Copper and Your Goat

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Some of these articles are very scientific so just hang in there with me if you can. I want you to get as much information as you can possibly get.

This page is going to be pretty lengthly because it covers the importance of copper in a goats diet and how it can help manage your goats health and condition and resistance to illnesses and parasites.

Now Im going to try to share some info that may be hard to understand at first but I will print more than one article of how people have explained this practice. I am incorporating this into my management program as well.

It is called Copper Bolusing (I may not have spelled it correctly). It is used in cattle but it can be used in goats and sheep as well. It is where you give a goat a Copper Bolusus with a pill gun. Now there are other ways you can give it to them so use your imagination if you dont want to give a pill. I know they already get copper in their feed and minerals, but it is Copper Sulfate which is a different form that what the pills are. The pills are Copper Oxide. Some of our feed and minerals have alot of iron which inhibits the absorption of copper like copper sulfate. Copper oxide is not hindered by iron so there fore it is absorbed better and stays longer in the body because it is slow releasing. There is no danger of Copper toxicity if used correctly. It is recommended to use twice a year. Once in spring and once in fall. I have seen pics and read of so many good results of this practice that Ill leave you with some articles from different people so you can see their opinions, research and results.

This has also been researched and proven by many universities and other farms to help cut down on parasites as well as they will explain. Keep in mind they do say that goats will always have a parasite count in them because hey are browsers and eat off the ground too, and it helps them build up some sort of immunity to them. It does not completely rid them of all parasites but it sure cuts down on them and slows them down to where you dont have to worm as often. Not only that look at all the other health benefits of copper.

You can also Google Copper Oxide Wire Particles and pull up many websites with this info alot have pdf formats where you can save to your computer.

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This article is from Veterinary Parasitology journal homepage: www.elsevier.com/locate/vetpar type in key word Copper Oxide Wire Particles and you can pull up a pdf format you can save to your computer.

1. Introduction:
Infection with gastrointestinal nematodes (GIN), primarily
Haemonchus contortus, a blood-feeder that can cause severe anemia in infected animals, is the primary constraint to profitable sheep and goat production where this parasite is endemic, including the southeastern USA.
Broad-spectrum drugs have been the basis of control strategies in the past, but these drugs now have reduced efficacy due to widespread development of anthelmintic resistance in sheep and goat GIN. Alternative GIN control methods are urgently needed to sustain small ruminant industries in the USA. One of these is treatment with copper oxide wire particles (COWP). These are commercially available in 25 g boluses (Copasure; Animax
Veterinary Technology, UK) that can be repacked into 2 g gel capsules for sheep and goats. The capsule is administered into the animalsrquote abomasum by inserting at the back of the throat using a pill gun.
A number of experiments with sheep has shown high efficacy of COWP against H. contortus, particularly in young animals. Results from a small number of COWP trials with GIN-infected goats have been reported, but often with apparent lower efficacy results than with sheep trials. These trials have been conducted in locations with differing GIN populations. To date, no direct comparison of COWP efficacy has been made between
sheep and goats grazing together and subjected to infection by the same GIN population. Therefore, a study was designed to test efficacy of 2 g COWP in gel capsules against GIN in sheep and goats grazing the same pasture area at the Fort Valley State University Agricultural Research Station in Central Georgia in the southern US.
2. Materials and methods. 2.1. Animal welfare.
All animal procedures used in this study were approved by the Fort Valley State University Institutional Animal Care and Use Committee.
2.2. Experimental design and protocol.
A grazing study with young goat bucks (Kiko Spanish cross, 6 months old; n = 12) and female lambs (Katahdin or Dorper Blackface crosses, 5 months old; n = 12) was completed at the Fort Valley State University Agricultural
Research Station, Fort Valley, Georgia, during August and September, 2007. Prior to starting the trial, the goats acquired a natural GIN infection by grazing perennial summer grass pasture {primarily bermudagrass [(Cynodon dactylon (L.) Pers)], and bahiagrass (Paspalum notatum Flugge)} for approximately 4 months. Fecal samples were
collected weekly from individual animals to monitor fecal egg counts (FEC). When FEC were sufficiently high (approximately 3000 and 1500 for lambs and kids, respectively), the lambs and kids were randomly assigned
to 1 of 2 treatment groups such that both lamb and kid groups had similar total eggs per gram (EPG). The treatments consisted of: (1) 2 g of COWP in a gel capsule administered per os using a pill gun, and (2) no COWP.
After treatment, all the animals were grazed together on the same pastures as described previously, for 28 days, after which half the animals in each treatment group were randomly selected and removed from the grazing area for slaughter. The remaining animals were allowed to continue
grazing for an additional 14 days, after which the trial was terminated.
2.3. Sampling procedures and analysis.Throughout the grazing period after COWP was administered, blood and rectal fecal samples were collected from individual animals weekly for PCV and FEC determination, respectively. All FEC determinations were made on fresh feces. Eggs per gram of feces were counted using a modified McMaster procedure and PCV was determined using a Marathon 6K micro-hematocrit centrifuge and reader.
2.4. Recovery and counting of adult nematodes Adult GIN from abomasum and small intestines were recovered, counted, and identified to species using the procedures described by Shaik et al. (2006). The abomasal and small intestinal contents for each animal were washed into plastic buckets, brought up to 3 L with tap water, vigorously mixed, and then subsampled (2 aliquots of 150 mL each). The adult GIN were preserved by adding 100 mL of 10% buffered formalin solution to each container. The GIN were recovered
from one of the aliquots and counted using a Leica Zoom 2000 phase contrast microscope.
2.5. Statistical analyses:
Fecal egg count and PCV data were analyzed as a repeated measures analysis in a completely randomized design using the mixed model procedure of SAS with treatment, species, and species treatment interaction in the model. Adult GIN data were analyzed as a completely randomized design using the GLM procedure of SAS. The FEC and adult GIN data were log-transformed prior to statistical analysis to normalize the data. When treatment effects were different at P < 0.05, means were separated using LSD test. Fecal egg count and adult GIN data are reported as least squares means of untransformed data, with statistical inferences based upon log-transformed data analysis.
3. Results
3.1. Fecal egg counts
In both sheep and goats, treatment with 2 g of COWP significantly reduced (P < 0.01) FEC compared with control animals during the 28-day trial period (Fig. 1). After 12 days, FEC of COWP-treated sheep and goats were 94.3 and 74.9% lower, respectively, than untreated animals, while these differences were 82.5 and 90.5% for sheep and goats 26 days after treatment. Following the removal of half the animals in each treatment group for slaughter and worm recovery, there were significant treatment (P < 0.01) and species (P < 0.05) differences in FEC in the remaining animals between 28 and 42 days after COWP administration. The FEC of COWP-treated sheep and goats were 87.2 and 83.5% lower than non-treated animals, respectively, by day 42 of the experiment. Throughout the whole trial, the average FEC was higher in sheep than in goats.
3.2. Blood packed cell volume
There were significant treatment (P < 0.01) and species (P < 0.01) effects on blood PCV values (Fig. 2). The animals treated with COWP had higher (P < 0.05) PCV values than controls from days 21 to 42 of the experiment. Sheep had higher (P < 0.01) PCV than goats throughout the study.
3.3. Adult nematodes
Treatment with COWP reduced total H. contortus counts in the abomasum of both sheep (P < 0.05) and goats (P < 0.01), but had no effect on Teladorsagia circumcincta (abomasum) or the small intestinal worm Trichostrongylus colubriformis (Figs. 3 and 4). The reduction in number of
adult H. contortus due to COWP treatment was 67.2 and 85.8% for sheep and goats, respectively. Because the overall worm burden in each species was over 90% H. contortus, there was also a significant reduction in total GIN in both sheep and goats (P < 0.01) due to COWP treatment. These differences were 62.7 and 78.7%, respectively.
4. Discussion
Treatment with 2 g of COWP in a gel capsule effectively reduced GIN burden in both lambs and kids in the current study. Similar results have been observed with young animals in the literature . Burke reported that 2, 4, and 6 g doses of COWP were all highly effective against a predominantly H. contortus infection in 5- 6 months old hair breed lambs. In a follow-up study with lambs, Miller found similar effectiveness using lower COWP doses of 0.5, 1.0, and 1.5 g. Treatment with COWP up to a 4 g dose may be
less effective in mature sheep than in lambs (Burke, although there was no direct comparison made. Previous studies on COWP effectiveness against GIN infection in goats have been variable as well, with better results reported for weaned kids than for more mature animals, although there were fewer H. contortus in the mature goats (Burke et al., 2007b). Doses of COWPfrom 0.5 to 4 g all reduced FEC of weaned Boer Spanish cross kids by 75- 85%, while COWP doses up to 10 g were less effective or not effective against GIN of more mature goats that had more intestinal than abomasal worms. In previous reports, there were no direct comparisons of COWP effectiveness in sheep and goats grazing the same pasture and exposed to the same GIN population. There were species differences in initial FEC and anemia scores in the current study, with higher FEC and PCV values in the
lambs compared with the kids. Sheep can generally tolerate a higher infection rate than goats and still be productive. Despite these differences in infection rate between lambs and kids, COWP appeared to be equally effective as an anti-parasite agent in both species in the current study. The initial reduction in FEC was more pronounced in the lambs, but on a percentage basis, there was not much difference between the two species. In both species, the reduction in FEC in COWP-treated animals compared to untreated controls ranged from 75 to 95% throughout the trial, and this reduction was maintained for 42 days after treatment. Blood PCV was markedly improved by COWP treatment in both the lambs and kids, although there was a slight decline over the course of the trial in lambs, whereas PCV increased by approximately four percentage points in the
kids. The reduction in adult H. contortus numbers in the abomasum of 67.2% for lambs is less than previously reported for lambs given 2- 6 g COWP boluses in a study by Burke, in which the lambs were slaughtered 26 days post-treatment. The longer posttreatment period prior to slaughter in the current study (42 days) may have allowed some reinfection to occur, which might account for these differences. Previous reports on goats given 0endash 10 g of COWP did not include adult nematode data, but 85.8% reduction in H. contortus indicates very good efficacy against this parasite at the 2 g COWP dose level in goats in the current investigation. Generally high efficacy of COWP for both sheep and goats in this study is most likely related to the overall GIN infection in each species being >90% H. contortus.
Because COWP are less effective against T. circumcincta or T. colubriformis than H. contortus , the season of the year when the trial incompleted makes a difference in the results, as T. circumcincta and T. colubriformis are more prevalent in the cooler months of the year. The current investigation was completed in the summer when the predominant infection was H. contortus.
5. Conclusions:
Copper oxide wire particles effectively reduced H. contortus populations in kids and lambs grazing the same pasture and sharing a genetically similar worm population. Treatment with COWP at the 2 g level appears to be a viable option for controlling GIN infection in weanlings for both species when a predominant H. contortus infection is present. Further investigation with mature sheep and goats grazing the same pasture would be needed to compare the difference in the efficacy of COWP between adults of the two species.
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Phew I know that was alot to ingest. And there is a whole long list of references too but I want print them just take my word for it….lol

