What is Toxoplasmosis?
The Healthy Herd
Note the heat effect on male animals. 71 days for bulls, 56 for rams and potentially bucks. He says that it is not expected to affect long-term fertility, just X-days from extreme heat.
From Dr.David Fernandez, U of AR
Livestock producers may see lowered fertility in herds this fall
Arkansas Division of Agriculture
Updated: August 28, 2012
PINE BLUFF, Ark. – As if drought damage to pastures and high hay and feed prices aren’t enough, livestock producers may see reduced fertility in their breeding herds this fall, says Dr. David Fernandez, University of Arkansas at Pine Bluff Cooperative Extension Program livestock specialist.
“The exceptionally high heat could impair the ability of bulls, bucks, rams and boars to produce viable sperm,” he says. Cows, does, ewes and sows may produce less viable eggs or experience higher levels of early spontaneous abortions.
Here’s why. Most male mammals’ testes are located in the scrotum outside their bodies. This allows the male to maintain his testes at a temperature several degrees below his body temperature which is essential for sperm production. When temperatures exceed 103 F for several days, the testes cannot be cooled adequately, and sperm production can be impaired, says Dr. Fernandez.
The damage to sperm production can be long term. Sperm production in the ram requires an average of 47 days plus another nine days for the sperm to migrate to the storage area. That’s 56 days. Similar time frames are believed to exist for bucks. For bulls, it is more than 70 days. The damage is not readily apparent, he says. In some cases, the number of sperm and their motility may be reduced.
“Much of the damage appears to be done to the DNA of the sperm,” he says. This means that a sire may appear to be normally fertile after a breeding soundness exam, but pregnancy rates of dams may be low, with many repeat breeders.
Compounding the problem are the effects of high heat on female reproduction. When temperatures are high, eggs may be less fertile and may not survive to form a viable embryo after fertilization. Fortunately, the effect of high temperatures on females tends to be limited to the estrus cycle in which it occurs.
“Unfortunately, no cost effective on-farm method exists to determine whether the problem is with the male or female,” says Dr. Fernandez, who advises that the best thing to do is to provide plenty of cool water and shade to help keep livestock cool. Also, monitor the herd’s nutrition as they may not eat enough feed when days are extremely hot.
Finally, producers should plan ahead so they are prepared if their herd’s breeding season begins and ends later than usual. And, investigate alternative marketing strategies and parasite management schemes for next spring and summer, he says.
In this neck of the woods the very first sign of spring is not crocuses, but daffodils. I am pleased to report that this past week I was able to pick daffodils on the south facing bank of a nearby road. So, spring is in the air!
With the advent of spring, we usually have a bunch of new arrivals on our farms, and while it is exciting and usually a joy filled time, we occasionally need to be right on top of things to preserve the lives of some of these little blessings that show up.
Because sheep and goats regularly have multiple births, all those legs can get a little tangled up, and we sometimes need to help the dam get those kids sorted out and delivered. If you have been involved with sheep or goats for any length of time, some of the info in this newsletter will seem like old hat to you. While that may be the case, from time to time going over someone else’s prepper list for birthing supplies may remind you of something you have forgotten about, or give you an additional item to include in your own preparations.
Kids and lambs often have their lives hanging in the balance in the first hours after their birth. It is always best to have what you may need in advance than to find you have forgotten something and cannot get it until the weekend is over or risk having to call a vet out at 3am to supply something you could have had on hand if you had only thought of it during the week. Because there are so many little things to think about that might mean the difference between life and death, this newsletter is devoted to Birther Preps of the critter kind.
We hope you enjoy the information and do feel free to send in your tips and tricks for this time of the year. We can always benefit from other ideas!
All of Us at Hamby Dairy Supply
Basic Birthing Kit
For Sheep and Goats
- Flashlight & batteries – For those night time deliveries.
- Latex gloves – In case you have to assist.
- OB Lube – In case you have to “go in” to assist.
- 7% iodine – To treat the umbilical cord to prevent navel ill.
- Small spray bottle or film container – for dipping or spraying the umbilical cord with iodine.
- Dental floss – To tie the umbilical cord, if necessary.
- Blunt nosed scissors – For cutting the umbilical cord if it is too long.
- Long Shoe String- to make a loop to pull leg into position
*Corn Oil and Turkey Baster- to help lubricate for a
large kid to come through you can flood the vagina
with corn oil.
*Vitamin E oil- 2cc of vitamin e will often help a kid nurse
- Alcohol – to sterilize tools
- Baby nasal aspirator – To remove fluids from newborn’s mouth & nose, if necessary.
- 3 old but clean towels & 2 washcloths – To dry kids to prevent chill & dry hands.
- Bottle & Pritchard Nipple – In case you need to bottle feed, I have had the best luck getting newborns to use the Pritchard Nipple over others.
- Lamb / kid puller – In case of a kid that is positioned wrong. (Usually just your hand is enough to help a doe that needs help but it is a good idea to have one).
- Weak lamb syringe & feeding tube – To feed kids too weak to nurse.
- Small scale – to get a birth weight on the kids.
- Feed bag or garbage bag – For afterbirth.
- Soap & warm water – for washing up in case you need to assist.
- Small notebook & Pen – to record birth weights, etc.
- Digital thermometer – To check the temperature of chilled kids.
- Quiet hair dryer – to warm a mildly chilled kid.
- Phone # of 2 goat knowledgeable keepers/veterinarians – in case of an emergency.
by Sue Beck
With our days getting longer and our pastures getting greener, many of us are looking forward to being able to put our goats out on grass. But with the fresh new leaves of spring come one of the biggest threats to our herds’ health – parasites.
During the winter, the parasite eggs in your pastures go dormant, and pose very little risk of infecting our goats, making it the ideal time to get parasite problems under control. Now is the time when you should be testing fecal samples and treating accordingly, or using a broad spectrum dewormer to eradicate the parasites currently in your goats. If you can begin the summer with a clean herd, you will end it with a clean pasture.
In a recent presentation, Dr. Donald Bliss, founder and owner of MidAmerica Ag Research, recommended the following procedure to eradicate parasites in your herd:
1. Use Safeguard at the rate of 7.5 mg/kg spread over 3 days, then give Cydectin cattle pour-on dewormer orally (1 cc/ 20 pounds) on day 4.
2. Check random fecal samples 7-10 days after deworming.
3. Retreat if necessary, using wormer specific to the worms your goats still have.
4. Continue this process until your samples are free of parasites.
Early spring (as soon as the grass starts to grow):
1. Treat your herd with Safeguard at the rate of 7.5 mg/kg spread over 3 days.
2. Wait three weeks and retreat with Safeguard again.
3. Wait three weeks and treat with Cydectin as above (1 cc/ 20 pounds).
Timing is critical in this process. Parasite larva load is extremely high in the spring as dormant eggs begin to hatch, but by June, almost all these eggs have hatched and emerged. By treating aggressively at the beginning of the grazing season, you eradicate almost all existing larva from your pasture. If your goats are not dropping new eggs, the rate at which they become reinfested with parasites should decrease dramatically, and continue to decrease each year until they are virtually nonexistent in your herd. Just remember – if you can get your goats worm-free in winter and your pastures worm-free in spring, the rest of your year will be trouble free, too!
(an often-misidentified worm that’s lethal if not treated for properly)
by Sue Reith.
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
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.)
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.