1. CNS.
Bilharziasis.
Dr/ ABD ALLAH
NAZEER. MD.
Spinal
Cord.
Lung.
Liver.
Genito-urinary.
Intestine
.

2. Schistosomiasis, also named bilharziasis (after
the German physician Theodore Bilhartz, who worked in Egypt
during the nineteenth century and was the first to discover the
life cycle of the parasite), is one of the most prevalent infectious
diseases in the world. It is endemic in more than 70 countries,
mainly in the less developed countries, and is estimated to place
approximately 20% of the endemic population at risk. The
number of people affected is estimated to be 200 million.
The schistosomes are a group of trematodes (flukes), some of
which are pathogenic to humans. The principal parasites that
affect humans are Schistosoma haematobium, Schistosoma
mansoni, and Schistosoma japonicum; less prevalent parasites
are Schistosoma intercalatum in Africa and Schistosoma mekongi
in the Far East. presents the global distribution of schistosomal
species. The most prevalent area for schistosomiasis is Africa,
where S haematobium and S mansoni dominate.

4. Schema shows the two-stage life cycle of S haematobium.

5. Acute schistosomiasis:
The symptoms of acute schistosomiasis are not directly caused by the
parasites, but by your immune system (the body's defence against
infection) reacting to the parasites.
Symptoms include: a high temperature (fever) above 38ºC (100.4ºF)
headache
joint and muscle pain
cough
bloody diarrhea
a dark red, blotchy, raised skin rash
pain in the abdomen
a general sense of feeling unwell
In many cases, the symptoms usually get better by themselves within a
few weeks. However, it is still important to seek treatment as the
parasites will stay in your body and chronic schistosomiasis will
develop. This does not always lead to symptoms, but the infection will
remain and problems may develop at a later date.

6. Chronic schistosomiasis:
If schistosomiasis is not treated, the parasites remain in your body and will go
on to cause further symptoms. The immune system reacting to the eggs may
damage your organs, but fails to kill the parasites. The symptoms of chronic
schistosomiasis depend on where in the body the parasites have travelled to.
If the parasites travel to the digestive system, they can cause the following
symptoms: feeling tired all the time (fatigue), abdominal pain, bowel
problems – such as mild or severe watery diarrhea that contains blood and
mucus If the parasites travel to the urinary system, they can cause the
following symptoms: symptoms of cystitis– such as pain when urinating
frequent need to urinate, blood in your urine.
If the parasites travel to the heart or lungs, they can cause the following
symptoms: persistent cough in some cases, people cough up blood , wheezing,
feeling breathless and very tired after physical activity .
If the parasites travel to the central nervous system or brain, they can cause
the following symptoms: seizures (fits), headache, back pain, urinary
incontinence, weakness and numbness in your legs, dizziness, feeling sick
The parasites can also sometimes travel to the female genitals, where they
can cause the following symptoms: bleeding after sex, genital ulcers, irregular
menstruation, pelvic pain.

7. Involvement of the central nervous system in
Schistosoma mansoni and S. haematobium infection.
involvement of the CNS in Schistosoma mansoni (SM) and S.
haematobium (SH) infection was undertaken. Deposition of
ova in the brain has been reported in SM infection and less of
SH infection. In uncomplicated schistosomiasis, SH ova are
more likely than SM ova to be deposited in the brain and may
be carried there by the vertebral venous plexus. The deposition
of SM ova in the brain and meninges is more frequent in
hepatosplenic schistosomiasis, especially with corpulmonale,
and the route to the brain may be through pulmonary
arteriovenous shunts. Asymptomatic deposition of ova is
common but epilepsy may occur. The formation of large
granulomas and cerebral hemorrhage are rare complications.
Adult SM and SH have been observed in cerebral vessels.

