The rabbit as an infection model for equine proliferative enteropathy

Francesca Sampieri, Andrew L. Allen, Nicola Pusterla, Fabio A. Vannucci, Aphroditi J. Antonopoulos, Katherine R. Ball, Julie Thompson, Patricia M. Dowling, Don L. Hamilton, Connie J. Gebhart

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)110-119
Number of pages10
JournalCanadian Journal of Veterinary Research
Volume77
Issue number2
StatePublished - Apr 2013

Fingerprint

digestive system diseases
Horses
Lawsonia Bacteria
rabbits
Rabbits
Lawsonia intracellularis
horses
Infection
infection
lesions (animal)
immunohistochemistry
Immunohistochemistry
Feces
feces
immunoglobulin G
Hematoxylin
Eosine Yellowish-(YS)
blood serum
cultured cells
Cultured Cells

ASJC Scopus subject areas

  • veterinary(all)

Cite this

Sampieri, F., Allen, A. L., Pusterla, N., Vannucci, F. A., Antonopoulos, A. J., Ball, K. R., ... Gebhart, C. J. (2013). The rabbit as an infection model for equine proliferative enteropathy. Canadian Journal of Veterinary Research, 77(2), 110-119.

The rabbit as an infection model for equine proliferative enteropathy. / 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.

In: Canadian Journal of Veterinary Research, Vol. 77, No. 2, 04.2013, p. 110-119.

Research output: Contribution to journalArticle

Sampieri, F, Allen, AL, Pusterla, N, Vannucci, FA, Antonopoulos, AJ, Ball, KR, Thompson, J, Dowling, PM, Hamilton, DL & Gebhart, CJ 2013, 'The rabbit as an infection model for equine proliferative enteropathy', Canadian Journal of Veterinary Research, vol. 77, no. 2, pp. 110-119.
Sampieri F, Allen AL, Pusterla N, Vannucci FA, Antonopoulos AJ, Ball KR et al. The rabbit as an infection model for equine proliferative enteropathy. Canadian Journal of Veterinary Research. 2013 Apr;77(2):110-119.
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. / The rabbit as an infection model for equine proliferative enteropathy. In: Canadian Journal of Veterinary Research. 2013 ; Vol. 77, No. 2. pp. 110-119.
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