Here is a funnier read. If all her pics dont show up go to her blog at http://noodlevilleadventures.blogspot.com/2012/01/noodleville-how-to-copper-bolusing.html She is just too funny.

A Noodleville “How To”: Copper Bolusing

I read many great blogs. I sit and read blogs more often than I post on my own.Why? Well, because most of them provide really useful info in an entertaining format. Throw in a healthy dose of life experiences/stories and I m a happy reader. My blog is mostly a place where I jot down various happenings in my life, but rarely do I post actual useable info. Not sure how this is going to go, but I m going to attempt to sporadically post useful How To’s in the future. Do note that I said sporadically this gets me & my sporadic, hectic, unscheduled self off the hook for posting specifics at particular times.

So todays How To is going to be about copper bolusing goats. In advance, Ill forewarn yall that this isnt necessarily the gospel, its not the ONLY way to do things and I wont be getting overly scientific on yall.

Copper has been linked to fertility, parasite resistance, growth, resistance to disease, & general over all health. Most minerals do not provide adequate levels of copper to meet the needs of goats. Copper bolusing is a fantastic way to give a slow release copper supplement.Copper deficiency can show itself in numerous ways. Also, blood samples are not a reliable way to check for copper levels in goats, the best way to check copper levels is by liver biopsy which can be performed during a necropsy (I personally dont know any vets willing to do it on a live goat, but it can be done). Handy for the goat owner to get a view on how things are going with their management. Not so handy for the goat having the necropsy. So, here are a few outward signs of copper deficiency I can show you from my own goats (do keep in mind, these are not the only signs, just sharing a few from my herd). Sabrina came to me looking a bit rough. Her diet had been a mineral block, heavy sweet feeds (covered in molasses, which is high in iron and high iron levels inhibit copper absorption), rationed alfalfa hay, unlimited grass hay and grazing/browse. If you look at her tail tip in this picture shortly after we brought her home you can see she has a fish tail with a bald tail tip and the remaining tail hair resembles a fish tail. Many goats will grow this hair back after proper mineral needs are met and maintained, some wont. Sabrinas has filled in some, though not fully so Im still waiting to see if hers will fill in.

