Schütte Daniela, Pluschke Gerd
Swiss Tropical Institute, Basel, CH 4002, Switzerland.
Expert Opin Biol Ther. 2009 Feb;9(2):187-200. doi: 10.1517/14712590802631854.
Buruli ulcer is a necrotizing skin disease caused by Mycobacterium ulcerans. Major necrosis with abundant clusters of extracellularly replicating mycobacteria and only minor leukocyte infiltration are characteristic histopathologic features of the disease. Mycolactone, a cytotoxic macrolide exotoxin of M. ulcerans, plays a key role in the development of this pathology. Antimicrobial therapy, such as rifampicin/streptomycin that was recently introduced, seems to lead to phagocytosis of mycobacteria and massive leukocyte infiltration, which culminates in the development of ectopic lymphoid structures in the lesions. Whereas the curative effect of the antibiotic treatment may be supported by immune defense mechanisms, persisting mycobacterial antigens and immunostimulators occasionally also seem to cause apparent reactivation of the disease. This seems to be related to excessive immunostimulation rather than to incomplete killing of the pathogen.
布鲁里溃疡是由溃疡分枝杆菌引起的一种坏死性皮肤病。主要坏死伴有大量细胞外复制的分枝杆菌簇且仅有少量白细胞浸润是该疾病的特征性组织病理学特征。溃疡分枝杆菌的细胞毒性大环内酯外毒素——分枝杆菌内酯，在这种病理发展过程中起关键作用。最近引入的抗菌疗法，如利福平/链霉素，似乎会导致分枝杆菌的吞噬作用和大量白细胞浸润，最终在病变部位形成异位淋巴结构。虽然抗生素治疗的疗效可能得到免疫防御机制的支持，但持续存在的分枝杆菌抗原和免疫刺激剂偶尔似乎也会导致疾病明显复发。这似乎与过度免疫刺激有关，而不是病原体未被完全杀灭。
