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Schistosomiasis in Travelers
By Mary-Louise Scully, MD
The growing awareness and interest in schistosomiasis among travelers to endemic areas was a topic of discussion at the recent eighth Conference of the International Society of Travel Medicine. In addition, there are several new relevant publications in this area.
Hewison and Jones from Edinburgh, Scotland, presented a study of the clinical aspects of 199 patients with positive Schistosoma haematobium serology, of whom 115 had swum in Lake Malawi (Abstract FC 08.02). Cough was the most common respiratory complaint occurring in two-thirds and in those with genitourinary (GU) symptoms; hematuria was present in 25% and urinary urgency or frequency in 20%. A subsequent discussion considered Eli Schwartz’s article on travelers with hematospermia due to schistosomiasis and the need to consider treatment with higher doses of praziquantel or a longer course of treatment.1 In Schwartz’s report, 3 of the 4 patients treated with praziquantel, at 40 mg/kg given in 2 divided doses, had an initial clinical response, but all 3 patients experienced relapse of S haematobium infection after several months. The 1 patient treated initially with a higher dose (60 mg/kg) did not experience a recurrence of infection. Unless a travel and exposure history are taken, the diagnosis of schistosomiasis can be easily missed.
Christoph Hatz of Switzerland gave an excellent overview of schistosomiasis (Sy 10.01). It is estimated that 200 million people are infected with schistosomiasis with at least 120 million being symptomatic and 20 million with severe disease. The European Network on Imported Infectious Diseases Surveillance (TropNetEurop) has just published its data of the first 3 years of sentinel surveillance for imported schistosomiasis.2 Not surprisingly, the majority of imported cases were from Africa, with the largest contributors at a country level being Malawi (14.4%), Ghana (13.5%), Mali (8.1%), Burkina Faso (5.7%), and Egypt (4.5%).
Turning toward prevention, data from N’Goran’s recent publication of the randomized, double-blind, placebo-controlled trial of oral artemether for the prevention of S haematobium infection were discussed.3 Artemether, a derivative of the antimalarial artemisinin, has been shown to have antischistosomal properties against the young developmental stages of schistosomal parasites. Praziquantel is not effective during this early period. Studies have previously demonstrated artemether to be safe and effective in preventing acute infection with Schistosoma japonicum and Schistosoma mansoni.4
N’Goran’s study was done in a village in the highly endemic area of Lake Taabo in the Ivory Coast. Artemether at a dose of 6 mg/kg, vs placebo, was given once monthly for 6 months to 322 children. These children had been pretreated with 2 systemic doses of praziquantel 4 weeks apart and found to be free of schistosome infection by examination of urine specimens. Previous work in the village had shown that at least 50% of placebo patients would become reinfected with S haematobium within 6 months. Surveillance for malaria parasitemia was performed every 4 weeks, and children who developed malaria were treated with a single oral dose of SP (25 mg/kg sulfadoxine and 0.75 mg/kg pyrimethamine). In the final cohort of 306 children, the incidence of S haematobium infection was 25% lower in the artemether group (artemether 76/156 vs placebo 97/150). Also, the patients who received artemether, but did become infected with S haematobium, had less intense infections than the placebo group (artemether, 3.4 eggs per 10 mL urine; placebo, 7.4 eggs per 10 mL urine). The incidence of reduction of S haematobium infection in this study was less than that previously reported for S japonicum and S mansoni. N’Goran suggests that the results might be improved by decreasing the artemether dosing interval to 3 weeks, which had been used in the S mansoni study.5
The potential use of artemether for prevention of schistosomiasis is only recommended in areas where schistosomiasis is endemic but malaria is not (certain parts of Brazil, China, Middle East, and North Africa). Artemether or other artemisinin derivatives should not be used for prevention or cure of schistosomiasis in areas where malaria and schistosomiasis are coendemic because of possible evolution of resistance in malaria parasites.
Another study of prevention was presented in a poster by Jackson et al, Schistosomiasis Prophalaxis Using DEET (PO 13.03). Fifteen subjects participated in an expedition to record the fauna of Lake Malawi, including the intermediate snail hosts for schistosomes. Their research would require wading, kayaking, and diving in wet suits into Lake Malawi. Previous in vitro studies in mouse tail skin had demonstrated that topical DEET in sufficient amounts will diffuse through skin and destroy cercariae as they migrate during the first 72 hours after exposure.6 A 50% DEET solution in ethyl alcohol (to achieve adequate dermal concentration) along with Ultrathon for mosquito protection, was applied nightly. Despite 2 patients reporting "swimmer’s itch," no new schistosome infections occurred during a 3-month follow-up. Two patients found to have positive serology on blood collected before the study were felt to be infected previously. More studies addressing the safety of such an approach and studies looking at different doses of DEET are clearly needed. However, this study raises some interesting possibilities in terms of potential product development that could combine protections against mosquitoes and schistosomes.
Edward Pearce, from the University of Pennsylvania, reported last month on the current situation in vaccine development for schistosomiasis.7 Many of the antigens that are still being tested in vaccine research were identified more than 10 years ago. One of these, glutathione S-transferase (GST), is in independent development by the Pasteur Institute. S haematobium GST, formulated as Bilhvax, has advanced through Phase I trials and is now in Phase II trials. However, all experimental vaccines for schistosomiasis to date have only been able to induce partial resistance to infection (ie, animals vaccinated harbor fewer parasites). Some encouraging studies in animals suggest a possible role for the cytokine, IL-12, as an adjuvant to induce complete protection. Pearce concludes by encouraging continued support for research in the basic biology and immune mechanisms of schistosomes, which hopefully will lead to advances in immunotherapy.
1. Schwartz E, et al. Hematospermia due to schistosome infection in travelers: Diagnostic and treatment challenges. Clin Infect Dis. 2002;35:1420-1424.
2. Grobusch M, et al. Imported schistosomiasis in Europe: Sentinel surveillance data from TropNetEurop. J Infect Dis. 2003;10:164-167.
3. N’Goran E, et al. Randomized, double-blind, placebo-controlled trial of oral artemether for the prevention of patent Schistosoma haematobium infections. Am J Trop Med Hyg. 2003;68:24-32.
4. Utzinger J, et al. The potential of artemether for the control of schistosomiasis. Int J Parasitol. 2001;31:1549-1562.
5. Utzinger J, et al. Oral artemether for prevention of Schistosoma mansoni infection: Randomized controlled trial. Lancet. 2000;355:1320-1325.
6. Salafsky B, et al. Evaluation of N, N-diethyl-m-toluamide (DEET) as a topical agent for preventing skin penetration by cercariae of Schistosoma mansoni. Am J Trop Med Hyg. 1998;58:828-834.
7. Pearce E. Progress toward a vaccine for schistosomiasis. Acta Tropica. 2003;86:309-313.
Mary-Louise Scully, MD Seattle.