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Post by karenp on Nov 2, 2018 20:17:26 GMT
Have any of you heard of this being an issue with Dexter? I just had my cow miscarry her second calf at 6 months out of the same bull. Testing didn't show any explanation for the miscarriage and the bull is proven. It was suggested that this might be an issue. Most testing has been done on commercial breeds, I was wondering if there was any anecdotal information.
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Post by Deleted on Nov 4, 2018 23:04:32 GMT
what is a haplotype?
Are you saying the cow has lost 2 calves? Has she had any live calves?
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Post by karenp on Nov 4, 2018 23:31:00 GMT
www.selectsires.com/resources/healthdocs/impactingfertility.html?version=20180803This article does a better job explaining it than I could. No live births, she's been tested for everything the vet could think of, the bull is proven. She's lost both at 6 months, comes into milk and is a joy to milk. Well behaved lets down nicely and went 10 months the first time around. The people on the KFC site suggested if I really like her (I do) to try a different bull, they may not be compatable.
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Post by jamshundred on Nov 5, 2018 0:21:02 GMT
Karen,
Is this Joy's daughter with Cmas? I have never had a stillborn calf on my farm. . . . . . . EVER, nor one that died shortly after birth. ( this precludes bulldog aborts). One of the things that puzzle me quite frequently when I see all these breeders who are posting about dead calves. . .. . and even sick and dying cows. . . . . . is WHAT in the hell is going on? There was one breeder, summer before last that had five cows, and the first four to give birth ended up with dead calves. This . . . . is. . . . . not the Dexter breed I have experienced.
Without a doubt I am convinced there is something amiss in the polled bloodlines yet to be discovered. It took almost 25 years before PHA created enough dead calves for there to be any notice of something wrong in the breed. We know there are many, many, defects in other breeds, and the polled lines have FOUR recorded outcrosses to unknown breeds, ( jersey is known in one of them), and who in the heck could even guess what might be floating in those genes?
Did you by chance save any portion of the fetus? Dr. Beever and his partner researchers do a lot of research on genetic defects in a number of breeds.
Judy
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Post by karenp on Nov 5, 2018 17:30:17 GMT
Yes, Candy is Christmas's daughter. I'm grasping at straws for an excuse not to get rid of her.
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Post by Deleted on Nov 5, 2018 18:15:27 GMT
dont get caught up on Haplotypes they are neither good or bad. Haplotypes are just multiple alleles that go together. It would only make a difference if trying to determine a dna test for a specific haplotype. In practice a haplotype would work the same as a single allele.
It is possible that your cow could have a recessive lethal but would seem unlikely. If that were the case both sire and dam would have to have the recessive and both would have to pass it. You would only have a 25% chance of a dead calf each time. So you would have hit that 25% chance on both of them. More likely there is something else wrong maybe environmental or maybe something wrong with the cow. It would not be wrong to switch up the bull and see if it made a difference but even if it does still will not answer the question as to your bull and cow having the same genetic condition.
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Post by cascade on Nov 6, 2018 1:40:53 GMT
Haplotypes are simply chunks of DNA that tend to travel somewhat stuck-together through the generations. The chunks of DNA (haplotypes) may include a good number of genes coding for various functions.
If a gene codes for an essential life function, and if that gene is broken via a mutation, then it is called a lethal gene. Animals and plants require at least one good working copy of each essential gene for essential life functions. Lethal genes can't exist (for long) in homozygous pairs because it means that the offspring has two broken genes and lacks a good working copy of the essential gene and the fetus dies.
Via mass analysis of population genetics, they can't always track and identify all individual genes, but they can track haplotype groups of genes without even understanding anything about the genes themselves that are in the haplotype group.
If a haplotype group of genes contains a lethal gene, then any offspring that are homozygous for that haplotype, will die during development. So, in population genetics studies, they can scan for haplotypes that only occur in heterozygous pairs and never appear in homozygous pairs, and they can assume that those haplotypes that never appear in homozygous pairs must almost certainly contain an unidentified lethal gene.
Not all lethal genes are equally problematic. Some lethal genes are so lethal (in homozygous pairs) that the newly fertilized egg quickly aborts and the mother simply re-breeds and still has a timely healthy calf with not much impact. Other lethal genes allow the calf to go near full-term before dying, and can even threaten the mother's life due to being so malformed that is near impossible to pass through the birth canal.
Every breed is going to have several not yet identified lethal genes contained in haplotype groupings. Some will be shared with other breeds, some will be unique to just one breed.
Karen, make certain you hang onto tail hairs of both parents, and all offspring including dead offspring. It could come in handy.
I'd love to see the pedigrees of the parents to see which ancestors they share.
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Post by cascade on Nov 6, 2018 2:02:06 GMT
Traditional and Legacy Dexters share tons of genetics with other British Isle breeds because Traditional Dexters started as cross-breeds of most every breed found in the British Isles.
The only identified lethal genes (PHA and BD Chondrodysplasia) found in Dexters so far came from legacy and traditional horned lines. PHA came from Woodmagic and Bull Dog Chondrodysplasia mostly came from Grinstead (and a few others).
