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Genital schistosomiasis now more accurately called Urogenital schistosomiasis (also known as bilharziasis) is a parasitic infection of the genitals which affects men and women, causing chronic illness. The infectious agent (one of five species of flatworms, Schistosoma haematobium) is transmitted via tainted water. It is the eggs shed by the worm and not the worm itself, however, which cause the damage.[dead link] An estimated 9–13 million women are afflicted with urogenital schistosomiasis, primarily in 53 countries in sub-Saharan Africa and the eastern Mediterranean. The disease may be controlled with antiparasitics and improved education and hygiene.
Mucosal grainy, sandy patches seem to be pathognomonic for S. haematobium infection in the female genitals. S. haematobium infection probably also causes mucosal bleeding and inflammation. Grainy, sandy patches are significantly associated with S. haematobium ova only (OR 4.89, 95%CI 2.14-11.17, p<0.001). Genital S. haematobium ova are also significantly associated with homogenous yellow sandy patches in the genital mucosa (OR 2.94, 95%CI 1.35-6.44, p=0.007), mucosal bleeding (OR 8.13, 95%CI 2.01-32.9, p=0.003) and abnormal blood vessels (OR 5.16, 95%CI 2.04-13.07, p=0.001). The three latter phenomena are, however, also associated with other reproductive-tract diseases. Ova presence is not a predictor for ulcers, papillomata, leukoplakia, polyps or cell atypia. The findings are the same in all adult age groups—indicating that genital lesions do not undergo a change with age, or that women by the age of 20 have already passed into a chronic state of infection. The full clinical significance of genital schistosomiasis has yet to be established. The concomitant blood-vessel friability and inflammation may give weight to circumstantial evidence for bidirectional transmission of HIV.
Up to 75% of women excreting S. haematobium ova in the urine may have schistosome ova in the uterine cervix, vagina or vulva. Furthermore, some women reportedly have genital schistosomiasis even without urinary schistosomiasis. Studies in Tanzania and Zimbabwe have shown that up to 41% of women may have involvement of the lower reproductive tract without schistosome ova in the urine. However, genital schistosomiasis as a cause of morbidity is only rarely accounted for in overview publications, although there are exceptions.
S. haematobium oviposition may be distributed in pathophysiologically-vital areas in the pelvis. Post mortem studies and histopathological material from surgery in the reproductive tract have shown that S. haematobium may be distributed in all the pelvic organs. Ova are most commonly found in the cervix, followed by the vagina, ovaries, Fallopian tubes, vulva and (rarely) the uterus. There are only a few case reports of severe acute disease (such as ascites) with ovarian schistosomiasis, ectopic pregnancy, and heavy infestation of the uterus during pregnancy.
The crushed biopsy of genital tissue is considered the gold standard for the parasitological diagnosis of genital S. haematobium. However, the ova are located in highly-focal clusters and may be missed, especially with histological sectioning of a biopsy. Because this method leaves a wound in the genital area, and because women in parts of the schistosomiasis- and HIV-endemic areas might not have any choice regarding sexual intercourse or be able to suggest the use of a barrier contraceptive method, taking a biopsy is an HIV transmission risk for the patient (and her partner) until the wound has healed.
Wet smears and Pap tests can contribute to the diagnosis, but have low sensitivity. In a cytology laboratory in Harare, Zimbabwe, 44 of 1901 Pap smears were found positive; in Kampala, Uganda, only 1 in 30,000 smears were positive. Urinary filtration or dipsticks are insensitive indicators for genital S. haematobium. Moreover, the techniques themselves have been proven to be of poor value (or untested) in women of childbearing age. Increased levels of eosinophil cationic protein, Neopterin or Immunoglobulin A in cervico-vaginal lavage have only limited value in the diagnosis of female genital schistosomiasis.
For clearance of urinary ova excretion and reduction of morbidity, a single oral dose of praziquantel 40 mg/kg (or 60 mg/kg in 2 divided doses) is recommended with food and drink in order to minimise gastrointestinal side effects. Based on a number of reports, WHO has decided to also recommend praziquantel to pregnant and lactating women. Treatment for urinary schistosomiasis has been found equally effective in HIV-positive and -negative patients. Praziquantel does not seem to influence plasma HIV viral load in S. mansoni-infected individuals.
As of 2011, one study has directly explored the treatment of genital schistosomiasis. Although urinary ova excretion decreased following treatment (OR, 10.3 95% CI 3.8-27.8, p<0.001), praziquantel was not associated with a significant reduction in genital lesions or contact bleeding (p=0.31-0.94). Sandy patches remained strongly associated with contact bleeding and vessel abnormalities, even after treatment, and findings were independent of HIV status. Such lesions (common, and apparently refractory to treatment for at least 12 months) may be an important risk factor for both the acquisition and transmission of the human immunodeficiency virus in sexually-active women.