Sabrina 2011. Note the coarse coat & “fish tail”

Next up is this burnt, coppery colored hair tips. No, this is NOT sun bleaching and it was also present on the dark hairs of her legs. Her previous home had loads of trees and shade was plentiful, where as here in the desolate, dry land of Noodle, trees and natural shade are sparse. For a fair comparison, I snapped pictures of her hair almost exactly one year apart so you can look at the difference and can compare winter hair to winter hair (In her before pics which were taken January 2011, she was pregnant & due in 2 months, in her after pics, taken January 2012, she only has 21 days left before her due date). Here we have minimal shade and if anything she spent MORE time in the sun than at her previous home, yet there are no burnt colored hair tips now. Her bald tail tip has filled in some as well, though not fully. The texture of the hair is also greatly improved. A year ago it was course and brittle, now its soft and has a healthy shine to it.

Before Copper. January 2011 Brittle, coarse hair. Discoloration affected all dark hairs
After Copper. January 2012. Hair has no discoloration, it’s sleek, smooth (and covered in hay bits)

I didnt think about it at the time, but I should have taken pictures of her feet. Good grief they were awful!! Her previous home kept her feet trimmed every 2 months, but the overall condition of the hoof material was very poor….. Now her feet are pretty normal and don’t require as much effort to trim properly, nor do they have the tendency to grow misshapen as they did when she first arrived..
Another sign of copper deficiency is a fading out of the coat, or what some folks call “ghosting”. Bleuberry shows deficiency this way. She has no noticeable “fish tail” or burnt hair tips. I can’t give you pictures of her as I shaved her down and don’t have the “before” pics to share…. Just keep in mind, that even within one herd, animals can display deficiencies differently.
To make a copper bolus I rely on the info provided by Joyce Lazzaro at Saanendoah. Her site will give you all the scientific, technical info on her copper studies (plus show you the other signs of copper deficiency not shown here). Fantastic read, great pictures and any goat owner really should take the time to read her information.
First youll need to buy a bottle of Copasure. I buy mine from Jeffers Livestock. These are copper boluses made up for cattle so youll need to break them down into smaller doses for goats. The $40+ may seem steep, but a little goes a long way so this should last you quite a while. I’ll have to double check, but we bolused my mom’s 3 miniature does, my 2 Lamanchas, and the 2 Alpine does & I think we used 3-4 of the boluses total and we typically bolus every 4 months.

Copasure & a calf sized bolus

Using a postal scale, you weigh out the appropriate dose of copper needed for your goat. Repackage the rods into smaller gel capsules. I place the lil’ foam pad from the Copasure container on my scale, zero it out, then pour on the copper rods.

Copper Oxide rods inside a bolus

I buy the smaller gel capsules at the health food store, but recently noticed Jeffer’s is now carrying them, as are several other online vendors. You can buy a variety of sizes but I personally prefer to package all my boluses in one size gel capsule & fill accordingly. I dose according to the data collected by Joyce Lazzaro which is 1 gram per 22lbs.

Next is the tricky part.
Ok, ok, I confess I seem to be the only bolusing challenged person in the whole world!!!!!!!
I was instructed to use the smallest baling gun. I tried that. I got chomped up, spit out boluses. I found it too long, bulky, and thought it did a very poor job of holding the smaller bolus (even with peanut butter!). The goal here is to get the entire bolus swallowed WHOLE. Which means, using the baling gun, you hold open the mouth, put the baling gun as far back as possible. Im not talking just in the mouth. I mean over the back of the tongue and into the throat. Once in position you push the plunger and shoot the bolus, whole, down their throat.
I saw videos. I had helpful folks walk me through the process and give me 10,000 pointers. Yet, while all my goaty friends were swiftly, happily bolusing their goats, I was not. I tried empty horse dewormer tubes still a no go. I gave up, and went for an alternative method. Hiding the rods in treats. Sabrina would swallow an orange slice with a bolus in it with no problem. My miniature doe liked marshmallows. The rest? Not so much they spit, chomped and basically did whatever possible to thwart me with every treat imaginable.
Sadistic lil critters! Then I found my life saver in the form of a $2 piece of plastic.

A bolusing challenged gals best friend!

This Pill Gun (known as the “Buster Pet Piller” from Jeffers) freaking rocks!!!!!
Granted, its not as long as a baling gun, so I have to hold their mouth open wide and get it back there but thats no biggey. This lil pill gun firmly holds the bolus with a rubbery grip end, plus it also holds about 2-3ccs of fluid so when you push the plunger, fluid also comes out to help push that sucker right on down their throat.
Follow up with a treat while saying Nummy, Nummy and youre all done! If you decide to use fluid in the pill gun (I do), make sure you dry the rubber gripper tip before putting the bolus in so it doesn’t slip and to prevent the moisture from breaking down the gel cap prematurely.

Just look at that nifty lil booger hugging my bolus!! Note- I wouldn’t use a capsule bigger than 00 with this gun.

I say Nummy, Nummy in a “sing-song” voice while giving all oral meds to goats & children. I think it helps the process, my kids contradict me.
Now, a few things to keep in mind. In the front, goats only have bottom teeth, no top teeth, instead on top they have a hard dental pad. However, in the back they have both top and bottom teeth that are SHARP! Your dogs molars have nothing on the molars of a goat and I promise you, you do not want to get your fingers caught!
Here is a handy picture showing you the anatomy of a goats mouth. You can see the lower incisors in the front, the gap, then the razor sharp molars in the back.

When bolusing, I straddle the goat, grab from the top and hold firmly in that toothless gap, careful to keep my fingers away from the chomping molars. Tilt the head back, push pill gun up over the tongue and as far back as I can get it, then push the plunger, close their mouth and shove a treat in!! With Bleuberry, I’m not tall enough to straddle her, so I lock her in the milkstand to bolus her. Easy Peasy! So easy in fact, that Clayton, my 8 year old, bolused Casper without a single problem. No spit out boluses, no chomped boluses, and no missing fingers.
Now, there is some debate on whether or not bolusing via treats is as reliable as the traditional baling gun (or pet pill gun) method, Im not getting into all that here. I did the treat method out of desperation, but in all honesty, I prefer the pill gun and giving full, un-chewed boluses. That way I KNOW without a doubt that they received their full dose.
Here is a nifty lil diagram illustrating how the bolus actually works:

How the bolus works. Photo courtesy of Joyce Lazzaro by way of Animax Vet

Now, do keep in mind that copper is just one part in the mineral equation. Depending on your area you may have other deficiencies to worry about. For my area, and my herd, I have best results copper bolusing every 3-4 months, and I also give Bo-Se which is an injectable Vitamin E/Selenium that you can obtain with a vet RX. In addition to this I feed a high quality LOOSE mineral.
Emphasis on LOOSE mineral, as in bagged and similar to coarse sand in texture. Yes, there are mineral blocks available, but have you ever been licked by a goat? If not, come over and Ill set Sabrina on ya.
Goats have very smooth tongues like a dog does which make it a bit more difficult to get all they need simply by licking at the block. Mineral blocks are typically full of cheap salts, so the goat needs to consume more of the block in order to meet its mineral needs. Problem is, the goat is attracted to the mineral block because of the salt and they typically get their fill of salt before theyve come close to consuming the necessary amount of minerals. So all in all, while its a convenient concept, to me, a mineral block is worthless.

