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Active
disease
Transitional
stage
Inactive
disease
11
a
b
de
f
c
. Fig. 11.10.2 An illustration shows the diff erent stages of hydatid cysts that may be encountered during CT examination: ( a ) pure cystic form,
( b ) a cyst with multiple hypodense lesions within it, ( c ) a cyst with internal septations, ( d ) fl oating water lily sign, ( e ) ball of wool sign, and ( f )
calcifi ed cystic wall
e hydatid cyst walls are composed of three layers. e
rst layer (pericyst) is made up of compressed host tissue and
in ammatory cells. e second and the third walls are the
true cyst walls. e second wall is an outer acellular layer
(ectocyst), and the third is an inner cellular wall (endocyst).
e daughter cysts arise from the endocyst wall.
5 Grade 1 lesion (purely cystic lesions): is grade is seen
on ultrasound, CT, or MRI as a pure cyst without
internal inhomogeneities. is grade is explained by
intact endocysts, and patients with grade 1 lesions
bene t from percutaneous aspiration and scolicidal
injection therapy.
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Signs on Chest Radiograph
Hydatid cyst lesions are seen as a well-circumscribed,
round mass, with no internal texture (
11.10.3 ). It mimics a solid pulmonary mass and may lead
to a false diagnosis of pulmonary tumor. Absence of
symptoms and presence of other cystic lesions within
the liver are important clues.
. Figs. 11.10.2 and
. Fig. 11.10.3 Posteroanterior plain chest radiograph shows
two large masses located at the right middle and lower lung
fi elds in a patient with hydatid liver disease. The masses
represent intact hydatid cysts within the lung
a
b
. Fig. 11.10.4 Axial abdominal CT images show a very large
hydatid cyst that occupies almost the entire right lobe of the
liver ( a ) and the cyst appearance after aspiration of the cyst
contents ( b )
Signs on US
On ultrasound, the hydatid cyst shows a double wall
( double - line sign ). This is an important sign that
diff erentiates a grade 1 hydatid cyst from a simple
hepatic cyst, which shows a thin single wall.
Signs on CT
The cyst appears as a simple cyst with no internal
septations, densities, or contrast enhancement
(
. Fig. 11.10.4 ).
5 Grade 2 lesions (lesions with complex morphology with
or without biliary dilatation around the lesion): is
grade is characterized by the appearance of di erent
intracystic textures. ese textures arise due to previous
rupture of an endocyst, with hydatid uid leakage into
the potential space between the endocysts and the
pericyst. Later, this uid causes di erent intracystic
textures seen on ultrasound, CT, or MRI.
Signs on US, CT, and MRI
5 Internal septations with honeycomb-like
appearance can be seen on ultrasound, CT, and
MRI (
. Fig. 11.10.2 ).
5 Small internal echoes may be seen on ultrasound,
reflecting floating protoscoleces ( snowflakes sign ).
5 The daughter cysts may be seen as multiple
hypodense lesions, compared to the density of the
original cyst on CT (
. Figs. 11.10.5 and 11.10.2 ) .
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. Fig. 11.10.5 Coronal abdominal CT image in a patient with
hepatic and splenic hydatid cyst shows hepatic hydatid cyst
with internal hypodense lesions ( arrowheads ) and splenic
hydatid cyst with calcifi ed wall ( arrow )
5 Grade 5 lesions : is grade is characterized by death of
the cyst (inactive disease). It is seen as collapse of the
hydatid membrane (pericyst) over the residual endocysts.
is is seen on plain radiographs, CT, and MRI as a thick
wall plus an irregular, wavy, water- uid level oating on
top of the residual hydatid uid.
is sign is known as the oating water lily sign
(. Figs. 11.10.8 and 11.10.2 ). Degeneration of cysts is seen as
11
5 Grade 3 lesions (lesions with intrabiliary rupture): Because
the cyst is originally formed within the liver tissue, which in
turn contains biliary canaliculi, cysto-biliary communication
may occur as an uncommon complication. is grade is
characterized by intrahepatic biliary dilatation with hydatid
vesicle escape from the mother cyst into the biliary radicals,
causing regional biliary obstruction (
. Fig. 11.10.6 ).
