemia, and respiratory distress.
In this case, malaria resulting from P falciparum infection was promptly diagnosed on the basis of the patient's travel history and the severity of his symptoms. He was admitted to the pediatric intensive care unit for close observation because of the potentially dangerous side effects of treatment. The patient received a bolus of intravenous quinidine and clindamycin. His parasitemia level was less than 0.5% on the second day of treatment, and the patient was switched to oral quinine therapy and clindamycin. His platelet and creatinine levels improved on hospital day 5, and he was discharged to home on oral therapy for a total of 7 days.
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