There are a variety of loose minerals on the market. Steer clear of Sheep & Goat minerals. Copper is toxic to sheep, while studies have shown that goats need a good bit of it, so a mineral safe for sheep just isnt going to come close to meeting a goats copper needs. I prefer to buy dark, loose minerals grey, brownish ones. The red ones usually contain higher levels of iron and iron inhibits copper absorption. Add in that many of the red minerals have iffy amounts and sources of copper to begin with and its just not worth the money. The best I could find, in my area is Cargill Right Now Onyx, a cattle mineral and the goats seem to do great on it and readily consume it, so Im happy.

My loose mineral of choice. A 50lb bag last FOREVER.

To be truly scientific I even tried a few for comparison…. And yes, by “tried”, I mean I went on a taste testing spree.
I licked a mineral block, a salt block and tried a pinch of the Cargill Right Now Onyx loose mineral. Salt block obviously was the saltiest. That mineral block was almost as salty as the pure salt block, with a hint of earthy undertones and the Right Now Onyx was just gross (or should I say “very earthly”?) I could taste a SLIGHT saltiness, but it was barely there. So given that controlled, uber scientific experiment, I have proven that my loose mineral of choice isnt chock full of cheap, filler salts.
True, I also read the labels as well, but the taste testing, IMO, made the whole thing more legit.

Also, a side note Copper boluses are made of copper OXIDE. I see some folks grabbing bottles of copper SULFATE and just pouring who knows how much into their water troughs, and some who even have fed it via syringe. Do keep in mind that there is such a thing as Too much of a good thing. The copper OXIDE rods in the bolus dissolve slowly over a period of MONTHS in the digestive tract of the goat and when used properly, pose no risk of copper toxicity. The copper sulfate CAN be toxic and it is not a gradual release form of copper supplementation….
Anywho, just look how pretty Sabrina is now!

No coarse hair, no coat discoloration, no more hoof issues

Before her diet was heavily processed sweet feed in huge amounts (4 1/2+lbs of 16% sticky sweet feed per day), browse, a flake of alfalfa hay, mineral block and grass hay free choice. Here we switched it up a bit.
She now gets 17% protein, Standlee alfalfa pellets, good quality coastal & sudan hay, LOOSE minerals and her grain ration is a 12% protein mix of 2 parts whole oats, 1 part Purina Strategy Healthy Edge horse feed (lower protein, high forage content high fat/calcium feed) top dressed with black oil sunflower seeds or rice bran pellets.When milking she consumes no more than 3lbs of grain per day (usually 1lb each milking) and last lactation she milked 14lbs at 2 weeks fresh. Plus she maintains great condition. So, in summary, she actually looks better on LESS feed.

The diet is made up of quality forage (alfalfa & hay), proper minerals and minimal grains. I find many folks will buy the poorest quality hay for goats, when in fact, I find my money better spent when I choose the best quality I can afford. Making the bulk of my herds diet alfalfa and quality hay enables me to have better production, better condition on a lot less of the concentrates (grain/pelleted rations) Not to mention the overall health of the herd is much, much better. Good forages make for a happy, healthy rumen. Proper minerals improve the overall health.

Sabrina’s pregnant belly January 2012. Such a huge difference in overall condition when compared to last year. Kids due January 26th.

Many people think Im nuts after all they are Just goats, they can eat anything but the proof is in the pudding my friends! Which, BTW, not a clue how this got started, but goats do NOT eat anything, nor should it be considered ok to feed them food stuffs unsuitable for other livestock. They are actually picky eaters, preferring browse to grazing and if you watch them at the hay feeder they are constantly picking through it to find the best bite (which is why I feed alfalfa pellets.. They pick through the alfalfa hay, eat the leaves and waste a ton of stems..No waste with my alfalfa pellets). A horse will consume hay spilled on the ground and walked on, a goat won’t unless that’s the only thing available….
Anywho….usually the folks who think I’m nuts and advise me to use outdated methods of poor grass hay, lots of heavy sweet feeds and inadequate minerals are those with scraggly looking goats and they are the ones losing does to hypocalcaemia every kidding season.

No scraggly looking goats here, and my does receive enough calcium from their alfalfa that Ive had no losses & no hypocalcaemia. Providing proper minerals i.e- copper, has also allowed me to deworm less frequently as well…..

Of course, each person has their own methods. I didnt invent this stuff folks. Im blessed to be advised by those who have decades of first hand experience and have been willing to help me out. In turn, Ive tweaked things to suit my herds needs and my budget and all in all, Im a happy goat owner with healthy goats.

Ive said it once, Ill say it again. If you have goats, I strongly urge you to read Joyce Lazzaro’s Copper Studies (think I’ve linked to it enough in this post? lol)...
There are some interesting pictures of animals suffering from extreme copper deficiency as well as more in depth info than the brief review I provided.
Good stuff!

