[Jacob-list] Congenital defects

Thu Apr 27 05:13:35 EDT 2006

There is some thinking that the Jacob Sheep is naturally inbred. That is: it arose from a rather small base, and those flocks tended to remain closed. The result of this is that there was a tendency for genetic recessives to be expressed and eliminated from those flocks early on. Much the same thing happens with inbred lines of chickens that have gone into the production of the modern poultry industry. In the almost twenty years that we have had sheep here, the only congenital defect that I can recall seeing was a "bulldog face" in a CROSSBRED lamb. 

We should also remember that genes are not static. There is a nasty little secret that is starting to come out in regards to BSE. Much of FDA and industry efforts have been to trace all Mad-cow to the consumption of tainted feed that originated with British imports, and maybe even scrapie sheep. But, it is very possible that the cases most recently seen in the US are the result of random new mutations that we would never have seen had we not been testing for it.

Neal Grose

"The world is always more complicated than we would like for it to be."
  ----- Original Message ----- 
  From: Jacobflock at aol.com 
  To: hettick1 at yahoo.com ; jacob-list at jacobsheep.com 
  Sent: Thursday, April 27, 2006 1:41 AM
  Subject: [Jacob-list] Congenital defects

  I think it is good that shepherds share problem episodes so that the breed may be conserved.  Congenital problems are not a new phenomenon nor a shepherd or breed stigma.  The committed shepherd will watch the flock and each sheep, note problems, search for causes and be willing to share the experience for the sake of the breed.  It is our "selfish" gene that says a defect should not be seen or reported, buried rather than necopsied.

  When Miss Shnickelgruber(sp?) saw her new-born son, she probably said he was a beautiful baby ... perfect ... he will be a success!  We look at lambs and see cute, a measure of perfection and it will be registered.  But perhaps the "perfect" lamb is really 20 years old that reproduced consistent, viable offspring that, in turn, reproduce consistent, viable offspring.  Lambs are far more a "hope" than a "promise"; they tell us about their parents, not their unborn offfspring.

  I am not advocating a "know-nothing" approach to the practice of husbandry but suggest tempering husbandry instinct with some realities such as "one robin does not make a spring", "stars are not only there at night", "the sun doesn't rise", "the major contributor to the OED was from an insane asylum" and "there'll be days like this".

  A single instance of atresia ani may be just that, a single instance of a genetic mutatioin caused by anything from the status of the egg or fetus getting hit by a neutrino to the ewe being stressed or ingesting skunk urine left in the pasture.  

  On the other hand, a gene is a predictable protein machine, always doing something (like producing copies of itself and the building instructions which get passed on) but we don't see gene efffects until the right conditions arise. Some effects are apparent at birth (black/white, horns, four cleft hooves and plumbing, even viability effects such as getting up, smell and sucking,and even congenital defects).  Some other effects such as ticking, stones, even parasite resistance or resilience are already there but are not typical lamb observations.  All breeds of sheep have positive breed outcomes as well as congenital and genetic problems. The Jacob is not that unique. 

  Most genetic problems are autosomal recessives (most are non lethal problems, some lethal).  Given the penchant for breeding pedigrees that dip deep to the imports rather than "unknowns", some genetic problems are results that would be expected from the gene puddle of the first 25-30 Jacobs. 

  You can create your own gene puddle ...Punnett saquare... like AAxAa where A is the "normal anus and run two lines, birth sex is 50/50 and assume that 4/5 rams are wethered or butchered.  I think you hit a aa with a 90% probability by the 4th generation.  You can repeat the breeding and see if it is repeatable.

  Defects can appear to come from "different" lines. On the one hand a line suggests a certain level of inbreeding greater than the general population; don't rely on flcok name prefixes for breeding distance; check the pedigree to great grandparents... on the other hand, did it ever previously occur in one line or the other ... ? 

  The severity, frequency and predictability of the problem is rather critical and that is why sharing information about congenital and genetic defects is so important ... how else does one collect information on defects per 100 births?  

  When a case of otognathia was reported...two more were reported ...  When cases of OCD were reported ... more were reported ... and atresia ani, stones, adactylly, intersex, jaw misalignments, ... etc.,  So there does exist a catalog of some Jacob congenital defects and a very crude measure of incidence.  On the other hand some defects are more clearly known; e.g., we did planned breeding to produce lysosomal storage problems over two years of breeding known and suspected carriers that, since genetics probably works, produced expected results. Texas A&^M identified the source(s), but the likelyl enzyme defect was not the expected beta galactosidase or the other betas associated with lysosomal problems in other breeds.  Perhaps the Jacob is unque!  

  Having come full circle, I must remeber that beyond the package of genes, management and environment also have an effect on the breed and congenital defects; e.g., over feeding and barn confinement are often noted. The task is to observe and study a problem, propose a casue, test the cause and proceed with a little bit of added knowledge and experience.  Sharing knowledge and experience helps the shepherd and the breed. 

  Fred Horak

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