Sampieri Francesca, Allen Andrew L, Pusterla Nicola, Vannucci Fabio A, Antonopoulos Aphroditi J, Ball Katherine R, Thompson Julie, Dowling Patricia M, Hamilton Don L, Gebhart Connie J
Department of Veterinary Biomedical Sciences (Sampieri, Antonopoulos, Ball, Dowling, Hamilton), Department of Veterinary Pathology (Allen), Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan; Department of Veterinary Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, California, USA (Pusterla); Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, Saint Paul, Minnesota, USA (Vannucci, Gebhart); Canadian Light Source, Saskatoon, Saskatchewan (Thompson).
Can J Vet Res. 2013 Apr;77(2):110-9.
The objective of this study was to demonstrate the susceptibility of rabbits to Lawsonia intracellularis obtained from a case of clinical equine proliferative enteropathy (EPE). This is a preliminary step toward developing a rabbit infection model for studying pathogenesis and therapy of EPE in horses. Nine does were equally assigned to 3 groups. Animals in 2 groups (Group 1 and Group 2) were orally inoculated with different doses of cell-cultured L. intracellularis. Controls (Group 3) were sham-inoculated. Feces and blood were collected before the rabbits were infected and at 7, 14, and 21 days post-infection (DPI). Serum immunoglobulin G (IgG) titers were measured using an immunoperoxidase monolayer assay (IPMA) and fecal samples were analyzed with quantitative polymerase chain reaction (qPCR). A doe from each group was euthanized at 7, 14, and 21 DPI for collection and evaluation of intestinal samples. Tissues were stained by routine hematoxylin and eosin (H&E) method and immunohistochemistry (IHC) with L. intracellularis-specific mouse monoclonal antibody. At 14 DPI, serologic responses were detected in both infected groups, which maintained high titers through to 21 DPI. Lawsonia intracellularis DNA was detected in the feces of Group 2 on 7 DPI and in both infected groups on 14 DPI. Gross lesions were apparent in Group 1 and Group 2 on 14 DPI. Immunohistochemistry confirmed L. intracellularis antigen within cells of rabbits in Group 1 and Group 2 on 7, 14, and 21 DPI. No lesions, serologic response, shedding, or IHC labeling were found in Group 3 rabbits. This study describes an EPE rabbit model that simulates natural infection, as typical lesions, immune response, and fecal shedding were present.
本研究的目的是证明家兔对从一例临床马增生性肠炎(EPE)病例中获得的胞内劳森菌的易感性。这是朝着开发用于研究马EPE发病机制和治疗方法的家兔感染模型迈出的初步步骤。将9只母兔平均分为3组。两组(第1组和第2组)动物经口接种不同剂量的细胞培养的胞内劳森菌。对照组(第3组)进行假接种。在兔子感染前以及感染后7天、14天和21天收集粪便和血液。使用免疫过氧化物酶单层试验(IPMA)测量血清免疫球蛋白G(IgG)滴度,并用定量聚合酶链反应(qPCR)分析粪便样本。在感染后7天、14天和21天,每组处死1只母兔以收集和评估肠道样本。组织用常规苏木精和伊红(H&E)方法以及用胞内劳森菌特异性小鼠单克隆抗体进行免疫组织化学(IHC)染色。在感染后14天,两个感染组均检测到血清学反应,这些反应一直维持到感染后21天仍保持高滴度。在感染后7天,第2组的粪便中检测到胞内劳森菌DNA,在感染后14天,两个感染组的粪便中均检测到该菌DNA。在感染后14天,第1组和第2组出现明显的肉眼病变。免疫组织化学证实,在感染后7天、14天和21天,第1组和第2组兔子的细胞内存在胞内劳森菌抗原。在第3组兔子中未发现病变、血清学反应、排菌或免疫组织化学标记。本研究描述了一种模拟自然感染的EPE家兔模型,因为出现了典型病变、免疫反应和粪便排菌情况。