Transmissible mink encephalopathy (TME)

TME is classified as a transmissible spongiform encephalopathy (TSE). Different TSE's &e caused by similar as-yet uncharacterized agents that produce spongiform changes in the brain. Other TSE's include scrapie, which affects sheep and goats; bovine spongiform encephalopathy (BSE); feline spongiform encephalopathy; chronic wasting disease of deer and elk; and five rare diseases in humans, kuru, both classical and variant Creutzfeldt-iakob disease (CM)), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia.

TSE9s have also been reported in Europe in captive wild ruminants, cats, and monkeys. The occurrence of TSE's in captive wild animals is believed to have resulted from BSE-contaminated feed. These rare, progressively degenerative central nervous system diseases are characterized by a very long incubation period, a short clinical course, and a 100 percent mortality rate.

The infectious agent responsible for TME is smaller than the smallest known virus and has not been characterized to date. There are three main theories on the nature of this agent: (1) the agent is a virus with unusual characteristics, (2) the agent is a prion6an exclusively host-coded protein that is modified to a protease-resistant form after infection, or (3) the agent is a virinoda small, noncoding regulatory nucleic acid coated with a host-derived protective protein.

The TME agent is extremely resistant to heat and to normal sterilization processes. It also does not evoke any detectable immune response or inflammatory reaction in host animals. Public interest surrounding TSE's soared when the United Kingdom announced in March 1996 that BSE may be linked to a variant form of CE). The fear of this disease prompted countries around the world to step up measures to ensure that they remain free of BSE.

BSE has not been detected in the United States, and the U.S. Department of Agriculture (USDA) works proactively to keep it that way. USDA's Animal and Plant Health Inspection Service (APHIS) and Food Safety and Inspection Service take aggressive measures in prevention, education, surveillance, and response.

Clinical Signs

TME has an average incubation period of more than 7 months before the onset of clinical signs. These signs can last from 3 days to 6 weeks. Early clinical signs, which can be quite subtle, include an increase in nest soiling and dispersal of droppings throughout the cage.

In addition, mink may step into their food often or eat with difficulty. As the disease progresses, an infected animal becomes increasingly excited, arching its tail over its back like a squirrel. TVTME-infected animals may exhibit severe incoordination, difficulty walking, and pronounced jerkiness of hind limbs.

The advanced cases, signs include rapid circling, compulsive chewing of the tail, and clenching of the jaw. Seizures rarely occur. Near death, affected mink become sleepy and unresponsive.

TME produces no changes in the body that are visible upon necropsy examination. However, microscopic examination shows that the disease is limited to the central nervous system, causing distinct spongel ike changes in specific areas of the brain. Currently, there are no validated tests to detect TSE's in a live animal. Veterinary pathologists confirm disease by microscopic examination of brain tissue or by the detection of the prion protein.

Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old.

The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.