Category: Nubians

DHI – Milk Testing

DHI – Milk Testing

Getting Started in DHI/ Milk Testing

Guinevere McIntyre, from original posting on the IDGA website

Here’s a good old cliche that is certainly true for the Dairy Herd Improvement (or DHI, DHIR, DHIA) program:  It is easier than you think!

Why would one be interested in the program in the first place?  You get tangible evidence of your herd’s milk production and can track each goat individually, getting information on quantity and butterfat and protein content percentages.   That all helps with management and breeding decisions, and can also earn your does some milking stars and Top Ten status, if you are doing it through ADGA.  And there’s more – not only are you learning about and promoting your own herd, the doe’s stats are entered into breed averages that help with the enhancement of that breed and dairy goats in general.  This is the type of info that the dairy cow world has in abundance – as dairy goat owners, we are working on getting there!

Here I will give you the very basics to get started, including links that will provide further details.

You will need:

  1. A tester
  2. A calibrated scale
  3. Contact with the DHI lab of your choice
  4. Enrollment with ADGA if desired

THE TESTER:  The requirements for a tester are simple, and once you’ve made contact with your DHI lab, they will help your tester get certified and ready to go. The tester cannot be a relative or anyone with a vested interest in your herd, but beyond those simple restrictions, it can be just about anyone.  Ideally you’ll want someone responsible (who will show up on test day!) and with an eye for detail for careful milk weight readings, getting sterile milk samples for each doe, and filling out the paperwork.  (Again, I promise, all very straight-forward stuff.)

THE SCALE:  You can spring for a digital scale, or go for a simpler hanging scale.  It does need to be calibrated – possibly at a local lab or your local post office may be able to do it.  I send mine in to my DHI lab, and they calibrate it for a nominal fee.  This has to be done annually, so I do it every January.

THE DHI LAB:  A good helpful DHI lab makes all of this easy.  Mine is wonderful and so accommodating with any question I have.  I use the lab at Langston University, managed by Eva Vasquez.  Follow this link for contact info for Langston as well as a complete list of labs that work with ADGA:  http://adga.org/forms/list-of-affiliates/

ADGA:  If you are doing this to improve your goat herd, most likely you will want to link your DHI testing through ADGA, so this information will get entered into their genetics website and your does will be eligible for Top Ten lists and milking charts.  Follow this link to set this up with ADGA:  http://adga.org/steps-for-adga-dhir/

There are different programs of ADGA testing that are outlined in the above link.  Owner sampler is very attractive to a lot of people as they do not have to coordinate with an outside tester, but does not qualify the does for Top Ten.  The standard program DHI-20, once described to me as the “gold standard,” involves once-a-month tests with your tester running the tests, taking the weights and pulling a milk sample from each doe.  Then you mail in the milk samples and the weight results and you’re done.  You indicate when the doe is dried up and then start up again a week after they freshen.  This is the test I use, and falling into a routine with it was quick and easy.

At first I was intimidated about starting a DHI program here, but in the end the process was (and continues to be!) smooth and straight-forward.  Along with ADGA’s linear appraisals, what I learn from the milk tests provides important insight as I continue to work to improve my herd.
ADDENDUM 4-20-14:  On the IDGA website, I reprinted an excellent write-up on starting DHI, with the kind permission of the author, Kristie of Land of Havilah Nubians.  Please visit this link to get more info:  http://www.iowadairygoat.org/dhimore.html

Polio

Polio

Judi Nayeri
Ma’s Acres Dairy Goats
Bondurant, IA

Originally appeared in the IDGA newsletter, reprinted here with kind permission of Judi Nayeri.

Foreword:  Judi Nayeri raises a lovely herd of Alpine and Nubian dairy goats in central Iowa, and is also a doctor for humans.  We experienced our first case of goat polio in the summer of 2014 – when I called Judi to tell her about the disorientation, diarrhea, drooling, and general weakness I was seeing in my then-7-month-old doe Naomi, she immediately said it sounds like polio.  I didn’t believe that was it at first, but I am very very glad that I treated with thiamin anyway, and lots of it, over a 3 day period. Naomi had entirely lost her vision and there was one scary low point where she was lying flat out on her side, and just generally looked like she was in very bad shape.  Her return to normalcy was rapid and by the end of 3 days, she was completely back to normal, literally as if nothing had happened.  I did treat with more thiamin than was prescribed – she received 8 cc every 3 to 6 hours for the first 48 hours, and every 12 hours for the next couple days.  If it ever happens again here, I will again treat with large quantities of thiamin, rather than risk not giving enough.  As Judi points out, you just can’t overdose on thiamin, they will pee out what they don’t need.  – Guinevere McIntyre

