Morbidity in schistosomiasis: An update
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.
Available from: Per Kallestrup
- "Chronic SH infection primarily affects the urogenital organs (Edington et al. 1975; Gelfand et al. 1970, 1971; Considering treatment of male genital schistosomiasis as a tool for future HIV prevention: a… Vennervald and Dunne 2004). Histopathological changes, including inflammatory lesions in the prostate and seminal vesicles without a correlation between egg load and grade of inflammation, have been established (Gelfand et al. 1970; Patil and Elem 1988). "
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ABSTRACT: Male genital schistosomiasis (MGS) is a neglected manifestation of Schistosoma haematobium infection with ignored implications on reproductive health and a differential diagnosis to sexually transmitted infections in endemic regions. MGS may have associations with HIV transmission and acquisition, and treatment could be a neglected chance of HIV prevention. This review summarizes current knowledge on epidemiology, clinical manifestations, diagnosis and treatment of MGS as a hypothesized risk factor for HIV transmission. Future research areas of global interest are suggested.
PubMed published literature was reviewed based on the MOOSE guidelines. All publications on MGS were included regardless of publication year and study design. Furthermore, all publications were searched for information on possible HIV association.
The 40 identified publications related to MGS were dominated by case reports and observational studies. No randomized clinical trials have been conducted to date, and very scant information related to possible associations with HIV transmission was presented.
Clinical, randomized studies and epidemiological studies covering the possible association between MGS and HIV are urgently needed. Furthermore, field diagnostic tools should be developed and future mass treatment programs should include adults to reduce morbidity and prevent HIV acquisition.
Available from: Michal Kuczma
- "A characteristic pathological manifestation of schistosomiasis is the granulomatous response against tissue-or organ-trapped parasite eggs (ova) (Pearce and MacDonald, 2002). In particular, the formation of hepatic egg granulomas and secondary hepatic fibrosis are the primary cause of death in schistosomiasis (Vennervald and Dunne, 2004). Soluble egg antigen (SEA) originating from the eggs of Schistosoma japonicum is potent enough to evoke pro-inflammatory responses by recruiting macrophages into the liver, which then initiate granuloma formation to limit the immune responses against SEA to the location of the trapped egg in the liver (Burke et al., 2010; Qiu et al., 2001; Shimaoka et al., 2007). "
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ABSTRACT: Acute schistosomiasis is featured by pro-inflammatory responses against tissue or organ trapped parasite ova along with granuloma formation. Herein in the present report we conducted studies in Cx3cr1(-/-) mice and demonstrated the role of Cx3cr1 in the pathoetiology of granuloma formation during acute schistosomiasis. Mice deficient in Cx3cr1 were protected from S. japonicum egg-induced granuloma formation and hepatic injury as manifested by reduced body weight loss, attenuated hepatomegaly along with preserved liver function. Notably, S. japonicum infection induced high levels of hepatic Cx3cr1 expression, which was predominantly expressed by infiltrating macrophages. Loss of Cx3cr1 rendered macrophages preferentially toward M2 polarization, which then led to a characteristic switch of host immune defense in the setting of acute schistosomiasis from a conventional Th1 to typical Th2 response. This immune switch caused by Cx3cr1 deficiency was likely associated with enhanced STAT6/PPAR-γ signaling and increased IDO expression. Together, our data provided feasible evidence supporting that CX3CR1 could be a viable therapeutic target for treatment of acute schistosomiasis.
© 2015. Published by The Company of Biologists Ltd.
- "The associated morbidity poses diverse challenges and a heavy impact on local public health services. S. haematobium associated morbidity range from subtle to severe (Vennervald and Dunne, 2004; Khalaf et al., 2012). It can typically present with anaemia, stunted growth, and cognitive impairment in children, as well as with organ specific manifestations such as genital and urinary tract lesions. "
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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.
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