Oh they did show up great pics if you ask me!
You can purchase these things also at Valley Vet and Jeffers Pet too.
Now last article I promise, this one is more in depth and has so many Universities backing the tests and results. This is more in depth and intense so buckle up:
Basic Information On Copper Deficiency In Dairy Goats In Southern California
Compiled by – Joyce Lazzaro/Saanendoah Dairy Goats
Winchester/Temecula, California

Here in southern-most Southern California (San Bernardino, Riverside, Orange and San Diego counties) and most of Arizona we have severe primary copper (Cu) deficiency (low levels in soil and feed) problem in the Swiss breeds and LaMancha dairy goats. As in cattle, we feel that genetic difference in both breeds and blood lines within breeds affects goats susceptibility to both deficiency and toxicity (research shows that Simmental and Charolais cattle need more copper in their diet than Angus, because they are less efficient absorbers of copper from the small intestine. And field experience suggests Simmental, Maine Anjou, Limousin and Charolais benefit from 1.5 times the copper intake of traditional breeds – Dennis Herd, Texas A&M beef cattle nutritionist). At first it appeared that Nubians were holding their own with the available copper, we now have comfirmation of copper deficiency in Nubians at the same rate as the Swiss breeds. Deficiency has also been comfirmed in the Boer, Pygmy and Nigerian Dwarf breeds in Southern, Mid and Northern California and Arizona. We have little laboratory or other information on the hair breed goats, though there are some old studies and perhaps recent lab work that indicate they may be more sensitive to excess copper than the dairy, miniature, and meat breeds. We know of hypocupric problems in both cattle and horses (foals), and occasionally sheep, in the area as well. In the last decade deficiency has been confirmed (via necropsy and/or laboratory work) in mid-state areas. While we only have a small amount of laboratory and other confirmation of copper deficiency in animals/herds in the high desert areas north of San Bernardino (where they feed mostly locally grown alfalfa) what we do have has shown goats in that area (including Nubians, who account for 95% of the data we do have) to be just as deficient as those in the lower areas. Indications are that in some mid and northern California areas theirs is a secondary deficiency (inducted by high levels of Cu-antagonists in the diet) from an excess in soil molybdenum. NOTE: See lab statistics for local animals (limited area) updated March 2006. Texas, Washington, Oregon, Missouri, Virginia, Colorado, South Dakota, Ohio, Wisconsin, Indiana, and the most of the New England states also have areas where copper deficiency in dairy, Pygmy, Boer, and Nigerian Dwarf goats has been confirmed.

Sandy soils have traditionally shown deficiencies, but high organic matter soils, degraded black soils, wooded calcareous and grey-wooded soils can also be severely deficient. Copper deficiency may occur when animals graze on soils deficient in copper, soils with high Molybdenum levels (+2PPM); copper intake should be 5 to 8 times molybendum intake, pastures with high sulphate levels (+0.35% total sulfur), iron exceeding 250 to 300 PPM, or some combination of these. Water (desired level for minerals in livestock drinking water), usually well water or hot springs water, may have substantial amounts of sulfur that reduce availability of copper. Water from alkaline soils is more commonly high in sulfur, which may add to interference. While all minerals can be involved in interactions, the effect other minerals have on the need for copper is more specific and unique than with many of the other minerals.

Coppers availability is reduced by iron, sulfur, molybdenum & zinc. The zinc/copper interaction is alleviated to a certain extent by maintaining the zinc:copper between 3:1 & 5:1. === Only a fraction of ingested copper is absorbed (average 4-5 per cent in adults) and is affected mainly by high levels of molybdenum, which binds with copper to make it insoluble, as well as high levels of iron and zinc. === Due to the large number of interactions, it is important to maintain a balance between trace minerals without over supplementing trace minerals. === Copper content of pasture can vary from spring to fall.

 

Soil copper is in two forms, Cu2+ and Cu(OH)+. In general the plant availability of copper in the soil decreases with an increase in pH of the soil. As pH rises adsorption increases and the solubility of the oxides decrease. Deficiencies can occur naturally in soils that are naturally high in pH or have been over limed. The opposite can occur in very acid soils. This is true of all the micronutrients except Selenium and Molybdenum. Studies have found that only 35% of pastures in the US have adequate copper levels. Other causes of copper deficiency appear when animals have heavy parasitism, which causes a loss of copper. Also Johnes disease. It may also occur when animals are given excess Zinc supplements. An 1999-2000 USDA-APHIS-VS-NAHMS (USDA’s National Animal Health Monitoring Service)source reports that blood (3,902 serum samples) and forage samples from 2,713 operations in the 23 top cow/calf states found copper deficiency to be either moderate or severe in 41.6 percent of the operations. And 1.7 percent were considered severely copper deficient. In addition moderate to severe zinc deficiency was found in 65.9 percent of all operations, with one percent considered to be severely deficient. Forage samples showed 77 percent and 67 percent of collected samples had levels of zinc and copper incapable of meeting the requirements of beef cattle.

In general, the Western states had lower mean serum copper concentrations compared to other regions.The mean serum copper concentration for operations in the Western regions was 0.63 ppm, while the Midwest and Southern regions recorded 0.70 ppm.
Almost half of Canadian feeds analysed at the Agricultural Soil and Feed Testing Laboratory (Canada) contain less than the estimated RDA of 10 ppm. Also, in the US 28.7% to 57.8% of pastures had molybdenum (Mo) and iron (Fe) levels high enough to cause copper malabsorption. To this can be added malabsorption through excessive sulfur intake.
NOTE: Alfalfa is notorious as a crop which is susceptible to copper deficiency. Wheat, barley and oats can also be deficient.
NOTE:: Molybdenum is common in alfalfa hays. Copper deficiency is likely if hay has less than four parts copper to each part molybdenum.
NOTE: Soil applied copper will generally have long-lasting residual effects. Beneficial effects from 1.3 to 2.7 pounds of copper per acre have persisted undiminished for up to 35 years (western Australia). Copper can be applied as organic compounds in the form of CuEDTA, copper ligninsulfonates, and copper polyflavonoids. Copper deficiency in grazing livestock has been recognized in most developed countries especially across Europe and North America as well as in Australia (pioneering work was done in Australia in the 1930s). As far back as the 1930s localized cases of copper deficiency were discovered in Florida, The Netherlands, New Zealand and parts of Australia.

Trace mineral concentrations in forages can vary among regions, within a state and even within a ranch. The following table demonstrates the variation measured among four pastures on a ranch in southwestern Montana. The table below demonstrates the variation in the Mineral Content of forage samples from one Southwestern Montana ranch. Forages were sampled during the late spring and early summer months. These analyses indicate adequate copper, zinc and manganese. But, the antagonistic effects of iron, sulfur and molybdenum have the potential to negatively affect the utilization of these minerals. Pasture

Mineral A B C D
Cu, ppm 7 19 7 0
Zinc, ppm 36 36 24 37
Mn, ppm 57 65 55 41
Mo, ppm 0.62 0.19 4.1
S, % 0.26 0.47 0.46 0.36
Fe, ppm 457 385 179 136

There can be little doubt that copper deficiency in ruminants is a worldwide problem. A recent survey on the nutrition of grazing ruminants in tropical regions has indicated that copper deficiency is a serious problem in many tropical countries:

ARGENTINA KENYA
BOLIVIA INDONESIA
BRAZIL PANAMA
COLOMBIA PERU
COSTA RICA PHILIPPINES
ETHIOPIA SAUDI ARABIA
EL SALVADOR SENEGAL
ECUADOR TANZANIA
DOMINICAN REPUBLIC SWAZILAND
CUBA SURINAM
GUATEMALA SUDAN
GUYANA SOUTH AFRICA
HAITI TRINIDAD
HONDURAS URUGUAY
INDIA VENEZUELA
MEXICO ZAIRE
MALAWI ZIMBABWE
MALAYSIA
COPPER DEFICIENCY A POSSIBLE CAUSE OF POLIOENCEPHALOMALACIA IN YOUNG GOATS
Prairie Diagnostic Services – Canada
During the spring of 1999, the Regina laboratory received submissions from a producer experiencing problems in pygmy kids between 1 1/2 – 2 months of age. The history presented for one kid included fever, depression, head pressing, circling and terminal opisthotonus. Another animal and several more at home exhibited generalized weakness and muscle tremors. weakness was most pronounced in the hindquarters.
At necropsy, the kid with seizures had severe cerebral edema with laminar necrosis of the cerebral cortical gray matter (polioencephalomalacia). The spinal cord from the kid with generalized weakness displayed extensive hypomyelination with neuronal chromatolysis and necrosis. Both kids had decreased numbers of Purkinje neurons and cells within the granular layer of the cerebellum with chromatolysis of medullary neurons. Hepatic copper level from the kid with weakness was 2.4 ppm, a level considered very deficient (normal range 25 150 ppm). A CBC indicated marked nonregenerative anemia (hemoglobin 82 g/L; hematocrit 0.10). Both goats had mild to moderate thyroidhyperplasia. One animal had moderate coccidiosis.
The owner housed sheep with the goats. Both were receiving hay, barley, sheep supplement and cobalt/iodized salt. Drinking water sulphate and phosphorus levels were within normal ranges.
When sheep and goats are fed together, it is not uncommon to feed supplements designed for sheep. The practice predisposes goats to copper deficiency as their requirements at 10 – 20 ppm are much higher than those for sheep at 5 – 10 ppm. Although dietary copper levels were not calculated, a copper deficient diet with respect to goat requirements was strongly suspected. Genetic or breed predisposition and the interfering role of dietary molybdenum were not ruled out. Thyroid hyperplasia may have also been genetically related as dietary iodine levels appeared normal.
Copper deficiency in young goats typically appears as “enzootic ataxia” related to spinal chord and cerebellar changes. Cerebellar changes noted in this case were consistent with copper deficiency. Low copper levels were suspected as contributing to polioencephalomalacia. Similar lesions have been reported in young lambs from England. Other causes of polioencephalomalacia include: thiamine deficiency, high sulphates, water deprivation, hypoxia and any condition causing cerebral edema.

 

Copper deficiency in Alaskan Moose and Finnish Reindeer have both been reported. In Finland the deficiency is so severe that winter survival is considerably impaired. Red Deer in North West Scotland and in the West Midlands of England have been found to suffer a swayback disease characterised by ataxia, paresis and spinal chord demyelination.

Copper is necessary for the absorption and utilization of Iron, it helps oxidize vitamin C and it works in conjunction with Vitamin C to form elastin, a chief component of muscle. It also helps with the formation of red blood cells and bone structure. A copper deficiency does not allow the bone marrow cells to reach maturity.

Sheep accumulate copper in the liver more readily than other farm animals and are highly susceptible to copper toxicity. Texel and Blue Faced Leicester sheep are known to be especially susceptible. Sheep should not be supplemented with copper above 10ppm, or allowed access to supplements containing high levels of copper.

Note: mineral mixes labeled for sheep AND goats will NOT contain adequate copper for goats. Generally goats should not be fed sheep minerals without some other form of copper supplementation.

Copper is actively transported through the intestinal wall and stored in the liver. Copper deficiency prevents iron from being incorporated in hemoglobin, resulting in anemia, indistinguishable from iron deficiency. Copper plays a role in iron absorption and mobilization. Copper deficiency impairs the formation of connective tissue proteins, collagen and elastin. Weak bones (osteoporosis), and defective arterial walls are the more obvious manifestations.

Many areas of the country with copper deficiency problems can correct a copper deficit by simply adding a mineral containing adequate copper for goats, such as a horse or cattle mineral mix.
Looking back to the early and mid 1980’s we can see that the problem actually began to manifest itself that long ago with an occasional animal exhibiting what we now know were signs of deficiency. In the beginning many of us had few if any classic copper deficiency symptoms, but testing has shown ALL our herds to be severely deficient. Some blood lines, and breeds appear to have more (Alpines) or less (Nubians) problems than others.

While liver biopsy is the most reliable test of the true copper status of the animal, few private practice or university affiliated veterinarians are willing to take the risk of performing liver biopsies on breeding stock. In the last few years there has been interest in the procedure and some successful caprine liver biopsies have been done at Texas A&M. The University of California at Davis has developed a procedure for doing liver biopsies on cattle that is proving successful. But for now, there is no reliable test readily available to the small goat keeper on a live animal; liver levels from the liver of deceased animals are still the only accurate indication of the Cu status that we have access to. Copper is carried in the blood in a variety of ways and conventional blood tests measure only the total copper content. Of this, usually only about 3% is available for use in enzymes. In cases of thiomolybdate toxicity, this will be grasped by the thiomolybdate ions. Blood serum and plasma copper levels are the last to fall, after Cu reserves fall to <30 mg/kg liver DM, so they seldom correlate to the actual levels in the liver. Blood levels can be normal, low, or even elevated, while the copper stores in the liver and kidneys are extremely deficient, blood testing for copper is a poor second choice, and we seldom test the blood levels anymore (NOTE: serum zinc levels can change rapidly in response to stress). Normal liver levels of copper for goats are 25ppm-150ppm. – unsupplemented animals in this area run 0.1ppm-15ppm. While liver copper and total blood copper are used alone as indicators of copper status, these do not take any account of the correction of the symptoms of clinical copper deficiency. The efficacy of copper supplementation of ruminants is the ability to correct the symptoms of clinical deficiency and should not be judged by the supplement’s ability to raise the copper content of the body. Copper levels in hair samples are highly variable.

