Genitourinary Schistosomiasis: Life Cycle and Radiologic-Pathologic Findings
Abstract
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. It rarely infects the colon or lungs. 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.
© RSNA, 2012
LEARNING OBJECTIVES
After completing this journal-based CME activity, participants will be able to:
| •. | Describe the pathogenesis of genitourinary schistosomiasis. | ||||
| •. | Recognize the clinical manifestations of genitourinary schistosomiasis. | ||||
| •. | Identify imaging features suggestive or indicative of genitourinary schistosomiasis. | ||||
Introduction
Schistosomiasis, one of the most protean diseases in humans, was known to the pharaohs more than 5000 years ago. The presence of snail species in the Paleolithic Age in Africa may indicate an even older history for this parasitic disease. The ancient Egyptians recognized schistosomiasis as a cause of bloody urine and stools and knew that the condition was due to worms (1).
In 1851, Theodor Bilharz described this parasitic infection, which consequently became known as bilharziasis but was later renamed schistosomiasis. Schistosomiasis (also known as “snail fever”) is a complex of parasitic infections that are caused by various trematodes of the genus Schistosoma, whose first hosts are aquatic or amphibious snail species that live in fresh water. Humans and other mammals may be infected through contact with water containing the parasites. Schistosomiasis is a major source of morbidity and mortality in the developing countries of Africa, South America, the Caribbean, the Middle East, and Asia; however, tourism to and immigration from endemic areas may lead to occurrences of the disease anywhere in the world (2,3).
In 1996, the World Health Organization (4) estimated that more than 200 million people worldwide were affected by schistosomiasis, mainly those living in rural agricultural and periurban areas. Of that number, it was estimated that 20 million were severely affected by the disease and that another 120 million were symptomatic.
According to the World Health Organization, schistosomiasis is one of the most widespread human parasitic infections, ranking second to malaria in terms of its effects on the socioeconomic status and health of populations living in tropical and subtropical regions. It is considered to be the most prevalent waterborne disease and a major occupational health risk in rural areas of developing countries, where it results primarily from the unsanitary disposal of human and animal wastes, combined with repeated daily contact of people with contaminated freshwater sources (eg, in fishing, farming, swimming, bathing, and recreation) (5).
Epidemiologic Characteristics and Forms of Schistosomiasis
Schistosomiasis is prevalent in tropical and subtropical regions, especially in poor communities with no access to safe drinking water or adequate sanitation. Of the 207 million people with schistosomiasis, 85% live in Africa (1,4).
Two major forms of schistosomiasis exist: intestinal and genitourinary. Intestinal schistosomiasis may be caused by any of five main species of blood flukes (Table). However, only Schistosoma haematobium affects the genitourinary system (5).
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S haematobium is endemic throughout Africa, Madagascar, Mauritius, the southern shore of the Mediterranean, and the Middle East, including Turkey. It primarily involves the urinary tract and the hepatic portal system, but it may also affect the colon and lungs (1,4,6).
Life Cycle of S Haematobium
The life cycle of S haematobium consists of two main stages, one of which is completed in freshwater snails, and the other, in humans and other mammals (Fig 1). Figure 1 Schema shows the two-stage life cycle of S haematobium.
First Stage: Freshwater Snails
The life cycle of S haematobium begins when eggs of the parasite excreted by a mammal host reach fresh water, where they hatch and release miracidia. The free-swimming miracidia can survive 1–3 weeks in fresh water. During this time, the miracidia must infect a snail of the genus Bulinus in order to complete their life cycle. These snails may be found in slow-moving freshwater streams, irrigation ditches, or nearly any other open water source (natural or artificial) in endemic regions.
In the snail, the miracidium develops into an adult sporocyst, from which thousands of larval cercariae are released 4–6 weeks after the initial infection (7,8). The cercariae, fork-tailed free-swimming larvae approximately 1 mm in length, can survive only 72 hours in fresh water. During that time, they must either attach themselves to and penetrate the skin of humans or other susceptible host mammals or die. Cercariae also may enter a human or other mammal host by penetrating the buccal mucous membrane; however, cercariae that are swallowed are digested in the stomach (9–12).
