History
Although filarial infection in endemic areas is generally acquired in childhood, the disease may take years to manifest before being diagnosed clinically in early adulthood. Therefore, in endemic areas, up to 50% of the population (more commonly men) may have subclinical infection and may develop pathologic sequelae (although rare). This is characterized by the presence of thousands or millions of parasites in the blood. However, this small number of infections in endemic areas with pathologic changes accounts for the bulk of clinical disease.
Many individuals with filarial infection develop fever due to immune reactions. Patients present with episodic fever associated with lymphangitis, lymphadenitis, funiculoepididymitis (ie, inflammation of the spermatic cord and epididymis), transient edema, and small hydroceles. Patients with secondary infections may also present with fever and a purulent reaction.
The hallmark of clinical disease is lymphedema. Patients in the prepatent period (50-150 d) may develop acute lymphedema of the scrotum that remits spontaneously or after medical treatment. In these patients, lymphatic tissues show typical changes of filarial infection, but adult worms are rarely found.
In contrast, patients with established infections develop permanent lymphatic scarring, resulting in progressive lymphedema. The genitals and lower extremities are the areas most commonly affected.
Physical Examination
Elephantiasis of the penis and scrotum in patients with filariasis is the most common clinical problem encountered by urologists. Secondary bacterial infections of the skin and local lymph nodes are common in these patients. Although bacteria play no role in chyluria or filarial hydrocele, elephantiasis and lymph scrotum are often superinfected. Bacterial or fungal infections (most commonly streptococci) lead to recurrent lymphangitis, erysipelas, chronic ulcers, or persistent fungal crusting, aggravating the clinical conditions.
Chyluria develops before elephantiasis in young adult patients. Chyluria results from obstruction of the retroperitoneal lymphatic channels, leading to dilatation and rupture in the urinary collecting system. Initially, chyluria may alarm patients; however, subsequently, it may be disregarded. Occasionally, urinary protein loss may be significant and may lead to hypoalbuminemia and anasarca. Most cases of chyluria are intermittent and respond to bed rest and abdominal binders to increase intra-abdominal pressure. Retrograde lymphangiography and lymphosclerosis can be used in an attempt to treat persistent cases.
Filarial hydroceles (see the images below) vary significantly in size. They can grow very large and may become socially unacceptable and cause significant morbidity and discomfort. Differentiating filarial hydrocele from idiopathic hydrocele is difficult in many cases. A history of exposure to infection from traveling to or residency in endemic areas is suggestive. The World Health Organization (WHO) estimates 69% of all hydroceles are filarial in origin. Since the prevalence of hydroceles in non-endemic areas is considerably low, all patients with hydroceles in W. bancroftiendemic areas should be should be examined for other manifestations of filariasis. [8]


Patients with filarial hydroceles often have a thickened spermatic cord and epididymis with firm nodules. During surgery, the tunica is thickened with calcifications in the wall, and the hydrocele fluid is milky. These findings are uncommon in patients with uncomplicated idiopathic hydroceles. Microfilariae and adult worms are rarely detected in hydrocele fluid.
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Filarial infection causing enlarged pubic lymph nodes.
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Laparoscopic view of enlarged lymphatics secondary to filarial infection.
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Lymphocele of the right spermatic cord.
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Microfilaria of Wuchereria bancrofti in a peripheral blood smear.
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Unilateral left hydrocele and testicular enlargement secondary to Wuchereria bancrofti infection in a man who also was positive for microfilariae.
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Bilateral hydrocele, testicular enlargement, and inguinal lymphadenopathy secondary to Wuchereria bancrofti infection in a man who also was microfilaremic.