Urology
Volume 54, Issue 6 , Pages 952-955, December 1999

Genital amebiasis: historical perspective of an unusual disease presentation

  • Suresh J Antony

      Affiliations

    • Texas Oncology PA, El Paso, Texas, USA
    • Corresponding Author InformationReprint requests: Suresh Antony, M.D., Texas Oncology PA, 7848 Gateway East, El Paso, TX 79915
    • ,
  • Patricia Lopez-Po

      Affiliations

    • Texas Oncology PA, El Paso, Texas, USA
    • Texas Tech University Medical Center, El Paso, Texas, USA

Received 11 January 1999; received in revised form 12 July 1999; accepted 12 July 1999.

Article Outline

 

Amebiasis is a disease with a worldwide distribution, especially in the tropics. An extraintestinal manifestation of this disease, genital amebiasis, is a rare presentation, often missed by clinicians because of the similarity of its presentation to genital carcinoma. This retrospective study of 148 cases of genital amebiasis was performed to define its clinical features and management.

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Material and methods 

Using a MEDLINE search (all languages), reports of 148 cases of genital amebiasis were identified in published reports between 1924 and 1997. Cases were included if the diagnosis was made by biopsy or direct smear for Entamoeba histolytica. The data were analyzed for patient demographics, clinical features, risk factors, mode of transmission, and clinical outcome.

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Results 

Epidemiology 

Of the 148 patients identified with genital amebiasis, 85% were women (n = 126) and 15% were men (n = 22). The average age of those patients for whom data were available was 39 years for the women and 44 years for the men. The country of origin included Mexico (n = 16) and New Guinea (n = 3), with the remainder from Asia and the United States. There were 116 Hispanic, 15 Asian, 13 African, and 2 white patients; in 2 patients, race was not reported.

Coexistent ailments 

Of the patients analyzed, 7.4% had associated ailments, such as genital cancer (n = 8), condyloma acuminatum (n = 1), syphilis (n = 1), and phimosis (n = 1). Seven cancers occurred in the cervix and one in the labia. All were squamous cell cancers.

Presentation and diagnosis in women 

In all female patients with genital amebiasis, a foul-smelling bloody vaginal discharge was the predominant presentation. In addition, approximately 37% presented with abdominal pain, 8.1% had ulcerative genital lesions, and 2.8% had weight loss (Table I). The diagnosis of genital amebiasis was made by direct smear (Papanicolaou smear) in 92% of the cases and by biopsy of the ulcerative lesions in the rest of the cases.

TABLE I. Clinical presentation of genital amebiasis
Women%Men%
Vaginal discharge100Painful penile ulcers86
Abdominal pain37Dysuria and urethral14
Genital ulcers8.1discharge
Weight loss2.8
Cervical squamous cell cancer5.5
Labial squamous cell cancer0.79

Presentation and diagnosis in men 

Eighty-six percent of the male patients presented with a penile ulcer; the remainder had dysuria and urethral discharge (Table I). Biopsy of the ulcerative lesions was necessary to make the diagnosis in 92% of the 22 patients, and culture, direct smear (Papanicolaou smear), or wet preparation for E. histolytica of urethral discharge was done in 2 patients.

Treatment 

Ninety-two percent of the patients were treated with antibiotics (metronidazole and other agents) alone and 4.8% received a combination of both medical and surgical treatment. In 3.2% of the patients, the treatment was not noted in the report. Of the 28 patients in whom the outcome could be documented, 26 were clinically cured (96%). One died of unknown causes and the other was lost to follow-up.

Risk factors 

The risk factors for these cases included homosexual and heterosexual contact with infected partners and concomitant intestinal amebic infection, poor genital hygiene, rectosigmoid amebic infection, and vulvovaginitis.