Second Stage: Humans and Other Mammals
After penetrating the skin of the human or mammal host, the larvae shed their tails and become schistosomula. The schistosomula enter the lymphatic system and pass through the thoracic duct into the right side of the heart. They then travel through the lungs to the left side of the heart and proceed along the mesenteric capillaries to the hepatic portal system and liver, where they mature and copulate. This journey takes 10–21 days. They then migrate along the endothelium, against the portal blood flow, to the vesicular venous plexus, which envelops the lower part of the bladder and the base of the prostate; there, they produce eggs. Maturation of the parasite also may occur in other organs, especially the lungs, but copulation outside the liver is uncommon (8,13).
The eggs are highly antigenic and may induce an intense granulomatous response in human hosts. After their excretion by the mature parasite, the eggs migrate through the host’s bladder wall and are shed in urine or feces. During this migration, which takes approximately 10 days, miracidia develop inside the eggs. Eggs that are not shed successfully may remain in the host’s tissues, where they soon become nonviable, or may be swept back from the mesenteric vessels to the portal circulation or from the vesicular vessels via the inferior vena cava to the pulmonary circulation (14).
Clinical Manifestations
Clinical manifestations reflect the parasite’s developmental stage and the host’s response to toxic or antigenic effects of the parasite and its eggs. During the early stage of infection, the patient may present with dermatitis caused by cercarial penetration of the skin (15). This self-limited process may recur more intensely with subsequent exposures to the same species. Cercarial dermatitis may be followed by bronchopulmonary manifestations that are attributed to the passage of schistosomula through the lungs (16–18). Approximately 5 weeks after infection, a condition known as Katayama disease may develop; this condition is characterized by marked clinical manifestations such as malaise, weight loss, gastrointestinal symptoms, eosinophilia, and fever. However, Katayama disease is uncommon in people infected initially by S haematobium and is more likely to occur in those who are reinfected (19,20). The stage of egg deposition is manifested by genitourinary symptoms of cystitis, dysuria with terminal hematuria, dull suprapubic pain, and hemospermia. In women, it also may be manifested by hypertrophic, ulcerative, fistulous, or wartlike vulval and perineal lesions that may be mistaken for another type of infectious genital lesion, particularly condylomata lata due to syphilis. Tubal infertility may be a late complication. Vulval schistosomiasis also may facilitate the transmission of human immunodeficiency virus.
Hematuria, the first clinical sign of established genitourinary schistosomiasis, appears 10–12 weeks after infection. Dysuria and hematuria are common in both early and late stages of disease. Proteinuria, often with values that are in the nephrotic range, may be a late manifestation. Definitive diagnosis is based on findings of ova at microscopic analysis of urine specimens (4,21) (Fig 2). Figure 2 Photomicrograph (original magnification, ×200; hematoxylin-eosin stain) shows a fresh ovum from S haematobium, floating in a human urine specimen. Note the terminal spine at one end of the ovum.
Histopathologic Findings
Adult schistosomes do not usually cause an inflammatory reaction in the venous system. In fact, their presence there is associated with increased protection of the host against reinfection by cercariae. In general, dead eggs and dead flukes cause a more severe inflammatory reaction than living ones do (22).
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 (23).
The deposition of eggs in the bladder and ureter induces a chronic granulomatous reaction (Fig 3) 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 (4,24) (Fig 4). The degree of calcification is roughly correlated with the number of eggs deposited.
Figure 3 Photomicrograph (original magnification, ×100; hematoxylin-eosin stain) of a histologic slice from the bladder wall of a patient with schistosomiasis shows a granuloma with multiple calcified ova at its center, surrounded by a zone of reactive inflammatory tissue containing giant cells.
Figure 4 Photomicrograph (original magnification, ×100; hematoxylin-eosin stain) shows multiple calcified ova of S haematobium with surrounding reactive inflammatory tissue in the submucosa of the bladder.
Chronic irritation of the urothelium causes it to proliferate, producing budlike or polypoid structures (Fig 5). 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.
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 (25,26).Ureteral lesions due to S haematobium infection. (a) Photograph shows a gross ureteral specimen that contains multiple mural projections. (b) Photomicrograph (original magnification, ×200; hematoxylin-eosin stain) of a slice obtained from the specimen in a shows many cystic lesions lined with multiple layers of low cuboidal cells.
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 (27).
