Hibiya Kenji, Higa Futoshi, Tateyama Masao, Fujita Jiro
Department of Medicine and Therapeutics, Control and Prevention of Infectious Diseases, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan.
Kekkaku. 2007 Dec;82(12):903-18.
Mycobacterium avium complex (MAC) causes respiratory tract infections and develops granulomatous lesions in the alveolar areas and bronchioles in humans. In contrast with the above, the intestinal tract is the primary infection site of immunocompromised hosts, such as patients with acquired immune deficiency syndrome (AIDS), or animals, such as pigs. Recent studies have revealed that hosts with hereditary dysfunction of mediators in the Th-1 cascade as well as hosts with a high titer of auto-antibodies against interferon-gamma are susceptible to MAC, and such hosts facilitate dissemination of MAC. However, their disseminated lesions are formed mainly in the lung or in soft tissues, and the mechanism of development of MAC in such host may be different from that of AIDS-related MAC infection. In this review, we specifically discuss the development mechanism of disseminated MAC disease in recently-identified several pathological conditions.
鸟分枝杆菌复合群（MAC）可引起呼吸道感染，并在人类的肺泡区域和细支气管中形成肉芽肿性病变。与此相反，肠道是免疫功能低下宿主（如获得性免疫缺陷综合征患者）或动物（如猪）的主要感染部位。最近的研究表明，Th-1级联反应中介质存在遗传性功能障碍的宿主以及抗干扰素-γ自身抗体滴度较高的宿主易感染MAC，并且此类宿主会促进MAC的播散。然而，它们的播散性病变主要形成于肺部或软组织中，此类宿主中MAC的发生机制可能与艾滋病相关MAC感染的机制不同。在本综述中，我们特别讨论了在最近确定的几种病理状况下播散性MAC疾病的发生机制。
