Friday, May 15, 2009
Home Made Yogurt
via videosift.com
I did two things today. I shopped Amazon for a flip camera and I made yogurt. I haven't gotten my flip camera yet but still wanted to treat you to this video.
Tuesday, May 12, 2009
New 2009 Junior Herdsire
This little guy is getting on a plane and flying from UC Davis in California to Dayton Inernational Airport sometime within this next week, probably Sunday. We can't wait to get him.
His dam is the lovely SGCH California Kalvin Special K and AI sire is White-Haven Remus, son of National GCH White Haven Misty. Special K is multiple top ten doe. She has classified 90EEEE and was #2 in her class in the 2005 National show. The ETA of this buck and his two brothers is 99/44 which should put him on the Elite Young Sire list.
Oberhasli Doe Giving Birth
This is video of an pretty Oberhasli doe giving birth to a large half boer buck. The doe yells a lot for a couple minutes, but if you stick with it you will see her afterwards taking care of the baby and obviously very proud of her little one.
Monday, May 11, 2009
Confusion Clears: Vaccines and how they work
Vaccines and how they work, generally but particularly as related to CL
This is a guest post from Bob Glass,Pan American Vet Labs
Hutto, TX
www.pavlab.com
I have posted on this before but this is a clear and easy to understand explanations. It is hard for me to achieve this, being trained in biology. I want to go into biochemistry and cell biology. This is called this and that is called that.
So I hope you understand this. If not, please comment here and I'll try to help. Or I'm sure Dr. Glass wouldn't mind you emailing him directly. This is his stock and trade.
************************
For the sake of simplicity I will use the term "vaccine" as a generic term
here. Actually the term vaccine is correctly used to described a
preparation which stimulates a protective immune response against a virus.
The term for the same type of product against bacteria is "bacterin" and
against toxins is "toxoid"
Vaccines are intended to "simulate" an actually infection in order to induce
the animal's immune system to react as if infected. In many (not all) cases
this will provide protection against future infections. This is the same
logic and mechanism which is employed with human vaccines.
If the same strain of a disease which causes disease were used, the vaccine
caused disease would be just as harmful as any "wild/natural" infection.
There are two strategies to overcome this problem. In some cases the
"vaccine" consists of a live but attenuated (greatly weakened) organism
which is not able to set up a persistent or disease causing infection.
Although weaker and less harmful than a natural infection this "vaccine"
infection will induce a protective immune response. A good example of this
is type of vaccine is sore mouth.
In other cases a killed vaccine is used. In this case the organism which
causes the disease is killed during the vaccine manufacturing process so
that no actual infection occurs. However the vaccine contains a large
number of these killed organisms which are able to stimulate the patient's
immune system. Often when a killed vaccine is used multiple doses are
required to sufficiently stimulate the patient's immune system. In both
these cases the goal of the vaccine is to stimulate an immune response that
kills the organism causing the infection.
In other cases a purified or semi purified vaccines is produced. A good
example of this is vaccines against toxins. Toxins are protein/carbohydrate
molecules produced by various organisms which have a pathologic effect on
the patient. Botulism is an organism which produces toxin. In these cases
it is not enough to kill the organism because the toxin will still be
present and cause life threatening illness. To combat this the toxins are
purified from the organism and "denatured" by various means
(heat/ph/chemicals) to make the toxin non harmful. This denatured toxin is
then injected into the patient who develops an immune response which
neutralizes the toxin. The antibody produced in the scenario is a
"anti-toxin". This is the same as the anti toxin you can buy and give to
animals that have not been vaccinated and become ill due to a toxin
producing bacteria. Anti Toxins are purified and concentrated antibodies
made by vaccinating animals with toxoids.
I have not read the article by Dr. Sparks, but I expect he referred to
introducing the disease organism into the goat (not the disease). In the
case of CL the organism is killed so the actual disease will not occur. In
some cases the patient may have a local immune response at the injection
site. In fact this is the body responding to the dead CL organism as if they
were "alive, thus the abscess, but in this case the CL is dead and the
abscess is "sterile".
I hope this helps;
Bob Glass
Pan American Vet Labs
Hutto, TX
This is a guest post from Bob Glass,Pan American Vet Labs
Hutto, TX
www.pavlab.com
I have posted on this before but this is a clear and easy to understand explanations. It is hard for me to achieve this, being trained in biology. I want to go into biochemistry and cell biology. This is called this and that is called that.
