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Loiasis is a filarial nematode infection (see Overview of Filarial Nematode Infections) with Loa loa. Symptoms include localized angioedema (Calabar swellings) and subconjunctival migration of adult worms. Diagnosis is by detecting microfilariae in peripheral blood or seeing worms migrating across the eye. Treatment is with diethylcarbamazine.
Loiasis is confined to the rain forest belt of western and central Africa. Humans are the only known natural reservoir for this parasite.
Loa loa microfilariae are transmitted by day-biting tabanid flies (Chrysops [deerfly or horsefly]). Microfilariae mature to adult worms in the subcutaneous tissues of the human host; females are 40 to 70 mm long, and males are 30 to 34 mm long. The adults produce microfilariae. Adults migrate in subcutaneous tissues and the eye, and microfilariae circulate in blood. Flies become infected when they ingest blood from a human host during the day (when microfilaremia levels are the highest).
Occasionally, infection causes cardiomyopathy, nephropathy, or encephalitis. Eosinophilia is common but nonspecific.
Most infected people are asymptomatic, but eosinophilia is common. Infection produces areas of angioedema (Calabar swellings) that develop anywhere on the body but predominantly on the extremities; they are presumed to reflect hypersensitivity reactions to allergens released by migrating adult worms. In native residents, swellings usually last 1 to 3 days but are more frequent and severe in visitors. Worms may also migrate subconjunctivally across the eyes. This migration may be unsettling, but residual eye damage is uncommon.
Nephropathy generally manifests as proteinuria with or without mild hematuria and is believed to be due to immune complex deposition. Encephalopathy is usually mild, with vague CNS symptoms.
Loiasis should be suspected in patients who have a history of travel in an endemic area and who present with eye worms, Calabar swellings, or unexplained peripheral eosinophilia. Microscopic detection of microfilariae in peripheral blood establishes the diagnosis. Blood samples should be drawn between 10 am and 2 pm, when microfilaremia levels are the highest. Many serologic tests for antibodies do not differentiate Loa loa from other filarial nematode infections. Loa-specific antibody tests have been developed, but they are not widely available in the US. A quantitative real-time PCR (qPCR) to confirm the diagnosis and determine the microfilarial burden is available at the Laboratory of Parasitic Diseases, National Institutes of Health.
People from endemic regions of Africa should be checked for Loa loa before they are treated with diethylcarbamazine or ivermectin for other disorders because these drugs can have substantial side effects in people with loiasis; people with > 8,000 Loa loa microfilariae mL/blood are at risk of potentially fatal encephalopathy.
Diethylcarbamazine (DEC) is the only drug that kills microfilariae and adult worms. In the US, it is available only from the Centers for Disease Control and Prevention (CDC) after laboratory confirmation of loiasis; clinicians should seek expert advice before they initiate treatment. Because DEC can worsen eye disease in patients with onchocerciasis, coinfection should be excluded before treatment.
Patients with symptomatic loiasis and < 8000 microfilariae/mL blood are given DEC 50 mg po on day 1, 50 mg po tid on day 2, 100 mg po tid on day 3, then 2.7 to 3.3 mg/kg tid for 21 days.
DEC transiently exacerbates proteinuria and, in heavily infected patients, may trigger encephalopathy, leading to coma and death. Patients with > 8000 microfilariae/mL blood are at risk of this effect and may benefit from apheresis or initial treatment with albendazole 200 mg po bid for 21 days; the goal is to reduce the microfilarial load to < 8000/ mL before DEC is initiated. Multiple courses of DEC may be necessary. Patients who have failed ≥ 2 rounds of treatment with DEC may be given albendazole 200 mg po bid for 21 days. Ivermectin has also been used to reduce microfilaremia, but albendazole is preferred because its onset of action is slower and risk of precipitating encephalopathy is lower.
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