Diagnostic markers in schistosomiasis

Deelder, André M.

doi:10.1590/s0074-02761992000900019

Cited by 6 publications

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“…1 Newer methods of diagnosis, including the detection of schistosomal antigens and eosinouria, are being explored. [8][9][10][11] However, the definitive diagnosis of S. haematobium infection usually is achieved by identification of the characteristic eggs in urinary and/or fecal sediment or tissue sections. The release of the miracidium from the egg is generally believed to occur in a fresh-water environment following egg passage.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic value of a miracidium in urinary sediment

et al. 1999

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Although rarely encountered in the United States, urinary tract schistosomiasis occurs commonly in many countries in the eastern hemisphere. Travel and immigration may contribute to imported cases of schistosomiasis. Excessive morbidity and increased mortality, including the development of urinary‐tract squamous‐cell carcinoma, are associated with untreated Schistosoma haematobium infection. Therefore, in the appropriate clinical context, all efforts should be made to rule out infectious and readily treatable causes of chronic hematuria. The presence of characteristic eggs in the urinary sediment is the usual means of diagnosing a S. haematobium infection. Additionally, the small and less commonly encountered miracidium stage of S. haematobium may also be present in the urine, which is another means of diagnosing urinary tract schistosomiasis. The present report describes a case in which a miracidium was detected in a fresh, unstained urine specimen. As detection of miracidia can be made in specimens also processed by routine cytologic methods, it behooves cytologists to be aware of this entity for the diagnosis of schistosomiasis. Diagn. Cytopathol. 1999;20:34–37. © 1999 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Diagnostic value of a miracidium in urinary sediment

et al. 1999

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“…A study reported that schistosomal carbohydrate antigens could be used as targets for vaccination and/or serodiagnosis of chronic schistosomiasis in humans (Nyame et al, 2003). Re-infection studies in schistosomiasis demonstrated increased levels of protective molecules like IgE which resist re-infection while increased IgG4 was related to high risk of re-infection (Deelder, 1992) this information can help in the treatment of patients in sero-epidemiological studies and vaccine trials.…”

Section: Diagnostic Markers or Biomarkers For Schistosomiasismentioning

confidence: 99%

Diagnostic Markers for Schistosome-Mediated Liver Disease

Manivannan¹

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<p>Chronic schistosomiasis presents with either a moderate or a severe form, termed intestinal (INT) or hepatosplenic (HS) schistosomiasis, respectively. The Schistosoma mansoni-associated hepatomegaly is estimated in 8.5 million people and ultimately results from liver granulomas induced by trapped parasitic eggs. The CBA/J mouse model replicates these two human disease forms and was used to understand the progressive pathology that leads to HS and to identify potential biomarkers. In this model 20% of infected mice spontaneously develop hypersplenomegaly syndrome (HSS) by 20 weeks of infection while the remaining 80% develop moderate splenomegaly syndrome (MSS). Using this model, we compared the liver protein patterns of control mice and mice infected for 6, 8, 12, or 20 (MSS and HSS) weeks. Two-dimensional differential in gel electrophoresis (2D-DIGE) was used to identify protein pattern variations and protein spots were identified using matrix adsorption laser desorption ionisation-time of flight (MALDI-TOF) mass spectrometry. In the first experiment, we found 124 protein spot unique changes for MSS and HSS compared to control mice of which 80 were identified and 35 changes were specific for HSS. In the second experiment, comparison between various time points with control mice revealed 76 significant protein spot changes of which 44 were identified using MALDI-TOF mass spectrometry. Importantly, we found that the abundance of liver keratin D, transferrin isoforms, collagen isoforms, hydroxyproline and Schistosoma mansoni-phosphoenolpyruvate carboxykinase increased while epoxide hydrolase isoforms, peroxiredoxin 6 and major urinary protein (MUP) isoforms decreased significantly with infection. To verify the changes in the liver 2D-DIGE analysis, candidate liver protein markers were measured in mouse serum using targeted biochemical assays. The mouse serum analysis showed MUP levels were decreased, while transferrin, connective tissue growth factor (CTGF), keratin D, hydroxyproline were increased in HSS mice compared to control mice or MSS mice supporting the liver 2D-DIGE analysis. Using targeted assays, serum samples from INT and HS patients were tested for the candidate liver protein markers: keratin D, CTGF, hydroxyproline and transferrin. The human serum analysis showed keratin D levels increased for HS compared to INT and normal sera. The CTGF levels were high in INT compared to HS and normal sera, while transferrin remained unchanged in INT and HS similar to normal sera. Additionally, in severe HS disease, serum hydroxyproline emerged as a strong indicator of fibrosis. We believe that these findings will have direct value in the development of diagnostic tools for early detection of hepatosplenic schistosomiasis in humans.</p>

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Genomic variation in Trypanosoma cruzi clonal cultures

1996

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Spontaneous changes in restriction DNA profiles and pulsed-field gel electrophoresis (PFGE) patterns, along with a concomitant loss of infectivity, were observed in infective clones of Trypanosoma cruzi strain Y either following a number of passages during the exponential growth phase of after subcloning in liver infusion tryptone (LIT) medium using as the probe a genomic fragment of the parasite (pMYP16), indicating naturally occurring rearrangements of DNA sequences. No variation could be detected when the genomic DNA was probed with conserved T. cruzi tubulin and actin genes. There was no correlation between such rearrangements and the life-cycle forms of the parasites, since trypomastigote forms showed the same karyotype and hybridization patterns as did epimastigote forms. The variations observed could be reverted and infectivity, recovered after inoculation of the parasites in newborn mice.

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Diagnostic markers in schistosomiasis

Cited by 6 publications

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Diagnostic value of a miracidium in urinary sediment

Diagnostic value of a miracidium in urinary sediment

Diagnostic Markers for Schistosome-Mediated Liver Disease

Genomic variation in Trypanosoma cruzi clonal cultures

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