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 (28,29).
Imaging Findings
Radiologic imaging manifestations of urinary tract schistosomiasis are observed mainly in the ureters and bladder. The kidneys appear normal until a late stage of disease.Ureters
Ureteral involvement in schistosomiasis has been reported in as many as 65% of cases (30,31). The earliest change visible at urography is persistent filling of the distal ureteral segment of the ureter, followed by distal ureteral dilatation (Fig 6, Fig 7). Early-stage ureteral dilatation results from ureteral dysfunction, not tissue damage; is generally unilateral; and ranges from slight to severe. At a later stage, ureteral fibrosis resulting from tissue healing may lead to ureteral strictures. More than 80% of the earliest ureteral strictures occur in the intravesical segment of the ureter (ie, the part within the bladder); the second most common location is 2–5 cm (1–2 inches) above the orifice. The part of the ureter affected by fibrosis extends above and below the stenotic ureteral segment. As fibrosis progresses, the entire length of the ureter may be involved, with multiple strictures (32,33) (Fig 8). Figures 6 Excretory urogram demonstrates bilateral distal ureteral dilatation secondary to early-stage urinary tract infection by S haematobium.
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.
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.
The peristaltic movement of the ureter is affected by two main factors: ureteral stricture due to fibrosis, and mural calcification that begins in the bladder wall. Fibrosis of the ureteral wall and periureteral tissue affects the nerve plexus of the ureter, causing hypotonia mainly in the distal ureteral segment; peristalsis in the proximal ureteral segment (the segment between the ureteropelvic junction and the iliac vessels) is normal until the advanced stage of fibrosis, in which the whole ureter is involved (31,34,35)Fine ureteral calcification may be observed at an early stage of schistosomiasis, initially with areas of sparing but eventually coalescing until the entire length of the ureter is calcified, from the bladder to the kidney. The fine ureteral calcification is visible as a linear or parallel linear pattern on radiographs and as a circular pattern on axial CT images. These radiologic imaging findings are considered pathognomonic (30,34) (Fig 9).
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).
Ureteritis cystica and pyelitis cystica, which are characterized by air bubble–like filling defects in the ureter and renal pelvis, respectively, also may be seen at intravenous urography, intravenous ureteropyelography, and CT urography (37) (Fig 10, Fig 11).
(a)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. (b) 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.
Figure 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.
Bladder
In the early stages of schistosomal infection, the bladder outline becomes hazy and ill defined at urography because of submucosal edema and pseudotubercles. The bladder wall becomes thickened and ulcerated with multiple small flat papillomas that can be distinguished from a malignancy at cystoscopy and bladder biopsy (38–40).
Schistosomiasis-induced changes in the bladder vary widely, depending on the geographic region. In Egypt, a syndrome called “bladder neck obstruction” has been described; the condition is relatively common and results from eggs entering the muscles of the urinary bladder and inducing partial hyperplasia that evolves into fibrosis. The trigone is the bladder region most severely affected by hypertrophy, which involves the formation of a prominent bulge between the ureteral orifices that protrudes into the bladder lumen. As the hypertrophic tissue undergoes fibrosis, it atrophies and shrinks, leaving the mucosa and muscularis as a mass that is pushed forward over the internal urethral orifice, leading to obstruction at the level of the bladder neck. Such marked bladder outlet changes have not been reported outside Egypt (41–43).
Schistosomiasis is the most common cause of bladder wall calcification in regions where S haematobium is endemic; it accounts for as many as 56% of cases of such calcification (30,44). Bladder wall calcification is due to the presence of a large number of calcified dead eggs in the submucosa. The degree of calcification is roughly correlated with the number of calcified eggs but not with the number of eggs discharged in urine, which depends on the activity of the parasite. A region containing as few as 100,000 calcified eggs per cubic milliliter can be detected at radiography. The number of eggs required to produce an amount of calcification detectable at CT is not known; however, calcification becomes detectable when attenuation exceeds 160 HU (30). At radiography, bladder calcifications are visible first at the bladder base, forming a linear pattern that parallels the upper border of the pubic bone; eventually, calcium deposits encircle the entire bladder (44).
