The Healthy Herd

LIVER FLUKE
(an often-misidentified worm that’s lethal if not treated for properly)
Update 12/08
by Sue Reith.

SYMPTOMS
Liver fluke damage is generally rather slow in appearing in mature goats… In a reasonably healthy goat, it can take years of gradual decline before the owner is even aware that Liver fluke is present.  Symptoms are some, if not always all, of the following: Gradual increase in unthriftiness (dry coat, guard hairs sticking up, ribbiness, pale eye membranes (indicating anemia caused by the worm’s activity), a swelling under the jaw (that has erroneously been considered among the veterinary community to be symptomatic of resistance to treatment for Haemonchus contortus), and, eventually, a possibly sub-normal temp (less than 102 degrees), a distended belly (symptomatic of last-stage liver disease), and fecal pellets that are almost black in color and shriveled up with pointy ends on them.
Often the victim goat is one that has been wormed routinely, and yet still continues its gradual decline. The problem is that there’s only one wormer on the market that will wipe out Liver fluke properly, Ivomec PLUS, (the PLUS part being clorsulon, specifically for eradication of Liver fluke) and many owners don’t even know this wormer exists! Sadly, even when the owner finally learns about it and starts treatment, by that time there has often already been too much damage to the goat’s liver for it to be saved even after proper worming.
BTW: While Liver fluke damage is often found in otherwise well-managed mature goats that despite good care continue to decline in appearance, in my experience this sudden appearance of anemia and weakness with either normal, or subnormal, temp (and sometimes swelling under the jaw as well) is not at all unusual to discover in young ruminants within the first few months of life as well.  At that age it commonly shows up when they’re heavily exposed to it in pastures containing wet areas,  before their immune systems can get up and going to protect them. In fact, it’s not uncommon for these young victims to die so fast they hardly have time to be sick.¹ This is especially true if there are any clostridial (Entero) organisms present in them, since they multiply and secrete their toxins fast in the already damaged, poorly oxygenated liver tissue .¹ 

TREATMENT:
I’m not one to quit without at least doing my best to save the goat… So if a goat of mine were affected with Liver Fluke I’d start it immediately on Ivomec Plus, using the appropriate worming approach as follows: All wormer packages note on the packaging that the product kills off ONLY the adult stages. So in order to get the worm load in the host down to a low enough level so that the immune system can take over and keep the problem under control, you need to worm 3X, with 10 days between wormings. The first dose will wipe out the adults already in there,  the second dose will wipe out the larvae that were in the gut, but not affected by the first worming, as they become adults (but before they can start laying eggs of their own), and the third dose kills off any eggs that were left over after you started the worming regimen,when they’ve passed thru the larval stage, when they, too, have become adults.

