Click on the edge of the Evaluation Sheet in order to make it bigger so you can read it.
Kinder Goats
A Kinder Goat is one that is bred according to the Kinder Score Card and the Kinder Breed Standard. As Kinder breeders we are breeding one type of goat and that is according to our standards. We do not have two or more types of goats but only one. The Kinder is a dual purpose animal that will milk and also provide a good meat carcass. The ideal Kinder doe is to be 26 inches at the withers and the bucks 28 inches. Those animals with longer more dairy type bodies and legs are not truly Kinder goats. There are many dairy animals for people to choose from, we do not need to try to make our Kinder one of those. If we are to continue to breed a dual purpose animal then we must breed according to our standards.
Dam Raised or Bottle Raised
I suppose I should say that this is the breeders preference but if you are selling Kinder stock then you might want to consider the buyers thoughts.
For my husband and myself this is very important because in general dam raised kids are not nearly as gentle are easy to handle as those raised on a bottle. We are in our 70’s and 80’s so animals that are easy to handle is quite important. We have owned both so we know first hand just how these animals act as kids and into adulthood. Those Kinder raised by their dams are never as gentle and trusting as those that are bottle raised. We have one older doe in our barn right now that was dam raised and to this day she is not nearly as easy to handle as the other older doe that was raised on a bottle. We have two doelings in our barn right now with one being raised by her dam and one raised on the bottle. The young doe that was dam raised is quite a challenge when trimming hooves, worming and etc..
I often hear breeders say that leaving kids on the dams is the natural and best way. It may be the natural way but it is not always the best way. When raising Kinder kids give some thought to the buyers that you plan to sell these animals too. I would almost always give more money for a bottle raised kid than one that was raised on their dam.
Here is a little hint that has worked for us: When wanting the dams to raise their kids then only leave those kids with their moms for the first week to ten days then move the kids to a separate area. Twice a day bring the does to the kid area and turn them in for the kids to nurse. Just as soon as they have finished nursing open the gate and doe will be very happy to return to the barn leaving her kids in their kid quarters. Doing it in this way the kids will become yours ( much more friendly)and they will also be able to be raised by their dams. It has always worked for us.
The evaluation is of this buck
A Genetic Defect and its Management
A Genetic Defect and its Management
By Dagny Vidinish ©
All animals, including dairy goats, have numerous genetic defects of varying severity. We are all familiar with the occasional multiple teats, for instance, and with such defects as undershot and overshot jaws. Other defects are rapidly fatal, and it often is unclear whether the death of a kid should be attributed to genetics or to misfortune. The exact inheritance of many of these defects is often obscure; for instance, although most people believe that multiple teats show up when both parents carry a gene for this trait there is evidence that in some cases they are actually caused by environmental factors. In order to manage these undesirable genes breeders usually have to fall back on the “don’t repeat that breeding” strategy, which is very crude and unsatisfactory.
This article will describe a recently discovered genetic defect which is easily managed and eliminated because its mode of transmission is straightforward and, more important, because a foolproof DNA test is available to identify carriers of the gene.
This defect’s full names are mucopolysaccharidosis IIID, or G-6-Sulfase deficiency, and it is usually referred to as G-6-S. It was first identified in 1987 at Michigan State University, and subsequently the researchers tested nearly one thousand goats in Michigan and concluded that about 25% of Nubians carry this gene. All cases are the result of a single mutation, and appear to be confined to Nubians and their crosses; other breeds were tested initially and they do not have this particular defect.
The affected goats lack an enzyme (G-6-S) and this results in a variety of symptoms of varying severity. The main symptom exhibited by affected goats is failure to grow. Sometimes the kid is smaller than normal at birth, and grows slowly. Some breeders have reported kids which grew normally for the first three months and then stopped growing. Other affected goats grow to what appears to be normal size but is in fact small for the particular bloodlines.
They lack muscle mass, appear “slab-sided”, sometimes with blocky heads. Immune function appears to be compromised, and sometimes they become deaf or blind. The longest-lived goat known to be G-6-S affected died at just under four years of age, and death is usually due to heart failure. Unfortunately affected animals can and do grow up to breed, although they often experience reproductive problems.
The same symptoms can have many other causes, so that affected animals are seldom recognized as having a genetic defect. Often they grow normally for the first few months and may be sold before any problems become apparent. In that case the breeder may blame the new owner for the goat’s failure to thrive and early demise.
Every animal has two genes for every trait, one inherited from the dam and one from the sire. In turn, that animal will pass only one of those genes to each offspring, and which one it will be is a matter of chance, like the flip of a coin. On the average, half the offspring will inherit one gene and half the other. If the two genes are different, then there is a question as to which of them will determine how the animal actually looks or functions. The defective G-6-S mutation is a simple recessive gene, which means that a goat which has only one copy of it will appear perfectly normal and will not show any of the symptoms described above. Such a goat is referred to as a “carrier.” A goat which inherits the defective gene from both parents shows symptoms and isreferred to as “affected”. A “normal” goat, in this context, is one who has two copies of the normal gene.
If a normal goat is bred to a carrier, then all offspring will inherit a normal gene from the normal parent. The carrier parent will pass a normal gene to half the offspring, and a defective gene to the other half. Thus such a mating will, on the average, produce half normal kids and half carriers, and no affected ones. If two carriers are bred to each other, then one quarter of the kids will be normal, one half will be carriers, and one quarter will be affected. If an affected goat is bred to a normal goat, all offspring will be carriers. An affected goat bred to a carrier will produce half carriers and half affected.