8. ETIOLOGY AND EPIDEMIOLOGY
The term neuroschistosomiasis (NS) refers to the symptomatic
or asymptomatic involvements of the central nervous system
(CNS) by schistosomes. When associated with clinical
symptoms, it is one of the most severe presentations of
schistosomal infection. NS can be caused by Schistosama
japonicum, S. mansoni, and S. haematobium. Considering the
symptomatic form, the last two species are almost always
associated with a myeloradicular syndrome and the first
species, with cerebral disease.
Symptomatic cerebral NS has been recorded in about 2-4% of
individuals infected with S. japonicum (Watt et al. 1986). On
the other hand, this form of presentation is very rare in
association with the other two species.

9. Noncontrast axial CT of the brain showing edema areas in the right cerebellum,
schistosomiasis (B) Axial T1-weighted MRI of the brain showing isointense signal
in the right cerebellum, (C) Axial T2-weighted MRI of the brain showing
hyperintense signal in the right cerebellum, (D) Axial T1-weighted MRI after
gadolinium injection showing intensely enhancing nodules in the right cerebellum.

10. schistosomiasis
with neurological
Complications.

11. Schistosoma mansoni cerebral schistosomiasis.
Brain magnetic resonance imaging shows a heterogeneously
enhancing lesion with surrounding edema.

13. Cerebral schistosomiasis. (A) Axial T2-weighted MR image shows vasogenic edema
and mass effect involving left frontal lobe. (B) Axial and (C) coronal contrast-enhanced
T1-weighted MR image shows typical pattern of enhancement with multiple areas of
central linear enhancement surrounded by enhancing punctate nodules.

14. Magnetic resonance images (A-D) and histologic features (E and F) in a patient with
cerebral schistosomiasis. A, Coronal T1-weighted gradient echo image. B, T2-weighted
gradient echo image. C, T1-weighted image after gadolinium injection, showing a
nodular irregular lesion in the right parietal and insular cortex with mass effect,
perilesional edema, and slight irregular contrast enhancement. D, T2-weighted image
obtained 1 month after treatment, showing complete resolution of the lesion

15. Symptomatic spinal cord involvement is a rare but well-documented
manifestation of schistosomiasis. A nonspecific
intramedullary expansion in the caudal spinal cord is the most
common finding in conventional and computed myelography.
The literature concerning MR imaging of spinal cord
schistosomiasis is scarce, and pathologically confirmed cases
are mainly limited to isolated case reports.
Schistosomiasis of the spinal cord should be considered in the
differential diagnosis of lesions affecting the lower thoracic
cord-conus medullaris-cauda equina in patients from endemic
areas with history of exposure to Schistosomal infestation. MR
imaging can reveal the true extent of the disease and can
suggest the diagnosis through recognition of its signal
intensity changes and enhancement forms. Accurate diagnosis
allows early treatment and results in better prognosis of
spinal cord schistosomiasis.

17. Schistosomiasis. A to D, MRI of lumbar spine revealed expansion of the medullary
cone associated with spinal cord edema in the affected area associated with
epidural enhancement adjacent to areas of medullary involvement. G and H, The
roots of the cauda equine are thickened. E, F, and I, Magnetic resonance images
after treatment reveal the lesions reduction.

18. Epidural bilharzioma. A, Axial T1-weighted MR image shows a homogeneous
epidural mass with extension through the intervertebral foramina with a
lobulated paraspinal mass. B, Axial T2-weighted MR image shows a mild
heterogeneous hyperintensity and a contralateral displacement of spinal cord. C,
Axial T1-weighted MR image after gadolinium injection shows a homogeneous
enhancing of the lesion. D, Photomicrograph of frozen histopathologic section
shows ovum of Schistosoma mansoni. Note characteristic broad lateral spine.

19. Sagital magnetic ressonance imaging in T1 phase (Figure 3a), no contrast T2 phase (Figure
3b), and contrast T2 phase (Figure 3c) in a spinal cord schistosomiasis patient.

20. Spinal cord schistosomiasis patient. It is observed a granular impregnation
of gadolinium magnetic contrast in thoracic-lumbar spinal cord.

