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Temporal distribution of transmissible mink encephalopathy virus in mink inoculated subcutaneously
Abstract:
Information was sought on the temporal distribution of transmissible mink encephalopathy virus in royal pastel mink inoculated subcutaneously with 10(3.0) 50% intracerebral lethal doses of the Idaho strain. As determined by intracerebral assay in mink, extremely little replication of the virus occurred during the preclinical stage of infection. It seemed largely limited to lymph nodes draining the site of inoculation. Virus first appeared in the central nervous system (CNS) at 20 weeks, when all mink were still clinically normal. Early spongiform degeneration, limited to the posterior sigmoid gyrus of the frontal cortex, was first found at 28 weeks, or a few weeks before onset of clinical disease in most of the mink. Once virus reached the CNS, where greater concentrations occurred than elsewhere, it appeared in many extraneural sites (spleen, liver, kidney, intestine, mesenteric lymph node, and submandibular salivary gland). These seemingly anomalous findings, especially the limited extraneural replication of virus as a prelude to infection of the CNS, suggest that mink are not natural hosts of the virus. The results of this study support the generally held view that transmissible mink encephalopathy arises from chance or inadvertent infection of ranch mink with an exogenous virus, most likely feed-borne wild scrapie virus.
Insights
Transmissible mink encephalopathy virus showed limited replication in mink before reaching the central nervous system (CNS). This suggests mink are not natural hosts, and infection likely stems from external sources like feed.
Area of Science:
- Veterinary Pathology
- Prion Disease Research
- Animal Virology
Background:
- Transmissible mink encephalopathy (TME) is a fatal prion disease affecting mink.
- Understanding the virus's temporal distribution is crucial for disease control.
Purpose of the Study:
- To investigate the temporal dynamics of transmissible mink encephalopathy virus (TMEV) in inoculated mink.
- To elucidate the early stages of TMEV infection and its spread within the host.
Main Methods:
- Subcutaneous inoculation of mink with a defined dose of TMEV (Idaho strain).
- Intracerebral virus assays to quantify viral load.
- Histopathological examination for spongiform degeneration.
Main Results:
- Minimal viral replication occurred in extraneural tissues during the preclinical phase.
- Virus first detected in the central nervous system (CNS) at 20 weeks post-inoculation.
- Spongiform degeneration observed in the frontal cortex shortly before clinical signs appeared.
Conclusions:
- Mink appear to be incidental hosts for TMEV, with limited intrinsic replication.
- The findings support the hypothesis of exogenous TMEV infection, likely feed-borne.
- Understanding TMEV pathogenesis is key to preventing outbreaks in ranch mink.