MCF virus is transmitted by sheep in most instances. There is no documented evidence of person-to-bison transmission. Normal veterinary infection control precautions should be followed when caring for a bison suspected to have this viral infection.

There is no reason at this time why such animals should be culled. An important question we are trying to answer is whether healthy test-positive bison are at a significantly higher risk of developing MCF compared to healthy test-negative bison.

Most infections are characterized by depression, separation from the rest of the herd, loss of appetite, and in many bloody diarrhea. Unlike MCF in cattle, discharge from the eyes and nasal passages of affected bison is minimal. Animals develop a fever and may pass bloody urine. The clinical course is generally 1 -7 days. Most animals die within 3 days of developing clinical signs.

Animals older than 6 months, particularly if stressed by bad weather, transportation and handling. Large outbreaks occur in feedlots, where stress due to crowding is likely.

Following transmission, the MCF virus is presumed to infect lymphoid tissues (spleen and lymph nodes) and cells lining the gut, urogenital tract and nasal passages. The severe inflammation generally causes gastroenteritis, with widespread formation of ulcers particularly in the large bowel. This is the basis for bloody diarrhea, a common and useful diagnostic sign of MCF in bison.

Natural infections occur in many species of deer such as elk, reindeer and moose, as well as a variety of exotic ruminants. The disease can be transmitted experimentally to laboratory species, but there is nothing to indicate these species are involved in natural transmission. MCF was recently reported in pigs for the first time.

Three tests are available: histopathology, serological testing for MCF and an OvHV-2 specific test using the polymerase chain reaction (PCR).

We are aware of cases in 11 states (Utah, Wyoming, Colorado, Montana, California, Oregon, Ohio, Kansas, Nebraska, North and South Dakota) and three Canadian provinces (Saskatchewan, Ontario and Alberta). The disease is widespread in the bison industry and is commonly misdiagnosed due to lack of specific clinical signs.

With currently available test methods, between 15 and 23%. This is a minimal figure. No test is perfect. It is entirely possible that the tests currently being used for identifying infected normal bison miss a significant percentage of animals. The true rate of subclinical infection could be significantly higher than this.

Our limited knowledge on this subject suggests that bison may be infected for extended periods, in some instances years, before developing MCF. More work is needed on this aspect of the disease.

We think it is rare. There are inherent problems in tracking diseases like MCF in wild bison. The number of studies of MCF in public herds is small.

The best one to use for diagnosing active disease is the PCR test. Blood collected into an EDTA-anticoagulant tube (purple-top tube) is the best sample to obtain from live animals. Both the PCR test and a newly developed serological test can be run on one purple-top blood sample. The carcass of an animal that dies of MCF-like signs should be examined post-mortem by your veterinarian or better still a pathologist at a veterinary diagnostic laboratory.

There is no evidence that transmission occurs horizontally from one bison to another. Currently we are doing a study supported in part by the National Bison Association to establish whether bison-to-bison transmission is a factor in natural outbreaks.

There have been rare instances where allograft tissues have transmitted infections to recipients. In most instances the infection was present in the donor at the time of death but was not detected. In some cases, tissues have been contaminated during removal, transport, processing, or storage.

Yes. There are generally no lesions in the fetus or placenta. It is assumed that abortion is a result of illness in the dam, rather than infection of the fetus. Dams die shortly after they abort.

The liver is the body's primary repository of glycogen, so most glycogen storage diseases have a direct adverse effect of the liver. These diseases also affect muscle tissue, which must comply with sudden demands for energy.

No. There is no effective treatment for MCF in bison or cattle. There are scattered reports in the scientific literature of animals recovering from MCF following medical treatment. In our experience treatment merely prolongs the clinical course without effecting a cure.

No. Attempts to develop a protective vaccine to MCF in cattle using the wildebeest virus, alcelaphine herpesvirus-1 (AlHV-1), were unsuccessful. No comparable studies have been done on bison to date.

Epidemiological studies of field outbreaks strongly suggest that sheep infected with OvHV-2 are the principal source of MCF outbreaks in bison and cattle. A strong association between outbreaks in cattle and recent exposure to sheep has been documented repeatedly since 1929. Recent data indicate that a similar pattern occurs in bison. In some outbreaks, however, no sheep were in the vicinity immediately prior to the first case being identified.

We are doing a study to establish this. It clearly happens, but the percentage is low. No precise figures are available yet. Many factors are likely to affect the probability that a subclinically affected bison will develop clinical disease. One of the most important of these is stress.

far as is known, the disease has been present for hundreds of years. However, it has been recognized as a defined disease only within the past 80 years or so in the U.S. Reports of an MCF-Iike disease in cattle in North America appeared as early as the 1920s. The first well-documented case of MCF in bison occurred in South Dakota in 1973 and was reported in the scientific literature in 1977.