5 Grade 4 lesions : is grade is characterized by rupture of
the pericyst and the endocysts, with spillage of the cyst
content into the neighboring organs or spaces. Leakages
of the hydatid uid into the peritoneum cause severe
irritation and peritonitis. Later, peritoneal calci cation
arises (
. Fig. 11.10.7 ).
. Fig. 11.10.7 Plain abdominal radiograph in a patient with previous
intraperitoneal ruptured hydatid cyst shows multiple calcifi cations
involving the mesentery and the intraperitoneal structures
. Fig. 11.10.6 Axial CT illustration demonstrates grade 3 hydatid
cyst disease. Notice the right lobe cyst with dilated biliary radicals
around it, with an intrabiliary daughter cyst ( arrow )
. Fig. 11.10.8 Posteroanterior plain chest radiograph shows
ruptured hydatid cyst with fl oating water lily sign ( arrowheads ). Notice
the cystic wall mimicking a cavity ( arrow )
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11
. Fig. 11.10.9 Ultrasound image of a liver hydatid cyst shows
internal, multiple, solid-like lesions within the cyst (ball of wool sign)
. Fig. 11.10.11 Axial CT illustration shows the hepatic atrophy–
hypertrophy complex. Notice the large hydatid cyst occupying a large
portion of the right lobe of the liver ( arrowhead ), with compensatory
hypertrophy of the left liver lobe ( arrow )
in atrophy of the hepatic segment supplied by this vein or
biliary branch. As the liver has the ability to regenerate, compensatory hypertrophy of the liver is usually seen when a
large segment of the liver parenchyma is atrophied. is phenomenon is known as the HAHC.HAHC may occur uncommonly as a complication of hydatid cyst disease, especially
when the cyst occupies a large area within the right lobe of
the liver. It is important for HAHC to be documented by the
radiologist, because it informs the surgeon that the cyst is
tightly involved with one or more of the portal triad structures or a major hepatic vein (. Fig. 11.10.11 ).
How does one di erentiate between ruptured hydatid cyst
and acute abscess ?
5 e wall of the abscess is enhanced a er contrast
injection on CT, while the hydatid cyst wall will not
enhance.
5 e air– uid level surface is straight in the abscess, while
in the hydatid cyst, it has a wavy water surface due to the
collapsed pericyst ( oating water lily sign).
. Fig. 11.10.10 Lateral plain radiograph of the thoracic spine shows
a calcifi ed hydatid cyst in the paraspinal region
multiple, solid-like lesions within the mother cyst, resulting
in a pseudotumor appearance on ultrasound or CT, known as
the ball of wool sign (
. Figs. 11.10.9 and 11.10.2 ). Finally, cir-
cular or curvilinear calci cation of the hydatid cyst wall is a
sign of inactive disease (. Figs. 11.10.10 and 11.10.2 ).
D i ff erential Diagnoses and Related Diseases
Hepatic atrophy – hypertrophy complex ( HAHC ): obstruction
of a major hepatic or portal vein or biliary tree branch results
Echinococcus alveolaris Disease
Infection with E. multilocularis is found in the United States,
Canada, Japan, and Central and Northern Eurasia. e de nitive hosts for E. multilocularis are foxes and rodents. Like E.
granulosus , humans are intermediate hosts who are infected
via ingesting food or water contaminated with the eggs or by
direct contact with the de nitive hosts.
In contrast to E. granulosus , E. multilocularis cysts are not
con ned within a pericyst layer and grow by external vesiculation. e cyst is small (1–10mm in diameter) and forms
multilocular alveolar cysts that resemble lung alveoli, hence
the name alveolaris . e external parasitic proliferation initi-
ates a broin ammatory response of the host within the
a ected organ, commonly the liver. is will later result in a
brous, tumor-like lesion composed of E. multilocularis
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embedded in a keloid scar and necrotic liver tissue. Stenosis
of the porta hepatic with the hepatic veins within the lesion is
commonly found. When the lesion heals, multiple, punctuate
calci cations arise within the lesion, which makes the lesion
increasingly resemble a malignant hepatocellular carcinoma
(HCC) or metastasis of the liver.