22. Masslike nodular enhancement
form in spinal cord schistosomiasis.
MR imaging of dorso-lumbar spine

23. Localization of spinal
cord schistosomiasis.
MR imaging of
dorso-lumbar spine
with moderate
expansion of the
distal cord and conus
medullaris. Linear
heterogenous
contrast uptake at
the enhanced study.

24. Radicular
enhancement
form in spinal
cord
schistosomiasis.
Peripheral enhancement form
of spinal cord schistosomiasis

25. Pulmonary involvement in schistosomiasis
Although the lungs are not an end organ in the life cycle of
schistosome infection in humans, pulmonary pathology exists. For
many years, pulmonary pathology was described mainly as a late
complication of the infection. It recently has been recognized that
pulmonary involvement also may occur in the early, acute stages.
Early-stage pulmonary involvement is unique to nonimmune
patients, that is, populations never previously exposed to
schistosomal infection, usually travelers from developed countries
to endemic areas. Physicians who practice in Western countries
who treat returning travelers are more likely to encounter
pulmonary involvement in the early stages of infection rather than
the later complications.
Early and late pulmonary schistosomiasis are two different diseases
with different clinical manifestations and different pathogenesis
and pathology, not merely a difference in time of onset.

26. Early (acute) pulmonary schistosomiasis:
Clinical manifestations.
Early pulmonary manifestations occur usually 3 to 8 weeks after
schistosome penetration. Patients with pulmonary schistosomiasis
reported shortness of breath, wheezing, and dry cough, mainly while
recumbent. Reports show that in some cases the pulmonary symptoms
coincided with febrile illness (Katayama fever). Most patients, however,
presented several weeks after the fever had subsided. Almost all the
patients could recall having had febrile disease before the onset of
pulmonary symptoms, but the pulmonary symptoms continued for
weeks after the fever subsided.
Pulmonary involvement can be divided into three types:
1. Symptomatic cases with radiologic findings (either chest
radiograph or CT scan). The radiologic findings may be evident at
presentation or, not uncommonly, may appear after antischistosomal
treatment. In either case, cough may persist for several weeks despite
the treatment.

27. 2. Symptomatic cases without radiologic findings.
In some patients, the clinical course is similar to the previous
one, but radiologic findings (either chest radiograph or CT
scan) are absent. This result may be caused either by the small
dimensions of the findings, which makes them invisible by
conventional methods, or their transient nature.
3. Asymptomatic cases with radiologic findings.
Cases in which there are pulmonary findings without a current
history of pulmonary symptoms are rare. The incidence of
these cases is unknown, because radiology is usually not
performed for asymptomatic patients. The author was able to
identify such cases since chest radiographs were performed as
part of the evaluation of patients with suspected early
schistosomiasis.

28. Pulmonary schistosomiasis. Chest radiography (pa) showing multiple small
pulmonary nodules scattered over both lungs without obvious predilection.

29. Pulmonary schistosomiasis. Chest CT of the upper lungs showing
blurred ground glass nodules scattered over both lungs

30. Chest radiograph that reveals several small round lesions in both lungs
(arrows). (B) Chest radiograph that reveals diffuse, increased lung markings
and prominent hilum with ill-defined nodules with pulmonary bilharziasis.

31. The progress
of pulmonary
hypertension
secondary to
S. mansoni.

32. pulmonary
hypertension
worsens, the
cardiovascular
changes become
more marked,
even in quite
young patients.
A In this 21-year
-old Puerto Rican
female, there is
marked dilatation
of the main
pulmonary artery
and the central
pulmonary
arteries, with
rapid tapering of
the peripheral
branches.

33. The end stage of cardiopulmonary schistosomiasis. There is massive enlargement
of the heart, and there are small bilateral pleural effusions, secondary to
congestive cardiac failure. Pericardiocentesis removed 320 cc of straw-colored
fluid. Thoracotomy showed multiple tiny nodules in the lungs and thick fibrous
plaques. The pericardium was greatly thickened. Histology showed granulomas
involving the lungs and pericardium and causing pulmonary arteriolitis.

