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苏丹的利什曼病。皮肤利什曼病。

Leishmaniasis in Sudan. Cutaneous leishmaniasis.

作者信息

el-Hassan A M, Zijlstra E E

机构信息

Department of Immunology and Clinical Pathology, Institute of Endemic Diseases, University of Khartoum, Khartoum, Sudan.

出版信息

Trans R Soc Trop Med Hyg. 2001 Apr;95 Suppl 1:S1-17. doi: 10.1016/s0035-9203(01)90216-0.

Abstract

Cutaneous leishmaniasis (CL) in Sudan is caused by Leishmania major, zymodeme LON-1. The disease is endemic in many parts of the country. The vector is Phlebotomus papatasi and the animal reservoir is probably the Nile rat Arvicanthis niloticus. Clinically, patients usually present with papules, nodules, or nodulo-ulcerative lesions, mainly on the exposed parts of the skin. In 20% of cases the parasite disseminates through the lymphatics, producing sporotrichoid-like lesions. The pathology of the lesion is described. Langerhans cells are the main antigen-presenting cells in CL. They pickup antigen from the dermis and migrate to regional lymph nodes where they present it to T cells. Antigen-specific activated T cells home to the dermis where they stimulate macrophages to eliminate the parasite. Peripheral blood mononuclear cells (PBMC) proliferate in response to Leishmania antigen in vitro and produce cytokines. PBMC of patients with mild and severe disease produce Th1- and Th2-like cytokine patterns, respectively. The criteria for the clinical diagnosis of CL are described. The diagnosis is confirmed by the demonstration of parasites in slit smears in 50-70% of cases and in histological sections in 70%. With primers specific for L. major, the polymerase chain reaction is positive in 86% of cases. Since CL is a self-limiting disease, treatment is confined to patients with severe disease.

摘要

苏丹的皮肤利什曼病(CL)由硕大利什曼原虫酶解模式LON-1引起。该病在该国许多地区呈地方性流行。传播媒介为巴氏白蛉,动物宿主可能是尼罗鼠。临床上,患者通常表现为丘疹、结节或结节溃疡性病变,主要出现在皮肤暴露部位。在20%的病例中,寄生虫通过淋巴管扩散,产生孢子丝菌样病变。描述了病变的病理学。朗格汉斯细胞是CL中的主要抗原呈递细胞。它们从真皮摄取抗原并迁移至局部淋巴结,在那里将抗原呈递给T细胞。抗原特异性活化T细胞归巢至真皮,在那里刺激巨噬细胞清除寄生虫。外周血单个核细胞(PBMC)在体外对利什曼原虫抗原产生增殖反应并分泌细胞因子。轻度和重度疾病患者的PBMC分别产生Th1样和Th2样细胞因子模式。描述了CL的临床诊断标准。在50%-70%的病例中,通过在刮片中发现寄生虫确诊,在70%的病例中通过组织切片确诊。使用针对硕大利什曼原虫的引物,聚合酶链反应在86%的病例中呈阳性。由于CL是一种自限性疾病,治疗仅限于重症患者。

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