Over the years I’ve received many calls about ill goats with polio-like symptoms. Many of those have been treated successfully, so I hope this will be helpful to you. My first experience with polio was about ten years ago. A Nubian yearling was in a breeding pen. When I did my routine check, she was “down” in her hindquarters. No matter how hard she tried the best she could achieve was a sitting position. She was immediately transported to the ISU Veterinarian Clinic in Ames. She was treated for tetanus, bacterial infection and polio. Happily she recovered fully. A few years later a goat “went down” at a very hot county fair. A vet was called and she was treated for polio. She was also blind but within the next few weeks she recovered fully including her sight.

Polio in goats is not a contagious disease but a vitamin deficiency. Goats and other ruminants are dependent on thiamine in the rumen which metabolizes glucose into carbohydrates. The carbohydrates are necessary to maintain healthy brain cells.  When something occurs to disrupt the pH balance in the rumen, “friendly” thiamine producing organisms can’t function causing a failure in the cascade causing brain cell death.  Subsequent brain edema occurs causing a variety of neurological symptoms.

Neurological symptoms may include one or more of the following: weakness, staggering, tremors, blindness ( which may last several weeks after recovery), posturing, diarrhea, decreased appetite, increased aggression, increased temperature, increased respiratory rate, decreased heart rate or nystagmus (rapid eye movement).  Rumen motility remains normal. Star-gazing is very common early symptom. Our goats are very attentive, when one stares past us, into space or ignores us (when not preoccupied) it is time for concern.  Remember, anything that negatively affects the rumen environment can disrupt the “good” microorganisms, bacillus sp., clostridium sporogenes, and b. aneurolyticus, and hinder their thiamine production. The other consequence is to encourage organisms that produce thiaminases which catabolize or break down the thiamine. Either way the result is thiamine deficiency. A major cause is feeding a diet rich in concentrate ration and low in roughage. Other causes may include but are not limited to prolonged treatment with higher than recommended doses of Corid (amprolium), deworming, grazing on recently fertilized pasture, high sulfur intake (as from water), and rarely published but one of the most common causes I have seen, STRESS.

There are several diseases which can mimic polio. CAE, listeriosis, enterotoxemia, toxemia of pregnancy, grain poisoning, plant poisoning, rabies and tetanus; most commonly tetanus and listeriosis. Tetanus can be differentiated by tickling the eyelid; if the third eyelid flashes across the eye that is pathonomic for tetanus otherwise it is Polio. Also in tetanus the joints cannot be manually bent while in polio they are flexible.  It is sometimes advantageous to treat with Procaine Penicillin to cover listeriosis, in doses high enough to cross the blood-brain barrier. Use 1.5ml/25# body weight or 6ml per 100# body weight of 300,000 Iu/ml. Tetanus can be covered with 1cc of tetanus antitoxin.

Treatment of the thiamine deficiency is simple. The literature varies greatly on dose, route and frequency of treatment.  I usually use 1-2cc of 200mg/ml on a small kid and 6-8 cc on an adult animal, IM. This can be repeated in 24 hours if needed. I called a ruminant veterinarian at ISU and he suggested 5mg/ # IM or if the animal is extremely ill 5mg/# IM and IV simultaneously. Repeat injection daily for 2-3 days if necessary.  Thiamine is cheap and it is water soluble so overdose is not a concern. The animal will excrete anything it doesn’t use. You won’t overdose.

Most of the literature talks of a winter disease, but actually, it is a year ’round disease. My cases have always been in the summer when they are in milk and pushing feed based on production. In the winter my goats are on maintenance only. In summer we are also under a lot more stress with showing and weaning. Remember, early treatment is the key. Last summer my son was walking through the barn and noticed a doeling standing in a corner with tremors and staggering when she walked. She was treated immediately, she was stronger in 10-15 minutes and fully recovered in about thirty minutes, but we did continue to watch her for 24 hours. Length of recovery will depend on how long the animal has been sick.  If unsure, it is better to treat the animal than risk losing the goat. If you wait, by 2-3 days it will be too late. Remember thiamine is water soluble; you can’t harm a goat by misdiagnosis or over treatment. If unsure, TREAT.

