Morbidity in schistosomiasis: an update.

Danish Bilharziasis Laboratory, Jaegersborg Alle 1D, 2920 Charlottenlund, Denmark.
Current Opinion in Infectious Diseases (Impact Factor: 5.03). 11/2004; 17(5):439-47. DOI: 10.1097/00001432-200410000-00009
Source: PubMed

ABSTRACT Schistosomiasis is an important poverty-related health problem and more than 200 million people are infected. This review summarizes papers from April 2003 to June 2004 with a focus on schistosomiasis morbidity and the various factors that affect the level of morbidity in endemic populations. The aim is to provide an update on the current state of knowledge and, hopefully, thereby stimulate continued research interest in this important area.
Research into the immune responses associated with severe morbidity has provided new insights into the mechanisms of immune regulation as well as the role of genetic predisposition to periportal fibrosis. Malaria and schistosomiasis are co-endemic and co-infection with malaria may increase the level of morbidity in hepatosplenic schistosomiasis, and alter the host immune response towards schistosome antigens. Schistosome infections may render the host more susceptible to human immunodeficiency virus infection by either interfering with immune responses or increasing the risk of transmission due to genital lesions. An important advance in schistosomiasis research, and parasite genomics, is the recent availability of two major Schistosoma mansoni and Schistosoma japonicum DNA bioinformatic resources.
Significant advances have been achieved in our understanding of the epidemiology, immunology and genetics of schistosomiasis, and the various factors that may influence morbidity. However, good research is vital for sustainable disease control, and continued progress requires a critical mass of researchers with a range of expertise from basic parasite biology to public-health interventions. It is therefore important to strengthen research capacity in endemic countries.

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    ABSTRACT: Schistosoma haematobium eggs can induce lesions in the urinary and genital tract epithelia, as eggs pass through or get trapped in the tissue. Local inflammatory reactions induced by S. haematobium eggs might affect the ability of bacteria to establish mucosal super-infection foci. S. haematobium infection and asymptomatic bacteriuria can both portray haematuria, proteinuria and leukocyturia. This shared set of proxy diagnostic markers could fuel routine misdiagnosis in S. haematobium endemic areas. Furthermore, S. haematobium infected individuals might be at a higher risk of contracting bacterial urinary tract infections, which could manifest either as symptomatic or asymptomatic bacteriuria. The aim of the current study was to explore whether schistosomal lesions are susceptible to super-infection by bacteria measured as asymptomatic bacteriuria. S. haematobium infection was determined by microscopy of urine samples. Furthermore, urine samples were tested with dipslides for asymptomatic bacteriuria and with dipsticks for haematuria, proteinuria and leukocytes. We found no association between asymptomatic bacteriuria and S. haematobium infection in a sample of 1040 female primary and high school students from a schistosomiasis endemic area in KwaZulu-Natal, South Africa. Furthermore, it was demonstrated that asymptomatic bacteriuria is not a bias for use of micro-haematuria as a proxy diagnostic measure for S. haematobium infection in this population.
    Acta Tropica 01/2015; 144:19-23. DOI:10.1016/j.actatropica.2015.01.008 · 2.52 Impact Factor
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    ABSTRACT: Schistosomes are parasitic worms that can survive in the hostile environment of the human bloodstream where they appear refractory to both immune elimination and thrombus formation. We hypothesize that parasite migration in the bloodstream can stress the vascular endothelium causing this tissue to release chemicals alerting responsive host cells to the stress. Such chemicals are called damage associated molecular patterns (DAMPs) and among the most potent is the proinflammatory mediator, adenosine triphosphate (ATP). Furthermore, the ATP derivative ADP is a pro-thrombotic molecule that acts as a strong activator of platelets. Schistosomes are reported to possess at their host interactive tegumental surface a series of enzymes that could, like their homologs in mammals, degrade extracellular ATP and ADP. These are alkaline phosphatase (SmAP), phosphodiesterase (SmNPP-5) and ATP diphosphohydrolase (SmATPDase1). In this work we employ RNAi to knock down expression of the genes encoding these enzymes in the intravascular life stages of the parasite. We then compare the abilities of these parasites to degrade exogenously added ATP and ADP. We find that only SmATPDase1-suppressed parasites are significantly impaired in their ability to degrade these nucleotides. Suppression of SmAP or SmNPP-5 does not appreciably affect the worms' ability to catabolize ATP or ADP. These findings are confirmed by the functional characterization of the enzymatically active, full-length recombinant SmATPDase1 expressed in CHO-S cells. The enzyme is a true apyrase; SmATPDase1 degrades ATP and ADP in a cation dependent manner. Optimal activity is seen at alkaline pH. The Km of SmATPDase1 for ATP is 0.4 ± 0.02 mM and for ADP, 0.252 ± 0.02 mM. The results confirm the role of tegumental SmATPDase1 in the degradation of the exogenous pro-inflammatory and pro-thrombotic nucleotides ATP and ADP by live intravascular stages of the parasite. By degrading host inflammatory signals like ATP, and pro-thrombotic signals like ADP, these parasite enzymes may minimize host immune responses, inhibit blood coagulation and promote schistosome survival.
    03/2014; 2:e316. DOI:10.7717/peerj.316
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    ABSTRACT: The effects of snail density on Biomphalaria alexandrina parasitized with Schistosoma mansoni were investigated. Laboratory experiments were used to quantify the impact of high density on snail growth, fecundity, and survival. Density-dependent birth rates of snails were determined to inform mathematical models, which, until now, have assumed a linear relationship between density and fecundity. The experiments show that the rate of egg-laying followed a negative exponential distribution with increasing density and this was significantly affected by exposure to parasitic infection. High density also affected the weight of snails and survival to a greater degree than exposure to parasitic infection. Although snail growth rates were initially constrained by high density, they retained the potential for growth suggesting a reversible density-dependent mechanism. These experimental data can be used to parameterise models and confirm that snail populations are regulated by nonlinear density-dependent mechanisms.
    Journal of Parasitology Research 06/2010; 2010(1-2). DOI:10.1155/2010/186792