REACTIVATION OF RICKETTSIA-RICKETTSII IN DERMACENTOR-ANDERSONI TICKS - AN ULTRASTRUCTURAL ANALYSIS

REACTIVATION OF RICKETTSIA-RICKETTSII IN DERMACENTOR-ANDERSONI TICKS - AN ULTRASTRUCTURAL ANALYSIS
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DOI:
10.1128/iai.37.2.779-785.1982
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发表时间:
1982-01-01
影响因子:
3.1
通讯作者:
BURGDORFER, W
BURGDORFER, W
中科院分区:
医学2区
文献类型:
--
作者:
HAYES, SF;BURGDORFER, W

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当豚鼠受到蜱虫媒介的生理应激(例如饥饿(越冬))时,安德氏立克次氏体中的强毒立克次体就会失去对豚鼠的致病性和毒力。受感染的蜱在高温(37°C)下孵育24-48小时或喂食一段时间(通常> 10小时)会诱导立氏立克次体恢复到有毒状态,这种现象被定义为重新激活。电镜显示,立克次体的微囊和粘液层会根据蜱虫媒介内的生理条件而发生变化。在充血的蜱虫中,微囊层很容易被识别为离散层,.apprx。 16 nm 厚,由周期性为 .apprx 的球状亚基组成。 10纳米。微囊层外部的粘液层在立克次体周围形成离散透明区域。在饥饿的蜱虫中,微囊层和粘液层都不是离散的实体。它们脱落并形成低电子密度的细丝、碎片和有点絮状的链,无周期性。 37℃孵育。 C或喂养饥饿的感染蜱会导致离散的微囊和粘液层的恢复。这些可逆的结构修饰与蜱宿主的生理变化有关,并与重新激活相关,即立克次体致病性和毒力的恢复。
Virulent R. rickettsii in D. andersoni lose their pathogenicity and virulence for guinea pigs when subjected to physiological stresses, such as starvation (overwintering), of its tick vector. Incubation of infected ticks at an elevated temperature (37.degree. C) for 24-48 h or feeding for a time (usually > 10 h) induces R. rickettsii to revert to a virulent state, a phenomenon defined as reactivation. EM reveals that the microcapsular and slime layers of R. rickettsii undergo changes dependent upon the physiological conditions within the tick vector. In engorged ticks, the microcapsular layer is readily identified as a discrete layer, .apprx. 16 nm thick, composed of globular subunits that have a periodicity of .apprx. 10 nm. The slime layer external to the microcapsular layer forms a discrete-lucent zone around the rickettsia. In starved ticks, neither the microcapsular layer nor slime layer remains a discrete entity. They are shed and form stringy, shredded and somewhat flocculent strands of low electron density without periodicity. Incubation at 37.degree. C or feeding of starved infected ticks results in the restoration of a discrete microcapsular and slime layer. These reversible structural modifications are linked to physiological changes in the tick host and correlate with reactivation, i.e., restoration of pathogenicity and virulence of R. rickettsii.