34. CT scan through the bifurcation of the trachea that shows multiple lesions of
different sizes in both lungs. (B) CT scan through a point just above the
diaphragm that shows diffuse ground-glass areas with some nodularity. The
findings are mainly at the lung periphery with pulmonary bilharziasis.

35. CT of chest showing peripheral nodular and patchy infiltrates
in both lung fields with pulmonary bilharziasis.

36. Chest X-ray of a patient with Sch-PAH
displaying the enlargement of the
main pulmonary arteries.

37. Chest radiograph (A), magnetic resonance imaging (B), and pulmonary
angiography (D) in patient with World Health Organization class IV
pulmonary hypertension secondary to schistosomiasis from Brazil. C,
Magnetic resonance imaging of the liver with typical Symmers’ fibrosis.

38. Hepatosplenic schistosomal disease and pulmonary hypertension
and the pulmonary artery systolic pressure of 68 mmHg.

39. Chronic schistosomiasis with pulmonary hypertension. Chest radiograph (A and
D)and CT demonstrate (B and C)marked dilatation of the main pulmonary artery.

40. Acute schistosomiasis in a 35 year-old man with fever, cough and dyspnea. Chest
CT scans demonstrate bilateral diffuse patchy areas of ground glass opacities.

41. HEPATIC SCHISTOSOMIASIS.
Schistosomiasis is caused by trematode blood flukes of the genus
Schistosoma. Five species are responsible for human infections and
numerous others only infect animals. The species that infect humans include
Schistosoma haematobium, S. mansoni, S. japonicum, S. intercalaturn, and
S. mekongi. Chronic infections with all Schistosoma species with the
exception of S. haernatobiurn can cause significant morbidity and mortality
as a result of granuloma formation in the intestine and liver. The resulting
hepatic fibrosis can lead to portal hypertension that eventually can be
complicated by splenomegally, esophageal varices, hematemesis, and
death. S. haematobium primarily affects the urinary tract, resulting in
chronic inflammation of the bladder, ureteral obstruction leading to
hydronephrosis, stone formation, and urinary tract infections that can be
complicated by gram-negative septicemia.% Although there have been
reports of liver disease due to S. haematobium,3 these are extremely
uncommon. Because the focus of this issue is on the liver, infection due to S.
haematobium is not reviewed. S. mansoni and S. japonicum have been most
intensely studied, and this article reflects available data on these two
species unless otherwise indicated.

42. Hepatic schistosomiasis, or schistosomal hepatopathy,
is the most common form of the chronic disease and
usually results from heavy S. mansoni infection
Clinical manifestations
Clinical presentation of hepatic schistosomiasis markedly
differs from that of cirrhosis. Although the symptoms and signs
of portal hypertension and hypersplenism are dominant in
schistosomiasis, the counter part of hepatocellular failure is
absent. However, some patients with schistosomiasis progress
to an end stage of the disease by exhibiting muscle wasting,
hypoalbuminemia, ascites and coma. These observations led to
the concept of compensated and decompensated
schistosomiasis to differentiate patients with the sole
manifestations of portal hypertension from those who, in
addition, presented signs of hepatocellular failure.

43. Ultrasound of the patient showing periportal thickening (yellow arrows
on the left side), thickening of the gallbladder wall (G = gallbladder;
yellow arrow = thickened wall) and the enlarged spleen (S).

44. Non–contrast enhanced computed tomography (CT) liver showing (a)
capsular calcifications (white arrowheads), an irregular hepatic contour, and
extension of peri-portal fat deep into the liver (white arrows), and (b) septal
calcifications (blackarrows) and junctional notches (white arrows).