Signs on US
In the liver, there are multiple echogenic nodules
embedded within irregular and indistinct margins from
the normal hepatic parenchyma ( hailstorm sign ).
a
11
Signs on CT
5 The liver often shows a hypodense mass with a
“geographic map” appearance and
inhomogeneous internal texture (
5 Areas of punctuate calcifications within the lesions
are very common in healed lesions (90 % of cases)
(
. Fig. 11.10.12 ).
5 Unlike HCC, the lesion shows no enhancement or
mild enhancement in the portal venous phase
because of the fibrous stroma within the mass
(characteristic and diagnostic).
5 Areas of central liquefaction may be seen.
5 There are no signs of retroperitoneal lymphadenopathy
(another diff erentiating point from HCC).
. Fig. 11.10.12 ).
. Fig. 11.10.12 Axial nonenhanced abdominal CT in a
patient with Echinococcus alveolaris disease aff ecting the left
lobe of the liver shows liver mass with geographic edges
( arrowheads ) and internal punctuated calcifi cations
Signs on MRI
The scan shows an inhomogeneous mass with
geographic margins and characteristically low T1 and
low T2 signal intensities, with no enhancement or mild
enhancement after contrast enhancement in the portal
venous phase (
. Fig. 11.10.13 ).
b
. Fig. 11.10.13 Axial T1W ( a ) and T2W ( b ) nonenhanced MR
images in a patient with Echinococcus alveolaris disease show a
mass that resembles HCC ( arrowheads ), with multiple cystic
lesions within the mass. Notice that the mass bulk is hypointense
on T2W image ( b ) due to the fi brous (keloid) nature of the lesion
Further Reading
Czermak BV, et al. Echinococcosis of the liver. Abdom
Imaging. 2008;33:133–4.
Etlik Ö, etal. Contrast-enhanced CT and MRI ndings of
atypical hepatic Echinococcus alveolaris infestation.
Pediatr Radiol. 2005;35:546–9.
Karabulut K, etal. Hepatic atrophy-hypertrophy complex due
to Echinococcus granulosus. J Gastrointest Surg.
2006;10:407–12.
Katranci N, etal. Correlation CT MRI and histological nd-
ings of hepatic Echinococcus alveolaris: a case report.
Comput Med Imaging Graph. 1999;23:155–9.
Rozanes I, et al. Grading of liver lesions caused by
Echinococcus granulosus. Eur Radiol. 1993;3:429–33.
Sasaki F, etal. Alveolar echinococcosis of the liver in children.
Pediatr Surg Int. 1994;9:32–4.
11.11 Chagas’ Disease (American Trypanosoma)
Chagas’ disease (CD) is an infectious, multisystemic disease
caused by Trypanosoma cruzi ( T. cruzi ), a blood-borne agel-
late. T. cruzi was rst described in Brazil by Carlos Chagas, in
11.11 · Chagas’ Disease (American Trypanosoma)
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1909. e disease is one of the most common public health
problems in South America from Texas to Argentina.
CD o en a ects children and young adults living in rural
areas and mud huts. T. cruzi is transmitted to humans by the
defecation of a vector bug known as the “kissing bug” (reduviid bug). e bite occurs around the face, o en at night, and
the parasite is found in the bug’s feces. e bite can be painless
or painful depending on the toxins found in the bug’s saliva.
At the bite site, T. cruzi penetrates the skin and travels via
the blood to the body organs. e parasite invades and enters
the host cells, particularly the muscles, the glia, and the reticuloendothelial system. Multiplication occurs by binary ssion until
the cells rupture, and the parasite enters the blood or invades
more tissues. At the site of multiplication, severe in ammatory
reaction occurs with local lymphangitis, which is known as cha-
goma . Soon a er that lymphatic spread to regional lymph nodes
occurs, which is usually seen in the rst 2 weeks postinfection.
Although the parasite can be found in any body tissue,
T. cruzi o en has a distinct predilection for striated and car-
diac muscles, glial, and nerve cells.
ere are four distinct phases of CD, each with its own
pathological and radiological features.
Signs on Cardiac MRI
5 Chagas’ myocarditis is seen as focal, segmental
high T2 signal intensity areas, with contrast
enhancement localized in the mid-wall or the
outer wall of the ventricle below the pericardium
(
. Fig. 11.11.1 ).
5 There are areas of wall motion abnormalities,
along with areas of aneurysmal wall dilatation.
