Ambrose N C
Centre for Tropical Veterinary Medicine, University of Edinburgh, Midlothian, Scotland.
Trop Anim Health Prod. 1996 May;28(2 Suppl):29S-37S. doi: 10.1007/BF02310696.
Pathogen, host and environmental factors must be considered in order to understand the pathogenesis of dermatophilosis. A frequently cited sequence of events involves physical damage to the skin, bacterial multiplication in the epidermis, repeated cycles of invasion by hyphae, infiltration by neutrophils and exudate, regeneration of epidermis and reinvasion. This paper is concerned with pathogen driven mechanisms involved in the origin and development of Dermatophilus congolensis infections. Primary infections of calves under controlled conditions at clipped, cleaned, defatted sites result in characteristic dermatophilosis crusts, illustrating that D. congolensis itself is pathogenic. Calves infected in this way develop protective immune responses to subsequent infections. In contrast first and second infections of calves simultaneously infested with Amblyomma variegatum result in more severe lesions that take significantly longer to heal than lesions on tick free calves. Immunity to D. congolensis is isolate specific, however the antigens that elicit immunity have not been defined, they might include pathogenic or virulence factors. Hyphae are the life-cycle stage most closely associated with the living epidermis. During in vitro growth hyphae secrete antigens and proteolytic enzymes into culture medium. Proteolytic activity has been linked to virulence of D. congolensis. The characteristics of proteases released into culture medium varies between isolates. This raises the possibility that proteases, with as yet undefined functions, act as pathogenic and virulence factors, that they are the targets for protective immune responses and that A. variegatum infestation interferes with host immune responses that normally inhibit their activity.
为了理解嗜皮菌病的发病机制，必须考虑病原体、宿主和环境因素。一个经常被引用的事件序列包括皮肤的物理损伤、表皮中的细菌繁殖、菌丝反复入侵循环、中性粒细胞浸润和渗出、表皮再生以及再次入侵。本文关注刚果嗜皮菌感染的起源和发展中由病原体驱动的机制。在可控条件下，对剪毛、清洁、脱脂部位的犊牛进行原发性感染会导致典型的嗜皮菌病结痂，这表明刚果嗜皮菌本身具有致病性。以这种方式感染的犊牛会对随后的感染产生保护性免疫反应。相比之下，同时感染变异革蜱的犊牛首次和第二次感染会导致更严重的病变，愈合时间比无蜱犊牛的病变明显更长。对刚果嗜皮菌的免疫力具有菌株特异性，然而引发免疫的抗原尚未确定，它们可能包括致病或毒力因子。菌丝是与活表皮关系最密切的生命周期阶段。在体外生长过程中，菌丝会向培养基中分泌抗原和蛋白水解酶。蛋白水解活性与刚果嗜皮菌的毒力有关。分泌到培养基中的蛋白酶的特性因菌株而异。这就增加了一种可能性，即功能尚未明确的蛋白酶作为致病和毒力因子起作用，它们是保护性免疫反应的靶点，并且变异革蜱的侵染会干扰通常抑制其活性的宿主免疫反应。
