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Mannose-binding lectin deficiency with eosinophilic meningoencephalitis due to Angiostrongylus cantonensis in children: a case series

Bárbara Padilla-Docal1, Alberto J Dorta-Contreras1, Raisa Bu-Coifiu-Fanego1, René H Martínez-Alderete1, Olga Susana de Paula-Almeida1, Hansotto Reiber2 and Jens Christian Jensenius3*

Author Affiliations

1 Faculty of Medical Sciences, "Dr Miguel Enriquez" Central Laboratory of Cerebrospinal Fluid (LABCEL), Havana Medical Sciences University, AP 10049, 11000 CP Havana City, Cuba

2 Neurochemistry Laboratory, Neurology Hospital, Georg August University, Göttingen, Germany

3 Department of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark

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Journal of Medical Case Reports 2011, 5:330  doi:10.1186/1752-1947-5-330

Published: 28 July 2011



Eosinophilic meningitis, a potentially fatal disease caused by Angiostrongylus cantonensis, is considered an emerging infectious disease.

Case presentation

Three Caucasian boys (aged five-years-old, 10-years-old and six-years-old) with a diagnosis of eosinophilic meningoencephalitis caused by Angiostrongylus cantonensis were studied. Serum immunoglobulin A (IgA), IgM, IgG, and complements C3c and C4 levels were quantified by using an immunodiffusion technique. Immunoglobulin E in serum was quantified by nephelometry and mannose-binding lectin by time-resolved fluorometry. Mannose-binding lectin deficiency was observed in the three patients. The first patient showed a reduction in the levels of IgA and IgM and an increase in the values of IgE and C4. The second patient showed a reduction in mannose-binding lectin level with increased IgG, C4 and IgE levels, and the third patient showed a decrease in mannose-binding lectin level and increased levels of IgM and complement C3c as well as a low level of C4.


To the best of our knowledge, this is the first report of mannose-binding lectin deficiency associated with Angiostrongylus cantonensis meningoencephalitis in children, and it may contribute to the understanding of the participation of this component of the lectin pathway in the development of the disease.