Apical aneurysm with thrombus formation is a
common finding.
467
11
Acute Chagas’ Disease
e main pathological process during this stage is chagoma
a ecting the heart and the central nervous system (CNS).
e acute stage is frequently seen in neonates, although it
may occur at any age.
A er an incubation period of 2 weeks, patients o en
present with fever that can persist for months, malaise, loss of
appetite (anorexia), vomiting, diarrhea, and muscle pain.
In the heart, there is severe lymphocytic myocarditis with
focal areas of endocardium and epicardium in ammation,
which leads to dilated cardiomyopathy and pericardial e usion. Hyaline necrosis of isolated myocardial bers ( Magarinos –
To r r es ’ lesion ) is a characteristic feature of Chagas’ myocarditis.
In the CNS, encephalitis or meningoencephalitis is o en
seen and may be the primary manifestation of CD. e trypanosomes may enter the conjunctiva in up to 50 % of patients,
causing upper or lower eyelid edema, conjunctiva chemosis,
and preauricular lymph nodes enlargement ( Romana ’ s sign ).
Hepatosplenomegaly, and pneumonia when the trypanosoma a ect the lungs, may be seen.
ECG Abnormalities
e most common changes in electrocardiogram (ECG) are
prolonged P-R interval, low voltage in an ECG rhythm showing electrical activity in the ventricles (QRS complex), and
prolonged Q-T interval.
Signs on Ultrasound
5 Hepatosplenomegaly that may persist for up to 5
months from the onset of the disease
5 Liver fatty infiltration
5 Regional lymph node enlargement
. Fig. 11.11.1 Sagittal short-axis, T1W postcontrast cardiac
MR illustration demonstrates the type of myocarditis
enhancement seen in Chagas’ disease (mid- to outer-wall
enhancement) ( arrowhead )
Subacute Chagas’ Disease
is stage is o en seen in young adults, and the patient presents without any fever, with severe heart failure that does not
respond to therapy.
Latent Chagas’ Disease
A er the acute stage subsides, many patients completely
recover, while others may pass into a latent or chronic stage.
In this stage, 2–5 % of patients become symptomatic
annually.
e number of ganglion cells in the Auerbach plexi in the
gastrointestinal (GI) tract starts to diminish in this stage. All
patients who recovered from the acute CD stage, or live in
endemic areas, have a positive complement xation test
( Machado – Guerreiro reaction ).
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Chronic Chagas’ Disease
is stage develops a er many years and is characterized by
dilated cardiomyopathy, with esophageal and colonic dilatation. e main pathology is attributed to reduction in the
motor ganglia of the GI tract, resulting in loss of motor function (aperistalsis), which results in dilatation and accidity of
the a ected organs.
In the esophagus, early stages are characterized by hypercontractility and hypertrophy of the circular smooth muscles. Later, denervation of the esophageal muscles results in
marked esophageal dilatation. Food may become lodged in
the esophagus. Carcinoma and esophageal abscess may
develop in 7 % of patients with chronic CD.
In the colon, massive dilatation and chronic constipation
is o en seen. Sigmoid volvulus may occur in 10 % of patients.
Signs on Plain Chest Radiograph
5 The dilated esophagus is seen as a mediastinal
mass along the entire right side of the
mediastinum with air or air–fluid level.
5 The heart is often dilated due to dilated
cardiomyopathy of chronic CD.
5 Raised left hemidiaphragm due to splenic flexure
dilatation may be found.
Further Reading
Barros MVL, etal. Doppler tissue imaging to access systolic
function in Chagas’ disease. Arq Bras Cardiol. 2003;80(1):
36–40.
de Souza AP, etal. Magnetic resonance imaging in experi-
mental Chagas disease: a brief review of the utility of the
method for monitoring right ventricular chamber dilatation. Parasitol Res. 2005;97:87–90.
Felippe L, etal. Radiological diagnosis of Chagas’ disease
(American trypanosomiasis). Semin Roentgenol. 1998;
33(1):26–46.
Ferreira-Santos R. Aperistalsis of the esophagus and colon
(megaesophagus and megacolon) etiologically related to
Chagas’ disease. Am J Digest Dis New Ser. 1961;6(8):700–26.
