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A. Dessein, Immunology and Genetics of Parasitic Diseases, INSERM, U. 399, Marseille, France,
B. Bucheton, Immunology and Genetics of Parasitic Diseases, INSERM, U. 399, Marseille, France,
L. Argiro, Immunology and Genetics of Parasitic Diseases, INSERM, U. 399, Marseille, France,
N. M. A. Elwali, Institute of Nuclear Medicine and Molecular Biology, University of Gezira, Wad Medani, Sudan,
V. Rodrigues, Laboratory of Immunology, University of Medicine, Triangulo Miniero, Uberaba, Brazil,
C. Chevillard, Immunology and Genetics of Parasitic Diseases, INSERM, U. 399, Marseille, France,
S. Marquet, Immunology and Genetics of Parasitic Diseases, INSERM, U. 399, Marseille, France,
H. Dessein, Immunology and Genetics of Parasitic Diseases, INSERM, U. 399, Marseille, France,
S. H. El-Safi, Institute for Tropical Medicine, PO Box 1304, Khartoum, Sudan,
L. Abel, Laboratory of Human Genetics of Infectious Diseases, INSERM, U. 550, Paris, France
SUSCEPTIBILITY TO SEVERE DISEASE DURING AN OUTBREAK OF VISCERAL LEISHMANIASIS IN A SUDANESE VILLAGE
Visceral leishmaniasis (VL) is caused by protozoan parasites of the Leishmania genus that are transmitted to humans by infected sandflies (Figure 10.1a). Parasites rapidly invade host phagocytes and multiply inside phagolysosomes. Clinical disease is primarily due to the uncontrolled multiplication of the parasite in many organs including the spleen and the liver; clinical symptoms include recurrent fever, considerable splenomegaly, hepatomegaly, and adenopathy (1). Death is certain if the patient is left untreated. Violent outbreaks of VL have occurred in regions of eastern Africa (2) (Kenya, Sudan) and in India (Bihar). VL is endemic in South America and in the Mediterranean basin. VL is caused by three Leishmania species: Leishmania donovani, L. chagasi/infantum, and L. archibaldi (L. donovani being the most pathogenic) (3). To identify the principal risk factors in VL, we carried out a five-year longitudinal study on 1,600 subjects from a village located on the Sudanese–Ethiopian border. The study was initiated in 1995 when the number of VL cases had just begun to rise in the village (4). Within five years, 28% of the population had been affected by VL. Most of these VL patients were treated and cured. Unfortunately, a small percentage either failed to respond to treatment or were not treated because of the difficulties involved in reaching them during the rainy season.
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