45. (a) Ultrasonography of the
liver showing diffuse
peri-portal
hyperechogenicity (white
arrows). (b) Contrast
enhanced computed
tomography (CT) arterial
phase image showing
septal calcification (white
arrow) in the right posterior
segment and a
hypervascular tumour in
the right anterior segment
(black arrowheads). (c)
Contrast-enhanced CT
porto-venous phase image
showing washout of
contrast in the tumour,
suggestive of
hepatocellular carcinoma
(black arrowheads)

46. Hepatic schistosomiasis with portal hypertension and splenomegally.

47. CT from two years prior demonstrating fatty liver and periportal fibrosis. These
images are similar in appearance to those of previous case reports demonstrating
CT appearance of schistosomiasis. A, B. Arterial phase images show hypoattenuated
round and linear branching lesions traveling adjacent to enhancing hepatic arterial
branches (arrows). C, D. These lesions enhance during portal phase (arrows). E, F.
The gallbladder wall is nodular and thickened and measures 4 mm.

50. MRI T2-weighted image of liver and spleen – a coronal section.
Liver with periportal thickening (yellow arrow) around the portal vein
(red arrow). There is a huge spleen (S). White arrow = stomach.

51. MRI T2-weighted image of liver and spleen – transversal section. There are four images
showing different aspects of periportal fibrosis in the liver (the vein in the center appears dark
– red arrow). Periportal thickening (yellow arrows). White arrows = stomach; S = spleen.

52. MRI T2-weighted image of liver and spleen – transversal section. The
vessels are easily identified. Black arrow = splenic vein; yellow arrow =
thickening around the gallbladder wall.G = gallbladder; S = spleen.

53. MRI T1-weighted image of liver and spleen with fat suppression – transversal section. S =
spleen; G = gallbladder. The white areas around the vessels (fibrosis) and gallbladder
(fibrosis) – yellow arrows - and also the blood inside the vessels, seen in previous images,
became black/gray on the two upper figures. Note, in the two lower figures, that there is
an enhancement of the gallbladder wall (yellow arrow) and of the periportal thickening
(yellow arrow) after the intravenous infusion of contrast (gadolinium).

54. Liver fibrosis in hepatosplenic schistosomiasis (white areas around
the vessels). There is a thrombus inside the portal vein (red arrow).

55. Angioresonance of the abdomen in hepatosplenic schistosomiasis with easy identification
of the portal vessels. The red arrow is pointing to a huge collateral vessel (left gastric vein).

56. Intestinal schistosomiasis:
Intestinal schistosomiasis is another well identified
form of chronic schistosomal affection. Egg deposition
and granuloma formation eventually leads to acute
then chronic schistosomal colitis and is commonly
associated with polyp formation. It frequently
presents as abdominal pain, diarrhea, tenesmus and
anal pain. Definite diagnosis of schistosomiasis
disease depends on microscopy and egg identification.
Marked progress regarding serologic diagnosis
occurred with development of recent PCR techniques
that can confirm schistosomal affection at any stage.

57. Schistosomal polyposis in the colon and rectum. A Multiple polyps throughout the rectosigmoid
colon, which was displaced out of the pelvis by a large pericolic bilharzial (schistosomal) abscess

58. Colonic and rectal polyps are usually multiple and associated with a
marked inflammatory reaction. A The hemicolectomy from an Egyptian
patient with combined S. haematobium and S. mansoni infections.

59. Schistosomiasis mansoni can cause marked granulomatous thickening of the bowel wall
and, eventually, strictures. A Transverse sections of a stenosed segment of bowel from an
18-year-old Egyptian male. Elsewhere in the colon there were multiple polyps.

60. The end results of schistosomiasis in the colon may be diffuse bowel wall thickening or local strictures.
In these patients with diffuse loss of haustrations, there is narrowing and rigidity of the colon.

61. Schistosomal calcification of the intestine. A non-enhanced CT scan of a 46-year-old
Egyptian showing dense calcification of the sigmoid colon.