In the urinary tract, the effect of praziquantel has largely been determined by resolution of lesions detectable by ultrasound scan and decreased ova excretion in the urine. Sandy patches in the bladder have been found post-mortem, in surgical specimens or as seen by cystoscopy; however, there have been no large-scale cystoscopic studies on the natural course of sandy patches or the effect of praziquantel on the clinical morphology of bladder lesions. The outcome of treatment in the urinary tract may be variable, depending on four factors:
- Age of the patient
- Pre-treatment intensity of infection
- Degree of fibrosis or calcification
- Site of the lesion
Urinary-tract lesions in younger patients are more responsive to treatment, and this may be so in the genital tract as well. However (as mentioned previously), given the same age group and exposure rates, lesions in the bladder decrease faster than lesions in the upper ureteres after treatment. Hence, the effects of treatment in the urinary tract cannot automatically be extrapolated to the genital tract.
Praziquantel (which kills the mature worm) is the standard treatment for all types of schistosomiasis, and there will be a decrease in S. haematobium ova excretion in the urine 4–26 weeks after treatment. Occasionally, repeated courses are be necessary to cure S. haematobium in the urinary tract—even in children, and sometimes in returned travellers long after the worm should have matured. Case reports indicate that praziquantel may have an immunomodulatory effect on lesions, so the lesions resolve. However, although praziquantel kills the egg-laying worms, lesions not yet visible may develop around ova already deposited in tissues. Once ova deposition has occurred in the cervix, ova excretion and lesion development are independent processes; praziquantel affects the former almost immediately, but possibly not the latter.
Egg excretion in the urine of lesions in genital mucosa are not directly comparable, and little is known about the effect of treatment in the genital tract. Prior to the Zimbabwean study there had been no longitudinal study, and only a few case reports on the effects of treating genital schistosomiasis. The case reports describe regression of sandy patches in lower-genital-tract schistosomiasis after treatment with praziquantel for a course of 1 week to 6 months. After less than two years, treatment has been described to resolve schistosomal infertility (with pregnancy) in up to 6 of 13 infertile women.
It has been hypothesised (and debated) that the release of worm fragments upon death enhances immunological protection against reinfection, and possibly also removes the immunosuppressive effect of the adult worm. Moreover, there is a second effect on transmission. By interfering with the cycle, there will be decreased infection of the snails and decreased excretion of cercaria and infection of humans, especially if mass chemotherapy is carried out in the low-transmission season. Other forms of treatment— such as arthemeter (recently tested), metrifonate (for S. haematobium, recently withdrawn from the market), niridazole, oxamniquine, hycanthone, amoscanate and antimony (no longer in use for schistosomiasis)—will not be discussed here.
WHO has recommended mass treatment for women and children in schistosomiasis-endemic areas, to prevent long-term morbidity. This is often done through schools, most often with the active participation of the teaching staff. Mass treatment has been recommended at six-month to three-year intervals, depending whether there is a continuous high or seasonal low transmission (more often with the former). Studies have found that the prevalence of schistosomiasis is higher in non-enrolled children. Moreover, girls are often underrepresented in schools; in an Egyptian study, it was estimated that 59% of infected boys but only 18% of infected girls were reached through school programmes.
Effects of travel
"Travellers" are defined as coming from non-endemic areas and exposed for a limited time, whereupon they return to a non-endemic site. Schistosomiasis (in particular genital schistosomiasis) has been neglected in travellers, despite the risk of infection with certain types of increasingly-common travels such as rafting and other forms of ecotourism. 18% of asymptomatic travellers to Africa, exposed to freshwater and subsequently screened at the Hospital for Tropical Diseases in London, were found to have schistosomiasis. Katayama fever, fatigue and dysuria are the commonest presentations in symptomatic travellers. There are, however, a few case reports where genital schistosomiasis has been found years after a reasonably short exposure.
The manifestations of schistosomal disease in non-genital organs, immunological considerations, immunodiagnosis, S. haematobium parasite adaptation, snail control and schistosomiasis’ relationship to cancer are beyond the scope of this article. Although S. mansoni, S. intercalatum, S. japonicum and S. matthei may affect the genital organs and the magnitude of the problem is not known.
- WHO fact sheet on schistosomiasis Retrieved 2011-08-02.
- Report of an informal working group meeting on urogenital schistosomiasis and HIV transmission
- Statement – WHO Working Group on Urogenital Schistosomiasis and HIV Transmission, 1–2 October 2009
- Examining the Relationship between Urogenital Schistosomiasis and HIV Infection. PLoS NTDs: December 2011, Volume 5, Issue12, e1396
- World Health Organization Partners for Parasite Control website
- Wellcome animation of the life cycle of the parasite
- Schistosomiasis Control Initiative
- CONTRAST, a research project on optimized schistosomiasis control in Sub-saharan Africa
- World Health Organization Tropical Disease Research programme
- Cambridge University Schistosomiasis Research Group
- York University Schistosomiasis Research Group
- Links to Schistosomiasis pictures (Hardin MD/Univ of Iowa)
- FIOCRUZ - Schistomiasis Research Group
- Vacine developed in Queensland, Australia