Rectal Prolapse Associated With Schistosomiasis

MAY 25, 2007


The etiology of rectal prolapse is not completely understood. Different mech?anisms have been postulated, most of which point to various anatomical ab?normalities of the pelvic floor. Schisto?somiasis, caused by parasitic trematode worms and common in many parts of the world, has been associated with rectal prolapse but is rarely reported in the United States. The authors report a case of rectal prolapse associated with schistosomiasis in a nulliparous Filipino woman. The patient underwent an un?eventful perineal rectosigmoidectomy.

Mirza Khurrum Baig, MD
Research Fellow
Department of Colorectal Surgery
Cleveland Clinic Florida
Weston, FL

Sherry Woodhouse, MD
Department of Pathology
Cleveland Clinic Florida
Weston, FL

Bruno Dipasquale, MD
Department of Pathology
Cleveland Clinic Florida
Naples, FL

Anthony M. Vernava III, MD
Department of Colorectal Surgery
Cleveland Clinic Florida
Naples, FL

Jonathan Efron, MD
Department of Colorectal Surgery
Cleveland Clinic Florida
Naples, FL

Rectal prolapse is full-thickness protrusion of the rectum through the anal sphincters. This condition can affect people of all ages. Children may present with partial prolapse, a condition more common in boys younger than 5 years.1 In adults, women are affected more often than men and commonly present with full-thickness rectal prolapse.1-3

Several causes of rectal prolapse have been described in the literature, most of which point to various anatomical abnormalities of the pelvic floor.4-7 Childbirth is a primary cause of rectal prolapse in women, but we could immediately rule this out in our patient because she was nulliparous. During perineal rectosigmoidectomy for her rectal prolapse, we discovered she had schistosomiasis. Along with this case report, we review the literature regarding schistosomiasis-induced rectal prolapse.


Case report
A 62-year-old Filipino woman presented with rectal prolapse, intermittent bright red bleeding from her rectum, and urinary incontinence. She had immigrated to the United States 30 years earlier and was married but had no children. Her medical history was significant for anxiety, chronic abdominal and back pain, hypertension, and diabetes mellitus. She had visited the Philippines within the past year.

Physical examination was normal except for full-thickness rectal prolapse. The patient underwent colonoscopy and an upper gastrointestinal endoscopy, both of which were normal. She had a thorough urological examination, and it was recommended that she receive conservative treatment for urinary incontinence. The patient subsequently underwent perineal rectosigmoidectomy for rectal prolapse.

The rectosigmoidectomy specimen consisted of a 16-cm length of bowel. The mucosal surface was smooth, glistening, tan, and intact; the wall appeared slightly thickened. Many irregular areas of yellow discoloration measuring up to 2 cm in diameter were seen throughout the bowel wall of the cut section. A microscopic examination showed numerous parasitic eggs measuring 65 to 75 microns in length, many of which were calcified, consistent with Schistosoma japonicum (Figure 1). The eggs were non?operculate and lacked both birefringence and lateral or prominent terminal spines (Figure 2), found in other species of Schistosoma.

In 1851, Theodor Bilharz described a parasitic infection (Bilharzia), currently referred to as schistosomiasis, caused by the presence of trematode worms (Schistosoma) in the venous system of the intestines.8 Man is the principal definitive host for this parasite. The adult worms of S japonicum inhabit the portal and mesenteric veins. The female worms occupy a groove in the lateral edge of the male worm's body and produce approximately 3,000 eggs each day.9 Egg production begins 4 to 6 weeks after infection and continues for the life of the worm, which is usually 3 to 5 years. Schis?tosome eggs find their way into the lumen of the bowel and bladder and are excreted in the feces (S mansoni and S japonicum) or urine (S hematobium).10

The eggs hatch in fresh water and release motile ciliated miracidia, which penetrate the body of an intermediate host snail (Oncomelania). The miracidia multiply asexually in the body of the snail, and within a few weeks hundreds of motile cercaria emerge. Cercaria enter humans by penetrating the skin, after which they lose their tails and evolve into schistosomula before migrating to the lungs and liver. Approximately 6 weeks after infection, they mature into adult worms, mate, and then pass through the venous system to their final habitat.

It is estimated that 200 million people throughout 74 countries have schistosomiasis. Of these, 120 million experience symptoms, 20 million of whom suffer severe illness. Three species are primarily responsible for human infections: S mansoni, S hematobium, and S japonicum. Despite major advances in controlling the parasite and decreases in morbidity and mortality, schistosomiasis continues to spread in humans with increasing frequency. Praziquantel is the mainstay of treatment and reliably cures 60% to 90% of patients; for those who are not cured, praziquantel substantially decreases the worm burden and egg production. After nearly 20 years of intensive use, resistance to praziquantel may be emerging.10 Despite substantial and successful control measures, S japonicum infection still occurs in China, Indonesia, and the Philippines.