Thiamine is cheap but it is prescription so get some from your vet as well as procaine Penicillin and Tetanus Antitoxin and keep these on hand. Goats never get sick when the vet is in. You can always call the vet in the morning to follow-up, but TREAT ASAP.
 

Coccidiosis

Coccidiosis

Causes, Prevention, Treatment, & More

Sue Reith
Carmelita Toggs
Bainbridge, WA

Followed by Reality Check!  By Bill Braun, DVM

printed here with kind permission of Sue Reith

What is the best preventative measure for coccidiosis……and if that doesn’t work what is the best treatment?

Very clean kidding pens and housing facilities for the new babies are the best preventative.  It is well known that the first kids born, if they are born on clean bedding and housed in clean pens, are very growthy in the spring, and their own immune systems, as they develop over the next few months, are very able to make antibodies to the few coccidia they are exposed to from the momentof birth.  If the next and subsequent kids are born on that same bedding and housed also in the same kid pens, without benefit of complete sanitization between groups, then the later in the season they are born, the more exposure they have to the coccidia building up in the bedding from that critical time ofbirth when they have absolutely no immune systems going for them at all, and by spring they are generally looking rather scrawny and undersized, a classic symptom of coccidiosis, in contrast to the first kids born that season in the clean environment, that are growthy and thriving.

It is important to add here that should those later kids fail to be treated to correct that scrawny and undersized condition, their future health will be permanently affected.  The presence of coccidia at the level which causes obviously impaired growth and condition in the kid will, at the same time, cause great damage to the walls of the intestinal tract through which the nutrients pass into the goat’s system.  When this sort of internal damage takes place it is irreversible, and the animal’s ability to absorb the nutrients it ingests will be permanently curtailed, subjecting it, should it survive, to a lifetime of unthriftiness.  It goes without saying that the sooner coccidiosis is treated in a kid during that first year of life, the more likely it will be to be able to live a productive life.

The best treatment is the oral sulfa.  You can buy Albon, or its generic, sulfadimethoxine, recommended over some of the other forms of sulfa for its only-one-dose-per-day property.  You can buy it in the catalogs. Sulfadimethoxine is available in the form of: gallons of oral sulfa (intended to put in large quantities into the cattle waterers, so it needs to be broken down into kid-sized individual doses); and boluses; and tablets (prescription item);and injectable… And you need to dose the INDIVIDUAL kids by weight, doubling the 1st dose, and then giving a regular dose the next 4 days after that, which will do a very good job of wiping out the coccidia in them at the time you treat.  The dose of oral Albon (generic is sulfadimethoxine) is 12.5 milligrams per pound. Remember, milligrams (mg) are not the same as millileters (ml). The label will tell you how many mg there are in every ml.

Overview of Coccidia Treatments Used Routinely for Goats by Sue Reith

Coccidiosis is treated in a variety of ways. Treatments with amprolium (CoRid is a common brand name), and decoquinate (Deccox is a common brand name), and sulfa, sulfadimethoxine, sulfamethazine (Albon is a common brand name),are all routinely used to control this problem.

Amprolium is a coccidiastat, which means that instead of killing off the coccidia it simply keeps it from producing for a couple of weeks to slow down its advance in the system.  A serious downside is that it is a thiaminase substance, so that when dosed in sufficient quantities it has the capability of destroying the necessary thiamine within a goat’s rumen, causing potentially lethal polioencephalomalacia in the goat as a result.

Decoquinate is generally fed routinely and long term to young kids to prevent the development of coccidia within them in the early stages, before the immune system kicks in.  Its downside is that it is expensive and requires daily dosing in the milk or the feed.

Sulfa is the most effective way to treat coccidia in the goat.  Sulfadimethoxine has the advantage management-wise over other forms of sulfa, because it requires only 1X daily treatment, as opposed to the 2X daily treatment required by all other forms of sulfa.  I am personally highly in favor of dosing each kid individually by weight, to ensure maximum efficiency in the treatment.  Also, while kids are being treated with sulfa it is essential to have plenty of freshwater available to them at all times.

Albon is the best known brand of sulfadimethoxine, and there are several generic brands as well.  Additionally, there are several non-prescription forms of sulfadimethoxine available for use. Sulfa in all of the available forms is dosed at the rate of 25mg/1lb of goat the first day, and 12.5mg/1lb of goat daily for the next 4 days.

