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Each parasite has a complex life cycle, and human infections are not readily established unless there is intense and prolonged exposure to infective larvae.
Early symptoms of filariasis include high fevers (filarial or elephantoid fever), lymphangitis, and lymphadenitis. Acute filarial lymphangitis occurs when the adult worms die, leading to severe localized inflammation. Serum: Current tests lack both sensitivity and specificity, and most people from the region of endemicity will have a positive serologic response. Adult: Adult worms are minute and threadlike, have a smooth cuticle, and are found in the lymph nodes and lymphatic channels. Since these helminths do not multiply within the human host, infection levels are related directly to the number of infective larvae to which humans are exposed. The microfilariae, which may survive for 1 to 2 years, are not infective for other vertebrate hosts, nor do they undergo any further development in the vertebrate host. After exposure, it may take years before significant pathological changes in the human host are evident. Filarial fever usually begins with a high fever and chills that last 1 to 5 days before spontaneously subsiding, and in many cases, patients with filarial fevers do not have a microfilaremia.
This response may be due to exposure to nonhuman filarial antigens from infected mosquitoes, and filarial antigens may cross‑react with antibodies to other parasitic diseases. The infections are transmitted to humans by the bites of obligate blood‑sucking arthropods that had become infected through ingesting larvae (microfilariae) contained in a blood meal obtained from a mammalian host.
In the adult stages, human filarial parasites inhabit the lymphatic system, subcutaneous tissues, or deep connective tissues. The intermediate host, a mosquito, acquires the infection by ingestion of microfilariae in the blood meal. The lymphangitis will extend in a distal direction from the affected nodes where the filarial worms reside.
Obstruction of the retroperitoneal lymphatics may cause the renal lymphatics to rupture into the urinary tract, leading to chyluria.
The inflammatory reaction evoked by the filarial infection is a result of host reactions to the products of the developing worm or its death.
PCR assays are becoming useful diagnostic tools because they can discriminate between past and present infection, can be used to monitor therapy, and can be used to detect and differentiate multiple filarial infections.

The asymptomatic incubation period can be from 6 months to 3 years; therefore, the chances of eliciting a relevant patient history are rare, at best.
In areas of endemicity, exposure begins early in childhood, with microfilaria rates increasing with age, although the infection may not be clinically apparent. Lymphadenitis and lymphangitis develop in the lower extremities more commonly than in the upper. Microfilariae do not appear to be responsible for the major sequelae of lymphatic filariasis. Once released by the female worm, microfilariae, which are highly motile and threadlike, can be detected in the peripheral blood or cutaneous tissues, depending on the species. Within hours after their arrival in the mosquito stomach, the microfilariae lose their sheaths. Almost half of the microfilaremia patients will have renal abnormalities characterized by proteinuria and hematuria. The microfilariae, which may survive for 1 to 2 years, are not infective for other vertebrate hosts, nor do they undergo any further development in the vertebrate host. The larvae then penetrate the wall of the gut, migrate to the thoracic muscles, and develop into infective (filariform) larvae over a period of 7 to 21 days. The larvae migrate to the labella (distal end of the proboscis) of the mosquito and enter the skin of the definitive host through the puncture wound when a blood meal is taken. The infective larvae enter the peripheral lymphatic system and migrate to lymph vessels distal to the lymph nodes, where they grow to mature female and male adults and mate.
The nodes are firm, discrete, and tender and tend to remain enlarged, while the lymph vessel is indurated and inflamed. The overlying skin is tense, erythematous, and hot, and the surrounding area is edematous. Microfilariae are released from the gravid female and can be detected in the peripheral circulation in 8 to 12 months postinfection; however, filariasis without microfilaremia is not uncommon.

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