Schistosomiasis
of the bladder
Geographical
distribution
The disease is endemic in many parts of Africa, in Israel, Syria, Saudi
Arabia, Iran, Iraq and along the shores of China’s great lakes. Dwellers of
the Nile valley have suffered for centuries. Marshes or slow-running fresh water
provide a favourable habitat for the particular freshwater snail (Bulinus
truncatus) which is the intermediate host.
Mode
of infestation
The disease is acquired while bathing in infected water. The
free-swimming, bifid-tailed embryos (cercaniae) of the trematode Schistosoma
haematobium penetrate the skin. Shedding their tails, they enter blood
vessels and are swept to all parts of the body, but flourish in the liver where
they live on erythrocytes. They develop into male and female worms. The female
is long, smooth and slender, and is furnished with two weak suckers anteriorly.
The male is broader, shorter (11 mm in length), bosselated and provided with a
strong sucker at either end. Sexual maturity having been attained, the nematodes
leave the liver and enter the portal vein. The male bends into the shape of a
gutter (the gynaecophonic canal), into which a female nestles and the pair makes
its way towards the inferior mesenteric vein. Schistosoma haematobium has
an affinity for the vesical venous plexus which they reach through the
portosystemic anastomotic channels.
Having
reached the bladder, the female moves forward until she enters a submucous
venule so small that she completely blocks it. She now proceeds to lay about 20
ova in a chain. Each ovum is provided with a terminal spine which penetrates the
vessel wall. A heavily infected subject passes many hundreds of ova a day. If
the ova reach fresh water, the low osmotic pressure causes their envelope to
Clinical
features
After penetration of the skin, urticaria lasting for about 5 days
can occur (swimmer’s itch). After an incubation period ranging from 4 to 12
weeks, high evening temperature, sweating and asthma, together with leucocytosis
and eosinophilia, occur. Usually, an asymptomatic period of several months
supervenes before the ova are released, causing the typical early sign and
symptom of intermittent, painless, terminal haematunia. Men are three times more
often affected than women. Patients often present at a very late stage.
Examination
of the urine
The last few millilitres of an early morning urine specimen are
collected and centrifuged in a dry container. Examination on several consecutive
days may be required, but a negative result does not exclude bilharziasis,
especially in patients no longer resident in bilharzial districts.
Cystoscopy
Dependent
on the length of time for which the disease has remained untreated, cystoscopy
will reveal one or more of the following.
1. Bilharzial pseudotubercles are the
earliest specific appearance. The pseudotubercles are larger, more prominent,
more numerous, more yellow and more distinctly grouped (Fig.
65.42) than those
of tuberculosis.
2. Bilharzial nodules (Fig.
65.43) are
due to the fusion of tubercles in the presence of secondary infection. They are
larger and greyer than those in 1.
3. ‘Sandy patches’ are the result of
calcified dead ova with degeneration of the overlying epithelium. They occur in
the first instance around one or both ureteric orifices (Fig.
65.44).
Considerable calcification of this nature is visible on the radiograph.
4. Ulceration is the result of sloughing
of mucous membrane containing dead ova or, what is even more common, sloughing
of a bilharzial papilloma. The ulcer is shallow (Fig.
65.45) and bleeds readily,
and its common position is the posterior wall of the bladder.
5.
Fibrosis is mainly the result of secondary infection. The capacity of the bladder
becomes much reduced and contracture of the bladder neck may be found.
6. Granulomas. Bilharzial masses are due
to an aggregation of nodules. They are sessile and soft, and bleed readily when
touched.
7.
Papillomas are distinguished
from those in 6, above, by being more pedunculated (Fig.
65.46). They vary in
size and may be single or multiple.
8. Carcinoma is a common end result in grossly infected bilharziasis of the bladder which has been neglected for years. It usually commences, not in a papilloma, but in an ulcer, and is therefore a squamous celled carcinoma (due to metaplasia). It is usually advanced and will require radical cystectomy (see the section on ‘Carcinoma of the bladder’).
Treatment
Lesions 1—6, inclusive, can be expected to heal in response to
systemic treatment by antimony or other preparations (e.g. praziquantel and
metriphonate). It takes many months for dead ova to be expelled, and even after
repeated courses and healing of the bladder lesion living bilharzial worms have
been found at necropsy in the portal system. In addition to general treatment,
healing of bilharzial ulcers and granulomas is expedited by light diathermy
coagulation. Bilharzial papillomas and carcinomas do not respond and require
the same surgical measures as nonbilharzial papillomas and carcinomas.
Other
complications and their treatment
• Secondary bacterial cystitis is commonly present and requires
treatment.
• Urinary calculi, especially vesical and ureteric, occur more
frequently when bilharzial lesions of the bladder are present.
• Stricture of the ureters affects the last inch of the ureters.
These often respond to dilatation, but sometimes re-implantation of the affected
ureter is necessary.
• Prostatoseminal vesiculitis.
• Fibrosis of the bladder and bladder neck (Fig.
65.47) should be
treated in the same way as that of nonbilharzial origin.
• Bilharzial urethral strictures are often accompanied by fistulae, and
can be cured only by excision of the fistulous tracks and urethroplasty.