The available (non-prescription) forms are:

  1. Oral liquid, 1 gallon, 12.5%, designed to be used in the water of cattle, or as an individual drench.
  2. Injectable, 40%, designed to be used intravenously, but routinely administered by owners to their goats subcutaneously.
  3. Boluses, 5 grams each, designed to be dosed orally with a balling gun.

Sulfadimethoxine 12.5% oral liquid is in a gallon bottle for use in drinking water when treating cattle, and it can be used as a drench as well.  It is dose done time daily for 5 days in a row.  When using it as a drench, the first oral dose (always double) is 20cc/100lbs of goat.  The next 4 oral doses are 10cc/100lb of goat.

Sulfadimethoxine 40% inj contains 400mg of sulfadimethoxine per ml, which at the rate of 25mg per pound of goat the first day, and then 12.5mg per pound daily for the next 4 days, would be injected SQ at the rate of 1ml per 16 lb of goat the first day, then 1ml per 32 lbs of goat daily for the remaining 4 days of treatment.

Sulfadimethoxine is also available in boluses, with each goat/sheep sized bolus containing 5 grams of sulfadimethoxine.  If using these, 1/2 bolus would treat 100lb of goat the first day, and 1/2 bolus would treat 200lb of goat daily for the next 4 days.  A balling gun would be used for administration.

Addendum 2016/ G. McIntyre – we have been using a product that was not common when this article was written.  Toltrazuril (Baycox) is very effective for us, a simple preventative in the form of 1cc/5lb doses given to kids starting at 4 weeks, and following up once a month until 6 months of age.  (Same dosage for treatment.)

Reality Check!!!

By Bill Braun, DVM.

Dr Braun is currently an associate professor of veterinary medicine in the College of Veterinary Medicine, University of Missouri. He previously taught at the School of Veterinary Medicine, Louisiana State University. He is a board certified theriogenologist, a recognized specialist in animal reproduction. In the past he has been an associate and contributing editor and author for the Dairy Goat Journal. Dr. Braun just finished as section editor and author for the section on goat reproduction to be published this year. (1996)

Coccidiosis is a disease and it is a parasite.  As a parasite it needs a host of some sort in order to live and reproduce. Coccidia DO NOT live in the ground, they eventually die in the ground.  The only part of their life cycle that is in the ground, and therefore outside of the host’s body is in the form of oocysts.  Think of these as eggs, as in intestinal worm eggs.  It’s the same sort of principle.  Oocysts on the ground will eventually die, the speed of that die off depends on the temperature, amount of sunlight and how much moisture is present.  Freezing (winter) will kill them and hot, dry conditions will also do them in. The reason it seems that coccidia are more active as the weather warms up and the rains come is because fewer of the oocysts are dying off, therefore, there are more present to infest or infect their next victim.

The victim: Each coccidia species has its own particular host and will not tolerate another.  There are coccidia for chickens, for sheep, for goats, for cows and so on. They typically do not cross to other species, other than sheep and goats share a few of the coccidia types.  Their usual victims are the young, in this case the current year’s kid crop.  The young pick up the oocysts from eating things that are contaminated with feces (goat berries) that contain the oocysts.  The parasite breaks free of the shell of the oocyst in the victims gut and begins its life’s cycle. The only place a coccidia can live is in the gut.  It usually takes 2-4 weeks for the life cycle to be complete to the point of that victim shedding its own oocysts in its feces.  Now you know why you don’t have trouble with coccidiosis in kids until they are 2.5 to 4 weeks old.

Immunity: As long as the coccidia doesn’t kill its host, the host will gradually become partially immune to the parasite.  So as the animal becomes older, it builds up its immunity until coccidia are usually no longer a problem.  Coccidiostats (rumensin, lascalocid, sulfas, etc) help the victim keep down the number of coccidia in its body so that the victim can live long enough to develop that immunity.  The coccidiostats don’t totally eliminate the coccidia from the body, just reduce their numbers and the severity of any clinical problems.  Coccidiostats like amprolium (Corid) tie up thiamin and make it unavailable to the host, thereby causing polio in some over-treated animals.  Adult goats have coccidia in their gut.  They have learned to live with the bug and have developed some immunity.  If the adult animal becomes debilitated from some disease or condition (starvation) it may break with coccidiosis.  Otherwise, the adult animal does not have clinical coccidiosis.