As stated above, research shows that 25% of Nubians carry the defective G-6-S gene. Almost all of these are carriers, since most of the affected animals which are born would be culled, and the rest die early. Most people find it surprising that something which is in one quarter of the population can have escaped notice for so long. However, random matings in such a population would result in only one out of sixteen being carrier to carrier, and only one quarter of the kids from these breedings would be affected. Thus only one kid in sixty-four (1.6%) would be affected. Given the variable and obscure symptomsof G-6-S affected kids, it really is understandable that most Nubian breeders believe that they have never encountered affected kids.
However, many Nubians are line-bred, and this practice will concentrate certain genes in some lines while eliminating them from others. It has been observed that the G-6-S mutation is very prevalent in the same lines which are known for high milk production. Thus breeders who have been selecting for milk may have inadvertently also been selecting for the G-6-S defect. Fortunately it appears that the two traits are actually independent, that you can cull the G-6-S carriers without at the same time culling the high producers.
Usually it is difficult to eliminate a genetic defect without losing all thegood genetics for which a line is known. For instance, if a buck throws double teats, then there is no way of knowing which of his offspring will do the same and which will not. You can cull him, but that seems rather heavy-handed since the bad gene will undoubtedly live on in some of his relatives. With G-6-S we are very fortunate to have a foolproof DNA test available which will tell us whether a goat is normal, or a carrier, or affected. This test makes it possible to save the good genetics and eliminate the defective gene if that is our wish. If a superior animal is a carrier, then we can test the kids and manage them in such a way as to avoid the birth of any affected individuals.
What is a good management strategy? What is the most efficient way to save the good and get rid of the bad? The usual recommendation for such testable defects is to cull carrier males, but not the females. Remember that if a normal buck breeds a carrier doe, then only half the kids will be carriers, and none will be affected. Thus if there are some carrier females in the herd, then using only normal bucks will reduce the incidence of carriers in the next generation by one half. The average herd would start with 25% carrier females, and if only normal bucks were used the next generation of females would be down to 12.5% carriers, and the next generation to 6.25%, etc. This is in sharp contrast to what a carrier buck would do in the same herd: if used to breed all the does, his daughters would be 50% carriers and 6.25% affected. Clearly there is much to be gained by testing buck kids and retaining only normal ones for breeding.
While it is relatively easy to cull a buck kid, one might hesitate to do the same with a proven sire. In particular, there are some very popular bucks whose semen commands a high price and who are carriers for the defective G-6-S gene.
A reasonable strategy here would be to use these bucks only on normal does, thus avoiding affected kids. Then one would test the kids and cull carrier bucks.
Although the DNA tests are expensive, if testing one’s bucks prevents the birth of even one affected kid then it is cost effective. Unlike tests for diseases, a genetic test does not need to ever be repeated. Also, the DNA tests are completely accurate, there are none of the gray areas which can be so frustrating. There is no need to test the kids if both parents are known to be normal. One can work back from one’s foundation animals and if there really is no problem in the herd then it may be possible to establish that at reasonable cost. Normally whole blood is used for the test, but semen can also be used. If an AI buck is a carrier, that can be established by finding a carrier offspring out of a normal doe, but no number of normal offspring will prove that a buckis normal.
A number of breeders have expressed the opinion that the G-6-S defect is no more of a problem than many other genetic defects, and therefore does not merit any particular attention. They evidently miss the point that it is the availability of a DNA test which makes this defect special. One can use goats from bloodlines which are known to have a high concentration of the G-6-S defect completely safely by just testing the particular individuals and either rejecting carriers or using them with proper precautions. There is nothing to be gained by trying to sweep G-6-S under a rug, and much to be gained by sharing information about it.
One may wonder why a DNA test has been developed for such an obscure defect, and no help is available for, say, multiple teats. The answer is simple – humans don’t have a problem with multiple teats, they do with G-6-S. The same genetic defect, when found in humans, is called Sanfilippo IIID; the affected child appears normal at birth but soon stops growing, looses muscle mass, has neurological deterioration and dies. When the same genetic defect was discovered in goats researchers used them as models for treatment, and goatbreeders in turn benefited from their discoveries.
Testing for G-6-S is done at the Texas Veterinary Medicine Diagnostic Lab (TVMDL) at a cost of $ (please call for current cost) US.
The Beginnings of the Kinder Breed
HISTORIC KINDERS
Zederkamm Liberty, first generation Kinder doe
Twiss Acres Thadius (Pygmy)
Born 10/05/80 – #80469M
Bred to Zederkamm Cocoa (Nubian), daughter of Brandy, producing Zederkamm Briar Rose
6/30/86
Bred to Zederkamm Brandy (Nubian) producing Zederkamm Liberty and Zederkamm Tia
7/04/88
Zederkamm Brandy (Nubian)
Born 01/84 – #BS850003D
Zederkamm Cocoa (Nubian)
No photo of Zederkamm Cocoa available
Born 04/85 – #BS840005D
Zederkamm Liberty
Born 7/04/86 – *M AR (FM) #1860007D
Sire: Twiss Acres Thadius #80469M
Dam: Zederkamm Brandy #BS850003D
Liberty was the first Kinder doe to earn her Milk Production Star
Zederkamm Tia
Born 7/04/86 #186011D
Sire: Twiss Acres Thadius #80469M
Dam: Zederkamm Brandy #BS850003D