And as soon as you’ve begun the repair process by giving the first dose of Ivomec Plus, the next step would be to immediately start the goat on subcutaneous injections of Ferrodex 200 (each 1 ml dose of which delivers 200 mg of elemental iron… BTW: If the Ferrodex 200 isn’t easily accessible, go to the local Rite Aid or other drug store and buy a bottle of Iron tablets (Ferrous Sulfate, ~321% or 65mg, crush them, and feed with yogurt) (1 Ferrous Sulfate tablet is equivalent to 1/3/ dose of Ferrodex200, so 3 iron tablets would be the equivalent of 1 daily dose provided in Ferrodex200), to restore the liver’s red cells, the loss of which was the cause of  have caused the anemia and the blackened, shriveled, pointy-ended fecal pellets. And at this very critical time, as adjunct (supportive) therapy, I’d give it subcutaneous doses daily of ‘Fortified’ B-complex’ (a combination of B vitamins needed for proper body function that has everything but B-12), essential because every time the patient urinates, it’s losing all of those vitamins that are needed to maintenance of its body functions, and BoSe (to support his stressed immune system so that the goat can help itself to get well from inside, while I work on it from the outside), and Banamine (to reduce the goat’s pain and cut the inflammation caused by the worm damage) which, once given, will encourage the goat to want to eat once again! And last but not least, I’d give the goat a preventative doe of C&D antitoxin (to prevent entero from taking this opportunity to sneak in and finish the poor victim off because while it’s down its stomach is not digesting food and moving it out of its body as it should.)
BACKGROUND :
Liver fluke is  found in most of the US, but it’s especially common in the Southern states due to the lack of good frosts to wipe out eggs and larvae in winter. We see it often up here in the Northern states as well, but because we have colder winters, the numbers, fortunately, are somewhat lower.  However during the rainy season, no matter what part of the country the goat lives in, the Liver Fluke problem becomes particularly pervasive each year!
Today, by far the most difficult problem that we as owners face with Liver fluke treatment/control is that the veterinary community in general isn’t even aware that it’s there.  As a result, they’re unable to recommend proper treatment for it. This is because the egg of the Liver fluke (Fasciola hepatica)² looks so similar to that of the Barberpole worm (Haemonchus contortus)² that when it shows up on the slide in the Vet’s office it’s routinely misidentified to BE that of the Haemonchus contortus (or perhaps by some general term like strongyles, stomach worms, et al).  And this is despite the fact that the Merck Veterinary Manual (8th Ed. Pp.197-198)³, which, BTW, is not a text used in Vet Schools, but in fact is instead a text available to Veterinarians and Goat owners as well, in discussing its prevelance, notes:  “Fasciola hepatic, the most important trematode of domestic ruminants, is the common cause of Liver Fluke disease in the USA and other temperate areas of the world. It’s endemic along the Gulf Coast, the West Coast, the Rocky Mountain Region, and other areas… IT is present in Eastern Canada, British Columbia, and South America… etc and so forth.. They have even found it in Europe, Australia,in NEw Zealand, Africa and Asia, and it’s been reported in Hawaii as well”…
Until just a few years ago the veterinarian, seeing what was thought to be Haemonchus contortus eggs on the slide, would recommend Ivomec to the owner as the wormer of choice to eradicate it. And rightly so, because the moment Ivomec appeared on the scene back in the early 1980’s, it was recognized as the most effective general wormer to show up ever! And frankly it  remains, in my view, still the best and most efficacious general wormer on the market today.
And largely because the real Haemonchus contortus has always responded very well to Ivomec, veterinarians, misidentifying Liver fluke eggs as those of Haemonchus contortus, quite logically continued recommending Ivomec for treatment. When the Liver fluke failed to respond to the Ivomec treatment, unfortunately the loss of the animal in question was assumed to be a sign of the Haemonchus contortus having developed ‘resistance’ to the Ivomec! This notion has now become so pervasive that the veterinary community in general believes these days that the worms affecting livestock have developed a resistance to Ivomec, the result being a recommendation to their clients that they (1) increase the doses, and (2) turn to other wormers.  Neither approach has even slowed down the deaths being caused, in fact, by Liver fluke. Since neither of those suggestions are working, the most recent approach has been to set up Famacha classes to instruct owners and veterinarians alike in how to check the eyelids of the downed animals to see if they’re anemic. If the animals have pale eyelids, indicating they’re anemic, owners are sometimes advised to destroy the victim, fearing that if it lives, the ‘resistance to wormers’ will spread even further.
Sadly, neither plain Ivomec, nor Panacur, nor any of the other general wormers on the market today, are effective against Liver fluke.  The fact is, this parasite can ONLY be eradicated efficiently by using a product called Ivomec Plus .  It’s not the Ivomec itself, but the PLUS part of the combined wormer, which is actually ‘clorsulon‘ , that effectively wipes out Liver fluke.. And (very critically) since it only kills the ADULT of the species, clorsulon (just as all wormers) must be used at regular doses, 3 X in a row, 10 days apart, to wipe out all stages of the worm. ¹
And it will no doubt be of particular interest for those owners who are worried about using milk from does being treated with Ivomec Plus that the Pharmaceutical companies have now run the required tests on those two products that officially clears them for use in lactating ruminants! 
So in my view, these days (particularly if the reader is having a hard time controlling internal parasites in his/her animals) Ivomec Plus (instead of plain Ivomec) should ALWAYS be used for general worming, ‘just in case’!  Just like regular Ivomec, it can be given orally although it’s actually an injectable. But since right now Ivomec itself is less readily being used by people (most of whom have never even heard of Liver fluke, and many of  whom have their vets ID their goats’ fecal samples as well) Ivomec Plus, while its importance is gradually growing among goat owners, may not yet be available in your local feed store… However it is readily available in livestock catalogs.

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.  