If, by chance (like being raised on wire or slats like little pigs), an animal makes it to adulthood without experiencing coccidia, they will die rapidly from exposure to the bug.  They have developed no immunity to the disease and are very susceptible. Most (all) producers want to have their animals exposed to coccidia at an early age so they can develop immunity and be protected later in life.

 

Enterotoxemia: How it Gets Started

Enterotoxemia: How it Gets Started

A Seasonal Reminder

Sue Reith
Carmelita Toggs
Bainbridge, WA

printed here with kind permission of Sue Reith

Spring is a dangerous time of the year for enterotoxemia because so many animals are let out on the new, lush spring grass and bloat is common under such circumstances.  The problem is, bloat is often just the beginning of the problem. Enterotoxemia is a common secondary invader that follows on its heels.  You need to be prepared now to give any goat that does become bloated from eating the spring grass a dose of antitoxin preventatively when this happens, as a stitch in time saves nine, and it is easier to prevent this disease than to treat it!

Enterotoxemia is a disease caused by the overproduction of toxins by the clostridium prefringens organisms that are found naturally in the rumen of the goat. As they multiply in the rumen, which they will do if it is slowed or shut down for any reason, the toxins quickly reach the level where they start to destroy the intestinal walls, eventually passing through them and into the peritoneal cavity where they systematically begin shutting the organs down, killing the host.  It is a very painful way to die.

The clostridial (enterotoxemia) organisms are always present in the goat’s gut, right along with everything else.  They usually cause no trouble because they just keep passing on out of the system in the feces.  The gut activity needs to be stopped by something else for a long enough time to give those little bugs a chance to build up sufficient numbers to cause enterotoxemia.  Some of the gut-stoppers that are common precursors to entero are grass bloat, too much carbohydrate, as in heavy feedings of milk replacers or milk/replacer + grain (slow to digest), Floppy Kid Syndrome, etc…

Some may have noticed that whenever anyone mentions that an animal has bloat or grain overload or etc I suggest, as a part of the corrective measures, that he/she administer a hefty dose of Enterotoxemia Antitoxin ASAP.  Owners often resist (as in ignore) that part of the treatment because they don’t keep Entero Antitoxin on hand and they know (or the vet has said) it is bloat, etc., not entero… (!)

When the problem begins, that’s no doubt true.  And if the animal is current on all its CD/T vaccinations and over 4 months of age that still may be true.  But any older animal that has not had its yearly boosters is at risk, as is a yearling that did not receive at least 2 vaccinations no earlier than 2 months of age AND a booster at 6 months of age, thus has NO antibodies left at 1 year of age.

The key here is that it takes just a few days (maybe 5 or so at the most) for whatever has stopped up the gut initially (such as FKS or grain overload or too much milk replacer or grass bloat or whatever) to turn into full-blown enterotoxemia.  You see, when the naturally occurring clostridial organisms stop passing routinely out of that now stopped-up rumen it takes that long for them to multiply within the rumen until they are in sufficient number to create enterotoxemia in the gut.

It is incredibly rewarding to me to learn that more and more owners have actually avoided enterotoxemia by giving the antitoxin preventatively when the goat’s gut is compromised in this manner.  By comparison, it’s so sad to learn of goats that have died unnecessarily but could have been saved, only because people (INCLUDING many vets!) didn’t realize the danger inherent in a stopped up gut and prepare ahead to have CD Antitoxin on hand for such emergencies.

Keep in mind that the CD Antitoxin has only one function.  That is to destroy on contact any entero toxins detected in the gut.  So if, due to the animal’s own immune system having sufficient antibodies present, there are NO entero toxins developing in the stopped-up gut, it has no other role to play and will just dissipate from the goat’s system.

Addendum: FYI:  Banamine kills the pain and cuts inflammation created by the toxins as they do their damage to the gut walls (whatever else you do, do not substitute dexamethasone for Banamine, as it will shut down the immune system while reducing the inflammation!);  BoSe stimulates the body’s own immune system so it can help itself to get better while you help it from outside;  Penicillin does its part to help kill off the toxins, but is not strong enough to do that without the help of the antitoxin;  electrolytes keep up the body’s natural chemical balance so it won’t die of dehydration while you are trying to kill off the entero;  baking soda reverses the acidosis created by the toxins as they destroy the walls of the intestines;  and Pepto Bismol coats the intestinal walls to help protect them from further damage by the toxins.