So I hope you understand this. If not, please comment here and I'll try to help. Or I'm sure Dr. Glass wouldn't mind you emailing him directly. This is his stock and trade.
************************
For the sake of simplicity I will use the term "vaccine" as a generic term
here. Actually the term vaccine is correctly used to described a
preparation which stimulates a protective immune response against a virus.
The term for the same type of product against bacteria is "bacterin" and
against toxins is "toxoid"
Vaccines are intended to "simulate" an actually infection in order to induce
the animal's immune system to react as if infected. In many (not all) cases
this will provide protection against future infections. This is the same
logic and mechanism which is employed with human vaccines.
If the same strain of a disease which causes disease were used, the vaccine
caused disease would be just as harmful as any "wild/natural" infection.
There are two strategies to overcome this problem. In some cases the
"vaccine" consists of a live but attenuated (greatly weakened) organism
which is not able to set up a persistent or disease causing infection.
Although weaker and less harmful than a natural infection this "vaccine"
infection will induce a protective immune response. A good example of this
is type of vaccine is sore mouth.
In other cases a killed vaccine is used. In this case the organism which
causes the disease is killed during the vaccine manufacturing process so
that no actual infection occurs. However the vaccine contains a large
number of these killed organisms which are able to stimulate the patient's
immune system. Often when a killed vaccine is used multiple doses are
required to sufficiently stimulate the patient's immune system. In both
these cases the goal of the vaccine is to stimulate an immune response that
kills the organism causing the infection.
In other cases a purified or semi purified vaccines is produced. A good
example of this is vaccines against toxins. Toxins are protein/carbohydrate
molecules produced by various organisms which have a pathologic effect on
the patient. Botulism is an organism which produces toxin. In these cases
it is not enough to kill the organism because the toxin will still be
present and cause life threatening illness. To combat this the toxins are
purified from the organism and "denatured" by various means
(heat/ph/chemicals) to make the toxin non harmful. This denatured toxin is
then injected into the patient who develops an immune response which
neutralizes the toxin. The antibody produced in the scenario is a
"anti-toxin". This is the same as the anti toxin you can buy and give to
animals that have not been vaccinated and become ill due to a toxin
producing bacteria. Anti Toxins are purified and concentrated antibodies
made by vaccinating animals with toxoids.
I have not read the article by Dr. Sparks, but I expect he referred to
introducing the disease organism into the goat (not the disease). In the
case of CL the organism is killed so the actual disease will not occur. In
some cases the patient may have a local immune response at the injection
site. In fact this is the body responding to the dead CL organism as if they
were "alive, thus the abscess, but in this case the CL is dead and the
abscess is "sterile".
I hope this helps;
Bob Glass
Pan American Vet Labs
Hutto, TX
Wednesday, May 6, 2009
Liver Fluke in Goats
LIVER FLUKE
(an often-misidentified worm that's lethal if not treated for properly)
Update 2/08 by Sue Reith.
SYMPTOMS:
Liver fluke damage is generally rather slow in appearing in mature goats... In a reasonably healthy goat, it can take years of gradual decline before the owner is even aware that Liver fluke is present. Symptoms are some, if not always all, of the following: Gradual increase in unthriftiness (dry coat, guard hairs sticking up, ribbiness, pale eye membranes (indicating anemia caused by the worm's activity), a swelling under the jaw (that has erroneously been considered among the veterinary community to be symptomatic of resistance to treatment for haemonchus contortus), and, eventually, a possibly sub-normal temp (less than 102 degrees), a distended belly (symptomatic of last-stage liver disease), and fecal pellets that are almost black in color and shriveled up with pointy ends on them.
Often the victim goat is one that has been wormed routinely, and yet still continues its gradual decline. The problem is that there's only one wormer on the market that will wipe out Liver fluke properly, Ivomec PLUS, (the PLUS part being clorsulon, specifically for eradication of Liver fluke) and many owners don't even know this wormer exists! Sadly, even when the owner finally learns about it and starts treatment, by that time there has often already been too much damage to the goat's liver for it to be saved even after proper worming.