HYPOCALCEMIA IN LATE-GESTATION (and lactating) DOES:
Feeding to Prevent it
By Sue Reith (2/07 update)

Hypocalcemia is a life-threatening condition that shows up when a doe is either pregnant or lactating, but getting fed an unbalanced diet that doesn’t provide her with enough calcium for both herself and her growing fetuses or for milk production.  It can appear at any time during the last 2 months of pregnancy, right up to the doe’s due date, as well as at any time while she’s lactating.
Symptoms:  The first thing she’ll do is refuse to eat her grain. Soon after that she won’t want her hay either.  Without quick intervention she’ll become weak and wobbly, lethargic and depressed. If still untreated by then, she’ll lie down and not want to get up. If you take her temperature when you first see these changes, it’ll be normal (102.3), but soon after that it’ll drop to sub-normal (below 102). Unless corrective measures are begun right away you’ll lose both the doe and her fetuses.
Treatment: If, because you’re unsure as to why the doe is behaving this way, you call a veterinarian in for advice, he or she will probably (and unfortunately) tell you that her problem is “pregnancy toxemia”, or “pregnancy disease”, or perhaps the most likely diagnosis will be “ketosis” a secondary condition that happens when the doe stops eating (in this case because she’s too weak to do so) thus has to start living on her own body’s reserves*. While ketosis was not the initial cause of the doe’s difficulty, after a couple of days  of being too weak to eat any food it will certainly become a major part of her problem! So it, too, must be dealt with fast!  A veterinarian, recognizing the ketosis but not the hypocalcemia that caused it, will want to treat with glucose, etc.  But it’s absolutely essential that the doe be treated with calcium supplements** at the same time, without which she will either end up dead, babies and all, or with a c-section, with babies too young to survive, and a hefty vet bill as well.  So it behooves the owner to take charge of this whole process right away, to treat the doe with calcium supplements for the hypocalcemia, and, if more than a day or two has passed before treatment was begun, with glucose for ketosis as well.

