Lammerding A M, Glass K A, Gendron-Fitzpatrick A, Doyle M P
Food Research Institute, University of Wisconsin, Madison 53706.
Appl Environ Microbiol. 1992 Dec;58(12):3991-4000. doi: 10.1128/aem.58.12.3991-4000.1992.
A pregnant mouse model was developed to follow the course of infection after peroral inoculation with six different strains of Listeria monocytogenes and one strain of Listeria innocua. Tissues were sampled and analyzed by microbiologic and histologic methods for 5 days postinoculation. In gnotobiotic pregnant BALB/c mice, L. monocytogenes Scott A (SA), serotype 4b, colonized the gastrointestinal tract, translocated to the livers and spleens of mice by day 1 postinoculation, and multiplied in these tissues until day 4. Infection of the placental tissues occurred by days 3 and 4 and was followed by infection of the fetuses. Little damage of colonic and cecal tissues was evident by histologic examination. Livers and spleens showed a cellular immune response; a similar immune response was not detected in the placentas or fetuses. A rough variant of L. monocytogenes SA which was as virulent as the parent strain in mice when injected intraperitoneally was less virulent perorally and did not consistently infect the fetuses. L. monocytogenes ATCC 19113, serotype 3a, did not colonize the gastrointestinal tract, nor was it isolated from any internal tissue. L. monocytogenes strains of serotypes 1/2a and 1/2b behaved like the SA strain in this mouse model. L. innocua colonized the gastrointestinal tract and translocated to the livers and spleens but did not survive in these organs and rapidly disappeared without infecting placental and fetal tissues. In comparison with gnotobiotic mice, conventional pregnant mice inoculated with L. monocytogenes strains showed less consistent infection. These results suggest that the gnotobiotic pregnant mouse is a useful model for detecting differences in virulence relating to colonization, invasiveness, and uteroplacental infection which cannot be detected by intraperitoneal inoculation of mice.
构建了一个怀孕小鼠模型,用于追踪经口接种六种不同单核细胞增生李斯特菌菌株和一种无害李斯特菌菌株后的感染过程。接种后5天,通过微生物学和组织学方法对组织进行采样和分析。在无菌怀孕BALB/c小鼠中,4b血清型的单核细胞增生李斯特菌斯科特A(SA)菌株定殖于胃肠道,接种后第1天转移至小鼠的肝脏和脾脏,并在这些组织中繁殖直至第4天。胎盘组织在第3天和第4天发生感染,随后胎儿受到感染。组织学检查显示结肠和盲肠组织几乎没有损伤。肝脏和脾脏表现出细胞免疫反应;在胎盘或胎儿中未检测到类似的免疫反应。单核细胞增生李斯特菌SA的一个粗糙变体,经腹腔注射时在小鼠中的毒力与亲本菌株相同,但经口时毒力较低,且不能持续感染胎儿。3a血清型的单核细胞增生李斯特菌ATCC 19113未在胃肠道定殖,也未从任何内部组织中分离出来。在该小鼠模型中,1/2a和1/2b血清型的单核细胞增生李斯特菌菌株的表现与SA菌株相似。无害李斯特菌定殖于胃肠道并转移至肝脏和脾脏,但在这些器官中无法存活,并迅速消失,未感染胎盘和胎儿组织。与无菌小鼠相比,接种单核细胞增生李斯特菌菌株的常规怀孕小鼠的感染情况不太一致。这些结果表明,无菌怀孕小鼠是一种有用的模型,可用于检测与定殖、侵袭性和子宫胎盘感染相关的毒力差异,而这些差异通过小鼠腹腔接种无法检测到。