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Comment 

E. histolytica, once more prevalent in the tropics, has now become increasingly common in the subtropical regions as well. In the United States, the incidence is higher in the immigrant populations from Asia, Africa, and Central and South America. Residents of the southeastern and southwestern United States appear to have a higher incidence of amebiasis, presumably because of the influx of immigrants from Mexico and South America.1

It was estimated in 1986 that approximately 480 million people or 12% of the population are infected with amebiasis and that the annual mortality is 40,000 to 110,000 persons.2 The incidence is widely variable in the population studied, from around 1% in industrialized countries to 50% to 70% in the tropics. People who are at recognized high risk include travelers, immigrants, migrant workers, immunocompromised individuals, sexually active homosexual men,3 institutionalized patients, and possibly children in day care centers. In homosexual men, the increase appears to be in the nonpathogenic strains.4 Transmission occurs by the fecal-oral route and from food and water contamination.5

In our study, the age ranged from 39 to 44 years, with women predominant. The latter may be because of the increased vigilance in the detection of pelvic diseases in women or because the presence of a vaginal discharge alerts physicians to an underlying disease process. Seven percent of the patients in this review were thought to have acquired the disease sexually.6, 7, 8, 9, 10, 11 There is an increasing body of evidence supporting sexual transmission of E. histolytica in the homosexual community in the United States, as well as in other countries.1, 6, 8, 11, 12 This might possibly be due to direct oral/anal contact or anal intercourse, although clear evidence regarding this mode of transmission was not available.

E. histolytica has the capacity of destroying almost all tissues of the human body, including bone and cartilage. It does this by means of several virulence factors such as adhesion molecules, toxins, contact-dependent cytolysis, protease, and phagocytic activity.13, 14 Damage is produced by the trophozoites, which adhere to the colonic mucosa after colonization (Fig. 1). The presence of bacteria is essential for the colonization, as they provide an environment low in oxygen tension and a supply of other metabolic needs. The trophozoites then penetrate the mucosa and adhere to the host cells. The trophozoites possess several receptors that recognize proteins in the extracellular matrix and induce the release of protease and collagenase. This substance then degrades the cellular attachment and produces a cytolytic effect.15, 16, 17

In the heterosexual population, other factors that could be responsible for the spread of genital amebiasis include perineal trauma during anal intercourse and anal and vaginal intercourse with partners who have active genital ulcers.6, 8, 12, 18, 19 Veliath et al.8 noted in their patients that cervical amebiasis was possible after vaginal intercourse, adding more support to this mode of transmission.

In women, the exact incidence and prevalence of genital amebiasis is unknown.12, 20, 21 Predisposing factors for genital amebiasis in women include vulvovaginitis, rectosigmoid infection, perianal trauma, and poor hygiene.12, 18, 20, 21 The ulcers produced by the trophozoite are deep and penetrating, allowing easy spread and transmission of the disease. Another postulated method of transmission is venous embolization by way of an anastomosis between perirectal and perivaginal veins.18, 20 It appears that local external spread from the gastrointestinal tract to the genital tract is more feasible as a mode of transmission in women. The largest series of genital amebiasis (n = 40) cases in women was reported by Fentenes and Bribiesca.20 In their series, the diagnosis was made by cytologic examination, with 18 cases confirmed by histologic examination. The lesions appearing in the cervix often resemble large carcinomatous ulcers,8, 12, 19, 22, 23, 24, 25, 26, 27 which can lead to diagnostic difficulties. The diagnosis of genital amebiasis in women can occasionally be made by standard Papanicolaou smear; only a small percentage require biopsy of the lesions for definitive diagnosis.12

Eight percent of the female patients in this series had coexistent genital amebiasis and malignancy (Table I). The clinical presentation was similar to the patients who had only amebiasis. The average age of this group was 46 years. All these patients had squamous cell carcinoma of the cervix, with the exception of one who had labial involvement. No predisposing factors were clearly documented, but all of these patients were sexually active.

In men, the classic presentation is painful penile ulcers that progress rapidly with a mucopurulent discharge. The best differentiating feature between penile cancer and amebic ulcer appears to be the absence of pain in the patients with cancer.6, 7, 9, 18, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37 Predisposing factors in men include homosexual and heterosexual contact and possibly concomitant intestinal infection. The diagnosis was made by biopsy in 91% of the patients and with direct examination of the Papanicolaou smear in the rest.

