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United States Department of Agriculture

Agricultural Research Service

Title: Clinical features in prion protein-deficient and wild-type cattle inoculated with transmissible mink encephalopathy (TME)

item Vargas, Francisco
item Kuroiwa, Yoshimi
item Greenlee, Justin
item Hamir, Amirali
item Kunkle, Robert
item Kangas, Tracy
item Kanthasamy, Anumantha
item Robl, James
item Richt, Juergen

Submitted to: Abstracts World Buiatrics Congress
Publication Type: Abstract Only
Publication Acceptance Date: 9/13/2010
Publication Date: 11/14/2010
Citation: Vargas, F., Kuroiwa, Y., Hamir, A.N., Greenlee, J.J., Kunkle, R.A., Kangas, T., Kanthasamy, A., Robl, J., Richt, J. A. 2010. Clinical features in prion protein-deficient and wild-type cattle inoculated with transmissible mink encephalopathy (TME) [abstract]. XXVI World Buiatrics Congress 2010, November 14-18, 2010, Santiago, Chile. Available:

Interpretive Summary:

Technical Abstract: Background: Transmissible spongiform encephalopathies (TSEs) or prion diseases are caused by the propagation of a misfolded form (PrP**d) of the normal cellular prion protein, PrP**c. Recently, we have reported the generation and characterization of PrP**C-deficient cattle (PrP-/-) produced by a sequential gene targeting system and also we reported that PrP-/-cattle are resistant to prion diseases. Objectives: In this study, we wanted to show the clinical features observed in prion protein-deficient and wild-type cattle inoculated with transmissible mink encephalopathy. Methods: Five PRNP+/+ wild-type and five PRNP-/- cattle were inoculated intracerebrally with a 10% brain homogenate derived from a bovine infected with a cattle-adapted TME isolate. Six other cattle (three each PRNP+/+ and PRNP-/-) were inoculated with normal brain material. All PRNP-/- and PRNP+/+ calves were further given an extensive clinical examination at the start of the experiment and each 3 months after inoculation with special emphasis in neurological examination. Additionally, the clinical assessment also included electrocardiography (EKG) and ophhtalmoscopic examination. All animals were monitored daily during the experiment. Results: All five PRNP+/+ cattle inoculated with TME were euthanized with clinical signs within 18 MPI and contained abnormal PrP**d in their CNS tissues. The most important clinical signs observed in the wild type inoculated group were: low body condition score, low response to cutaneous reflex, lordosis, hyperreaction to stimulations (menace, sounds and light), hypersensitivity in the head; abnormal attitudes and movements (excessive licking, movements of ears and teeth grinding), slow response to pupilar reflex; head lowered, hypersensitivity in the trunk and locomotion alteration. Retinal examination revealed, neovascularization in the optic disc (NVD) and atrophy in the retinal pigment epithelium (RPE). All five PRNP-/- cattle inoculated intracerebrally with a cattle-adapted TME isolate and normal brain homogenate are clinically normal at 36 MPI. However, some PRNP-/- cattle inoculated with TME and normal brain showed mild reaction to some stimulation from the beginning of the experiment. Conclusion: PRNP+/+ wild type inoculated with TME showed nervous clinical signs similar to BSE at 18 MPI. PRNP-/- inoculated with TME did not develop clinical signs consistent with prion disease. Mild reaction to stimulation observed in some PRNP-/- (inoculated with TME and normal brain) may be associated with alteration of Purkinje cells degeneration.

Last Modified: 08/18/2017
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