Fong I W, Chiu B, Viira E, Fong M W, Jang D, Mahony J
Department of Medicine, St. Michael's Hospital, Toronto, Ontario, Canada.
J Clin Microbiol. 1997 Jan;35(1):48-52. doi: 10.1128/jcm.35.1.48-52.1997.
A rabbit model was established for Chlamydia pneumoniae infection that may be helpful to understand the pathogenesis of disease in humans. Twelve, pathogen-free, 1-month-old New Zealand White rabbits were inoculated with 1.0 x 10(7) to 5.0 x 10(7) CFU of purified C. pneumoniae (ATCC strain VR 1310) via the nasopharynx (1 rabbit died immediately postinoculation, and 11 were available for study). Five controls were inoculated with the carrier buffer. Ten of the 11 study rabbits demonstrated serological evidence of acute infection (immunoglobulin G antibodies, 1:8 to > 1:16), with the weakest response at 7 days and the strongest response at 28 days, whereas none of the controls showed any seroconversion. Study animals were sacrificed in batches of three, on days 7, 14, 21, and 28, but controls were sacrificed on days 7 and 28. Two-thirds of the animals demonstrated evidence of bronchiolitis and pneumonia on days 7 and 14 and resolution by day 21. Two study rabbits demonstrated, on histology, early and intermediate lesions of atherosclerosis: one animal (day 7) showed the accumulation of foamy macrophages (fatty streak) in the arch of the aorta, and the other animal (day 14) showed spindle cell proliferation of smooth muscle cells (intermediate lesion). Focal periaortitis was seen in the same animal (day 7). C. pneumoniae elementary bodies were demonstrated by immunocytochemical stain in the lungs (n = 2), liver (n = 3), spleen (n = 5), and aorta (n = 2), one of which corresponded to the intermediate lesion. C. pneumoniae was cultured from the lungs (n = 2), liver (n = 2), spleen (n = 2), and aortic arch (n = 1). All histopathological, immunocytochemical, and cultural studies were negative in the controls. Hence, the rabbit provides a useful animal model for the study of C. pneumoniae infection and its complications, particularly atherosclerosis.
建立了肺炎衣原体感染的兔模型,这可能有助于了解人类疾病的发病机制。12只1月龄的无特定病原体的新西兰白兔经鼻咽接种1.0×10⁷至5.0×10⁷CFU的纯化肺炎衣原体(ATCC菌株VR 1310)(1只兔子接种后立即死亡,11只可供研究)。5只对照兔接种载体缓冲液。11只研究兔中有10只出现急性感染的血清学证据(免疫球蛋白G抗体,1:8至>1:16),7天时反应最弱,28天时反应最强,而对照兔均未出现血清转化。研究动物在第7、14、21和28天分批处死3只,但对照兔在第7天和28天处死。三分之二的动物在第7天和14天出现细支气管炎和肺炎的证据,并在第21天消退。2只研究兔在组织学上表现为动脉粥样硬化的早期和中期病变:1只动物(第7天)在主动脉弓处出现泡沫巨噬细胞积聚(脂纹),另1只动物(第14天)出现平滑肌细胞梭形细胞增殖(中期病变)。同一只动物(第7天)可见局灶性主动脉周炎。通过免疫细胞化学染色在肺(n = 2)、肝(n = 3)、脾(n = 5)和主动脉(n = 2)中发现肺炎衣原体原体,其中1例与中期病变相对应。从肺(n = 2)、肝(n = 2)、脾(n = 2)和主动脉弓(n = 1)中培养出肺炎衣原体。所有组织病理学、免疫细胞化学和培养研究在对照兔中均为阴性。因此,兔为研究肺炎衣原体感染及其并发症,特别是动脉粥样硬化提供了有用的动物模型。