62. Genitourinary schistosomiasis is produced by Schistosoma haematobium, a
species of fluke that is endemic to Africa and the Middle East, and causes substantial
morbidity and mortality in those regions. It also may be seen elsewhere, as a result of
travel or immigration. S haematobium, one of the five fluke species that account for most
human cases of schistosomiasis, is the only species that infects the genitourinary system,
where it may lead to a wide spectrum of clinical symptoms and signs. In the early stages,
it primarily involves the bladder and ureters; later, the kidneys and genital organs are
involved. A definitive diagnosis of genitourinary schistosomiasis is based on findings of
parasite ova at microscopic urinalysis. Clinical manifestations and radiologic imaging
features also may be suggestive of the disease, even at an early stage: Hematuria,
dysuria, and hemospermia, early clinical signs of an established S haematobium infection,
appear within 3 months after infection. At imaging, fine ureteral calcifications that
appear as a line or parallel lines on abdominopelvic radiographs and as a circular pattern
on axial images from computed tomography (CT) are considered pathognomonic of early-stage
schistosomiasis. Ureteritis, pyelitis, and cystitis cystica, conditions that are
characterized by air bubble-like filling defects representing ova deposited in the ureter,
kidney, and bladder, respectively, may be seen at intravenous urography, intravenous
ureteropyelography, and CT urography. Coarse calcification, fibrosis, and strictures are
signs of chronic or late-stage schistosomiasis. Such changes may be especially severe in
the bladder, creating a predisposition to squamous cell carcinoma. Genital involvement,
which occurs more often in men than in women, predominantly affects the prostate and
seminal vesicles.

63. Pathologic changes in the urinary tract due to schistosomiasis are far
more common in chronic infections than in acute ones. Such changes result
from the deposition of eggs (not adult flukes) in and around vessels, which
leads to chronic inflammatory lesions and induces an immune response with
granuloma formation and associated fibrotic changes . The deposition of
eggs in the bladder and ureter induces a chronic granulomatous reaction.
The disease usually starts at the urinary bladder trigone and base, with the
formation of submucosal granulomas leading to inflammatory patches and
hematuria. Cystitis resembling that in tuberculosis results in “sandy
patches” on the bladder wall that, in severe cases, may become a network
of dense concentric calcifications . The degree of calcification is roughly
correlated with the number of eggs deposited.
Chronic irritation of the urothelium causes it to proliferate, producing
budlike or polypoid structures. These structures differentiate into cystic
deposits of cystitis cystica or intestinal columnar mucin-secreting glands,
resulting in cystitis glandularis, which may develop into adenocarcinoma.
Cystitis cystica, ureteritis cystica, and cystitis glandularis can be observed as
polypoid filling defects on radiographs . Ureteral lesions due to S
haematobium infection.

64. In long-standing infections, a cellular reaction to dead ova produces
calcification and fibrosis, which are important contributors to squamous metaplasia
and squamous cell carcinoma. Severe fibrosis classically involves the bladder and
ureteral segments distal to the iliac vessels (hereafter referred to as “distal ureters”),
diminishing their elasticity. Severely fibrotic ureters have a ragged outline and a
beaded internal appearance, with irregular dilatation due to pseudotubercles in the
submucosa. As the pseudotubercles heal, they may become fibrotic, a condition that
may lead to ureteral stricture. Renal involvement in late-stage fibrosis, which usually
results from vesicoureteral reflux, is manifested by renal calculi and hydronephrosis
or pyonephrosis secondary to ureteral obstruction. Urethral involvement usually
occurs in the form of fossa navicularis polyps, periurethral abscesses, and perineal
and scrotal fistulas; strictures are uncommon .
Schistosomal infection of the prostate gland and seminal vesicles is found at
autopsy in 58% of male cadavers in geographic regions where S haematobium is
endemic. The epididymis, spermatic cord, and testes are rarely affected. Prostatic
involvement leads to initial enlargement of the prostate, followed by fibrosis and
shrinkage with calcification of the gland. The seminal vesicles may become
enlarged and calcified. Ejaculatory duct dilatation may result from distal fibrosis
and obstruction. Genital schistosomiasis is not as common in women as in men,
but lesions may be found in the vulva, vagina, and cervix, and more rarely in the
ovaries, fallopian tubes, and uterus .