Deworming

Deworming

WORMING:
A Simple Approach to Success

Sue Reith
Carmelita Toggs
Bainbridge, WA

printed here with kind permission of Sue Reith

Jasper Farm –  We have actually experienced a resistance on our farm to Ivomec, and in most recent years have had good success with Valbazen.  We have not experienced a problem with liver fluke.  What’s so important about this article is to understand HOW to deworm effectively and WHY you do it.  Don’t get hung up on the brand/type of dewormer, other than that you need to use something that is effective for your animals.

Resistance to wormers is a ‘catch all’ term that’s very popular these days.  What’s really happening is a failure to understand the proper approach to worming.

The directions on any wormer package invariably say it wipes out ONLY the ADULT worms.  (Well, some claim to wipe out ‘4th stage larvae as well, but they’re only a day away from adulthood by then so the wormer will still be in the system to get them the next day.)

The time it takes for the average worm egg to pass thru the larval stage, and mature to lay its own eggs, is only about 14 days.  If your goats have a pretty serious worm problem and you worm them once, and then check a fecal sample a month later, you’re still going to find a bunch of worm eggs on the slide.  And it’ll be quickly determined that your goat is ‘resistant’ to the wormer.  But the catch is that the eggs on the slide this time aren’t from those original worms, which most definitely are long dead. Instead, they’re being produced by new adult worms that were just eggs and larvae when the previous worming was done, so were not affected by it. Now they’re adults themselves, producing their own eggs!

To avoid that confusion (and to be sure you’ve actually reached your goal of wiping out a serious worm load as well) proper worming must be done 3X in a row, allowing about 10 days between each dose, to destroy as many newly matured adults as possible before they start producing eggs of their own to start yet another worm cycle.

After doing all that you should be able to do another fecal check and find that lo and behold, these worms assumed to be ‘resistant’ have all but disappeared entirely!  (BTW: It’s important to recognize that the body needs to maintain a very low level of worms, not even enough to show up on the slide in most cases, so the immune system will have something against which to continue developing antibodies.)

There’s one big exception to that, and it’s the existence of the Liver fluke.  This is a highly lethal, difficult to eradicate worm that can only be done-in sufficiently by using that 3X worming regimen.  The Liver fluke eggs closely resemble those of the Haemonchus contortus (barberpole worm).  But unfortunately for goat owners, while Haemonchus contortus responds well to general wormers, the Liver fluke does not.  It will, however, respond readily to a relatively new product, Ivomec PLUS.  The PLUS part is clorsulon, specific to Liver fluke eradication.

This is where (albeit unintentionally) the problem falls squarely on the shoulders of the veterinary community, in the form of misidentification of worm eggs.  However, that was not always the case. Early on there was excellent photo reference material available for microscopic ID of eggs /oocysts in a book entitled Veterinary Clinical Parasitology, by Sloss and Kemp.  But following the release of the 5th Edition in 1982 the publishers, Iowa State University Press, changed the format entirely, ruining it for parasite egg /oocyst ID.  Unfortunately for us all, to date they haven’t seen the need to re-issue the 5th Ed., and while a few others have tried unsuccessfully to replicate the quality of that book for use in microscopic ID of parasites, no one has yet succeeded.  Idealized artists’ renditions have been made available in the hope they’ll ‘fill the gap’, but they simply aren’t useful for making those crucial, accurate ID’s out here in the real-world.  So unless / until someone else successfully takes on this important challenge, the fact is that Veterinary offices don’t have access to good photos for accurate ID of the eggs / oocysts seen on slides that would enable them to make that vital distinction between the egg of a Liver fluke and that of a Haemonchus contortus.

And many years of ongoing mistakes in ID have now fostered a shocking veterinary protocol wherein it’s assumed that all eggs ‘looking like’ Haemonchus contortus ARE Haemonchus contortus, thus failure to wipe them out, despite the vet’s recommendation that the owner increase the doses of the wormer he has initially recommended caused the vet to automatically assume that the worms have become resistant to worming, period. So the vets began recommending to their clients the use of larger and larger amounts of the wormers they recommended, but to no avail!  The conclusion, then, is that the only practical method of control is to destroy the animals harboring these worms as a means to prevent further spread.  This is interesting, an approach that ignores information in the Merck Veterinary Manual, which is NOT text used in vet school, but instead is a vet text that’s available to Veterinarians in practice, and lay persons like myself.  (In the 6th Ed. Pp.210-211, it states that “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.”