The losses to local goat breeders were immeasurable, one year in the early ’90s a herd in Arizona lost all but three kids to copper deficiency (confirmed by Arizona U and Cornell), they were either stillborn or died within the first few weeks. The loss in mature animals was tremendous to herds experiencing the most severe problems. On the other hand, many of us did not have specific or classic copper deficiency symptoms, but rather a multitude of miscellaneous problems such as frequent staph lesions on the udder, nose, mouth, and chin (occasionally the entire body) and thin/rough/faded (achromotrichia) hair coats (odd “prickly” coats in the case of some Saanens), maybe nothing more than bald tail tips or light spots on the nose. Other herds had serious problems with increased cases of mastitis including gangrene mastitis (more than a dozen cases of gangrene mastitis in this area in a two year period, when it was virtually unheard of before – and since), ruptured uterus’ and pre-pubic tendons (abdominal wall hernia) , hugh hematomas following injections or even a minor injury. What acts like spinal cord injuries in adults (osteoporosis), twisting or bending of the front legs and/or feet in kids and pregnant yearlings (osteoporosis – see photo #1), anemia …. just about anything your can imagine ….. we were all mystified (our veterinarians and professionals in academia included) that our seemingly well managed animals were so plagued; again, some herds experienced NO obvious problems. We now realize that many of these situations were/are a direct effect of a compromised immune system resulting from the hypocupric condition. While other problems (bone disorders – ataxia – hair – cardiovascular) were a direct result of the low levels of copper. Young kids are most often and severely affected, with everything from the classic symptoms of swayback (congenital copper deficiency) andenzootic ataxia (delayed-onset ataxia) caused by demyelination of the spinal cord (a breakdown of the insulating fatty coverings [myelin sheaths] that surround the nerves in the brain and spine), this ataxia is NOT reversable by treatment with copper. to light colored rings around the eyes, thin hair over the nose and/or around the eyes and/or ears, small size, general weakness or sore joints and general failure to thrive. The does are not able to get kids on the ground with adequate levels of copper to maintain them in good health. Often they are so extremely deficient that they suffer from osteoporosis (soft, porous bones that bend and fracture easily i.e neonatals with rib fractures), severe anemia, or other health problems, some are unable to survive at birth, some appear normal at birth with symptoms showing soon after or weeks/months later depending on the level of the deficiency and the individual animal.

If copper nutrition was as simple as determining the copper levels in the base diet and adding a highly available copper source/supplementation, copper deficiency would not be a problem. However, because copper absorption and metabolism can be affected by molybdenum, sulfur, calcium, zinc, iron, manganese, cobalt, lead, cadmium, and selenium, deciding how much supplemental copper is required is not always easy.

Early on (after we identified the problem) we tried via oral supplementation of different mineral mixes high in copper (up to 1100ppm) and feeding of other than goat specific feeds (horse pellets, horse minerals, etc.) to correct the problem, to date none of them has succeeded in bringing up the body stores of copper. Absorption of copper can vary from zero to as high as 75% (Linder, 1991) depending on a number of factors. Copper availability in most feedstuffs fed to farm animals is between 1% and 15% (Hemken et al. 1993). Most minerals contain copper oxide in powder form, availability is poor when used in this form, the mineral passes through the gut with little absorption. (note: other areas of the US have had excellent results with just the addition of a mineral mix high in copper) in our area we have found copper boluses (copper oxide wire boluses) dosed to weight to be the most effective means of elevating the liver copper levels to within normal limits. We had the first boluses brought into the US from New Zealand in the spring of 1994; since that time we have found a source of cattle copper boluses that we can downsize to goat doses. In this area 2000 to 2500+ goats have been on these boluses for nine years now (early ’02). Continuious laboratory work on bolused animals indicates we are achieving normal liver concentrations of copper. To this date (June 2006) we have not had a single case of copper toxicity, and only one elevated liver copper level. Liver concentrations remain in the low normal (30-80ppm) with only three animals testing above that range in the twelve years we’ve been using the boluses. We’ve found that the boluses need to be administered at 5-6 month intervals to maintain adequate levels. After about 4 months, liver stores start to fall rapidly. In order to best protect the neonatal kids, we strive to use the boluses at times that will keep the does levels up during her entire pregnancy. Minnesota research with mice showed that perinatal brain development was affected by copper concentration in the mothers diet. Mice born to copper deficient dams had permanent brain disorders even when fed adequate copper after birth. Some breeders are routinely giving boluses (0.625 to 1.35 grams) to kids early on (2-4 weeks old) and it’s proven to be very satisfactory (I’ve done this the last six years in my herd).

This is an ongoing program. We get additional/new information, ideas, etc., constantly. As time goes on the regime may change to less or more frequent bolusing or perhaps a completely different method of correcting the problem. After more than a decade we’ve still not found a more satisfactory source of copper supplementation than copper boluses, nor a solution to the primary source of the problem (hay/feed). Until then, its imperative that we work together to keep on top of the situation and keep our animals healthy. We have veterinarians, both private and university affiliated, still interested and working on the problem. Our laboratory work has been done primarily by the California Animal Health & Food Safety Laboratory System [ CAHFS/UCDavis, was California Veterinary Diagnostic Laboratory Sytem, CVDLS/UCDavis] in San Bernardino and Davis, and the University of Arizona. Unfortunately, there are still veterinarians in the area that are unaware of the problem and even argue against its existence, though as time goes by more and more are seeing both the problem and our results and are recommending copper supplementation to goats in these areas.

Additional information, copies of laboratory work and veterinary information is available (your veterinarian is welcome to contact the veterinarians working with us for additional/specific information and confirmation as well).


One Example
(Photos & history of Toggenburg buck by Linda Colquitt – Eders Toggs, Alpines & Colquitt’s Saanens) This Toggenburg buck was born 3/92 in a herd having severe copper deficiency problems. Other animals in this herd were put down due to limb paralysis. This buck was a normal medium brown Toggenburg color at birth and left the herd at 3 months. The entire herd was blood tested for copper several months later and his twin sister was the lowest in the herd (0.06ppm). Only 6 of 17 animals were in the normal range of 0.8- 1.2ppm. At six months of age the buck was entirely white.

After seeing the blood tests above, he was given a MolyCu injection of 0.25mL. There were no other changes made in his care or nutrition. In about 10 days, he had dark roots. The picture below was taken about 1 month after the injection. In Februrary 93 he was given a copper Bolus of 2.5gms (the only size available at the time). In May, he was clipped for the shows and was a normal Toggenburg brown. The clippings showed a definate change in color with 1/3 of the hair nearest the skin being dark and the other 2/3 nearly white.

It is important to stress that color change might not be present in animals with a copper deficiency and that more serious problems can result from copper deficiency.


