334

Practical Urology: EssEntial PrinciPlEs and PracticE

Thus, surgical intervention must be applied

with cutaneous plaque-like lesions with associ-

on a case by case basis with consideration for

ated ascending lymphangitis and local adenitis.

the specific resistant clinical manifestations

In contrast, patients may also present with local

caused by schistosomiasis. Persistent obstruc-

distinct well-circumscribed nodular areas of

tive uropathy, for example, has been shown to

local lymphadenitis and lymphangitis with a

respond well to balloon dilation, but with distal

centrifugal pattern of spread. These may mani-

ureteral involvement, techniques such as the

fest in the nematode’s preferred lymphatic dis-

Leadbetter-Politano reconstruction may be nec-

tribution or their nesting areas causing “sterile”

essary.46 Deep bladder ulcers tend to be resistant

abscess, funiculoepididymitis or orchitis.

to fulguration, and partial cystectomy might

Funiculoepididymits causes testicular pain

provide more definitive resolution. Contracted

with local edema, hydrocele, and palpable cord-

bladders might necessitate augmentation or

like swelling with possible pampiniform throm-

diversion to provide symptomatic relief.10

bosis. These findings may simulate malignancy,

Bladder cancer is treated and monitored with

and histological specimen at orchiectomy

standard resection techniques.

shows marked eosinophilia and may reveal

adult worms. This may resolve spontaneously,

Filariasis

or may progress or worsen chronic lymphoe-

dema. These patients will likely not have detect-

able microfilaremia. As the local inflammation

Filariasis is a classification of diseases caused

resolves, the local area will be replaced by scar

by one of three nematode parasites. While

tissue, causing local lymphatic obstruction

Wuchereria bancrofti cause 90% of human

which initially will be compensated for by local

lymphatic filarial illness, other organisms such

lymphatic collaterals that with repeated chro-

as Brugia malayi, of Southeast Asia and the

nic infection will further obstruct worsening

Pacific Isilands, and Brugia timori may also be

lymphedema.10,51

the culprit. The life cycle of these parasites

The most common sequelae of chronic infec-

depend upon mosquito vectors that breed in

tion are hydroceles. The hydroceles of filariasis

pools of polluted, stagnant water in endemic

present with a milky fluid, often sediment rich

areas spanning 76 countries, with 40% of the

and gross specimens may be distinctive with

cases occurring in India, affecting over 120

calcium or cholesterol deposits in a fibrous,

million people worldwide.50 The larvae dwell

thick tunica vaginalis. Chronic infections also

in the salivary glands of their mosquito vectors

lead to lymphedema and elephantiasis as the

and traverse the bite site, conjunctival or buc-

superficial lymphatics obstruct. Secondary bac-

cal mucosal barriers of their human hosts.

terial superinfection is a major contributing

From there, adult worms migrate into lym-

factor to the worsening and development of

phatic vessels. W. bancrofti remains in the cen-

severe lymphedema and elephantiasis.52 As the

tral, inguinal, or scrotal channels, while W.

deep lymphatics obstruct, they rupture spilling

malayi navigates toward inguinal or distal

chylous fluid into urinary tract resulting in chy-

lymphatics. The female worm will then secrete

luria, the peritoneum causing chylous ascites or

microfilaria into the lymphatics and blood

into the tunica vaginalis with chylocele.53

stream maintaining a constant level. Both cel-

lular and humoral immune responses, likely to

Diagnosis

dead or dying worms cause local inflammatory

and granulomatous responses that damage and

The diagnosis of filariasis begins with a thor-

obstruct local lymphatic channels.

ough history and physical. Transmission of

filariasis requires long-term repeated exposure,

Clinical Manifestations

so patients will have a history of living in

endemic areas as well as any of the classical

Early filarial infection may be asymptomatic,

physical findings discussed above. Blood sam-

or present with “filarial fever,” a clinical syn-

ples may demonstrate microfilaremia, but must

drome characterized by episodic fever, tran-

be drawn at midnight, the peak of microfilaria

sient edema, hydroceles, and lymphangitis/

release. Histologic specimens that demonstrate

lymphadenitis or dermatolymphangioadenitis

adult worms surrounded by graunlomas are