Thus the reality is, in fact, is that the eggs that are not responding to treatment for Haemonchus contortus are actually those of the Liver fluke instead, a worm that doesn’t respond to any of the goat wormers they’re using, but can be eradicated if just treated with the proper wormer!   A pathetic situation, I must say.

Having said that, in my view the easiest way to overcome this whole problem of egg misidentification and get the job done right once and for all is to use only Ivomec Plus (at a regular dose of 1cc / 100lbs, SQ), and to repeat the wormings 3X in a row with 10 days’ lapse between each one, for ALL general worming.  The result will be an excellent broad-spectrum worming, and the only worms you won’t be able to wipe out by that method are tapeworm (easily recognized by little flat white segments in the feces, and treated effectively with Praziquantal) , and pinworms (easily recognized by tiny, hairlike, wiggly white worms in the anal opening, and treated effectively by repeated daily doses of any of the benzamidazoles.)

I raise Toggenburgs. .. After having been continuously on the ‘show circuit’ for about 25 years, I’ve now retired.  My goats, housed in their lovely ‘Goatie Condo’, are no longer being exposed to worms from outside goats.  Every now and then (If I’m lucky enough to be in the right place at the right time) I scoop up a few ‘nanny berries’ from specific animals and run a fecal check on them right here in my office… And I have to tell you, I have not seen a worm egg in any of my goats for 4 years now!

I don’t necessarily recommend that you close your herd, but I do want you to know that if, when you do worm, you worm appropriately, you really can keep your animals worm-free.

Drawing Blood

Drawing Blood

We do our own blood draws for our annual herd health testing.  It’s definitely a 2-person job, and as I tend to be a fainter (ugh), I hold the goat and my husband does the actual draw.  When we were first researching how to do this ourselves, we found a video showing a little girl holding the goat that was totally charming and confidence-inspiring – that was years ago and I can’t find that video now!  Let me know if you find it.

Here I will include a link to another excellent video and also an article by Sue Reith – I recommend checking them both out.  Also links to buy the syringes and the vacutainers…

The video:
How to Draw Blood on a Goat

Syringes

Red Top Vacutainers
Plastic is fine – they are available on Amazon too but for more $$$

Guide to Drawing Blood for Testing Purposes
By Sue Reith (reprinted with kind permission)

Materials needed

  • One sterile 10-12cc syringe per animal
  • One sterile 1-inch X 20 gauge needle per syringe
  • One Red-top 10cc Vacutainer per animal
  • One black pen to write a goat ID on each vacutainer
  • Clippers with stripping blade
  • Bottle of Isopropyl alcohol and cotton balls
  • One courageous person to draw blood
  • One sturdy person to restrain goat

Procedure

I suggest doing this early on a Monday morning, so that it can be taken to the Post Office by noon and shipped Next-Day-Air to WADDL at WSU, because testing is only done on Wednesday.

It’s important that the goat not be able to dance around, as that would make the effort to draw the blood somewhat difficult, if not dangerous. The person designated to restrain the goat plants his/her feet firmly, pulling the goat up close for support, and firmly but gently lifts and holds the goat’s head up and away from the person that will be making the blood draw.

Prepare the needles on the syringes, and have the red-top vacutainers right there beside them.

In the drawing here you will see a ‘jugular’ furrow. That runs up the length of the goat’s neck and can be felt thru the hair coat. The jugular vein, of course, is found along that furrow.

BTW: There is a jugular furrow in the same spot on EACH side of the goat’s neck. So this procedure can be conducted from either the right or the left side of the goat, depending on which is more comfortable for the person doing the blood drawing to use…

Clip away about a 2-inch wide, 3-inch high strip of hair from a mid-section of that jugular furrow area so that you can see what you are doing, and then swab the clipped area with alcohol.

Grasp the syringe in whichever hand you plan to use to do the blood draw (I do so with my left hand, with the hole in the point of the needle facing outward so I can see it), and press the thumb of the other hand firmly in the jugular furrow and hold it there until the jugular vein, with the blood flow stopped, starts to fill up and become apparent. This may take a few tries…

Gently insert (slide) the tip of the needle upward into the swelled vein, and slowly withdraw the plunger, in so doing withdrawing blood from the vein, until ~10cc have been drawn out.

