Sheep and goat TSE

By Michael Fisher

Golden Plains Area Livestock Extension Agent

There are several transmissible spongiform encephalopathy diseases in the world today. The most famous of these is probably bovine spongiform encephalopathy. A sampling of other TSE's that you may hear of from time to time include the mink's transmissible mink encephalopathy, feline spongiform encephalopathy in cats, and chronic wasting disease among deer and elk. There is a whole list of TSE's that can affect humans. Creutzfeld-Jakob disease and variant CJD are the most talked about human versions, but there is also Gertsmann-Straussler-Scheinker Syndrome, fatal familial insomnia, and for the human cannibal lurks the TSE called kuru.

The TSE's are sometimes referred to as the prion diseases. This is because prions are at the root of the problem. Prions are misshapen proteins that affect the brain and nervous system of the infected animal. They cause tiny holes to develop giving the brain a sponge-like appearance. The tissue is damaged to the point that proper function is unattainable and death becomes eminent.

TSE's are a unique set of diseases in the fact that their etiology (the cause of the disease) can be traced back to multiple reasons. Genetics can play a large role. This is not through inheritance of the disease but rather by contributing to how susceptible the offspring are to a given TSE. There are cases in which a TSE is caused by a sporadic mutation of a prion, which then replicates itself within the animal's gray matter. Ingestion of infected feedstuffs has been shown to be a common cause of the diseases transmission. Most people assume that this is through the feeding of mammalian by-products but it has also been shown to be of relevant concern through the consumption of placental materials. Research has also shown that the TSE family of diseases can be transferred by iatrogenesis; meaning through medical procedures, like blood transfusions or improperly sterilized medical instruments.

Based on documented records, the oldest of the TSE diseases is scrapie. It was first diagnosed in Scotland in 1732 after shepherds observed that some ill sheep were "scraping" their heads against trees prior to dying. Scrapie affects both sheep and goats and is considered to be world-wide, with only New Zealand and Australia recognized as being currently "scrapie free". The first U.S. diagnosis of scrapie was in 1947 with cases being discovered around the same time in Australia and Canada. These outbreaks were the catalysts for a great deal of scrapie research in the 1950s which vastly increased our understanding of the TSE's.

Today, we know that in sheep there is one pair of genes that holds the genetic code for susceptibility to scrapie. I will try to explain this very briefly without sounding too much like a geneticist. It is important to state that this information is what we know about how sheep get scrapie. Less is understood about how the goat contracts the disease, although that research is currently ongoing and the USDA expects to make more goat information available in 2008.

The gene pair is known as the Prion Protein Gene (PRPN). They contain 254 codons and four of these are involved in determining how likely it is that a sheep can contract scrapie. Those four are codons 136, 141, 154 and 171. Researchers consider the role of codons 141 and 154 to be minor but they still need to be monitored. In the United Kingdom, codon 136 is the primary contributing codon. The U.S. strain of scrapie usually relies on a mutation of codon 171.

Codon 136 can have one of two amino acids at that position, while Codon 171 can have one of four. In the case of both codon locations, the offspring will receive one amino acid from the sire and one from the dam. At codon 136, they are valine (V) and alanine (A). In the case of codon 171, they are arginine (R), glutamine (Q), histidine (H), or Lysine (K). The latter three are considered to be similar in their susceptibility to scrapie, so the letter Q is often used to signify any of them.

When you have a lamb tested for genetic susceptibility of scrapie, the report may read as two pairs of letters or as a number followed by a pair of letters. If it is in the form of all letters, the first pair represents codon 136. In this pair, alanine is considered resistant to scrapie; so you will hope to see two A's. The second pair represents codon 171. Argnine is the resistant amino acid at this codon; so you will hope to see a pair of R's. An R and a Q would indicate that the lamb was susceptible to scrapie, while a pair of Q's would suggest a high level of susceptibility to the disease. As mentioned previously, most U.S. cases of scrapie are due to issues with the codon 171. Therefore, many U.S. tests will simply report the results in the format of 171RR, 171RQ, or 171QQ.

All of this is used to determine the animal's susceptibility of contracting scrapie if exposed to it. The exposure still has to occur. In the case of sheep and goats, that exposure often times come through contact with infected placental tissue. A two to five year period of incubation is needed following exposure before the sheep or goat actively exhibits signs of the disease.

It is estimated that scrapie costs American sheep producers $20 million plus annually in lost marketing opportunities. Partially for this reason, the USDA established the National Scrapie Eradication Program in 2001, with a goal of eliminating the disease in the U.S. by 2010. In the state of Colorado, the program requires that all sexually intact sheep and goats have a scrapie surveillance flock ID tag at the time of ownership change, slaughter, or when at a livestock show or exhibition. This requirement also pertains to any wether once it has reached 18 months of age. Also, all breeding flock sheep must be identified in the program regardless of ownership changes.

For more information on the program or to obtain scrapie tags for your flock, contact Colorado's USDA-APHIS Area Veterinary Services office at 303-231-5385.

3/10/08
3 Star CO\17-B

Date: 3/5/08

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