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• W2609772453 abstract "Current Concepts in MedicineGenito-Urinary Schistosomiasis (Bilharziasis). Part 3: Endoscopic and Pathologic Diagnosis Kamal A. Hanash, MD FACS Nabil K. Bissada, MD FACS David B. Lewall, and MD FRCP(C) John T. GodwinMD FCAP Kamal A. Hanash Chief, Service of Urology, Vice Chairman, Department of Surgery Search for more papers by this author , Nabil K. Bissada Service of Urology, Department of Surgery Search for more papers by this author , David B. Lewall Chairman, Department of Radiology Search for more papers by this author , and John T. Godwin Chairman, Department of Pathology and Laboratory Medicine; King Faisal Specialist Hospital and Research Centre Search for more papers by this author Published Online:1 Jan 1982https://doi.org/10.5144/0256-4947.1982.31SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutENDOSCOPIC DIAGNOSISSecond only to the presence of schistosome ova in the urine, endoscopy may be considered as the most accurate diagnostic test for genito-urinary bilharziasis. When supplemented by a trans-uretheral biopsy of suspicious vesical lesions, it helps confirm the diagnosis in about 70 percent of the cases. It is also important in staging the disease, in relating the degree of infestation, and in excluding a coexistent cancer. It eventually leads to a better selection of proper therapy.Because the active or acute stages of the disease are usually responsive to medical treatment, in contrast to chronic stages, proper endoscopic staging carries an important therapeutic value.1 In this section, specific endoscopic findings are classified into active and chronic stages and are related to histologic vesical changes.Active LesionsMost active lesions are located over the posterior vesical wall and the trigone. The bilharzial granulomas, or tubercles, are usually visualized endoscopically as an irregular patch of shiny, refractory, granular, whitish or yellowish fine nodules of less than one millimeter in diameter. They have been compared to sugar powder in appearance. They are usually surrounded by areas of hyperemia and inflammation which bleed on overdistension of the bladder thus resembling interstitial or hemorrhagic cystitis. These lesions correspond histologically to granulomatous epithelial changes caused by the ova's penetration of the epithelial wall. These changes denote acute activity of the lesions and are usually responsive to medical therapy.Bilharzial nodules are formed by a coalescence of the granulomas or tubercles. Cystoscopically, they appear as whitish or yellowish nodules of one to two millimeters in diameter and resemble grains of rice. They are usually associated with diffuse areas of cystitis. The tubercles may involve a large surface of the vesical epithelium in a patchy or linear pattern along the blood vessels. Histologically, they correspond to an aggregation of the tubercles or granulomas.Bilharzioma is a lesion that, endoscopically, resembles a strawberry laid over the bladder mucosa to which it is usually attached by a narrow pedicle. Figure 1. It is multinodular, hyper-vascular, and bleeds easily on contact. When reaching a large size, it may fill up the entire lumen and resemble a malignant tumor. Histologically, it represents a proliferative and hyperplastic epithelial reaction with hypervascularity. It is infiltrated by numerous bilharzial follicles.Figure 1. Endoscopic view of a bilharziomaDownload FigureChronic LesionsLesions commonly involve the trigone and posterior vesical wall and denote a chronic infection which is poorly responsive to medical therapy.Fibrosis and calcification of the primary tubercles in the submucosa, “the sandy patches,” are pathognomonic of bilharziasis. Figure 2. Cystoscopically, they appear as whitish or yellowish, dull, fine, granular, nodular patches resembling sand under water.Figure 2. Fibrosis and calcification of the primary tubercules in the submucosa, “sandy patches.”Download FigurePapillomas represent mucosal growths secondary to a proliferative process. They usually contain ova at their bases but are not specific for bilharziasis.The cicatricial lesions, with sclerosis and calcification, appear endoscopically as whitish, grayish, or brownish patches with rigid walls. A decrease in bladder capacity accompanies these lesions.Other chronic lesions include chronic ulcers, atrophic mucosal changes, and ureteral orifice rigidity. Such rigidity leads either to stenosis or to reflux.It is important to remember that several, active, chronic lesions, of different stages of the disease, can co-exist in the bladder. This co-existence depends primarily upon the degree and rate of the initial and subsequent infestations.Nonspecific LesionsNonspecific lesions are commonly encountered in bilharziasis and are produced by toxic or chemical irritants, inflammation, secondary infection, and stasis of urine. They include the different types of cystitis, cystica, glandularis, hemorrhagic, ulcerative, and pseudo-membranous. Other nonspecific lesions commonly seen are mucosal hemorrhages, ulcerations, bullous