Laboratory findings of extraintestinal amebiasis include leukocytosis, the absence of eosinophilia, and the presence or absence of pathogens in the stools. More recently, the presence of antibody against E. histolytica may prove to be more useful in the diagnosis because an antibody response is present in 80% to 90% of patients with invasive disease. Some of the serologic tests include immunofluorescent antibody test, radioimmunoassay, countercurrent immunoelectrophoresis, and enzyme-linked immunosorbent assay. The enzyme-linked immunosorbent assay is the most sensitive and does not give false-negative results in patients with amebic abscesses. It is also specific, giving only 3.6% false-positive results in controls living in endemic areas. One must interpret these results with caution, as patients may remain positive for more than 10 years after infection.5, 38, 39 Culture of the tissue is 100% sensitive and 100% specific. The more recently developed polymerase chain reaction is around 87% sensitive and specific in detecting E. histolytica.

The treatment of this unusual disease appears to be either metronidazole or a combination of metronidazole and an intraluminal agent such as puromycin or iodoquinol. Surgical treatment such as skin grafts may occasionally be required in severely deformed cases.

The clinical outcome appears to be excellent in patients treated with medical treatment alone and should probably be instituted empirically while awaiting results of diagnostic studies. An early Papanicolaou smear in addition to the other routine studies could be an option in both sexes. If metronidazole therapy fails, then biopsy of lesion is necessary. The relationship between genital amebiasis and cancer is unclear. However, Leroy et al.40 recently found indications that in the mucosa of the colon, there were molecules released by the trophozoites immediately after adhesion to epithelial monolayers that bind to elements of the epithelial intracellular junctions. This phenomenon may lead to functional disturbances of this junction. Down-modulation of cell-to-cell adhesion molecules promotes invasion of colon cancer cells as well.40 Other studies have noted that trophozoites cause a decrease of transfilter electrical resistance, resulting in the formation of holes in the enteric cell layer and transfilter migration of trophozoites.41 In light of the above data, it is possible that the trophozoites cause disruption of the genital epithelium, with possible invasion by cancer cells as well.

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Conclusions 

This disease process is difficult to diagnose and must be distinguished from genital cancer, especially in countries in which the incidence of amebiasis is high. The risks factors for the development of the disease are unclear, but appear to be related to sexual activity, poor hygiene, and intestinal amebiasis. The reason for the coexistence of genital amebiasis and cancer is not well understood. The diagnosis is made with cytologic or histopathologic examination or a combination of both, looking for active trophozoites. Medical treatment is almost 100% effective, but surgery may be required when there is coexistent carcinoma or deformity.

