1. Presented By: Devin & Matt & Bruce
Human Schistosomes
Presented By:
Devin & Matt & Bruce

2. *Background*
Schistosome: A parasitic trematode worm contracted from infested water that is capable of causing liver, gastrointestinal tract and bladder disease.
Three main species of these trematode worms (flukes) Schistosoma mansoni, S. haematobium, and S. japonicum, that produce disease in humans.
Schistosomiasis or bilharzia after the German physician Theodor Bilharz ( ). Nickname “Bill Harris” by British soldiers serving in Europe during WWI.

3. *Morphology*

4. Morphology

5. *Morphology (eggs)* S. haematobium S. mansoni S.japonicum
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Trends in Immunology Volume 24, Issue 4, April 2003, Pages Abstract Full Text + Links PDF (59 K)         Related Articles in ScienceDirect Hepatic Changes in Congenital Schistosoma japonicum Inf... Journal of Comparative Pathology
 Hepatic Changes in Congenital Schistosoma japonicum Infections in Pigs Journal of Comparative Pathology, Volume 136, Issue 4, May 2007, Pages T. Iburg, M.V. Johansen, P.S. Leifsson, A.L. Willingham and R. Lindberg Abstract Summary
The inflammatory response in liver tissue from piglets congenitally infected with Schistosoma japonicum was examined at two different timepoints after infection. The piglets, which were the offspring of three sows infected with 9000 S. japonicum cercariae in the 10th week of gestation, were allocated into two groups (n=9 and 17) killed 5 or 11 weeks after birth, respectively. All piglets developed a low level infection,with no significant difference between the groups. Inflammatory lesions in the liver consisted mainly of granulomas in portal areas, often obliterating the portal veins, and frequently with central eggs or egg remnants. The granulomatous reaction consisted of epithelioid cells and occasional giant cells surrounded by layers of lymphocytes, eosinophils, plasma cells, and various amounts of collagen and fibroblasts. Mild to moderate infiltration of portal and septal connective tissue with eosinophils and lymphocytes was common, but the connective tissue was generally not increased. At the two timepoints, slight differences were observed in the numbers of eosinophils and lymphocytes in the granulomas and in the size of the granulomatous reaction. The same pattern of immunohistochemical labelling was seen in both groups. CD79α+ B cells were scarce except in granuloma-associated lymphoid follicles;the majority of lymphocytes in granulomas and at other sites were CD3ε+ T cells. The granulomatous reaction in the livers of piglets to schistosoma eggs from prenatal S. japonicum infection was similar to that seen in postnatal infection. Signs of immunomodulation of granulomas between the two timepoints of infection were not demonstrable.
Abstract | Full Text + Links | PDF (860 K)
The schistosome egg granuloma: immunopathology in the c... Transactions of the Royal Society of Tropical Medicine ...
 The schistosome egg granuloma: immunopathology in the cause of host protection or parasite survival? Transactions of the Royal Society of Tropical Medicine and Hygiene, Volume 80, Issue 4, 1986, Pages M. J. Doenhoff, O. Hassounah, H. Murare, J. Bain and S. Lucas Abstract The granulomatous inflammatory response induced by schistosome eggs entrapped in the microvasculature of host tissues is considered responsible for much of the symptomatology of schistosomiasis. However, the evolutionary role of the egg granuloma in the host-parasite relationship is not yet well defined. Some evidence indicates that the lesion may protect the host, either by shielding tissues against toxic egg products, or by interfering with the migration patterns of secondary infections, and thereby non-specifically contributing to the host's acquired “immunity”. We here review earlier work concerned with the role of the egg granuloma in the host-parasite relationship in schistosomiasis, and we present new experimental evidence to suggest that the function of this cell-mediated immune response might, in addition to its putative host protective function, facilitate the extravasation of parasite eggs in the mesenteries, and thereby contribute directly to the continuation of the schistosome life-cycle.
Abstract | Abstract + References | PDF (2801 K)
The host's genetic background determines the extent of ... Acta Tropica
 The host's genetic background determines the extent of angiogenesis induced by schistosome egg antigens Acta Tropica, Volume 99, Issues 2-3, October 2006, Pages Koen K. Van de Vijver, Cecile G. Colpaert, Werner Jacobs, Kristel Kuypers, Cornelis H. Hokke, André M. Deelder and Eric A. Van Marck Abstract Schistosomiasis is characterised by periovular granuloma formation within the portal tract and presinusoidal venules. As inflammation wanes, continued attempts to wall off and repair hepatic injury, lead to the development of extensive fibrosis. The codependence of chronic inflammation and angiogenesis is a well-known phenomenon. Neovascularisation is a complex process of endothelial cell proliferation and remodelling of the extracellular matrix. Previous studies demonstrated the ability of schistosome soluble egg antigens (SEAs) to stimulate endothelial cell activation in vitro. In the present study, we investigated the angiogenic potential of SEA in Swiss and BALb/c mice, after infection with Schistosoma mansoni or S. haematobium and by implanting SEA-coated beads into the murine liver. Anti-CD34 and anti-Ki-67 immunohistochemical stainings demonstrated newly formed blood vessels within and at the periphery of the granulomas. However, in one third of the granulomas the pre-existing portal stroma was not destroyed by the granulomatous inflammation, angiogenesis was minimal or absent and further growth of the granuloma was prevented. In C57BL/6J and C3H/HeN inbred mice, this polarisation was even more pronounced. In 91% of the granulomas in C57BL6/J mice the portal stroma was preserved. These mice had significantly smaller granulomas, less fibrosis and less mortality as compared to the high pathology C3H/HeN mice, where 87% of the granulomas were of the angiogenic type with destruction of the pre-existing stroma, leading to more severe chronic pathology. Thus, host's genetic mechanisms regulating the degree of angiogenesis and fibrosis, determine the severity of schistosome-induced pathology.
Abstract | Full Text + Links | PDF (890 K)
Immunoregulation within the granulomas of murine schist... Microbes and Infection
 Immunoregulation within the granulomas of murine schistosomiasis mansoni Microbes and Infection, Volume 1, Issue 7, June 1999, Pages Joel V. Weinstock, David Elliott, Ahmed Metwali, Arthur Blum, Jie Li, Khurram Qadir and Matyas Sandor Abstract | Full Text + Links | PDF (230 K)
Subcutaneous implantation of the spleen as a new techni... Transactions of the Royal Society of Tropical Medicine ...
 Subcutaneous implantation of the spleen as a new technique for experimental induction of hepatic Schistosoma mansoni egg granulomas Transactions of the Royal Society of Tropical Medicine and Hygiene, Volume 80, Issue 4, 1986, Pages SanaàS. Botros, Nawal El-badrawi and E. H. El-raziky Abstract Schistosoma mansoni egg granulomas were induced in the livers of mice by injecting eggs into spleens which had been surgically exposed with their vascular beds intact. Subsequent return of the spleens to a subcutaneous site allows repeated injections of eggs into the liver if necessary.
Abstract | Abstract + References | PDF (177 K)
View More Related Articles View Record in Scopus Cited By in Scopus (1) doi: /S (03)        Copyright © 2003 Elsevier Science Ltd. All rights reserved.
Letters
Granulomas are not just gizmos for immunologists
S.japonicum

