Malaria

Malaria is a parasitic infection transmitted by the Anopheles mosquito that leads to acute life-threatening disease and poses a significant global health threat. Two billion people risk contracting malaria annually, including those in 90 endemic countries and 125 million travelers. The Plasmodium parasite has a multistage lifecycle, which leads to characteristic cyclical fevers. With timely treatment, most people experience rapid resolution of symptoms; however, significant complications may occur, including cerebral malaria, severe malarial anemia, coma, or death. This activity reviews the epidemiology, presentation, and complications of Plasmodium malaria and the role of the interprofessional team in evaluating and managing patients with this life-threatening infection.

Objectives:Review the epidemiology of malaria infection.Describe the pathophysiology of malaria infection.Summarize the pharmacologic treatment strategies for malaria infection.Outline the importance of collaboration amongst an interprofessional team to improve outcomes for patients receiving malaria treatment.Access free multiple choice questions on this topic.

Malaria

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Malaria is a parasitic infection transmitted by the Anopheles mosquito that leads to acute life-threatening disease and poses a significant global health threat. Two billion people risk contracting malaria annually, including those in 90 endemic countries and 125 million travelers, and 1.5 to 2.7 million people die in a year.[1] The Plasmodium parasite has a multistage lifecycle, which leads to characteristic cyclical fevers. With timely treatment, most people experience rapid resolution of symptoms; however, significant complications may occur, including cerebral malaria, severe malarial anemia, coma, or death. Preferred antimalarial therapeutic and chemoprophylactic regimens get dictated by species, geography, susceptibility, and patient demographics. Latent or reactivating infections may be reported years following exposure.

The incubation period, and therefore time to symptom development, varies by species: 8 to 11 days for P. falciparum, 8 to 17 days for P. vivax, 10 to 17 days for P. ovale, 18 to 40 days for P. malariae (though possibly up to several years), and 9 to 12 days for P. knowlesi.[1] The periodicity of the Plasmodium lifecycle creates the classic "malarial paroxysm" of rigors, followed by several hours of fever, followed by diaphoresis, and a drop to normal body temperature (P. vivax infection establishes a 48-hour cycle), though this is less commonly seen today due to rapid identification and treatment.[1]

Forty percent of the global population resides in or visits malaria-endemic regions annually.[1]P. falciparum is present in Western and sub-Saharan Africa and displays the highest morbidity and mortality of the Plasmodia species.[2]P. vivax is present in South Asia, the Western Pacific, and Central America.[2]P. ovale and P. malariae are present in Sub-Saharan Africa.[2] P. knowlesi is present in Southeast Asia.[2] As many as 500 million malaria cases occur annually, with 1.5 to 2.7 million deaths.[1] Ninety percent of fatalities occur in Africa.[1] Those at highest risk include children under age 5, pregnant women, and disease nave populations, including refugees in Central and Eastern Africa, nonimmune civilian and military travelers, and immigrants returning to their place of origin.[2]

Of the 125 million travelers who visit endemic locations each year, 10000 to 30000 develop malaria, and 1% of these will die from complications of their disease.[2][3] Rising average global temperatures and changes in weather patterns are projected to expand the burden of malaria; a rise of 3 degrees Celsius is postulated to increase malaria incidence by 50 to 80 million.[1]

Five Plasmodium species possess the ability to infect humans: P. falciparum, P. ovale, P. vivax, P. malariae, and P. knowlesi.[2] The female Anopheles mosquito ingests gametes during a blood meal, which form sporozoites that replicate in the gut.[1] During subsequent bloodmeals, saliva containing sporozoites gets released into a human host's bloodstream.[1] Within 60 minutes, sporozoites reach the liver, invade hepatocytes, and then rapidly divide, forming merozoites. In an active infection, organisms reenter the bloodstream and invade erythrocytes.[1][4] Within erythrocytes, Plasmodia consume hemoglobin and develop from immature trophozoites (ring stage) to either mature trophozoites or gametocytes (CDC Malaria 2019). Mature trophozoites replicate, forming schizonts, disrupting erythrocyte cell membrane integrity, and leading to capillary endothelial adherence and cell lysis.[1]