Rochitte CE, etal. Myocardial delayed enhancement by mag-
netic resonance imaging in patients with Chagas’ disease:
a marker of disease severity. J Am Coll Cardiol.
2005;46:1553–58. Originally published online 22 Sep
2005. doi: 10.1016/j.jacc.2005.06.067.
11.12 Schistosomiasis (Bilharziasis)
Schistosomiasis is an infectious disease caused by freshwater
Schistosoma. Schistosoma are atworms that do not have a
digestive tract and are commonly known as trematodes or
blood ukes. Schistosomiasis is commonly known as “bilharziasis,” a er Bilharz, the discoverer of the parasite in 1815.
Signs on Barium Swallow and CT
5 The esophagus is massively dilated (>7 cm), with
bizarre, dysrhythmic contractions that mimic
achalasia (
lodged within the esophagus.
5 On CT, megacolon with massive rectosigmoid
dilatation is usually found.
. Fig. 11.11.2 ). Food may be found
. Fig. 11.11.2 Axial thoracic CT in a patient with chronic Cha-
gas’ disease shows massive dilatation of the esophagus, with
food lodged inside the esophagus, mimicking achalasia
Schistosoma Life Cycle
Schistosoma release their eggs in freshwater. Later, the eggs
are hatched into larvae, which maturate in freshwater snails.
A er maturation, the mature larvae (cercariae) leave the
snails and enter into humans by penetrating the exposed
human skin in the freshwater. A er skin penetration, the parasites travel within the lymphatic system through the thoracic duct to enter the circulation. e parasites lie in the
lymphatic system for almost 21 days before they enter the
hepatic portion of the portal venous system into the liver,
where they further mature and mate. Depending on the type
of the Schistosoma , the parasites migrate into the intestinal or
the bladder venous system to lay their eggs. e adult worms
are strictly intravenous and do not evoke the immune system,
while both the cercariae and the eggs stimulate the immune
system, resulting in the formation of granulomas around the
eggs and the systemic cercariae, which will cause tissue brosis and calci cation of the a ected organ in advanced stages
of the disease. Dead worms can be embolized almost anywhere within the body.
ere are four types of Schistosoma worldwide:
5 Schistosoma japonicum is found within eastern Asia, is
located within the intestinal tract veins, and releases its
eggs in the feces.
5 Schistosoma mansoni is found within South America and
Africa, is located within the intestinal tract veins, and
releases its eggs in the feces.
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5 Schistosoma haematobium is found within Africa and the
Middle East, is located within the bladder and ureters
venules, and releases its eggs in the urine.
5 Schistosoma intercalatum is found only in equatorial Africa
and mainly a ects the intestinal tract and the portal system.
e rst symptom of the disease starts when patients
develop itchy skin a er larvae penetration, due to hypersensitivity reaction type 1 and type 4 (cercarial dermatitis or swimmer’s
urticaria). Weeks later, systemic manifestations like hematuria,
fever, weight loss, diarrhea, and abdominal pain arise.
e living worm lives between 4 and 30 years. e living
worm engulfs the red blood cells (RBCs) and excretes them
as hemozoin, which is engulfed later by the macrophages. e
other action by the living worm is laying eggs (ova). As the
ova penetrate the wall of the intestine or the urinary bladder,
they may cause chronic bleeding (resulting in anemia), be
trapped in the wall of the organ, or enter the blood and circulate as emboli. e dead worms initiate a severe in ammatory reaction within the veins, causing thrombophlebitis,
which can block the a ected vein.
Diagnosis of schistosomiasis is con rmed by identifying
the Schistosoma eggs in urine or feces and eosinophilia in the
complete blood count (CBC).
e clinical and radiological manifestations of schistosomiasis can be classi ed according to the parasite type.
469
Signs on Ultrasound
The liver shows an internal echogenic polygonal network
due to periportal fi brosis and calcifi cation, which causes
a “fi sh-scale” appearance (30 % of cases).
Signs on Abdominal CT
There is internal periportal fi brosis (low-density bands)
or calcifi cation (high-density bands) within the liver
parenchyma, along with liver contour irregularities
(turtleback appearance) (
. Fig. 11.12.2 ).