BTW: While Liver fluke damage is often found in otherwise well-managed mature goats that despite good care continue to decline in appearance, in my experience this sudden appearance of anemia and weakness with either normal, or subnormal, temp (and sometimes swelling under the jaw as well) is not at all unusual to discover in young ruminants within the first few months of life as well. At that age it commonly shows up when they're heavily exposed to it in pastures containing wet areas, before their immune systems can get up and going to protect them. In fact, it's not uncommon for these young victims to die so fast they hardly have time to be sick.¹ This is especially true if there are any clostridial (Entero) organisms present in them, since they multiply and secrete their toxins fast in the already damaged, poorly oxygenated liver tissue .¹
TREATMENT:
I'm not one to quit without at least doing my best to save the goat...So if a goat of mine were affected with Liver Fluke I'd start it immediately on Ivomec Plus, using the appropriate worming approach as follows: All wormer packages note on the packaging that the product kills off ONLY the adult stages. So in order to get the worm load in the host down to a low enough level so that the immune system can take over and keep the problem under control, you need to worm 3X, with 10 days between wormings. The first dose will wipe out the adults already in there, the second dose will wipe out the larvae as they become adults (but before they can start laying eggs of their own), and the third dose kills off those eggs that were already in there when you started the worming, after they've passed thru the larval stage, when they, too, have become adults.. That leaves just a very low level of the parasites still in the host, the ones that from sheer timing
(good luck?) missed being wiped out by the worming onslaught... And that's just enough for the immune system to keep under control from then on. Having begun the repair process by giving the first dose of Ivomec Plus, the next step would be to immediatelystart it on subcutaneous injections of Ferrodex 200 (each 1 ml dose of which delivers 200 mg of elemental iron), to restorethe liver's red cells, the loss of which was the cause ofthe anemia and the blackened, shriveled, pointy-ended fecal pellets.And at this very critical time, as adjunct (supportive) therapy, I'd give it subcutaneous doses daily of 'Fortified' B-complex' (a combination of B vitamins needed for proper body function that has everything but B-12), essential because every time the patient urinates, it's losing all of those vitamins that are needed to maintenance of its body functions, and BoSe (to support his stressed immune system so that the goat can help itself to get well from
inside, while I work on it from the outside), and Banamine (to reduce the goat's pain and cut the inflammation caused by the worm damage) which, once given, will encourage the goat to want to eat once again! And last but not least, I'd give the goat a preventative doe of C&D antitoxin (to prevent entero from taking this opportunity to sneak in and finish the poor victim off because while it's down its stomach is not digesting food and moving it out of its body as it should.)
BACKGROUND:
Liver fluke is found in most of the US, but it's especially common in the Southern states due to the lack of good frosts to wipe out eggs and larvae in winter. We see it often up here in the Northern states as well, but because we have colder winters, the numbers, fortunately, are somewhat lower. However during the rainy season, no matter what part of the country the goat lives in, the Liver Fluke problem becomes particularly pervasive each year!
Today, by far the most difficult problem that we as owners face with Liver fluke treatment/control is that the veterinary community in general isn't even aware that it's there. As a result, they're unable to recommend proper treatment for it. This is because the egg of the Liver fluke (Fasciola hepatica)² looks so similar to that of the Barberpole worm (Haemonchus contortus)² that when it shows up on the slide in the Vet's office it's routinely misidentified to BE that of the Haemonchus contortus (or perhaps by some general term like strongyles, stomach worms, et al).
Until just a few years ago the veterinarian, seeing what was thought to be Haemonchus contortus eggs on the slide, would recommend Ivomec to the owner as the wormer of choice to eradicate it. And rightly so, because the moment Ivomec appeared on the scene back in the early 1980's, it was recognized as the most effective general wormer to show up ever! And frankly it remains, in my view, still the best and most efficacious general wormer on the market today.
And largely because the real Haemonchus contortus has always responded very well to Ivomec, veterinarians, misidentifying Liver fluke eggs as those of Haemonchus contortus, quite logically continued recommending Ivomec for treatment. When the Liver fluke failed to respond to the Ivomec treatment, unfortunately the loss of the animal in question was assumed to be a sign of the Haemonchus contortus having developed 'resistance' to the Ivomec! This notion has now become so pervasive that the veterinary community in general believes these days that the worms affecting livestock have developed a resistance to Ivomec, the result being a recommendation to their clients that they (1) increase the doses, and (2) turn to other wormers. Neither approach has even slowed down the deaths being caused, in fact, by Liver fluke. Since neither of those suggestions are working, the most recent approach has been to set up Famacha classes to
instruct owners and veterinarians alike in how to check the eyelids of the downed animals to see if they're anemic. If the animals have pale eyelids, indicating they're anemic, owners are sometimes advised to destroy the victim, fearing that if it lives, the 'resistance to wormers' will spread even further.