Pull out the needle and place a dry cotton ball over the hole that was made, applying pressure to stop the blood flow. The person restraining the goat can then take over that job while you put the needle into the top of the vacutainer and plunge the entire 10cc of blood into it. Write the identity of that goat on the container before continuing on to the next draw…

As soon as you’re sure the bleeding has stopped, return the goat to its pen and bring out another one, repeating the whole process again until you have finished the entire blood draw!

Box up and take the Red-top vacutainers to the Post Office ASAP for shipping to WADDL.

WSU-WADDL FAQs for CAE testing

Measuring Tape Conversion Chart

Measuring Tape Conversion Chart

The measurement should be taken at the heart girth.  This is just behind front legs up to withers, but not including the shoulder blades. It should be snug, but not overly tight. These are reasonable estimates of the weight of standard dairy goats (not for pygmies or nigerian dwarves).  If done properly, in research these have been proven to be accurate within 5 pounds, plus/minus.

INCHES CENTIMETERS POUNDS     KILOGRAMS
10 ¾         27.3                 5               2.27
11 ¼        28.6                 5 1/2         2.49
11 ¾        29.9                 6               2.73
12 ¼        31.1                 6 1/2         2.95
12 ¾        32.4                 7               3.17
13 ¼        33.7                 8               3.63
13 ¾        34.9                 9               4.08
14 ¼        36.2                10              4.54
14 ¾        37.5                11              4.99
15 ¼        38.7                12              5.44
15 ¾        40.0                13              5.90
16 ¼        41.3                15              6.8
16 ¾        42.7                17              7.71
17 ¼         43.8                19             8.62
17 ¾        45.1                21             9.52
18 ¼        46.4                23            10.43
18 ¾        47.6                25            11.34
19 ¼        48.9                27            12.24
19 ¾        50.2                29            13.15
20 ¼        51.4                31            14.06
20 ¾        52.7                33            14.97
21 ¼        53.9                35            15.87
21 ¾        55.3                37            16.78
22 ¼        56.5                39            17.69
22 ¾        57.8                42            19.05
23 ¼        59.1                45            20.41
23 ¾        60.3                48            21.77
24 ¼        61.6                51            23.13
24 ¾        62.9                54            24.49
25 ¼        64.1                57            25.85
25 ¾        65.4                60            27.21
26 ¼        66.7                63            28.57
26 ¾        67.9                66            29.93
27 ¼        69.2                69            31.29
27 ¾        70.5                72            32.65
28 ¼        71.7                75            34.01
28 ¾        73.0                78            35.37
29 ¼        74.3                81            36.73
29 ¾        75.6                84            38.10
30 ¼        76.8                87            39.46
30 ¾        78.0                90            40.82
31 ¼        79.4                93            42.18
31 ¾        80.7                97            44.0
32 ¼        81.9             101             45.8
32 ¾        83.2             105             47.62
33 ¼        84.5             110             49.89
33 ¾        85.7             115             52.15
34 ¼        87.0             120             54.42
34 ¾        88.3             125             56.69
35 ¼        89.5             130             58.96
35 ¾        90.8             135             61.22
36 ¼        92.1             140             63.49
36 ¾        93.4             145             65.76
37 ¼        94.6             150             68.08
37 ¾        95.9             155             70.29
38 ¼        97.2             160             72.56
38 ¾        98.4             165             74.83
39 ¼        99.7             170             77.10
39 ¾       101.0            175             79.37
40 ¼       102.2            180             81.63
40 ¾       103.5            185             83.90
41 ¼       104.8            190             86.17
41 ¾       106.1            195             88.44
42 ¼       107.3            200             90.7
42 ¾       108.6            205             92.9
43 ¼       109.8            210             95.3
43 ¾       111.1            215             97.5
44 ¼       112.4            220             99.8
44 ¾        113.7            225           102.1
45 ¼       114.9            230           104.3
45 ¾        116.2            235           106.6
46 ¼        117.5            240          108.8
46 ¾        118.7            245           111.1
47 ¼        120               250           113.4
47 ¾       121.2            255           115.6
48 ¼       122.5            260           117.9
48 ¾       123.8            265           120.2
49 ¼        125.1            270           122.5
49 ¾        126.4            275           124.7
50 ¼       127.6            280           127
50 ¾        128.9            285           129.3
51 ¼       130.2            290           131.5
51 ¾        131.4            295           133.8
52 ¼       132.7            300           136.1