Schistosomiasis or bilharzia is a tropical disease caused by worms of the genus Schistosoma. The transmission cycle requires contamination of surface water by excreta, specific freshwater snails as intermediate hosts, and human water contact. The main disease-causing species are S haematobium, S mansoni, and S japonicum. According to WHO, 200 million people are infected worldwide, leading to the loss of 1.53 million disability-adjusted life years, although these figures need revision. Schistosomiasis is characterised by focal epidemiology and overdispersed population distribution, with higher infection rates in children than in adults. Complex immune mechanisms lead to the slow acquisition of immune resistance, though innate factors also play a part. Acute schistosomiasis, a feverish syndrome, is mostly seen in travellers after primary infection. Chronic schistosomal disease affects mainly individuals with long-standing infections in poor rural areas. Immunopathological reactions against schistosome eggs trapped in the tissues lead to inflammatory and obstructive disease in the urinary system (S haematobium) or intestinal disease, hepatosplenic inflammation, and liver fibrosis (S mansoni, S japonicum). The diagnostic standard is microscopic demonstration of eggs in the excreta. Praziquantel is the drug treatment of choice. Vaccines are not yet available. Great advances have been made in the control of the disease through population-based chemotherapy but these required political commitment and strong health systems.

a v a i l a b l e a t w w w . s c i e n c e d i r e c t . c o m j o u r n a l h o m e p a g e : h t t p : / / w w w . e l s e v i e r . c o m / l o c a t e / t r s t m h Summary Soil-transmitted helminths of the genus Strongyloides (S. fuelleborni and the more prevalent S. stercoralis) are currently believed to infect an estimated 30-100 million people worldwide. The health consequences of S. stercoralis infections range from asymptomatic light infections to chronic symptomatic strongyloidiasis. Uncontrolled multiplication of the parasite (hyperinfection) and potentially life-threatening dissemination of larvae to all internal organs is found among individuals with compromised immune system functions. This paper provides an overview of the current state of the art in relation to diagnostic methods for detecting the infection, the morbidity caused by the infection and the recommended treatment. It further discusses some of the reasons why this infection is so neglected and the consequence of this for the estimated global prevalence. The paper finally points to the gaps in our knowledge and future research needs related to this infection. As Strongyloides infections have the potential to develop into severe disease in certain population subgroups, untreated infections could cause serious problems in the community. Therefore, we need to carefully investigate this parasite in order to develop and implement effective control programmes. REVIEW Strongyloidiasis

A real-time PCR method targeting the small subunit of the rRNA gene was developed for the detection of Strongyloides stercoralis DNA in faecal samples, including an internal control to detect inhibition of the amplification process. The assay was performed on a range of well-defined control samples (n=145), known positive faecal samples (n=38) and faecal samples from a region in northern Ghana where S. stercoralis infections are highly endemic (n=212), and achieved 100% specificity and high sensitivity. The use of this assay could facilitate monitoring the prevalence and intensity of S. stercoralis infections during helminth intervention programs. Moreover, the use of this assay in diagnostic laboratories could make the introduction of molecular diagnostics feasible in the routine diagnosis of S. stercoralis infections, with a two-fold increase in the detection rate as compared with the commonly used Baermann sedimentation method.

Schistosomiasis is a disease of great medical and veterinary importance in tropical and subtropical regions, caused by parasitic flatworms of the genus Schistosoma (subclass Digenea). Following major water development schemes in the 1980s, schistosomiasis has become an important parasitic disease of children living in the Senegal River Basin (SRB). During molecular parasitological surveys, nuclear and mitochondrial markers revealed unexpected natural interactions between a bovine and human Schistosoma species: S. bovis and S. haematobium, respectively. Hybrid schistosomes recovered from the urine and faeces of children and the intermediate snail hosts of both parental species, Bulinus truncatus and B. globosus, presented a nuclear ITS rRNA sequence identical to S. haematobium, while the partial mitochondrial cox1 sequence was identified as S. bovis. Molecular data suggest that the hybrids are not 1st generation and are a result of parental and/or hybrid backcrosses, indicating a stable hybrid zone. Larval stages with the reverse genetic profile were also found and are suggested to be F1 progeny. The data provide indisputable evidence for the occurrence of bidirectional introgressive hybridization between a bovine and a human Schistosoma species. Hybrid species have been found infecting B. truncatus, a snail species that is now very abundant throughout the SRB. The recent increase in urinary schistosomiasis in the villages along the SRB could therefore be a direct effect of the increased transmission through B. truncatus. Hybridization between schistosomes under laboratory conditions has been shown to result in heterosis (higher fecundity, faster maturation time, wider intermediate host spectrum), having important implications on disease prevalence, pathology and treatment. If this new hybrid exhibits the same hybrid vigour, it could develop into an emerging pathogen, necessitating further control strategies in zones where both parental species overlap.

keywords Schistosoma mansoni, praziquantel, resistance correspondence Y.S. Liang, Jiangsu Institute of Parasitic Diseases, Meiyuan, Wuxi, Jiangsu 214064, P. R.China.The tolerance of Schistosoma mansoni to praziquantel has been reported in some endemic regions (Fallon et al. 1995;Stelma et al. 1995;Ismail et al. 1996;Guisse et al. 1997). To establish the reasons for clinical failures of praziquantel, a simple, quick and economic assay is required to detect resistance. Ideally this will involve the use of eggs or miracidia since these are the stages of the parasite life cycle which can easily be obtained from the faecal material of infected humans. As praziquantel causes changes in the shape of miracidia (Coles 1979), this was used as the basis for designing a test for resistance.In 24-well flat bottom microplates we observed the effect of praziquantel on miracidia hatched from eggs obtained from the faeces of mice infected with six isolates of S. mansoni. Two isolates were praziquantel-susceptible (one from Puerto Rico and one a mixture of isolates from Puerto Rico, Brazil, Egypt and Kenya), and four isolates were praziquantelinsusceptible, including a laboratory-selected praziquantelresistant population (Fallon & Doenhoff 1994) and three Senegalese isolates. The cessation of swimming of miracidia was observed in different concentrations of praziquantel at various times and then the morphological changes were checked by adding a drop of Lugol's iodine.When the miracidia of both the susceptible and insusceptible isolates were exposed to 10 -3 and 10 -4 M praziquantel, they immediately contracted in the middle part of their bodies, giving the shapes of an unequal dumbbell or calabash, with the greater mass at the anterior end. In 5 ϫ 10 -6 M praziquantel 100% of miracidia from the susceptible isolates immediately changed shape, whereas only 11-15% of those from the insusceptible isolates did. Thus by addition of Lugol's iodine immediately after administering praziquantel, an objective measure of susceptibility could be obtained. After 1 minute in 10 Ϫ6 M praziquantel 52% to 100% of susceptible miracidia had changed shape, and after 5 min 100% had done so compared with 3% to 15% and 9% to 18% of the insusceptible miracidia. Susceptibility could also be detected by determining whether miracidia had stopped swimming but this was less easy to read as a test than change in shape.By exposing freshly hatched miracidia to 10 Ϫ6 M praziquantel and observing change in shape over one minute it should be possible to determine whether failed therapy is due to the presence of praziquantel-tolerant worms. It is planned to investigate this in field trials in China. The work was supported by the UNDP/World Bank/WHO Special Programmme for Research and Training in Tropical Diseases. ReferencesColes GC (1979) The effect of praziquantel on Schistoma mansoni. Journal of Helminthology 53, 31-33. Fallon PG, Sturrock RF, Niang AC, Doenhoff MJ (1995) Short report: diminished susceptibility to praziquantel in a Senegal isolate of Schistosoma ...