The classic presentation of a calcified bladder, which resembles a fetal head in the pelvis, is pathognomonic of chronic urinary tract schistosomiasis (Fig 12). Various calcification patterns have been reported, depending on the state of bladder filling: In the empty bladder, calcifications appear coarser and thicker because the collapsed bladder wall has thick folds. Other patterns that may be seen include fine granular, fine linear, and thick irregular calcification. Calcification may encircle the bladder or may affect only parts of it; calcification may be more marked on one side than the other, or more marked at the base than at the vault. A shell-like rim of calcification, an appearance produced by the submucosal deposition of eggs and not caused by fibrosis, has little to no effect on bladder capacity or emptying. Later in the course of infection, when the bladder wall becomes fibrotic and the bladder contracts, leading to a reduction in capacity, marked changes become visible at cystography (37,45–47).
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.
Bladder calcification may resolve partially or completely because of the reabsorption of calcified eggs in situ or the rupture of eggs from the submucosa into the bladder and their excretion in the urine. An excretion rate of about 2,000,000 eggs per year is necessary to allow bladder decalcification. If all calcified eggs are discharged, the bladder wall may return to relative normality. Bladder calcification is less common in the elderly than in young people (48).
Schistosomal Bladder Masses.—Chronic irritation of the bladder mucosa leads to an inflammatory reaction in the tissue (24). The urothelium proliferates into buds (von Brunn nests), which grow into the connective tissue beneath the epithelium in the lamina propria. These buds then differentiate into cystic deposits leading to cystitis cystica (Fig 10b), or intestinal columnar mucin-secreting glands (goblet cells) producing cystitis glandularis (49,50). Cystitis glandularis and cystitis cystica may occur at any age; the reported prevalence is 2.4% in children with urinary tract infections, including schistosomal infections (51). At cystoscopy in patients with either of these forms of cystitis, the mucosa usually has a cobblestone-like appearance. In addition, in late-stage cystitis glandularis, a papillary or polypoid mass may arise that mimics carcinoma and demonstrates a predilection for the bladder neck and trigone (25,26).
Squamous Cell Carcinoma.—In geographic regions where schistosomiasis is not endemic, squamous cell carcinomas account for less than 5% of all bladder malignancies (52). In regions where schistosomiasis is endemic, it constitutes a major risk factor for bladder malignancies, predominantly for squamous cell carcinomas, which account for more than 50% of bladder cancers (53). Chronic S haematobium infection induces squamous metaplasia, which may evolve into squamous cell carcinoma. Among people who do not have chronic schistosomiasis, squamous cell carcinomas of the bladder tend to manifest in those older than 60 years, with a slight male predominance; patients with chronic schistosomiasis and squamous cell carcinoma of the bladder tend to be younger and are five times more likely to be male. Clinical manifestations of squamous cell carcinoma of the bladder include gross hematuria and irritative voiding symptoms (54).
The imaging findings of squamous cell carcinoma in the bladder are nonspecific. A nodular or fungating mass is visible on radiologic images in 80% of cases. Tumors may appear as a single enhancing mass or as diffuse or focal regions of bladder wall thickening (55,56). Multiplicity of tumors is seen in 25% of cases. Squamous cell carcinoma is sessile, not papillary like urothelial cell carcinoma, and purely intraluminal growth is not seen. Bladder wall thickening and calcification due to a coexistent chronic S haematobium infection may complicate the diagnosis. Muscle invasion is present in 80% of cases, and extravesical spread may be extensive (56). Tumors are most commonly found in the trigone and lateral wall of the bladder but may also arise in bladder diverticula (57). At cystoscopy, a squamous cell carcinoma of the bladder appears as a large, often ulcerated, infiltrating mass that usually spreads laterally from the mucosa into the bladder wall and surrounding tissues and abdominal wall (Fig 13); the usual route of lymphatic spread is via the paraaortic lymph nodes (58).
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.
Given the large percentage of patients with extravesical extension at the time of diagnosis, the overall prognosis for squamous cell carcinoma of the bladder is generally poor. Two-thirds of the tumors are poorly differentiated and are diagnosed at an advanced stage, likely because of the similarity between the symptoms of bladder carcinoma and those of previously diagnosed urinary tract schistosomiasis. Death usually results from local extension, with metastases found in only 8%–10% of cases. Aggressive local treatment with radical cystectomy is the treatment of choice. Given the poor prognosis, physicians should consider performing regular screening with cytologic urinalysis and cystoscopy in high-risk patients (59).