Cause:  It’s all about the food!  Most cases are seen in does that are getting a hefty grain ration along with their hay, especially when they’re getting grass hay instead of alfalfa. During the last 2 months of the doe’s pregnancy, this type of grain/grass hay diet does not provide enough Calcium for both the fast-growing fetuses’ bone development and for her own muscle tone as well, so depending on how many fetuses are draining calcium from her to build their little skeletons, at some point the babies will drain ALL of her calcium from her for their own needs, leaving her nothing to keep her heart going (the heart is a muscle) or to go into labor (the uterus is ALSO a muscle).  And the more fetuses she’s carrying, the sooner this will happen!  With just 1 or 2 fetuses she may make it until she goes into labor, but then be too weak from lack of muscle tone to expel the babies in a timely manner***. Or if she  does succeed in birthing the kids (often requiring the owner’s assistance), starting lactation in a calcium-deficient state can lead to a sudden (and very surprising!) loss of milk production at some unexpected point during lactation.
Prevention:  You CAN prevent this, just by feeding your pregnant does a proper diet during pregnancy!  Pregnant does need a great deal of calcium in their diets, particularly in the last two months of gestation. That’s when the fetuses, now having fully developed all their little parts, focus all their energy on growing rapidly, and in so doing drain large amounts of calcium from the mother’s body. Calcium is only available in the diet if the doe is ingesting at least 2 parts (and no more than 5 parts) of calcium-providing food to every 1 part of phosphorus-providing food. “The calcium-to-phosphorus ratio of a food or supplement determines how much of the calcium is absorbed.” (http://www.askdrsears.com/html/4/T040600.asp, bottom of the article, #8 under “12 ways to boost your calcium”.)
The only really good Calcium-providing feeds are alfalfa and clover, because grass hay contains barely any at all. OTOH, ALL forms of grain contain a great deal of phosphorus (and almost no calcium whatsoever). So if you feed grain without the calcium available from alfalfa or clover, OR if you feed alfalfa or clover without the phosphorus available from grain, there will be NO   calcium available in the diet you feed for the developing babies….
During the doe’s pregnancy, there are three basic feeding approaches that will prevent hypocalcemia.
(1)  Provide her daily with a small amount of grain (for a mature dairy-sized doe that would be no more than one cup per feeding) along with a regular ration of alfalfa, or,
(2)  If feeding a grass hay or pasture instead of alfalfa, give her NO grain at all. That’s because while grass hay does in itself contain a proper ratio of calcium to phosphorus, the total amount of each is exceedingly low.  But adding a heavy-phosphorus grain ration to it would turn the balance of calcium to phosphorus upside down to something like 1 Ca to 4 (or more) P, making NO calcium available to the doe, and setting her up for hypocalcemia in late gestation. To increase the availability of Calcium in this instance, provide a good free-choice loose supplemental trace mineral mixture that contains at least 16% protein (grass hay has only ~5%), along with a ratio of no lower than 2 parts of Calcium to each 1 part of Phosphorus (the amount of which could be nicely increased with the addition of powdered Di-Calcium Phosphate, available through feed suppliers as well as online.)
(3)  For those who would prefer to feed both grain and hay in late gestation, but because they don’t have ready access to free choice alfalfa must instead either pasture their goats or feed them grass hay,  if alfalfa pellets can be bought locally at a reasonable price, a perfect late gestation diet for prevention of Hypocalcemia would be a ration of 1 cup (by measure) of grain, added to (using the same cup) 3 cups of alfalfa pellets, fed 2X daily, along with all the free choice pasture or grass hay the does want to eat between meals, and free choice access to a good, loose, trace mineral supplement, and baking soda.
In an effort to help owners figure out just how much of what feed to give their late gestation does to provide that minimum 2:1 ratio, I recently wrote a technical nutritional analysis of how the 2 CA to 1 P balance works out in real-time farm-feeding measurements. (I’ll be happy to forward a copy of that analysis to readers who’d like to read it.)
And then to translate the technical information in the article into useful terms, I calculated the actual weight of the (minimum) 2Ca:1P ratio diet I feed to my own Togg does. In so doing I found that at mealtime they each get 1 lb of alfalfa (a combination of 12 oz alfalfa pellets, ALL of which is devoured eagerly, and roughly 24 oz loose alfalfa free choice, some of which is generally wasted) along with 1 cup (1/4 lb by weight) of grain. That’s roughly a per-meal ratio of 1 lb of calcium-containing food to each 1/4 lb of phosphorus containing food, translating to a daily ration of 4:1 (4 Ca to every 1 P), well-within the parameters of the acceptable calcium to phosphorus ratios of 2Ca:1P to 5Ca:1P that are needed to make calcium available in the diet.  
Because when measuring them pound for pound we can see there’s a difference in the volume of grain and alfalfa pellets, after calculating the above feeding ratio by weight I went back again and re-calculated it by volume.  When I filled up my 1-cup grain-measuring container with alfalfa pellets instead, I discovered that it took exactly 3 of them to fill up my larger, alfalfa-measuring container.  So, when measuring out a feeding of grain and alfalfa pellets for one animal, to provide the essential minimum of 2 Ca to 1 P ratio in that meal all you need to do is put 3 of the small scoops (or a larger scoop that holds the equivalent) of alfalfa pellets into the dish, and top it off with 1 small scoop of grain****! 
Addendum: For readers that while feeding to prevent Hypocalcemia are concerned about other nutrients, such as protein, being available to their does as well, according to Ensminger and Olentine’s Livestock Feeds and Nutrition Complete the average digestible protein content in grain is 11.2%, whereas in alfalfa it’s 15.9%, in clover 10.5%, in beet pulp it’s 14.1% and in grass hay 5.1%. The average digestible energy level in grain is 1.38%, in alfalfa it’s 1.13%, in clover it’s 0.93%, in beet pulp it’s 1.32%, and in grass hay it’s 1.8%. And, last but not least, the average crude fiber content in grain is 6%, in alfalfa it’s 27.2%, in clover it’s 25.7%, in beet pulp it’s 15.17%, and in grass hay it’s 28.2%.
Sue Reith
Carmelita Toggs
Bainbridge Island WA
suereith@msn.com
*When the goat doesn’t get food from outside, it tries to stay alive by using its own reserves.  Its own fatty tissue is used to provide energy, and in so doing it releases ‘ketones’ into the system.  The ketones soon shut down the liver, hence the name ‘ketosis’.
**The most effective calcium supplementation is done with CMPK, because it’s made up of not just Calcium, but also Magnesium, Phosphorus, and Potassium, formulated to work together as a team to make Calcium more quickly available to the body, and at the same time prevent an overdose of the Calcium (which when given alone can result in cardiac arrest) during restoration. For those that have no access to CMPK, A ‘homemade recipe’ for it follows: 

To re-create the equivalent of a 30 cc CMPK dose (650 mg calcium; 500mg potassium; 150 mg phosphorus; and 96 mg magnesium) right in your kitchen, go to the Supplements department of any large chain-type drugstore and buy a bottle of Posture-D tablets (containing 600mg calcium, 266mg phosphorus, and 50mg magnesium), and bottles of Potassium tablets (500 or 550mg) and Magnesium tablets (150 or 250mg).  Calculate the amount of each pill needed to come up with an equivalent to one 30cc dose of CMPK as spelled out above, and, using a pill cutter of some kind, create that amount, crush it up to a powder and serve it orally in a little yogurt. Or add some water to the mixture and dose it in a drenching syringe.
***This delayed labor brought about by a lack of sufficient calcium to provide the uterus with proper muscle tone is also the cause of Floppy Kid Syndrome!  The babies remain in the birth canal for too long before gaining access to oxygen, a process which sets up an acidosis in the brain tissue.  This is why Sodium Bicarbonate is the treatment of choice to save the ‘Floppy Kid”, which it does by neutralizing the acidosis in the kid’s brain.
****If the pregnant doe is lactating and still being milked, you can serve that grain/pellets combo to her while in the stanchion
Sue Reith

Lets talk about CAE.