Sadly, neither plain Ivomec, nor Panacur, nor any of the other general wormers on the market today, are effective against Liver fluke. The fact is, this parasite can ONLY be eradicated efficiently by using a product called Ivomec Plus . It's not the Ivomec itself, but the PLUS part of the combined wormer, which is actually 'clorsulon' , that effectively wipes out Liver fluke. And (very critically) since it only kills the ADULT of the species, clorsulon (just as all wormers) has to be used at regular doses, 3 X in a row, 10 days apart, to kill it off completely. ¹
And it will no doubt be of particular interest for those owners who are worried about using milk from does being treated with Ivomec Plus that the Pharmaceutical companies have now run the required tests on those two products that officially clears them for use in lactating ruminants!
So in my view, these days (particularly if the reader is having a hard time controlling internal parasites in his/her animals) Ivomec Plus (instead of plain Ivomec) should ALWAYS be used for general worming, 'just in case'! Just like regular Ivomec, it can be given orally although it's actually an injectable. But since right now Ivomec itself is less readily being used by people (most of whom have never even heard of Liver fluke, and many of whom have their vets ID their goats' fecal samples as well) Ivomec Plus, while its importance is gradually growing among goat owners, may not yet be available in your local feed store... However it is readily available in livestock catalogs, and online as well, at about the same price as Ivomec.
END
¹ Georgi's Parasitology for Veterinarians, Dwight Bowman, 7th Ed. P116.
² Veterinary Clinical Parasitology, Sloss & Kemp, 5th Ed. P.41, Fasciola hepatica eggs; P.46, Haemonchus contortus eggs
Sue Reith
C Carmelita Toggs
Bainbridge Island WA
(While I urge you to share this information with other individual goat owners, please do not reproduce the article for publication without my specific permission. Thank you. Sue Reith.)
(an often-misidentified worm that's lethal if not treated for properly)
Update 2/08 by Sue Reith.
SYMPTOMS:
Liver fluke damage is generally rather slow in appearing in mature goats... In a reasonably healthy goat, it can take years of gradual decline before the owner is even aware that Liver fluke is present. Symptoms are some, if not always all, of the following: Gradual increase in unthriftiness (dry coat, guard hairs sticking up, ribbiness, pale eye membranes (indicating anemia caused by the worm's activity), a swelling under the jaw (that has erroneously been considered among the veterinary community to be symptomatic of resistance to treatment for haemonchus contortus), and, eventually, a possibly sub-normal temp (less than 102 degrees), a distended belly (symptomatic of last-stage liver disease), and fecal pellets that are almost black in color and shriveled up with pointy ends on them.
Often the victim goat is one that has been wormed routinely, and yet still continues its gradual decline. The problem is that there's only one wormer on the market that will wipe out Liver fluke properly, Ivomec PLUS, (the PLUS part being clorsulon, specifically for eradication of Liver fluke) and many owners don't even know this wormer exists! Sadly, even when the owner finally learns about it and starts treatment, by that time there has often already been too much damage to the goat's liver for it to be saved even after proper worming.