HOW THE COPPER BOLUSES WORK

When copper deficiency has been recognized, attempts to remedy it by provision of extra oral copper has proved unsatisfactory because of the unpredictable intake, rapid excretion, and variable effect. With an element such as copper, which is a cumulative poison, the risk of chronic copper poisoning from parenteral or oral copper treatment is positively correlated with its effectiveness in combating deficiency. Existing methods of treatment for copper deficiency have limitations. Mineral licks and supplementals are unpredictable because of the individual refusal of some animals and over indulgence of others. Copper sulfate (CuSo4) drenches are not only astringent (Cu sulphate drench, if it accidentally enters the lungs, can cause shock and death) but more than 90% of the copper is rapidly excreted from the body. Animals need to be drenched every 2-3 weeks. Boluses (glass) of copper that lodge in the rumen or reticulum can form unusable complexes with molybdenum, sulfur and iron. Compounding copper salts with concentrate rations can be effective (though it has not proven so with our animals). Injectable copper (copper glycinate, CuCa-EDTA, copper methionates and Cu-oxyquin) can be acutely toxic (seen most often w/Cu EDTA which is no longer available), so inectable doses must be limited, the dose is often partly encapsulated at the injection site and thus prevented from achieving its objective. Side effects such as injection site abscesses (copper glycinate) and hepatic necrosis are potential problems with this method of treatment. Repeated injections are needed to maintain adequate protection. note: we only use copper glycinate (Molycu) injections in emergency situation, usually in young kids from unbolused dams. Gelatin capsules containing copper oxide needles provide relatively long term protection against copper deficiency. The sustained activity after oral dosing with copper oxide needles as a means of alleviating hypocupremia in goats has been widely reported.

The gelatin capsules contain thousands of minute, blunt copper oxide rods. When give orally, the gelatin capsule dissolves in the rumen, releasing the copper oxide rods, which then pass into the abomasum where they lodge. There they release copper for the animal’s immediate requirements and reserves. The rods dissolve completely over a period of time.
NOTE: There is at least one study (Attempted Induction of Chronic Copper Poisoning in Boma Confined Impala. Research and Development, Kruger National Park, Skukuza, South Africa, ’99) that indicates, via fecal copper concentrations, that a good portion of the of the copper oxide particles are excreated from the body. Dispite deliberate attempts to overdose the study Impalas with one time doses ranging between 125 mg/kg to 1000 mg/kg, less than 20% of the animals were found to have elevated liver copper levels after 52 and 105 days.

Copper oxide needles are brittle rods (1 to 8 mm long , and 0.5+/- 0.1mm in diameter) made by oxidizing fine copper wire. They are nontoxic when given orally, and they can be given in doses sufficient to establish long-lasting reserves of copper in the liver. Their properties were discovered by Australian scientists, who found that a combination of small particle size and high specific gravity (2.0 and 7.0) caused them to become trapped in the folds of the abomasum. Copper oxide particles, released in the rumen pass through to the abomasum where they remain in the folds of the abomasum. CSIRO (1978) and Judson et al., (1982) demonstrated that the particles remained for a period of at least 32 days. CSIRO (1978) showed that the excretion rate of copper from the copper oxide particles was about 0.2 grams by weight per day which allowed for the safe absorption of copper without toxicity being apparent. The accumulated hepatic stores of the absorbed copper can protect the animal against copper deficiency for periods of months (our lab work indicates 4.5-6 months).To be effective the Copper particles must be swallowed, administer by a conventional balling gun which delivers the capsule direct into the gullet. The gauge and weight of the copper particles is calculated so that they sink and lodge properly. Chewing rods/wires/particles will change both the gauge, weight, specific gravity, causing the particles to pass on through the animal in greater amounts than the dose is adjusted for.


(photo of Copasure bolus and stomach chart courtesy of Animax Limited)

To get the most out of your copper supplementation program

Heavy worm burdens can affect copper uptake by altering the pH in the gut, making the copper less soluble. An effective worming program is therefore an important aspect of copper supplementation. Internal parasites can:

    • Reduce the solubility of copper in the abomasum (fourth stomach), by up to 70 per cent.
  • Reduce the subsequent uptake of dissolved copper by the liver by up to 50 per cent.
  • Increase copper losses from the animal.

While the use of cupric oxide rods has been shown to produce significant anthelmintic effects, their efficacy may be reduced by a heavy abomasal parasite burden. It is important that adequate selenium (Se) levels are also maintained. See: U.S. Geological Survey Selenium in Counties of the Conterminous States . Selenium testing: Whole blood (EDTA or heparin) is the best sample since most of the selenium is located on red blood cells. Serum selenium analysis is possible but does not reflect long-term status of the animal.
North Dakota:Areas With High Concentrations of Selenium in the Soil and Forage Produce Beef With Enhanced Concentrations of Selenium

PAY ATTENTION!
Copper can be toxic, it is important to stress again, that this is a local problem and solution, and though both primary and secondary Cu deficiency problems of different magnitudes may be found in other areas we do not recommend supplementation using these methods or doses without complete evaluation of your herd’s copper status via laboratory work and veterinary consultation.
Dose rates:
The animals are dosed to weight at the rate of 1 gram copper oxide in bolus form per 22 pounds at five to six month intervals, laboratory work has shown that liver and kidney concentrations start to fall rapidly after about four months. Copasure downsize guide

Valley Vet Supply in Kansas carries both Copasure boluses and the #13, 1/8th oz empty gel caps. 800-360-4838
Jeffers – Dothan, Alabama 1-800-533-3377 – fax 1-334-793-5179 has Copasure boluses on an on and off basis.
Animal Health Express, Tucson, Arizona, 1-800-533-8115 has Copasure boluses in both 12.5 gram and 25 gram sizes.
Walco International in Ontario, California (1-909-947-4957) has Copasure boluses (25 gram only) in stock. NOTE: The Walco in Ontario, California will NOT sell for use in goats.
Smaller size capsules:
“000” (1.37 mL) – “00”(0.95 mL) “0” (0.68 mL)par
“1” (0.50 mL)“2” (0.37 mL)“3” (0.30 mL) – “4” (0.21 mL)par
For smaller doses or multiples (an adult dose of 6.25 grams or 1/2 of a 12.5 gram boluse will fit into two “000” capsules). These can be found at health food stores, pharmacys or online at various herb and vitamin sites like Herbal Remedies

 

#13 1/8 oz gel cap
see link of other sizes

Conversion Factor
0.1% = 1000 ppm (Move decimal four places to the right)
1 ppm = 1 mg/kg
1 ppm = 0.45 mg/lb
1 mg/lb = 2.2 ppm or 2.2 mg/kg


www.aphis.usda.gov/vs/ceah/cahm

The National Geochemical Survey


Phew that was a long one too, glad you made it through. I hope you get some kind of idea of how important copper is in our goats diet.

10 Responses to Copper and Your Goat

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