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332

Practical Urology: EssEntial PrinciPlEs and PracticE

Schistosomiasis

 

 

 

 

that characterize chronic schistosomiasis.10

 

 

 

 

 

 

 

 

 

 

 

 

Patients may be asymptomatic, or present dysu-

Urinary schistosomiasis is caused by the blood

ria, hematuria, frequency, colic, incontinence,

retention, and stones (Lehman 1973).

trematode Schistosoma

haematobium. It

is

Obstructive uropathy is also a long-term

endemic to areas of the Middle East and most of

sequelaeof urinaryschistosomiasis.Hydroureter

Africa with 90 million infected worldwide, and

usually precedes hydronephrosis and is typi-

has become more prevalent in the USA with the

cally bilaterally asymmetrical (Lehman 1973).

increased international travel.10

 

 

 

 

 

 

As the obstructive uropathy progresses and

The life cycle of S. haematobium in the human

ascends to hydronephrosis, long-term dilation

host begins with the deposition of ciliated lar-

leads to atrophy

and

finally renal failure

vae into fresh water from eggs excreted through

(Lehman 1973).

 

 

urine and feces of infected human hosts. The

 

 

Chronic urinary schistosomiasis also pro-

larvae use an intermediate host, Bulinus snails,

duces bladder hyperplasia, metaplasia, dyspla-

to produce cercariae in freshwater which, using

sia, and eventually cancer. Metaplasia and

vibratory locomotion, penetrate the unbroken

dysplasia are usually associated with bladder

skin of human hosts to become a schistosomu-

cancer caused by

the

chronic inflammatory

lum. Following maturation of 80–110 days, the

state. Squamous

cell

carcinomas make up

schistosomulum microembolize to the liver and

50–90% of bladder cancer lesions, with adeno-

lung before settling into the pelvic and perivesi-

carcinoma accounting for 5–15%. Most are exo-

cal venous plexus where paired male and female

phytic,but 25% can be endophytic and ulcerative.

worms now their adult size of 1.5 cm adhere to

They tend to occur most frequently on the pos-

the endothelial

lining of

veins

and

begin

to

terior and lateral

walls, typically sparing the

release eggs into the blood stream. These eggs

trigone.47 Unlike other squamous cell carcino-

are ovoid, distinctly terminally spined, and

mas, those associated with schistosomiasis tend

80–150 mm in length. Twenty percent of these

to be well differentiated, have a good prognosis,

eggs will cross directly into the bladder or rec-

and have low metastatic potential.45

tum where they will be excreted to continue the

In addition to malignant sequelae, the blad-

cycle of infection. The presence of terminally

der can develop painful ulcers with the slough-

spined eggs in the urine or feces is the gold

ing of necrotic papules. More common with

standard for the diagnosis of schistosomiasis.

chronic schistosomiasis, patients may present

Adult worms have a typical life span of 3–6

with suprapubic or pelvic pain and dysuria.47

years, but have been demonstrated to live up to

During the very late stages of the disease pro-

3 decades, and may release as many as 100 eggs

cess, the detrusor can become indurated and

per pair daily. During active infection, eggs of

thicken, markedly

reducing bladder capacity

all stages are excreted, but in active or cured

causing the patient abdominal pain and voiding

infections, only

degenerated

eggs

will

be

dysfunction. As with bladder cancers, the trigo-

excreted.10,44

 

 

 

 

 

 

 

 

 

 

nal region is typically spared.10

 

 

 

 

 

 

 

 

 

 

 

 

S. haematobium eggs can invade epididymal

Clinical Manifestations

 

 

 

structures and ejaculatory ducts, and blood and

 

 

 

 

 

 

eggs may be present in the ejaculate even before

The clinical sequelae of schistosomiasis come

the urine. A painful scrotal mass may be mis-

from the eggs which cause significant cellular

taken for cancer and only discovered after

and humoral host responses that result in the

orchiectomy. Women with schistosomiasis may

granulomatous encasement of eggs.45 This

manifest eggs on routine Papanicolaou smear

inflammatory reaction results in the presence of

due to asymptomatic cervicitis or vaginitis.45

hyperemic, large, bulky polyps surrounding

Patients with urinary schistosomiasis may

localized areas of large egg burden within host

also have concurrent superinfections with a

tissue.46 As the eggs are destroyed and urinary

variety of pathogens. In endemic regions,

excretion of eggs ceases, calcification and

chronic infections with Salmonella commonly

fibrosis occurs resulting in tan colored flat

recur and are resistant to antimicrobial therapy

mucosal lesions, known as the “sandy patches”

alone (Lehman 1973).

 

333

nonBactErial infEctions of tHE gEnitoUrinary tract

Diagnosis

The diagnosis of schistosomiasis requires a high index of suspicion. Information elicited during the history may increase suspicion for schistosomiasis, such as time spent in or near those regions where the trematode is endemic. Typically, patients require chronic exposure to water, but recent travelers may be more likely to present with acute symptoms.

The gold standard to diagnose schistosomiasis is the demonstration of terminally spined eggs in urine sediment. Egg excretion is highest midday, and the proportion of eggs excreted in the urine is an indication of overall egg burden. Eggs may also be demonstrated on pathologic specimens from bladder biopsy (Fig. 24.3b), which may be necessary in latent infections where active eggs are no longer being excreted in the urine. The schistosomiasis eggs also invade rectal tissue, thus when negative urinalysis necessitates the need for pathologic diagnosis, rectal biopsies might be preferential and less invasive.10,47 Western blot assays are available, and have a high sensitivity and specificity, but do not differentiate between acute and chronic infections, but this method can make the diagnosis in cases with low egg excretion.48

The long-term sequelae of schistosomiasis may be very apparent on x-ray of the kidneys, ureter, bladder (KUB). The presence of rim of calcified bladder resembling a fetal head is pathognomonic for urinary schistosomiasis (Fig. 24.3). In addition, calcifications may also be seen in the wall of the distal ureters, prostate and seminal vesicles, posterior urethra, and even the colon. CT will demonstrate these calcifications with or without concurrent obstructive uropathy.49 Ultrasound reveals a thick walled, calcified bladder, while voiding cystourethrogram (VCUG) may show vesicoureteral reflux, which can be present in as many as 25% of ureteral infections.10

Treatment

The mainstay of treatment of urinary schistosomiasis is medical treatment with Praziquantel (Table 24.2). Generally well tolerated, it produces cure rates approaching 100%. Many of the clinical manifestations respond to medical therapy alone including obstructive uropathy caused by

a

b

Figure 24.3. schistosomiasis. (a) coronal non-contrast ct images demonstrating bladder calcifications in 20-year-old african student with hematuria and schistosomiasis.(b) Histologic demonstration of fibrosis and terminally spined eggs in bladder biopsy.

polypoid lesions, with marked improvement in obstruction and resulting renal impairment in about 2 weeks. For this reason, surgical intervention should be withheld until after the initiation of medical therapy and applied only to those sequelae resistant to medication, or those requiring acute intervention such as severe hematuria.10,44