BTW: While Liver fluke damage is often found in otherwise well-managed mature goats that despite good care continue to decline in appearance, in my experience this sudden appearance of anemia and weakness with either normal, or subnormal, temp (and sometimes swelling under the jaw as well) is not at all unusual to discover in young ruminants within the first few months of life as well. At that age it commonly shows up when they're heavily exposed to it in pastures containing wet areas, before their immune systems can get up and going to protect them. In fact, it's not uncommon for these young victims to die so fast they hardly have time to be sick.¹ This is especially true if there are any clostridial (Entero) organisms present in them, since they multiply and secrete their toxins fast in the already damaged, poorly oxygenated liver tissue .¹
TREATMENT:
I'm not one to quit without at least doing my best to save the goat...So if a goat of mine were affected with Liver Fluke I'd start it immediately on Ivomec Plus, using the appropriate worming approach as follows: All wormer packages note on the packaging that the product kills off ONLY the adult stages. So in order to get the worm load in the host down to a low enough level so that the immune system can take over and keep the problem under control, you need to worm 3X, with 10 days between wormings. The first dose will wipe out the adults already in there, the second dose will wipe out the larvae as they become adults (but before they can start laying eggs of their own), and the third dose kills off those eggs that were already in there when you started the worming, after they've passed thru the larval stage, when they, too, have become adults.. That leaves just a very low level of the parasites still in the host, the ones that from sheer timing
(good luck?) missed being wiped out by the worming onslaught... And that's just enough for the immune system to keep under control from then on. Having begun the repair process by giving the first dose of Ivomec Plus, the next step would be to immediatelystart it on subcutaneous injections of Ferrodex 200 (each 1 ml dose of which delivers 200 mg of elemental iron), to restorethe liver's red cells, the loss of which was the cause ofthe anemia and the blackened, shriveled, pointy-ended fecal pellets.And at this very critical time, as adjunct (supportive) therapy, I'd give it subcutaneous doses daily of 'Fortified' B-complex' (a combination of B vitamins needed for proper body function that has everything but B-12), essential because every time the patient urinates, it's losing all of those vitamins that are needed to maintenance of its body functions, and BoSe (to support his stressed immune system so that the goat can help itself to get well from
inside, while I work on it from the outside), and Banamine (to reduce the goat's pain and cut the inflammation caused by the worm damage) which, once given, will encourage the goat to want to eat once again! And last but not least, I'd give the goat a preventative doe of C&D antitoxin (to prevent entero from taking this opportunity to sneak in and finish the poor victim off because while it's down its stomach is not digesting food and moving it out of its body as it should.)
BACKGROUND:
Liver fluke is found in most of the US, but it's especially common in the Southern states due to the lack of good frosts to wipe out eggs and larvae in winter. We see it often up here in the Northern states as well, but because we have colder winters, the numbers, fortunately, are somewhat lower. However during the rainy season, no matter what part of the country the goat lives in, the Liver Fluke problem becomes particularly pervasive each year!
Today, by far the most difficult problem that we as owners face with Liver fluke treatment/control is that the veterinary community in general isn't even aware that it's there. As a result, they're unable to recommend proper treatment for it. This is because the egg of the Liver fluke (Fasciola hepatica)² looks so similar to that of the Barberpole worm (Haemonchus contortus)² that when it shows up on the slide in the Vet's office it's routinely misidentified to BE that of the Haemonchus contortus (or perhaps by some general term like strongyles, stomach worms, et al).
Until just a few years ago the veterinarian, seeing what was thought to be Haemonchus contortus eggs on the slide, would recommend Ivomec to the owner as the wormer of choice to eradicate it. And rightly so, because the moment Ivomec appeared on the scene back in the early 1980's, it was recognized as the most effective general wormer to show up ever! And frankly it remains, in my view, still the best and most efficacious general wormer on the market today.
And largely because the real Haemonchus contortus has always responded very well to Ivomec, veterinarians, misidentifying Liver fluke eggs as those of Haemonchus contortus, quite logically continued recommending Ivomec for treatment. When the Liver fluke failed to respond to the Ivomec treatment, unfortunately the loss of the animal in question was assumed to be a sign of the Haemonchus contortus having developed 'resistance' to the Ivomec! This notion has now become so pervasive that the veterinary community in general believes these days that the worms affecting livestock have developed a resistance to Ivomec, the result being a recommendation to their clients that they (1) increase the doses, and (2) turn to other wormers. Neither approach has even slowed down the deaths being caused, in fact, by Liver fluke. Since neither of those suggestions are working, the most recent approach has been to set up Famacha classes to
instruct owners and veterinarians alike in how to check the eyelids of the downed animals to see if they're anemic. If the animals have pale eyelids, indicating they're anemic, owners are sometimes advised to destroy the victim, fearing that if it lives, the 'resistance to wormers' will spread even further.