11
Schistosomiasis by S. japonicum
S. japonicum lives in the mesenteric veins and mainly a ects
the liver, small bowel, and lungs. In the small bowel, the duodenum and the jejunum are mainly a ected.
In the liver, the parasite eggs are deposited in the portal
venules along the liver periphery. When the eggs die, brosis
within the venules results in a polygonal network of periportal brosis that makes the liver look like a “turtle back” on
gross appearance (. Fig. 11.12.1 ). e eggs are also deposited
within the liver capsule, resulting in capsule thickening and
brosis. ere is a high incidence of liver carcinoma with
S. japonicum infection.
. Fig. 11.12.1 An illustration demonstrates the gross turtleback
appearance of S. japonicum liver schistosomiasis
. Fig. 11.12.2 Axial CT illustration of the liver in S. japonicum
schistosomiasis demonstrates the internal periportal
calcifi cation and fi brosis causing the turtleback appearance
Schistosomiasis by S. mansoni
S. mansoni mainly a ects the liver, bowel, central nervous system, and lungs. In the bowel, the parasite causes granulomatous colitis, which causes loss of haustration and strictures later
on, mimicking Crohn’s disease. If the small intestine is a ected,
regional ileitis and protein-losing enteropathy may develop. In
uncommon cases, when the calci cation is so severe as to
include all the layers of the colon wall, the ova start to accumulate freely within the peritoneal cavity outside the wall. is
causes in ammation and brosis within the peritoneal cavity
and the pericolic region, resulting in a pericolic mass that cannot be di erentiated from carcinoma on imaging.
In the liver, the parasite deposits its eggs around the main
portal vein at the liver hilum, later resulting in Symmers’
pipestem brosis. Symmers’ pipestem brosis is a condition
that arises when egg granulomas aggregate around the portal
vein, resulting in vascular brosis that causes obstruction of
the small veins and presinusoidal cirrhosis. Portal hypertension (HTN), esophageal varices, and splenomegaly are common complications of this type of brosis.
In uncommon cases, angiomatoid lesions can develop
within the liver. ese angiomatoid lesions emerge as a
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470
secondary action taken by the body against severe brosis of
the hepatic veins and portal HTN. e emergence of such
lesions can be explained by the fact that in severe portal
HTN, the blood within the veins cannot ow normally, which
results in opening of sideway channels and collaterals to
decrease liver congestion. is can result in angiomatoid formation of lesions (e.g., hemangiomas). ese lesions seen in
the liver represent a severe stage of portal HTN.
Splenomegaly in bilharziasis occurs at an early stage due to
antigen stimulation, causing splenic parenchymal hyperplasia,
and later in the course of the disease due to portal hypertension.
If eggs are embolized into the pulmonary vessels via the
venous system, they damage the vascular wall by initiating an
in ammatory reaction. e in ammatory reaction results in
a characteristic “dumbbell” granuloma blocking the vessel or
forms a pseudoaneurysm. Pulmonary hypertension may
develop in advanced stages (20 % of cases). All Schistosoma
species can a ect the lungs.
Rheumatic manifestations are uncommonly seen with
bilharziasis, resembling reactive arthritis or seronegative
spondyloarthropathies and sacroiliitis. Rheumatoid-like disease a ecting the metacarpophalangeal (MCP) and proximal
interphalangeal (PIP) joints, wrists, ankles, and knees have
been reported. Some of these manifestations are due to
immune complexes or direct infection by the parasite.
In the central nervous system, S. mansoni produces conus
medullaris thickening and arachnoiditis ( bilharzioma ).
Signs on Ultrasound
5 Hyperechoic lesions are noticed around the portal
vein due to Symmers’ pipestem fibrosis.
5 Thrombosis of the portal vein may be seen as loss
of Doppler signal flow within the portal main stem.
5 Signs of liver cirrhosis and portal hypertension
(e.g., splenomegaly).
5 Gallbladder wall thickening is found in 80 % of
cases.
Signs on Abdominal CT
5 The portal venous tracts are replaced by fibrous
tissue, seen as low-attenuation bands or rings,
with peripheral fibrosis radiating from the center
of the liver around the main portal vein branches.
Marked enhancement is noticed on postcontrast
images.