65. Excretory urogram demonstrates
bilateral distal ureteral dilatation
secondary to early-stage urinary tract
infection by S haematobium. (7) Urinary
tract schistosomiasis. (a) Excretory
urogram shows substantial dilatation of
the distal left ureter, likely a result of
ureteral narrowing at the level of the
pelvic bone. (b) Postmicturition
radiograph shows persistent filling of the
left ureter with a nondilated right ureter.

66. Urinary tract schistosomiasis. (a) Excretory urogram shows marked left hydroureteronephrosis.
(b) Coronal three-dimensional urographic image obtained with computed tomography (CT)
shows a long-segment stricture with proximal dilatation of the left ureter.

67. Urinary tract schistosomiasis. (a, b) Negative (a) and positive (b) anteroposterior radiographs
show thin calcification of the bladder wall and the entire length of the left ureter (arrows in a).
(c) Unenhanced axial pelvic CT image more clearly depicts the bladder wall calcification. (d)
Sagittal reformatted CT image more clearly shows the distal left ureteral calcification (arrow).

68. (10a) Excretory urogram obtained in a 46-year-old
woman shows multiple filling defects along
the course of the distal left ureter (arrows).
These findings represent ureteritis cystica due to
schistosomiasis. (10b) Postmicturition radiograph
shows multiple filling defects in the bladder,
findings indicative of cystitis cystica due to
schistosomiasis. The T-shaped object is an
intrauterine contraceptive device. (11) Coronal
three-dimensional CT urogram obtained in an 83-
year-old man with hematuria shows multiple
bilateral filling defects along the course of both
ureters (arrows). These findings represent
ureteritis cystica due to schistosomiasis.

69. Extensive bladder calcifications due to late-stage
schistosomiasis. (a) Pelvic radiograph shows the classic
appearance of the calcified bladder, which resembles a
fetal head in the pelvis, with associated faint calcification
of the distal right ureter (arrows). (b) Axial pelvic CT
image shows thick calcification of an extensive region of
the bladder wall and ringlike calcification of the wall of
both ureters, with patent ureteral lumina. (c) Axial pelvic
CT image obtained in another patient shows a completely
calcified bladder wall and calcifications obstructing both
ureteral lumina.

70. Squamous cell carcinoma of the bladder. (a) Axial T2-weighted magnetic
resonance (MR) image shows a soft-tissue mass arising from the left lateral wall
of the bladder with multiple small diverticula. (b) Axial T2-weighted MR image at
the level of the bladder neck shows extension of the mass through the urinary
bladder wall to the perivesical fat with infiltration of the left seminal vesicle.

71. Left hydroureteronephrosis due to schistosomiasis. (a) Coronal T2-weighted MR urogram
shows marked left hydroureteronephrosis with a normal right kidney and right ureter. (b)
Axial T2-weighted image depicts dilatation of the left ureter at the level of the bladder.

72. Calcification due to schistosomiasis of the
seminal vesicles and vasa deferentia. (a)
Unenhanced axial CT image shows
calcification of both seminal vesicles. (b)
Postmicturition radiograph from excretory
urography shows calcification of the vasa
deferentia and iliac vessels (arrows). (c)
Coronal three-dimensional reformatted
pelvic CT image shows calcification of both
seminal vesicles (arrowheads) and the left
vas deferens (arrow).

73. Transrectal US image of the prostate in a patient with genitourinary schistosomiasis shows
a region of dense prostatic calcification that produces an anterior acoustic shadow.

74. Seminal vesiculitis due to schistosomiasis. (a) Transrectal US image of the seminal
vesicles shows bilateral wall thickening (arrows). (b) High-resolution axial T2-
weighted MR image of the pelvis shows thickened seminal vesicle walls (arrows).

75. Thank You.