Sadly, neither plain Ivomec, nor Panacur, nor any of the other general wormers on the market today, are effective against Liver fluke. The fact is, this parasite can ONLY be eradicated efficiently by using a product called Ivomec Plus . It's not the Ivomec itself, but the PLUS part of the combined wormer, which is actually 'clorsulon' , that effectively wipes out Liver fluke. And (very critically) since it only kills the ADULT of the species, clorsulon (just as all wormers) has to be used at regular doses, 3 X in a row, 10 days apart, to kill it off completely. ¹
And it will no doubt be of particular interest for those owners who are worried about using milk from does being treated with Ivomec Plus that the Pharmaceutical companies have now run the required tests on those two products that officially clears them for use in lactating ruminants!
So in my view, these days (particularly if the reader is having a hard time controlling internal parasites in his/her animals) Ivomec Plus (instead of plain Ivomec) should ALWAYS be used for general worming, 'just in case'! Just like regular Ivomec, it can be given orally although it's actually an injectable. But since right now Ivomec itself is less readily being used by people (most of whom have never even heard of Liver fluke, and many of whom have their vets ID their goats' fecal samples as well) Ivomec Plus, while its importance is gradually growing among goat owners, may not yet be available in your local feed store... However it is readily available in livestock catalogs, and online as well, at about the same price as Ivomec.
END
¹ Georgi's Parasitology for Veterinarians, Dwight Bowman, 7th Ed. P116.
² Veterinary Clinical Parasitology, Sloss & Kemp, 5th Ed. P.41, Fasciola hepatica eggs; P.46, Haemonchus contortus eggs
Sue Reith
C Carmelita Toggs
Bainbridge Island WA
(While I urge you to share this information with other individual goat owners, please do not reproduce the article for publication without my specific permission. Thank you. Sue Reith.)
Wednesday, April 22, 2009
NAIS and the Family Farm
NAIS ~~~ And the Family
From the National Assn. of Farm Animal Welfare, 4.22.09
Life is precious, even more so when a little life is hanging by a thread. Here at Dickinson Cattle Company Inc., near Barnesville, Ohio, USA, every life is priority, the people and the livestock. When every breath of oxygen and ounce of colostrum is life or death, tender love, and on the spot management is drastically important.
Unbounded Symbol Family Unbounded Symbol Little Girl with Baby Calf
Herd health doesn’t come out of a bottle, or because of a federal law. It certainly is not about ear tags, or about Humane Society animal rights theory. It comes from devoted livestock management by the people who appreciate and respect livestock the most, the owners. Herd health is not a fourth of July rally. It goes all year long with generous amounts of clean hay, water and minerals during cold winter days.
Ranchers know their stock. Genetics are planned with special traits for many generations. Not only do producers know every herd animal, they often know their planned mating genealogies for 20 to 50 years deep back into historic pedigrees. The mind of a true stockman evaluates every trait of every animal. The herd sires receive multiple scrutiny. Frozen semen is a special tool for breed improvement. Check DCCI sires available at http://www.texaslonghorn.com/inventory/semen/index.cfm
Over 1000 livestock producing families per month go broke or terminate their businesses. This is caused by excessive enforcements, taxes, regulations of governments beyond reason, and the cost of labor having to compete against union salaries and the government's high paying jobs. Each day Congress and the Senate pass more laws to increase cost of agriculture production. Look close at these American families and realize they are a vanishing species. They work day and night to excel. The elderly fear the future; youth innocently dream of the grandeur to come. As children prepare for the cattle shows of this coming Summer, Washington regulators prepare to force mandatory NAIS compliance to strap livestock owners with one more hard financial blow.
You may have called your elected federal officials hundreds of times and robotically treated like a borrowed mule, never receiving the dignity of a returned call. Try another hundred emails, letters, fax and phone calls. Call your state veterinarians who have all taken massive bribes (cooperative agreements) from the USDA to promote NAIS. As the elected and employed ones vote themselves increases of salary, insurance and retirements annually, thousands of food producers in the USA depart. Please try a few more times to contact your enforcers. Someday, one may listen to the people affected by their onerous legislations and do the right thing. Please say --- NO to NAIS.
For more info www.naisSTINKS.com, or e-mail Ag.Ed@NAFAW.org
Thursday, April 2, 2009
Marily Burgess--Discussion of Changes in Breeds Since 1960s
Guest Host: Marilyn Burgess-Goodridge
Robla Dairy Goats
mabgrobla@aol.com
I guess I could describe myself as an old timer inbreeding dairy goats. My history with dairy goats goes back to about 1963 when I was introduced to my first dairy goats - a herd of Nubians and Saanens.
