Transmissible Mink

Encephalopathy 

Transmissible mink encephalopathy (TME) is a rare

illness that affects the central nervous system of

ranch-raised mink. It was first detected in the United

States in 1947. Since then, TME outbreaks have

been reported in numerous locations worldwide,

including the United States, Canada, Finland,

Germany, and the republics of the former Soviet

Union.

Related Diseases

TME is classified as a transmissible spongiform

encephalopathy (TSE). Different TSE’s are 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–Jakob

disease (CJD), Gerstmann–Straussler–Scheinker

syndrome, and fatal familial insomnia. TSE’s 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 prion—an exclusively hostcoded protein that is modified to a protease-resistant

form after infection, or (3) the agent is a virino—a

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 CJD. BSE,

widely referred to as “mad cow disease,” has devastated the cattle industry in the United Kingdom. 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.

TME-infected animals may exhibit severe incoordination, difficulty walking, and pronounced jerkiness of

hind limbs. In 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.

Diagnosis

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 spongelike 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.

Epidemiology

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

Factsheet

Veterinary Services February 2002

APHIS
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.

The 1985 Stetsonville Outbreak

The most recent TME outbreak occurred on one

mink ranch in Stetsonville, WI, in 1985. In the herd of

7,300 adult mink, 60 percent of the animals died.

Clinical signs included tail arching, incoordination, and

hyperexcitability. At the most advanced stages of the

disease, the animals were in trancelike states and

eventually died.

The outbreak lasted 5 months. Microscopic

examination of sections of the brain confirmed the

spongelike changes characteristic of TME. Diagnostic

tests identified the prion protein. The following year,

mink born during the outbreak showed no signs of

TME.

The late Richard Marsh, a veterinary virologist at

the University of Wisconsin who studied the transmission of TME and other TSE’s, investigated this outbreak. Marsh learned that the mink were fed a diet

composed of fresh meat products from “downer cattle”

and commercial sources of fish, poultry, and cereal.

Downer cattle are nonambulatory and cannot rise

because they are affected with a condition such as a

metabolic disease, broken limbs, or a central nervous

system disorder. Marsh theorized that the meat from

these downer cattle introduced a TSE agent to the

mink in which TME resulted.

Although Marsh’s hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted

its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of

more than 20,141 cattle have been examined at

APHIS’ National Veterinary Services Laboratories and

other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another

TSE in cattle.

Additional Information

Veterinarians and livestock and poultry owners

who suspect an animal may be affected with a TSE

should immediately contact State or Federal animal

health authorities.

For further information, contact 

USDA, APHIS, Veterinary Services

Emergency Programs

4700 River Road, Unit 41

Riverdale, MD 20737–1231

Telephone: (301) 734–8073

Fax: (301) 734–7817

Current information on animal diseases and suspected outbreaks is also available on the Internet at

http://www.aphis.usda.gov.

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United States Department of Agriculture • Animal and Plant Health Inspection Service • Safeguarding American Agriculture