LEYITER TO THE EDITOR
TESTICULAR
SCHISTOSOMIASIS
To the Etlitor: In the July issue (vol. 12, page 87) of UROLOGY, Dr. A. Elbadawi ct (I[. present an interesting case of benign testicular enlargement due to intratesticular schistosomiasis. A few years ago I reported a similar case of painless testicular swelling secondary to solitary epididymal schistosomiasis in a Canadian missionary, who had spent many years in the Sudan.’ The diagnosis came as a surprise on pathologic examination of the orchiectomy specimen. I agree with the authors that preoperative diagnosis of these unusual manifestations of schistosomiasis will be achieved only by greater physician awareness, but I doubt if diligent search for the parasite in the excreta will be of value. It appears that the absence of ova in stool and urine is a distinctive feature of the solitary form of schistosomiasis.‘*3 The use of a reliable skin test may be more rewarding, especially in nonendemic areas. The authors stress that the testicular enlargement resulted not from the parasitic orchitis itselfbut from the concomitant massive peritesticular fibrosis. Yet they gloss over its pathogenesis with the simple remark that it was “the late sequel to a hydrocele which had existed earlier and had been completely resorbed with obliteration of the vaginal cavity.” Hydroceles are common and do not usually cause massive peritesticular fibrosis. The description of the sclerosing periorchitis and periepididymitis without inflammatory cell infiltration suggests that the process may be the fibrotic end stage of a chronic lymphedema, that is, the Eppinger phenomenon. Two possible pathogenetic mechanisms come to mind. The
first is related to peritesticular lymphatic obliteration secondary to the parasitic orchitis. This seems unlikely since there was no periand the testicular spread of the infestation spermatic vessels were normal. The second mechanism, which I recently proposed,” is COIIgenital hypoplasia of the peritesticular lymphatics, which eventuates at a variable tempo into chronic lymphedema, noninflamlnatory peritesticular fibrosis, and symptomatic testicular enlargement. I would like to suggest that this patient presented clinically because of this mirelated and concurrent process. This suggestion fits with the observation that testicular schistosomiasis per se is asymptomatic and is usually detected at autopsy” or incidentally,” unless secondary complications develop, such as testicular infarction.’
Louis H. Honor+, F.R.C.P.(C) Department of Laboratories Grace General Hospital St. John’s, Newfoundland. Canada
1, Honor& LH and Ck~lemarr GU: Solitary cpididymal schistosomiasis, Can. J. Surg. 18: 479 (1975). 2. Eltayeb AA: Schistosomiasis of the epididymis, Br. J. Surg. 56: 522 (1969). 3. Boulos PB and Karim Oh: Schistosomiasis of rpididynis, J. H. Cdl. Surg. Edinb 18: 158 (1973). 4. Honort LH: Nonspecific prritesticular fibrosis manifested as testicular enlargement. Arch. Surg. 113: 814 (1978). 5. Gelfand 51, et al: Schistosomiasis of the male pelvic organs. Severity of infection as determined by digestion of tissue and histologic methods in 300 cadavers, An. J, Trap. bled. Hyg. 19: 779 (1970). 6. Houston \V: Bilharziasis of the testis. Br. J. Ural. 36: 220 (1964). 7. Joshi RA: Total granulomatous infarction of testis tlrw to Schistosoma hacmatobium. J. Clin. Pathol. 20: 273 (1967).
UROLOC:Y
i
OCTOBEH
19%
i
\‘OLL’\lE
X11
\L.\lHEH
.1
TESTICULAR
SCHISTOSOMIASIS
To the Etlitor: In the July issue (vol. 12, page 87) of UROLOGY, Dr. A. Elbadawi ct (I[. present an interesting case of benign testicular enlargement due to intratesticular schistosomiasis. A few years ago I reported a similar case of painless testicular swelling secondary to solitary epididymal schistosomiasis in a Canadian missionary, who had spent many years in the Sudan.’ The diagnosis came as a surprise on pathologic examination of the orchiectomy specimen. I agree with the authors that preoperative diagnosis of these unusual manifestations of schistosomiasis will be achieved only by greater physician awareness, but I doubt if diligent search for the parasite in the excreta will be of value. It appears that the absence of ova in stool and urine is a distinctive feature of the solitary form of schistosomiasis.‘*3 The use of a reliable skin test may be more rewarding, especially in nonendemic areas. The authors stress that the testicular enlargement resulted not from the parasitic orchitis itselfbut from the concomitant massive peritesticular fibrosis. Yet they gloss over its pathogenesis with the simple remark that it was “the late sequel to a hydrocele which had existed earlier and had been completely resorbed with obliteration of the vaginal cavity.” Hydroceles are common and do not usually cause massive peritesticular fibrosis. The description of the sclerosing periorchitis and periepididymitis without inflammatory cell infiltration suggests that the process may be the fibrotic end stage of a chronic lymphedema, that is, the Eppinger phenomenon. Two possible pathogenetic mechanisms come to mind. The
first is related to peritesticular lymphatic obliteration secondary to the parasitic orchitis. This seems unlikely since there was no periand the testicular spread of the infestation spermatic vessels were normal. The second mechanism, which I recently proposed,” is COIIgenital hypoplasia of the peritesticular lymphatics, which eventuates at a variable tempo into chronic lymphedema, noninflamlnatory peritesticular fibrosis, and symptomatic testicular enlargement. I would like to suggest that this patient presented clinically because of this mirelated and concurrent process. This suggestion fits with the observation that testicular schistosomiasis per se is asymptomatic and is usually detected at autopsy” or incidentally,” unless secondary complications develop, such as testicular infarction.’
Louis H. Honor+, F.R.C.P.(C) Department of Laboratories Grace General Hospital St. John’s, Newfoundland. Canada
1, Honor& LH and Ck~lemarr GU: Solitary cpididymal schistosomiasis, Can. J. Surg. 18: 479 (1975). 2. Eltayeb AA: Schistosomiasis of the epididymis, Br. J. Surg. 56: 522 (1969). 3. Boulos PB and Karim Oh: Schistosomiasis of rpididynis, J. H. Cdl. Surg. Edinb 18: 158 (1973). 4. Honort LH: Nonspecific prritesticular fibrosis manifested as testicular enlargement. Arch. Surg. 113: 814 (1978). 5. Gelfand 51, et al: Schistosomiasis of the male pelvic organs. Severity of infection as determined by digestion of tissue and histologic methods in 300 cadavers, An. J, Trap. bled. Hyg. 19: 779 (1970). 6. Houston \V: Bilharziasis of the testis. Br. J. Ural. 36: 220 (1964). 7. Joshi RA: Total granulomatous infarction of testis tlrw to Schistosoma hacmatobium. J. Clin. Pathol. 20: 273 (1967).
UROLOC:Y
i
OCTOBEH
19%
i
\‘OLL’\lE
X11
\L.\lHEH
.1