I've bred well over 200 polled Dexters with no sign of problems. I can even breed short to short with no problems, because my shorts are tested free of problem lethal genes.
My first bull (polled) is going on age 15 and is still healthy and still breeding in the pasture
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Post by genebo on Nov 6, 2018 15:28:55 GMT
Low selenium levels are known to cause this problem. Low selenium causes the uterus to be stiff and resist stretching. If the embryo gets too cramped, the cow may expel it.
Low selenium also causes calves to be born with bent legs due to the cramped space in the uterus. It also causes dystocia due to improperly placed calves that can't get into proper position to be born. It is responsible for "white muscle disease", that leaves the newborn calf so weak it cannot stand. A shot of BO-SE is advised at birth.
Proper selenium levels should be maintained in the cow throughout pregnancy. That insures that the calf is not selenium deficient.
Google a selenium map to determine if you are in a low-selenium area. If so you should be feeding minerals that contain up to 40 ppm of selenium and putting out a selenium 90 block for the cattle to lick.
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Post by karenp on Nov 6, 2018 23:25:41 GMT
Haplotypes are simply chunks of DNA that tend to travel somewhat stuck-together through the generations. The chunks of DNA (haplotypes) may include a good number of genes coding for various functions. If a gene codes for an essential life function, and if that gene is broken via a mutation, then it is called a lethal gene. Animals and plants require at least one good working copy of each essential gene for essential life functions. Lethal genes can't exist (for long) in homozygous pairs because it means that the offspring has two broken genes and lacks a good working copy of the essential gene and the fetus dies. Via mass analysis of population genetics, they can't always track and identify all individual genes, but they can track haplotype groups of genes without even understanding anything about the genes themselves that are in the haplotype group. If a haplotype group of genes contains a lethal gene, then any offspring that are homozygous for that haplotype, will die during development. So, in population genetics studies, they can scan for haplotypes that only occur in heterozygous pairs and never appear in homozygous pairs, and they can assume that those haplotypes that never appear in homozygous pairs must almost certainly contain an unidentified lethal gene. Not all lethal genes are equally problematic. Some lethal genes are so lethal (in homozygous pairs) that the newly fertilized egg quickly aborts and the mother simply re-breeds and still has a timely healthy calf with not much impact. Other lethal genes allow the calf to go near full-term before dying, and can even threaten the mother's life due to being so malformed that is near impossible to pass through the birth canal. Every breed is going to have several not yet identified lethal genes contained in haplotype groupings. Some will be shared with other breeds, some will be unique to just one breed. Karen, make certain you hang onto tail hairs of both parents, and all offspring including dead offspring. It could come in handy. I'd love to see the pedigrees of the parents to see which ancestors they share. The fetus didn't have enough hair to pull, just a few whiskers starting. The sire and dam are both listed on the Legacy site FF Freedom's Lakota and Homefront Candy Cane if you want to take a look. |
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Post by karenp on Nov 6, 2018 23:29:46 GMT
Low selenium levels are known to cause this problem. Low selenium causes the uterus to be stiff and resist stretching. If the embryo gets too cramped, the cow may expel it. Low selenium also causes calves to be born with bent legs due to the cramped space in the uterus. It also causes dystocia due to improperly placed calves that can't get into proper position to be born. It is responsible for "white muscle disease", that leaves the newborn calf so weak it cannot stand. A shot of BO-SE is advised at birth. Proper selenium levels should be maintained in the cow throughout pregnancy. That insures that the calf is not selenium deficient. Google a selenium map to determine if you are in a low-selenium area. If so you should be feeding minerals that contain up to 40 ppm of selenium and putting out a selenium 90 block for the cattle to lick. Yes, we are on the lower end for selenium, she has loose minerals with selenium available. I know she eats it. |
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Post by Deleted on Nov 7, 2018 15:15:07 GMT
I thought I remembered you had a necropsy done on one of them? If so they would have caught it if it had been low selenium
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Post by brynmawr on Nov 7, 2018 20:38:42 GMT
I have no personal experience with this but here is a thought.
Due to the time of the year a lot of nut trees are dropping nuts. Buckeyes and acorns are known to abort cattle. An experienced lifelong cattle farmer recommend fencing them away from the wood line where buckeyes are untill the nuts are done for the season. He said on on years like this with all the nuts he has lost calves.
One more thought...
If she is a milk cow, you are most likely getting more milk from her than a calf would take. Is she getting what she needs for the extra milk and calf?
Of course many people who have dairy
Cows have little to no interest in calves and justify keeping the cow just for milk. With a Dexter not producing as much I'd still want the calf, for her to be worth keeping.
Hope you get to the bottom of it!
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Post by otf on Nov 8, 2018 13:02:13 GMT
karenp, what testing was done? Your vet might recommend bloodwork to test for trace minerals. If it's a selenium issue, perhaps she needs more than what is provided in loose minerals.