Vesicoureteral reflux may occur as a late complication of schistosomiasis, resulting from fibrosis and ureteral stenosis; it eventually occurs in approximately 30% of patients with a substantially calcified bladder. Voiding cystourethrography is the examination of choice for detecting vesicoureteral reflux, focal bladder wall thickening, large polypoid lesions in the urinary tract, hydroureter, and hydronephrosis (60).
Kidneys
The kidneys are not the main target of S haematobium, but they may be affected in cases of ureteral obstruction and vesicoureteral reflux. Renal disease develops slowly, even in the setting of hydronephrosis, hydroureter, and chronic vesicoureteral reflux. MR urography is the modality of choice for assessing the morphologic characteristics and function of the urinary tract, especially in patients with hydronephrosis and poor kidney function (1,4) (Fig 14).
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.
Genitals
Schistosomal infection of the prostate gland and seminal vesicles has been found at autopsy in as many as 58% of male cadavers in regions where S haematobium is endemic (28). This diagnosis should be considered when calcifications of the prostate gland, seminal vesicles, or bladder wall are seen on transrectal ultrasonography (US) or CT (Fig 15) in patients presenting with a change in ejaculate color or quality (eg, a yellow color or watery consistency), particularly in young men who are known to have traveled to or lived in endemic areas (61–63). At US, echogenic foci may be visible in the prostate gland, with occasional dilatation of the ejaculatory ducts or seminal vesicles because of distal fibrosis and obstruction. In some patients, no changes are apparent at radiologic imaging (28) (Fig 16, 17).
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).
Figure 16 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.
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).
Chronic prostatitis is common in the setting of schistosomiasis and is often associated with seminal vesiculitis (64–66). On MR images, the size and signal intensity of the prostate gland may be normal. However, low signal intensity may be visible in the peripheral zone of the gland on T1- and T2-weighted MR images. This signal intensity abnormality may be focal or diffuse and is not usually accompanied by deformation of the prostate contour, although it may appear nodular, mimicking prostate carcinoma (67).
Seminal vesiculitis is usually seen in the subacute or chronic phase of genital schistosomiasis. Vesiculitis appears as diffuse wall thickening of the seminal vesicle, which has low signal intensity on T2-weighted MR images and may demonstrate dilatation, cystic change, atrophy, convolution loss, proteinaceous and hemorrhagic fluid content with variable signal intensity on T1- and T2-weighted images, and surrounding inflammatory changes (68–72). US in patients with vesiculitis usually reveals dilatation and wall thickening of both seminal vesicles (Fig 17). The diagnosis can be definitively established at microscopy with visualization of S haematobium eggs in seminal fluid (28,61,73).
Schistosomiasis of the testis (also known as bilharzial orchitis) commonly causes testicular edema. In some patients, a testicular schistosomal granuloma may simulate a mass (74). The schistosomal lesion appears on US images as a solid testicular mass with a heterogeneous echotexture or hypoechogenicity and shows increased vascularity at color Doppler flow imaging, an appearance identical to that of most testicular malignancies. Epididymal lesions may simulate neoplasms, infarcts, or foci of inflammation (75–77).
The male genitals are more commonly affected by schistosomiasis than the female genitals.Conclusions
Schistosomiasis is a complex of parasitic diseases with varied manifestations caused by different Schistosoma species. Most cases of human schistosomiasis are caused by S haematobium, S mansoni, or S japonicum. Only S haematobium infects the human urinary tract. The article reviews the life cycle of S haematobium, the modes of its transmission to humans, and the clinical manifestations and imaging features secondary to its infection of the urinary tract and genital organs.
The authors thank David Bier, medical illustrator at the University of Texas M. D. Anderson Cancer Center, for providing the schematic of the life cycle of S haematobium.
Presented as an education exhibit at the 2010 RSNA Annual Meeting.
For this journal-based CME activity, the authors, editor, and reviewers have no relevant relationships to disclose.
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Article History
Received: Sept 16 2011Revision requested: Oct 12 2011
Revision received: Dec 20 2011
Accepted: Jan 10 2012
Published online: June 27 2012
Published in print: July 2012