Schistosomiasis is the principal cause of rectal prolapse in certain parts of the world.9 In Egypt, the disease occurs almost exclusively in rural populations among young men, who are exposed to the parasite while cultivating and irrigating fields with water from the Nile, which is infested with S mansoni.

El Sebai reported that schistosomiasis of the rectum and colon can cause rectal prolapse due to frequent severe attacks of dysentery, passage of mucus and blood in the stool, and dragging tension of schistosomal polyps on the mucosa of the rectum.11 Hammam also reported a relationship between schistosomiasis of the colon and rectum and the development of rectal prolapse.12

Several mechanisms have been proposed for schistosomiasis-induced rectal prolapse. Chronic straining due to dysentery, along with the passage of blood and mucus in the stools, may weaken the pelvic floor, muscles, and sphincters. Repeated prolapse of schistosomal polyps with resulting venous congestion and secondary infection may greatly increase the bulk of the polyps. This, and the constant dragging effect of these polyps when present with lax ampullary mucosa of the rectum, may lead to prolapse. Continuous and repeated passage of mucus and blood in the stools can render these patients severely anemic and hypoproteinemic, resulting in weakness and hypotonia of the pelvic muscles and sphincters. This results in a lack of fixation of the rectum and can lead to rectal prolapse.9,13,14 Our patient presented with bleeding but no dysentery or anemia.

The presence of schistosomal polyps is not a constant finding in patients with schistosomiasis presenting with rectal prolapse; in these patients, myopathy may be a major contributory factor.13 In addition, positive immune fluorescence reaction for S mansoni egg antigen along the sarcolemmal membrane of human myocardial fibers suggests a role for im?mune complexes in the pathogenesis of the muscle lesions in S mansoni.14

Schistosomiasis results from the host's immune response to schistosome eggs and the granulomatous reaction caused by secreted antigens. Most granulomas develop at the sites of maximal egg accumulation: the intestine, genitourinary tract, and liver. Eggs retained in the bowel wall cause inflammation, hyperplasia, ulceration, and polyposis. As was the case with our patient, rectal prolapse may result. Chronic granulomatous le?sions may lead to portal hypertension, massive splenomegaly, and gastrointestinal bleeding. Patients experience fatigue, abdominal pain, and diarrhea; in severe cases, they may suffer from jaundice and liver failure.10

Schistosomiasis is diagnosed when evidence of schistosome eggs is found in the feces, urine, or a biopsy specimen (usually of the rectal mucosa). The extent of egg shedding may fluctuate, and as many as three specimens may be re?quired in some patients to make the diagnosis.10 We made our diagnosis after examining the rectosigmoidectomy specimen taken to repair the rectal prolapse. Since our patient had never borne children, we were able to eliminate one of the primary causes of rectal prolapse from consideration. The possibility of schistosomiasis should be considered for patients who present with rectal prolapse and have a history of living or traveling in an endemic region.

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2. Goligher JC. Surgery of Anus, Rectum and Colon. 2nd ed. London, England; Bailliere Tindall:1967;289.

3. Altemeier WA, Culbertson WR, Schowengerdt C, et al. Nineteen years' experience with the one-stage perineal repair of rectal prolapse. Ann Surg. 1971;173(6):993-1006.

4. Moschcowitz AV. The pathogenesis, anatomy and cure of prolapse of the rectum. Surg Gynecol Obstet. 1912;15:7-21.

5. Broden B, Snellman B. Procidentia of the rectum studied with cineradiography. A contribution to the discussion of causative mechanism. Dis Colon Rectum. 1968;11(5):330-347.

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7. Goldberg SM, Gordon PH, Nivatvongs S. Essentials of Anorectal Surgery. Philadelphia, Pa: Lippincott; 1980.

8. Schadewaldt H. The first report and drawings of schistosoma haematobium and monsori by Theodor Bilharz. Z Tropenmed Parasitol. 1953;4(3):410-414.

9. Abul-Khair MH. Bilharziasis and prolapse of the rectum. Br J Surg. 1976;63(11):891-892.

10. Ross AG, Bartley PB, Sleigh AC, et al. Schistosomiasis. N Engl J Med. 2002;346(16):1212-1220.

11. El Sebai I. Advanced Bilharzial intestinal manifestations: the relation to cancer. Kasr El-Aini J Surg. 1961;2: 905-933.

12. Hammam A. Treatment of complete prolapse of rectum in adults. Kasr El-Aini J Surg. 1964;15:209-214.

13. Hussein AM, Helal SF. Schistosomal pelvic floor myopathy contributes to the pathogenesis of rectal prolapse in young males. Dis Colon Rectum. 2000;43(5):644-649.

14. Rashwan MA, Ayman M, Ashour S, et al. Endomyocardial fibrosis in Egypt: an illustrated review. Br Heart J. 1995;73(3): 284-289.

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