Open Access Highly Accessed Research article

Exposure to malaria affects the regression of hepatosplenomegaly after treatment for Schistosoma mansoni infection in Kenyan children

Mark Booth1*, Birgitte J Vennervald2, Anthony E Butterworth3, Henry C Kariuki4, Clifford Amaganga5, Gachuhi Kimani6, Joseph K Mwatha6, Amos Otedo6, John H Ouma7 and David W Dunne1

Author Affiliations

1 Division of Microbiology and Parasitology, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK

2 Danish Bilharziasis Laboratory, Jægersborg Alle 1D, 2920 Charlottenlund, Denmark

3 Biomedical Research and Training Institute, P.O.Box CY 1753, Causeway, Harare, Zimbabwe

4 Division of Vector Borne Diseases, Ministry of Health, P. O Box 54840, Nairobi, Kenya

5 Kakamega Provincial Hospital, P.O. Box 560, Kakamega, Kenya

6 Kenya Medical Research Institute, Nairobi, Kenya

7 Maseno University, Kisumu, Kenya

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BMC Medicine 2004, 2:36  doi:10.1186/1741-7015-2-36

Published: 27 September 2004



Schistosoma mansoni and malaria infections are often endemic in the same communities in sub-Saharan Africa, and both have pathological effects on the liver and the spleen. Hepatosplenomegaly associated with S. mansoni is exacerbated in children with relatively high exposure to malaria. Treatment with praziquantel reduces the degree of hepatosplenomegaly, but the condition does not completely resolve in some cases. The present analysis focused on the possibility that exposure to malaria infection may have limited the resolution of hepatosplenomegaly in a cohort of Kenyan schoolchildren.


Ninety-six children aged 6–16, from one community in Makueni district, Kenya, were treated with praziquantel. At baseline, all children had hepatomegaly and most had splenomegaly. The source of S. mansoni infection, a river, was molluscicided regularly over the following three years to limit S. mansoni re-infection, whereas malaria exposure was uninterrupted. Hepatic and splenic enlargement was assessed annually outside the malaria transmission season.


Children living in an area of relatively high exposure to both infections presented with the largest spleens before treatment and at each follow-up. Spleens of firm consistency were associated with proximity to the river. The regression of hepatomegaly was also affected by location, being minimal in an area with relatively low S. mansoni exposure but high exposure to malaria, and maximal in an area with relatively low exposure to both infections.


The outcome of treating cases of hepatosplenomegaly with praziquantel in this cohort of Kenyan children depended strongly on their level of exposure to malaria infection. Furthermore, a residual burden of hepatosplenic morbidity was observed, which was possibly attributable to the level of exposure to malaria. The results suggest that exposure to malaria infection may be a significant factor affecting the outcome of praziquantel treatment to reduce the level of hepatosplenic morbidity.