Epidemiology

Loiasis occurs only in Africa, primarily in rainforest areas of Central and West Africa. Isolated cases have been reported in West Africa from Ghana to Guinea, and in Uganda, Malawi, Ethiopia, and Zambia (Fig. 35.1). Chronic infection may occur in 3–13 million residents of these endemic areas. Distribution of disease is affected by the predilection of the vector flies to reside in the forest canopy and lay their eggs in swamps and at river edges. The flies are attracted by movement, dark colors, and wood smoke. Rain forests, with relatively low canopies and scant undergrowth, seem to constitute a particularly desirable habitat for Chrysops flies.^1–3 Infection rates are higher in adults than in children, and, in endemic areas, tend to be higher in males.

Fig. 35.1 Distribution of Loa loa.

(Klion AD, Nutman TB. Loiasis and Mansonella infections. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical infectious diseases. 2nd edn. Philadelphia: Churchill Livingstone; 2006:1163)

Etiology

Chrysops silacea and Chrysops dimidiata are the most important vector species. Day-biting females inject larvae and pick up microfilariae of Loa in their blood meals. Larvae develop into adult worms in 6–12 months; adult worms may live up to two decades (Fig. 35.2). Adult worms migrate through subcutaneous tissue. Microfilariae are released into the bloodstream by adult female worms, but are found most commonly at midday, corresponding to the maximal biting time of the vector flies. Microfilaremia is seen less commonly in travelers or expatriates compared to individuals native to endemic areas.⁴

Fig. 35.2 Life cycle of Loa loa. The vector for Loa loa filariasis are flies from two species of the genus Chrysops, C. silacea and C. dimidiata. During a blood meal, an infected fly (genus Chrysops, day-biting flies) introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound (1). The larvae develop into adults that commonly reside in subcutaneous tissue (2). The female worms measure 40–70 mm in length and 0.5 mm in diameter, while the males measure 30–34 mm in length and 0.35–0.43 mm in diameter. Adults produce microfilariae measuring 250–300 μm by 6–8 μm, which are sheathed and have diurnal periodicity. Microfilariae have been recovered from spinal fluid, urine, and sputum. During the day they are found in peripheral blood, but during the noncirculation phase, they are found in the lungs (3). The fly ingests microfilariae during a blood meal (4). After ingestion, the microfilariae lose their sheaths and migrate from the fly’s midgut through the hemocoel to the thoracic muscles of the arthropod (5). There the microfilariae develop into first-stage larvae (6) and subsequently into third-stage infective larvae (7). The third-stage infective larvae migrate to the fly’s proboscis (8) and can infect another human when the fly takes a blood meal (1).

(Adapted from Centers for Disease Control and Prevention DPDx.)

Clinical Manifestations

Many of the clinical manifestations of Loa infection tend to be more prominent in the recently exposed. Eosinophilia and increased levels of serum IgE are characteristic and are usually more pronounced in symptomatic individuals. Disease manifestations range from asymptomatic infection associated with microfilaremia to severe and life-threatening complications such as encephalitis, cardiomyopathy, and renal failure. Allergic-type symptoms tend to be prominent, especially in those recently exposed. These include pruritus, urticaria, and transient migratory nonpitting edema (Calabar swellings). These swellings are thought to be a hypersensitivity reaction to adult worm antigens and are most common on the extremities. They appear and disappear spontaneously, usually lasting a few days to several weeks.

Adult worms may migrate under the conjunctiva, giving rise to the name eye worm for this infection. An intense conjunctivitis may accompany this migration, and most episodes resolve without sequelae. Worms may occasionally be seen migrating under the skin. Unlike the slow progress and intense itching of cutaneous larva migrans (caused by dog or cat hookworm larvae) migration of Loa loa is rapid and causes little or no reaction.² Complications of infection with Loa loa include peripheral neuropathy, encephalopathy, and renal involvement. Peripheral neuropathy tends to occur in association with Calabar swelling and commonly presents as entrapment neuropathy. Encephalopathy occurs most often in the setting of significant microfilaremia and is most often seen following treatment. Microfilariae have been found in the spinal fluid. Encephalitis has also been associated with ivermectin treatment given in mass treatment programs for onchocerciasis.⁵ Renal involvement, usually hematuria or proteinuria with a clear sediment, occurs in as many as one-third of those infected. Transient worsening may occur with treatment but is almost always reversible; progression to renal failure is rare.