edema, black granular dots, and mucosal atrophy.Ureteral OrificesThe endoscopic appearance of the ureteral orifices is of importance for proper staging of the disease and for the initiation of proper therapy which should prevent damage to the kidneys and restore renal function. The orifices may be indirectly obstructed by adjacent vesical hyperplastic lesions or directly involved by the bilharzial vesical pathology. The sclerosis and calcification of the bladder wall may lead to ureteral rigidity resulting in gaping with secondary reflux or to sclerosis with secondary obstruction.In summary, cystoscopy is essential for the diagnosis, staging, and treatment of bilharziasis. It is also of primary importance in the diagnosis of bladder tumors which may be present. Transurethral biopsy and resection of the bilharzial lesions have definite diagnostic and therapeutic values. Endoscopy may be complemented by, but not replaced by, other diagnostic tests.PATHOLOGYThe principal pathological changes of bilharziasis are in the urogenital and digestive tract although any organ system may be involved. The lesions produced by cercariae, schistosomula, the adult schistosomes, ova, or metabolites are similar in the various species.2The extent of disease depends upon the host burden of parasites. The lesions produced depend upon the number of invading parasites, the stage of infection, and the type of tissue response. Penetration of the epidermis by cercariae produces an inflammatory reaction. After cutaneous invasion, incubation occurs during which there may be multiple organ involvement due to circulating schistosomulea. The schistosomes develop into adults within the veins although only the dead worm produces vascular lesions. After copulation, the resulting ova are eliminated or die. The ova produce tissue damage related to the number of ova retained. The quantity of ova relates to the species because each species produces differing numbers of ova. The most prolific is Schistosoma japonicum.The ova may be lost via the bladder or intestinal mucosa. Figure 3. This is believed due to enzymatic action by the miricidia and by the action of the spines impinging upon and damaging the vein wall. This in turn produces hemorrhage and an inflammatory reaction. Of course, many ova do not escape and are thereby retained in the tissues where they produce both local and systemic reactions.Figure 3. Adenocarcinoma of the bladder containing schistosome ova within necrotic tissue being shed into the lumen.Download FigureThe ova incite a mononuclear cellular reaction including monocytes, lymphocytes plasma cells, and eosinophils.With the degeneration of the miracidia, there is calcification although the shell may remain unchanged. There is foreign body giant cell production which engulf the chitinous shells. There may be little or no reaction about the ova and they merely appear within the various tissues which may at times be easily overlooked if not searched for carefully. Figure 4.Figure 4. Schistosome ovum (Hematobium) in bladder musculature with severe fibrosis.Download FigureThe inflammatory reaction may incite necrosis with evolving fibrosis which may be dense and/or have a fairly characteristic concentric or lamellar pattern. The latter is particularly noticeable in the liver.In hollow viscera, there may be polypoid proliferations of granulation tissue and epithelial hyperplasia. This may, in time, become scar tissue. Figure 5.Figure 5. Schistosome ova in hyperplastic bladder mucosa.Download FigureThis is particularly true of the urinary bladder and is commonly produced by Schistosoma haematobium which incites lesions of the genitourinary tract of males and females. It is thought that the extensive exudative reactions about disintegrating worms and ova are most likely of allergic origin.The worms apparently spread along the mesenteric veins to reach the genito-urinary tract. Ova are deposited in almost any of the organs and in different sites within the organs. It is common to see a myriad of ova associated with extensive inflammation in the superficial layer of the bladder. Figure 6.Figure 6. Adenocarcinoma of the bladder with heavy infestation by schistosome ova.Download FigureKidney deposition is infrequent but may involve the parenchyma and pelvis. Various pelvic inflammatory lesions may develop. Secondary change due to involvement of the ureter and bladder are common. Ureteral involvement is common and generally occurs along with bladder infection, usually bilaterally. Figure 7.Figure 7. Schistosome ova within the ureter showing no significant tissue reaction.Download FigureThere may be epithelial hyperplasia and metaplasia even to the formation of carcinoma. There is partial obstruction due to the inflammation, polypoid hyperplasia with calcification, and scarfing. There may be marked hydroureter with dense fibrosis of ureteral wall and stricture formation.Within the bladder, the trigone is most commonly involved. In the bladder, ova may be extremely numerous forming large clusters with associated chronic inflammation. The epithelium