5 Shrunken liver, portal venous thrombosis,
splenomegaly, and esophageal varices are
commonly noticed (
5 Splenic siderotic nodules ( Gamna – Gandy bodies )
are commonly seen within the enlarged spleen.
a
. Fig. 11.12.4 ).
Signs on Plain Chest Radiograph
5 Signs of pulmonary hypertension and enlarged
pulmonary trunk in advanced stages.
5 Localized bilharzias granulomas within the lung
may be mistaken for a neoplastic nodule or mass.
5 Calcification of the bowel walls may be seen
(rarely) on plain radiographs (
. Fig. 11.12.3 ) .
. Fig. 11.12.4 Portal cavography ( a ) and axial CT urography
( b ) in a patient with schistosomiasis and portal vein thrombosis
shows a severely dilated portal vein, with development of
esophageal varices ( arrowhead ) and splenic varices ( arrows )
. Fig. 11.12.3 Plain abdominal radiograph shows
calcifi cation of the transverse colon walls in a patient with
schistosomiasis ( arrowheads )
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b
. Fig. 11.12.4 (continued)
Signs on Spinal Cord MRI
Bilharzioma is seen as localized conus medullaris
thickening, with high signal intensity on T2W images and
heterogeneous contrast enhancement postgadolinium
injection (
. Fig. 11.12.5 ).
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Schistosomiasis by S. haematobium
S. haematobium mainly a ects the bladder and the ureters.
e posterior part is the most vascular area of the bladder,
and it is the area where most ova within the vesical veins are
seen. S. haematobium lays more ova than S. mansoni . e eggs
are trapped within the ureter and the bladder mucosa as they
are carried by the urine to be excreted. e immune system
surrounds the eggs and starts an aggressive granulomatous
reaction that causes death and calci cation of the eggs. As the
disease advances, calci cation can occur within the ureters,
bladder, and seminal vesicles. When the ureters are calci ed,
obstructive uropathy and renal hydronephrosis may occur.
Complications of the ova within the bladder and intestinal
walls are as follows:
5 Sandy patch occurs when a huge number of ova die and
calcify, causing the overlying mucosa to degenerate and
atrophy.
5 Bilharzial polyp occurs due to localized deposition of a
huge number of ova, with hyperplasia of the wall. is is
mainly seen in the intestine ( S. mansoni ).
5 Bilharzial ulcers can arise due to penetration of huge numbers
of ova, due to falling of the atrophic mucosa over a sandy
patch lesion, or due to detachment of a bilharzial polyp.
5 Fibrosis can arise as a consequence of chronic
in ammation of the organ wall.
5 Urothilial changes (only seen in the bladder) comprise a
chronic reactive in ammatory disorder characterized by
transitional epithelial hyperplasia in the form of nests
called von Brunn’s nests, due to an irritant (e.g.,
schistosomal ova). ese nests may undergo central cystic
degeneration, forming a condition called “cystitis cystica.”
e cystitis cystica transitional epithelium may undergo
metaplasia into columnar mucin-secreting epithelium,
causing another condition called “cystitis glandularis.” e
ova may cause squamous metaplasia of the transitional
cell nest, causing leukoplakia, which may transform into
dysplasia and carcinoma in situ. Leukoplakia is a thick,
white patch of skin, commonly seen on the tongue, vulva,
or the bladder. It is composed of thick layers of strati ed
epithelium with keratin, with chronic in ammation of the
submucosa. Pathologically, it is explained by squamous
metaplasia followed by cellular hyperplasia.
11
. Fig. 11.12.5 Sagittal T2W lumbar MR illustration
demonstrates enlarged conus medullaris with multiple high
signal intensities representing bilharzioma ( arrowhead )
Signs on Plain Abdominal Radiographs
5 There is striking calcifi cation of the ureters or the
bladder (
calcifi cation of the schistosomiasis bladder is
pathognomonic. In contrast, bladder calcifi cation due
to tuberculosis or radiation is often patchy and focal.
5 Bilateral ureters calcification (. Fig. 11.12.6 ) with
hydronephrosis are a common finding.
5 Calcification of the seminal vesicles, testes, and
spermatic cords may be seen (
5 Fallopian tubes or cervical calcifications may occur
in women.
. Fig. 11.12.6 ). The uniform and linear
. Fig. 11.12.7 ).
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