Lest someone thinks that I was a newbie to livestock, I was raised on a ranch where my parents had a cow dairy when I was very young that was changed to a beef cattle operation and
a commercial fryer/broiler chicken ranch.
There was never a time in my life except for a year and a half break when I was in college when I have not had something to milk. I was in 4-H for most of my youth. So I do know livestock. My heart has always been with the dairy stock.
Now, I was introduced to Betty Nordfelt (long time head of the Judges' Training Committee) in the mid 1960's. It was her pronouncement that if you put a paper bag over the heads of dairy goats they should all look alike. Betty was the queen then. Wes Nordfelt was long time president of AMGRA that finally became ADGA.
They pretty much ruled our part of the dairy goat world. Even at my young age I was not comfortable with this idea.
My first dairy goats were Nubians of the dual purpose style heavy on the Da Ruth/Oakwood bloodlines. In 1965 I started my own goat dairy with my husband and those Nubians plus a small family of Saanens. A year later French Alpines were added. The next year a Rio Linda Toggenburg doe was added. The next year the rest of her family was added plus a small handful of Rio Linda and Indian Rock Saanens were added.
Shortly after that Hazel Tate of the Law-Zel Goat Dairy gifted my husband and myself with a La Mancha doe as a belated wedding gift. My mentors in the dairy goat world were Gene and Lousie Geiger (Peg's Nubians), Effie Evans (Evania Nubians), Mrs. V. E. Thompson (Oakwood Nubians), Hazel Tate) and N. S. & E. L. Goodridge (Rio Linda Dairy Goats). I had a very good start in the dairy goat world.
I saw the breeds in my area back then. They were quite different from what they are today. A lot of the difference is in the loss of what I call true breed character.
Alpines were quite tall and rangy and lacking in real body width. The head was long with long upright ears that tended to point more out than up.
Nubians were chunky of body style tending to be easy in the chine and while wide in rump more sloped to the pins. The heads were strong of jaw. The eyes tended to be almond shaped. And of course there was that high Roman nose not the convex nose of today. Jaws did not always match. And the ears were very pendulous lying flat to the head with a bell at the end.
Saanens were the "Holsteins" of the dairy goat world. They were big and thicker than the animals we see today. Many tended to have soft pasterns and bad feet. The head was fairly short
with breadth between the eyes. The face was often dished. Many were polled and had wattles. The ears were the largest of the Swiss breeds tending to be set lower and opening wider at the base of the head.
The Toggenburg had two styles. The old-fashioned which was smaller and wider of body. Mammaries were highly attached with teats to the outside of the udder. The other style was a much taller,longer type. Both styles had a broad head with a wide muzzle and a dished face and were more often than not polled. The ears were small and set higher on the head to make a very alert appearance.
The La Mancha was a newly accepted breed to the registry. According to N.S. Goodridge, who was on the original sifting committee for the La Mancha breed, many of the early bucks used on the sport Spanish La Mancha does were Alpines because
the Alpines were known for their higher production and they had more color to offer. A few Saanens and Toggenburgs were used but were frowned upon because of the color factor.
La Mancha heads were longer. There were a number of
ear types. The elf ear was a brief ear with a flap that hung down. The Pixietype had a tab that pointed up. The gopher ear was the one we typically see today. Then there was a very tiny Swiss type ear that was about a quarter the size of the Alpine ear. There was a herd of these does not far from my dairy.
Now we come to the Swiss Alpines which is what we now call the Oberhasli. Via Hazel Tate I was introduced to Esther Oman and her "Swissies" who was living with Hazel at the time. When I first saw them I thought they were the dairy goat world version of the Jersey cow. They had the same color pattern though the goats were red while the cows were fawn. They had very similar black markings. And they had that very short broad dished face.
Ears were tiny and very erect. Stick-up ears my husband called them. There was also a certain body style of a shorter body but very wide sprung ribs. Rumps were broad and flat from the hips to the pins. They did tend to be hocky. Teats were small as were the udders. Like the Jersey cow they were small.
Thus my remembrances of the dairy goat breeds circa the mid 1960's.