6. *Geographic Distribution*
S. mansoni -South America,Caribbean, Africa, Middle East
S. haematobium -Africa, Middle East
S. japonicum -Philippines, Japan,South Asia, Taiwan

8. *Definitive Host/ Intermediate Host*
Definitive host: Human
Intermediate host: Snail
Biomphalaria (S. mansoni)
Bulinus (S. haematobium)
Oncomelania (S.japonicum)
Reservoirs: monkeys, rodents, cats, dogs, cattle, horses, swine, wild mammals.

9. *Life Cycle*

10. *Pathogenesis* S. mansoni most pathogenic
site of infection: veins of large intestine
S. haematobium
bloody urine
site of infection: veins of bladder
S. japonicum  
high morbidity
site of infection: veins of small intestine

11. *Clinical Symptoms* Migratory phase Symptomless
Acute phase (Katayama fever)
Chills, fever, fatigue, headache, muscle aches, cough, abdominal pain, diarrhea, and eosinophilia. 
Chronic phase
Bloody diarrhea, enlargement of liver and spleen, ascites, bloody urine, bladder cancer, kidney problems, CNS lesions

13. *Control & Prevention*
Education of the public
Sanatation of drinking water
Diagnosis and treatment
Management of the environment
Control of the intermediate hosts (freshwater snails)

16. *Diagnosis*
Microscopic identification of eggs in stool or urine (most practical)
Tissue biopsy- rectal or bladder biopsy may demonstrate eggs when stool or urine examinations are negative.
Antibody detection
Morphologic comparison with other intestinal parasites

17. *Treatment*
praziquantel -drug of choice, effective in the treatment of all forms of schistosomiasis, with virtually no side effects
Oxamniquine -used exclusively to treat intestinal schistosomiasis in Africa and South America
Metrifonate - effective for the treatment of urinary schistosomiasis
No vaccinations currently available

18. References