Epidemiology of visceral leishmaniasis in Atbara River area, eastern Sudan: the outbreak of Barbar El Fugara village (1996-1997)

被引:27
作者
El-Safi, SH
Bucheton, B
Kheir, MM
Musa, HAA
El-Obaid, M
Hammad, A
Dessein, A
机构
[1] INSERM, U399, Fac Med La Timone, F-13385 Marseille 05, France
[2] Univ Khartoum, Fac Med, Dept Microbiol & Parasitol, Khartoum, Sudan
[3] Univ Gezira, Fac Med, Wad Madani, Sudan
关键词
epidemiology; visceral leishmaniasis; Sudan; LST; DAT;
D O I
10.1016/S1286-4579(02)00026-6
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
An outbreak of visceral leishmaniasis (VL) started in 1995 in the Atbara River area in eastern Sudan. This article reports on this outbreak and on the clinical and immunological studies that were carried out in a village, with the highest incidence of VL cases, from 1996 to 1997. A significant increase in VL incidence was recorded in a dozen villages in this area; one village, Barbar El Fugara accounted for half of the total number of cases recorded at the regional hospital. A total of 152 VL and 61 post kala-azar dermal lesion (PKDL) cases were diagnosed and treated in Barbar. Household (n = 671) and school (n = 276) surveys were performed using the leishmanin skin test (LST) and the direct agglutination test (DAT). LST positivity was 23.1 and 15.7%, whereas DAT positivity was 8.9 and 26.4% in both surveys, respectively. No gender differences were observed in either test. Unlike DAT, LST positivity was predominant in the higher age groups that also exhibited lower prevalence of VL. Few individuals were positive by both tests (1.3%, 5.2%) while the majority (68.8%, 64.8%) had no evidence of acquired immune response, suggesting either a role of innate immunity in preventing parasite establishment or, unexpectedly, lack of exposure to Leishmania. Subclinical parasitism was also demonstrated, as evidence of both acquired Immoral and cellular immune responses was observed in individuals with no past history of the disease. The wide spectrum of L. donovani/human interactions may be explained by differential exposure to environmental risk factors, parasite strain polymorphisms or host genetic makeup. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved.
引用
收藏
页码:1439 / 1447
页数:9
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