Free heme is released into the peripheral blood, which stimulates endothelial activation.[5][6] Untreated malaria lasts 2 to 24 months.[1] P. vivax and P. ovale infections may display "dormant schizogony," where inactive intrahepatic parasites (hypnozoites) remain until reactivation months to years in the future.[1] Although hypnozoite parasites do not routinely develop in the liver in the setting of P. falciparum and P. malariae infection, there are few reports of resurgent P. falciparum infection years after initial exposure.[7]

Low arginine, low nitric oxide, and elevated arginase activity have been observed in severe malaria in peripheral blood.[9] Studies have shown that the parasite's arginase enzyme may contribute to low arginine in severely ill patients, thus reducing nitric oxide production. Low nitric may lead to subsequent pulmonary hypertension and myocardial wall stress in children. Therefore, peripheral arginine or inhaled nitric oxide are possible treatment options.[10]

In taking a history, it is essential to inquire about the location of residence, recent travel and use of chemoprophylaxis, exposures (including sick contacts, fresh water, caves, farm/wild animals, insects/arthropods), HIV status, history of current or recent pregnancy, history of G6PD deficiency, history of sickle cell disease, history of anemia, history of blood or other cancers, and history of prior malarial infections (including successful or failed treatments).

The clinical features of infection in pregnancy vary from asymptomatic to severe, depending on the degree of (incomplete) immunity that a woman had acquired by the time she got pregnant. In semi-immune pregnant women, only a few infections result in fever or other symptoms.[12] Malaria in pregnancy has a devastating effect on maternal health and has been associated with increased infant mortality due to low birth weight caused by either intrauterine growth restriction or preterm labor, or both.[12] P. falciparum infections are associated with complications such as maternal anemia, low birth weight, miscarriage, stillbirths, and congenital malaria.[13][12] It is more likely for a pregnant woman in the second or third trimester to develop severe malaria with complications such as hypoglycemia and pulmonary edema compared to non-pregnant adults.[14]

Initial evaluation of undifferentiated fever in stable patients with possible malaria exposure includes a complete blood count, comprehensive metabolic panel, coagulation panel, blood culture, urinalysis, chest radiograph, and thick and thin blood smears. In patients with altered mental status, when cerebral malaria is suspected, a lactate level, arterial blood gas, and lumbar puncture may also be indicated.[2]

In patients with malaria, complete blood count reveals thrombocytopenia in 60-70% of all cases and varying degrees of anemia in 29% of adults and 78% of children.[2] Anemia is more severe in P. falciparum due to invasion of all aged erythrocytes and capillary and splenic erythrocyte sequestration secondary to decreased flexibility and cytoadherence.[1] Anemia is typically moderate with P. vivax and P. malariae due to preferential invasion of reticulocytes and older erythrocytes, respectively.[1] A comprehensive metabolic panel may reveal hepatocellular injury secondary to parasitic invasion, indirect hyperbilirubinemia due to hemolysis, electrolyte abnormalities secondary to the release of intracellular contents, concomitant dehydration, and kidney injury secondary to glomerular damage.[2] The coagulation panel may reveal coagulopathy concerning bleeding risk in patients with severe thrombocytopenia or liver dysfunction. Urinalysis may show proteinuria indicative of nephrotic syndrome.[1]

The gold standard for malaria diagnosis is a microscopic evaluation of Giemsa-stained thick and thin smears of a free-flowing venipuncture blood specimen.[2][1] Examination with oil immersion must be completed at 100-times and 1000-times magnification to avoid missing low-level parasitemia or "delicate ring forms."[1] The extent of parasitemia is estimated by the number of organisms per high-powered field.[1] Varying microscopic appearance of infected erythrocytes guides speciation:

An initial negative smear does not rule out malaria, as infected erythrocytes may become intravascularly sequestered; if clinical suspicion of malaria is high, smears require repetition in 12 and 24 hours.[2] The malarial pigment in monocytes and neutrophils may also manifest on the blood smear, particularly in patients with cerebral malaria.[1]

Treatment for patients diagnosed with malaria includes schizonticidal medications, supportive care, and hospitalization for high-risk patients. Nave adult and pediatric patients receiving active antimalarial treatment should remain inpatient for at least 24 hours to ensure adequate and correctly timed medication dosing and to trend parasitemia to evaluate treatment response. Higher initial parasitemia and poor downtrend are associated with fluid imbalance, renal dysfunction, and respiratory distress syndrome.[2] Unstable patients, particularly those with cerebral malaria or significant respiratory sequelae, require intensive care.[2] 2351a5e196