At the very beginning of my Kinder breeding program I was just like lots of others, looking for more genetics for my Kinder herd without using caution when buying new stock for that program.

Sure I had read all the warnings of bringing in new stock without asking about CAE, CL and etc. but just as I have already stated, I threw all caution to the wind. All I could think about was wanting new bloodlines to increase my gene pool.

Well in 1994 the chickens came home to roost, so to speak. After coming back from the Missouri State Fair, with a blue ribbon for the Kinder doe that milked the most in the milking competition, it was time for CAE testing. This was the first time for my testing the doe that had won the milking competition. It was then that my night mare started.

I had the vet to come and draw blood for CAE.The vet called when he received the test results. All negative except for one doe. This was the doe that had won the milking competition. This was the one that tested positive for CAE. I will always remember how sick I felt. I could not believe this, she didn’t have enlarged knee joints, she was in great condition and her coat shown like a bright new copper penny. There had to be some mistake, the test had to be wrong. So I ask the vet to draw more blood and send it to another lab.

I held my breath waiting for those results but no amount of wishing was going to change the results of the first testing. The doe once again tested positive. Just hoping against all hope I ask to have more blood drawn and sent to a third lab. The results were the same, positive for CAE.

What was I going to do? Not only did I have a CAE doe in my herd but I had put all the rest of the herd at risk. I would not be able to sell Kinder; my reputation was ruined. No one would ever want to buy a Kinder goat from me. My time for breeding Kinder seemed to be at an end. I was sick and sick at heart.

I called a friend in the Kinder Association and confided in her. She convinced me to do what every lab had suggested. Put down the doe with CAE then use CAE prevention with all the other Kinder in my herd. This would mean that I must be there at every birth and never allow a doe to touch any of her kids. I would need to heat treat the colostrum and pasteurize all the milk then bottle all the kids. The labs had told me that I would need to do this for some years because, even if no other Kinder had tested positive for CAE, it could at any time raise it ugly head again. The one doe had CAE and I had exposed all the others to this monster.

We put the doe down that had CAE, then my work began to try to stop CAE from infecting my other animals. It was lots of work and heart breaking to never let a doe see her babies. When Harvey would come to evaluate and even mention that a knee joint might be a little enlarged I would immediately send that animal for meat. We tested every year for CAE.

Years passed and never another animal positive for CAE. My life breeding Kinder did continue. My reputation had not been destroyed and I watched with such pride with many does being first in their class, winning championships and winning stars in one-day testing.

What is my point for writing about all this? I want to tell others how important it is to ask questions when buying animals. I want to impress on everyone that you cannot be too careful. It is important to have a gene pool but not at the expense of all your herd. It would have been so much better to have had fewer genetics than to expose all my goats to CAE. It didn’t wipe out all my Kinder but it surely could have. God was good! It was only by the grace of God that I was able to continue my Kinder breeding. Breeding Kinder goats is something that I have just loved since the very first day and I am so thankful for the experience to have done that. I always keep in mind that it was almost cut short by my wanting more and better genetics. Be very careful!

Abnormalities and all sort of disease like Johne’s, CAE and CL can quickly deplete the Kinder gene pool. Selling animals with any of the above will decrease the gene pool all across the country. Great care needs to be taken when selling animals and when buying stock from others.

This is true of all breeds but the Kinder is much more vulnerable because their gene pool is so small compared to the other breeds.

We need to be vigilant in our breeding practices so we sell only animals with good genetics, those that are healthy in every way and those that conform to the Kinder Breed Standard.

Several studies suggest that 60% of all cattle dairies Nation-Wide have at least 10% of their herd infected with Johne’s. Studies also say that most cow dairymen are not even aware of the disease. If you are thinking that by using cow milk you will avoid exposing your kids to CAE then you should read more on these studies.
While trying to avoid CAE you may be inadvertently exposing your kids to Johne’s which is just as devasting.

For more articles about Johne’s
http://www.johnes.org/handouts/index.shtml#general_articles