may be hyperplastic and metaplastic with cystitis cystica and cystitis glandularis forming. There are usually polypoid formations and incrustations, and there may be extensive scarring of the bladder wall with obstructive manifestations. There may be ova deposits in seminal vesicles, prostate and urethra with attendant, pathological alterations although many ova show no surrounding reaction. Occasionally, fistula may be produced via the skin, bowel, and ischiorectal fossa. In the urethra, the ' inflammation may develop with polypoid formations, ulcerations, abscesses, and fistula formation. In the prostate and seminal vesicles, there may be ulceration and later scarring and calcification.The testes are rarely involved but, if they are, it is usually accompanied by epididymal infection. Involvement of the body of the uterus, cervix, and ovary is also infrequent. The vagina may develop polypoid masses with scarring and malignant changes. Fistula between the bladder and vagina may occur. The vulva may show extensive inflammation with epithelial hyperplasia.One of the more important complications of genito-urinary schistosomiasis is the development of urinary bladder carcinoma. It appears that the chronic inflammation with epithelial hyperplasia and metaplasia precede and progress to neoplasia as is thought to occur in the development of carcinoma in other organs nonschistosomally related.I. El Sebai, et al. in a review of 655 cases of bladder carcinoma associated with bilharzial infection reported 483 tumors (73.7 percent) to be squamous carcinoma, 19 of which were verrucous type.3 H. N. Tawfik, et al. recorded 17 adenocarcinomas in which schistosomal ova were present in all cases. Figure 8. The general incidence of bladder adenocarcinoma is about two percent of malignant epithelial tumors whereas Egyptian material indicates ranges up to 4.75 percent.4Figure 8. Adenocarcinoma of bladder with associated schistosomiasis fibrosis. Hematoxylin and eosin stain.Download FigureM. E. El Boulkany indicated in a series of 304 bilharzial-associated bladder cancers 66.7 percent were squamous carcinoma, 23.4 percent transitional, 8.1 percent adenocarcinoma, and 1.8 percent unclassified.5 He also indicated that the bilharzial cancers were nodular, fungating, squamous type and usually did not involve the trigone in contrast to the nonbilharzial cancers which are papillary, transitional type and frequently involve the trigone.A. M. A. El Asfahani et al. have attempted to determine certain immunological aspects of bilharzial associated bladder cancer through a study of T lymphocytes, however, without established results.6A recent study by M. Magzoub and A. A. Kasim recorded the infection rate in snail vectors and the widespread distribution of bilharziasis in Saudi Arabia ranging up to 55.7 percent in the Gizan area population.7 This is borne out by the presence of schistosome ova in routine stool examinations and the frequent occurrence of ova in surgical specimens at this Hospital.Much basic research relative to bilharziasis is being supported by the United Nations Development Programme, World Bank, and World Health Organization which may hopefully elucidate some of the many problems related to this serious parasitic disease.8The importance of a team effort, including the microbiologist, biochemist, urologist, pathologist, radiologist, gastroenterologist, and, more important, the referring primary physician for the early diagnosis and proper treatment, should be emphasized. This would certainly improve the prognosis of this lethal disease.ARTICLE REFERENCES:1. Chatelain C: La Bilharziose Uro-gènitale. Masson, ed., Paris, 1977 pp 65–75. Google Scholar2. Abdallah A, Mousa AH: Schistosomiasis and other trematode infections. In: Woodruff AW, ed: Medicine in the Tropics. London, Churchill Livingstone. 1974 pp 173–220. Google Scholar3. El Sebai I, Sherif M, El Bolkainy MN, et al.: Verrucose squamous carcinoma of bladder . Urology 4: 407–101974. Google Scholar4. Tawfik HN, Abdin FH, Latif MEA, et al.: Histogenesis of adenocarcinomas of the urinary bladder . Al-Azhar Med J 6: 11–17, 1977. Google Scholar5. El Boulkany MN, Ghoneim MA, Mansour MA: Carcinoma of the bilharzial bladder in Egypt . Br J Urol 44: 561–701972. Google Scholar6. El-Asfahani AMA, Hammouda F, Tawfik HN, et al.: Thymus derived lymphocytes in patients with bilharzial urinary bladder cancer: brief communication. In: Selected Reports on Cancer. National Cancer Institute, Cairo, 1978 pp 57–59. Google Scholar7. Magzoub M, Kasim AA: Schistosomiasis in Saudi Arabia . Ann Trop Med Parasitol 74 (5): 511–131980. Google Scholar8. UNDP/World Bank/WHO: Fourth Annual Report. Special programme for research and training in tropical diseases. 1979-80 pp 89–98. Google Scholar Previous article Next article FiguresReferencesRelatedDetails Volume 2, Issue 1January 1982 Metrics History Published online1 January 1982 KeywordsSchistosomiasisEndoscopySchistosoma haematobiumUrologic diseasesInformationCopyright © 1982, Annals of Saudi MedicinePDF download" @default.
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