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References 

  1. Centers for Disease Control: Intestinal Parasite Surveillance. Annual Summary, 1978.
  2. Walsh JA. Problems in recognition and diagnosis of amoebiasis (estimation of global magnitude of morbidity and mortality). Rev Infect Dis. 1986;8:228–238
  3. Markell EK, Havens RF, Kuritsubo RA. Intestinal protozoa in homosexual men of the San Francisco Bay area. Prevalence and correlates of infection. Am J Trop Med Hyg. 1984;33:239–245
  4. Gathiram V, Jackson TFGH. Frequency distribution of E (histolytica zymodemes in a rural South African population). Lancet. 1985;1:719–721
  5. Farthing MJG, Cevallos A, and Kelly P: Intestinal protozoa, in Mansens Tropical Diseases, 20th ed. Philadelphia, WB Saunders, 1996, pp 1255–1298.
  6. Thomas JA, Antony AJ. Amoebiasis of the penis. Br J Urol. 1976;48:269–273
  7. Chantarakul N, Sook-Anek M, Tantiwonse A, et al.  Amebiasis of the penis on top of giant condyloma acuminata (report of a case). J Med Assoc Thailand. 1979;62:387–393
  8. Veliath AJ, Bansal V, Rajaram P, et al.  Genital amoebiasis. Int J Gynecol Obstet. 1987;25:249–256
  9. Purpon I, Jimenez D, Engelking RL. Amoebiasis of the penis. J Urol. 1967;98:372–374
  10. Parkarsh S, Ananthkrishnan N, Ramakrishnan K, et al.  Amoebic ulcer of the penis. Postgrad Med J. 1982;58:375–377
  11. Mylius RE, Ten Seldam RE. Venereal infection caused by Entamoeba histolytica in a New Guinea native couple. Trop Geogr Med. 1962;14:20–26
  12. Munguia H, Franco E, Valenzua P. Diagnosis of genital amoebiasis in women by standard Papanicolaou technique. Am J Obstet Gynecol. 1966;94:181–188
  13. Adams SA, Robson SC, Gathiram V. Immunological similarity between the 170KD amoebic adherence glycoprotein and human B2 integrans. Lancet. 1993;341:17–19
  14. Guillen N. Cell signaling and motility in Entamoeba histolytica. Parasitol Today. 1993;9:364–369
  15. Reed SL, Keene WE, McKerrow JH. Thio protease expression and pathogenicity of Entamoeba histolytica. J Clin Microbiol. 1989;27:2772–2777
  16. Munoz M, Lamoyi E, Leon G. Antigens in electron dense granules from Entamoeba histolytica as possible markers for pathogenicity. J Clin Microbiol. 1990;28:2418–2424
  17. Schulte W, Scholze H. Action of the major protease from Entamoeba histolytica on proteins of the extracellular matrix. J Protozool. 1989;36:538–543
  18. Grigsby WP. Surgical treatment of amoebiasis. Surg Gynecol Obstet. 1969;128:609–625
  19. Hingorini V, Mahapatra LN. Amoebiasis of the vagina and cervix. J Int Coll Surg. 1964;42:662–667
  20. Fentenes EF, Bribiesca LB. Cytological detection of vaginal parasitosis. Acta Cytol. 1973;17:252–257
  21. Fentenes E, Benitez L. Amoebiasis en eltracto genital femenino. Rev Inst Nal Cancerol Mex. 1969;21:654–656
  22. Weinstein BB, Weed JC. Amoebic vaginitis. Am J Obstet Gynecol. 1948;56:180–183
  23. Bhaduri KP. Entamoeba histolytica in leukorrhea and salpingitis. Am J Obstet Gynecol. 1957;74:434–435
  24. Jayaweera FRB. Amoebic ulceration of the cervix uteri and penis. Ceylon Med J. 1975;20:117–121
  25. Carter B, Jones CP, Thomas ML. Invasion of squamous cell carcinoma of the cervix uteri by Entamoeba histolytica. Am J Obstet Gynecol. 1954;68:1607–1610
  26. Heinz KPW. Amoebic infection of the female genital tract. S Afr Med J. 1973;47:1795–1798
  27. Majumder B, Chaiken ML. Amoebiasis of the clitoris mimicking carcinoma. JAMA. 1976;236:1145–1146
  28. Cooke RA, Rodriguee RB. Amoebic balanitis. Med J Aust. 1964;1:114–115
  29. Camacho BS, Bierana L. Amebiasis cutanea genital. Dermatologica. 1959;3:127–133
  30. Herman HB, Berman LS. Penile ulcer caused by Entamoeba histolytica. JAMA. 1942;120:827–828
  31. Velasco DJ, Engleking RL, Purpon I, et al.  Amibiasis de pene, presentacio de un caso. Rev Mex Urol. 1965;24:527–534
  32. Talwalker GV. Amoebiasis of the penis. J Ind Med Assoc. 1962;39:103–104
  33. O’Leary RK, Posen J. Amoebiasis of the penis. S Afr Med J. 1984;65:113
  34. Quevedo AM, Dib EJ. Un caso de amoebiasis del pene. Medicina. 1963;43:240–243
  35. Shih HE, Wu YK, Lieu VT. Amoebiasis of the penis. Chin Med J. 1939;55:139–145
  36. Lee SW. Amoebiasis of the penis. Chin Med J. 1932;46:1096
  37. Straub M. Amoebiasis penis (venerica). Geneeskundig Tijdschrift Voor Nederlandssch Indie. 1922;64:989–990
  38. Patterson M, Healy GR, Shabot JM. Serological testing for amoebiasis. Gastroenterology. 1980;78:136–141
  39. Proctor EM. Laboratory diagnosis of amoebiasis. Clin Lab Med. 1991;11:829–859
  40. Leroy A, Mareel M, De Bruyne G, et al.  Metastasis of Entamoeba histolytica compared to colon cancer (one more step in invasion). Invasion Metastasis. 1994;14:77–91
  41. Leroy A, De Bruyne G, Verspeelt A, et al.  Bacterium assisted invasion of Entamoeba histolytica through human enteric epithelia in 2 compartment chambers. Invasion Metastasis. 1997;17:38–48

PII: S0090-4295(99)00343-X

Urology
Volume 54, Issue 6 , Pages 952-955, December 1999

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