Genetically, it refers to an extremely heterogeneous group of clinical conditions associated with the presence of parasites of the Onchocercoidea family (Filarioidea superfamily) in the human body. More specifically, lymphatic filariasis is caused by two different nematode parasites: Wuchereria bancroftii and Brugia malayi. These parasites are transmitted in their larval stage by different types of Arthropoda (Anopheles, Aedes togoi, Mansonia), they then grow inside the human body, initially in the form of microfilarias and, at a later stage, about 90 days later, they become adults and stay so also for many years. Their entire growth takes place in subcutaneous tissues at the level of lymphatic collectors. Clinical manifestations associated with this parasitosis of the lymphatic structures may range from acute lymphangitis, to lymphadenitis, and the development of chronic lymphedema, as well as elephantiasis. The pathologic process often begins when the parasite dies, and granulomatous fibrosis is triggered by microorganism debris and by the products released during their maturation, causing thrombolymphangitis with eosinophylic invasion and, therefore, subsequent mechanical occlusion of the affected collectors, while setting up the physiopathological conditions for the development of chronic secondary post-infection lymphedema. Filariasis is endemic in India, China, South-East Asia, and Korea. Its diagnosis is mainly based on the patient’s medical history and clinical examination (in some specific and initial cases of W. bancroftii infections, microfilarias can be isolated in the blood during the night). Medical therapy against parasitic infection is mainly based on diethyl carbamazepin and other anti-parasitic drugs. Conversely, therapies in case of lymphangiologic complications (e.g. chronic secondary lymphedema) do not differ from the combined therapy successfully employed in the treatment of other chronic secondary lymphedemas.
Figure: Edema by past filiaria infection on an Ethiopian patient (posterior view).

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