Marilyn Burgess-Goodridge
Robla Dairy Goats
Robla Dairy Goats
mabgrobla@aol.com
I guess I could describe myself as an old timer inbreeding dairy goats. My history with dairy goats goes back to about 1963 when I was introduced to my first dairy goats - a herd of Nubians and Saanens.
Lest someone thinks that I was a newbie to livestock, I was raised on a ranch where my parents had a cow dairy when I was very young that was changed to a beef cattle operation and
a commercial fryer/broiler chicken ranch.
There was never a time in my life except for a year and a half break when I was in college when I have not had something to milk. I was in 4-H for most of my youth. So I do know livestock. My heart has always been with the dairy stock.
Now, I was introduced to Betty Nordfelt (long time head of the Judges' Training Committee) in the mid 1960's. It was her pronouncement that if you put a paper bag over the heads of dairy goats they should all look alike. Betty was the queen then. Wes Nordfelt was long time president of AMGRA that finally became ADGA.
They pretty much ruled our part of the dairy goat world. Even at my young age I was not comfortable with this idea.
My first dairy goats were Nubians of the dual purpose style heavy on the Da Ruth/Oakwood bloodlines. In 1965 I started my own goat dairy with my husband and those Nubians plus a small family of Saanens. A year later French Alpines were added. The next year a Rio Linda Toggenburg doe was added. The next year the rest of her family was added plus a small handful of Rio Linda and Indian Rock Saanens were added.
Shortly after that Hazel Tate of the Law-Zel Goat Dairy gifted my husband and myself with a La Mancha doe as a belated wedding gift. My mentors in the dairy goat world were Gene and Lousie Geiger (Peg's Nubians), Effie Evans (Evania Nubians), Mrs. V. E. Thompson (Oakwood Nubians), Hazel Tate) and N. S. & E. L. Goodridge (Rio Linda Dairy Goats). I had a very good start in the dairy goat world.
I saw the breeds in my area back then. They were quite different from what they are today. A lot of the difference is in the loss of what I call true breed character.
Alpines were quite tall and rangy and lacking in real body width. The head was long with long upright ears that tended to point more out than up.
Nubians were chunky of body style tending to be easy in the chine and while wide in rump more sloped to the pins. The heads were strong of jaw. The eyes tended to be almond shaped. And of course there was that high Roman nose not the convex nose of today. Jaws did not always match. And the ears were very pendulous lying flat to the head with a bell at the end.
Saanens were the "Holsteins" of the dairy goat world. They were big and thicker than the animals we see today. Many tended to have soft pasterns and bad feet. The head was fairly short
with breadth between the eyes. The face was often dished. Many were polled and had wattles. The ears were the largest of the Swiss breeds tending to be set lower and opening wider at the base of the head.
The Toggenburg had two styles. The old-fashioned which was smaller and wider of body. Mammaries were highly attached with teats to the outside of the udder. The other style was a much taller,longer type. Both styles had a broad head with a wide muzzle and a dished face and were more often than not polled. The ears were small and set higher on the head to make a very alert appearance.
The La Mancha was a newly accepted breed to the registry. According to N.S. Goodridge, who was on the original sifting committee for the La Mancha breed, many of the early bucks used on the sport Spanish La Mancha does were Alpines because
the Alpines were known for their higher production and they had more color to offer. A few Saanens and Toggenburgs were used but were frowned upon because of the color factor.
La Mancha heads were longer. There were a number of
ear types. The elf ear was a brief ear with a flap that hung down. The Pixietype had a tab that pointed up. The gopher ear was the one we typically see today. Then there was a very tiny Swiss type ear that was about a quarter the size of the Alpine ear. There was a herd of these does not far from my dairy.
Now we come to the Swiss Alpines which is what we now call the Oberhasli. Via Hazel Tate I was introduced to Esther Oman and her "Swissies" who was living with Hazel at the time. When I first saw them I thought they were the dairy goat world version of the Jersey cow. They had the same color pattern though the goats were red while the cows were fawn. They had very similar black markings. And they had that very short broad dished face.
Ears were tiny and very erect. Stick-up ears my husband called them. There was also a certain body style of a shorter body but very wide sprung ribs. Rumps were broad and flat from the hips to the pins. They did tend to be hocky. Teats were small as were the udders. Like the Jersey cow they were small.
Thus my remembrances of the dairy goat breeds circa the mid 1960's.
Marilyn Burgess-Goodridge
Robla Dairy Goats
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