Gale
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Post by cddexter on Nov 8, 2018 23:10:22 GMT
Karen, I've also had some experience with leptospirosis. Pomona is a subset that's carried by deer. If a cow somehow manages to lick up dew or eat grass that's been peed on, she has a good chance of picking up lepto. It causes abortions. L. harjo is carried by rats; if you feed grain that's been peed on by rats, you might have a similar problem. You don't say if your cow and the bull have been tested for pha? I haven't checked the pedigree, any chance they are both chondro carriers? You can get chondro abortions around 6 months. With nuts and lepto and pha, there's lots of choices for trouble.
You haven't mentioned the condition of the foetus: was it normal, just dead? Heatbreaking...keep us informed, please. Your disaster might be just the thing someone else needs to hear about to help them with a similar problem. cheers, c. |
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Post by cddexter on Nov 9, 2018 16:24:09 GMT
Oh, and...
Judy, you've blamed polled for just about every problem known to man. Remember your definite knowledge based on your 'research' that pha came from polled? Oops. Ditto large calves, except there's a whole bunch of legacy animals with large calves, too. Oops.
Then there's Platinum's outcrossing record: it is misleading to take one cross way back, and then add the number of generations so it becomes 4 or 5 crosses. Oops.
This is not a challenge, just a heads-up. Keep up the (other) good work. Cheers, Carol. |
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Post by karenp on Nov 9, 2018 22:23:56 GMT
She came up as exposed to the rodent lepto, but titers were not high enough to be considered positive. Vaccinated twice before rebreeding, both sire and dam are PHA free. Fetus looked normal, premature but appropriate for gestational age. I'll have to look at the paperwork again to see if she was tested for selenium. I'm not sure what I'm going to do, she's so nice to milk.
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Post by cddexter on Nov 9, 2018 23:52:52 GMT
It's not fair that this sort of thing most often happens to the nice guys. My heart goes out to you. cheers, c.
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Post by jamshundred on Nov 14, 2018 0:02:54 GMT
Carol . . . . I'm taking the bait. There are newer breeders here who do not know the back story, and I am always up for a history lesson!  The truth is. . . . in the USA. . . . . the PHA . . .. . . was primarily coming from POLLED animals. Why was that? In 2002, John Potter was head of the genetics committee in ADCA. He had access ( and I dare say, copies) of all genetic tests that were submitted through ADCA to labs and contacts and samples from breeders who were having aborted/deformed calves. At that time, most all tests were going through ADCA. By 2002, the test for chondro was available, and in that year, a breeder out west, posted on the DC2 chat board, she had a "bulldog type" calf, with long legs, from non-chondro tested Dexters. The genetics committee was aware of this calf.. . . and she also mentioned in her post, the term, anasplasia. Remember, this was 2002, and the genetics committee of ADCA ( and likely all the leadership, but for sure some) were aware as well. There was discussion over a period of time, and two other breeders reported the same issue. One of them was a guy named Charles, who reported the same type of dead calf, and along with the Dexters in the first herd, and his herd, I noticed there was polled in the mix. Unbeknownst to us "regular" folks, there were members of leadership, including the head of the genetics committee quite familiar with "long leg aborted or dead calves" from PHA, ( though the defect had yet to be named or identified). So familiar, Dr. Jon Beever of Illinois Univ was enlisted to research and identify what was causing these aborts/deaths. In 2004 a prominent breeder gave me more information, and AT THAT TIME, I asked leadership to alert the membership. . . . . . to make members aware and thus gather more information which could help research. NOTHING WAS DONE to advise the membership. IT WAS KEPT HIDDEN. I began gathering what info I could, and it was ALL tracing back to POLLED cattle. The reason being that there were polled herds with the problem, they were in leadership, and no one was talking to the membership about it! In 2005, unknown to me, I purchased some cattle from the west who eventually turned out to be carrying PHA, and before that knowledge was known. .. . . . . my herd had PHA all through it. I am both analytical and pretty good at digging up information when I'm interested. . . . . . . . and IF. .. . . PHA had not been PURPOSELY hidden from the membership. . . . . . just the names of animals who had aborted these calves, would have been enough to start connecting dots and arriving at earlier answers that may have saved some small breeders whose entire herds experienced tremendous loss. I knew one owner with five Dexters, all turned out to be carriers. No one ever discusses all the little guys who were victimized by the secrets kept. By the time Julie Cavanagh identified the PHA in Australian cows, the Canadian bull who was the source via AI was identified, and the defect traced back to an imported Woodmagic cow and a test developed, there were hundreds of Dexters in the USA that were carriers, and it could have been fewer. In fact, I was pretty astute early on to identify polled as a source, ( which it was), since overwhelmingly it first came to light in the US from polled lines descended from Cranworth Xanadu , ( there was more impact on polled lines) his ancestor Aldebaran Priapus was more a factor in Canada, and Cranworth Toby was used by the Piehota herd, and I have never heard that there was a problem with dead calves in his herd from PHA, although there were animals that were definitely carriers. It took a scientist in Australia attending two cows who had aborted PHA fetuses, to identify a genetic defect, (which by the time was WIDESPREAD in the USA, with the membership never advised. Those of us who suffered loss, ( for me it was thousands of dollars), should have sued ! ! I didn't know until later, the bigger picture of who knew what and when. You may recall the PHA calf, ( I just saw a photo of it in a book published in the UK a couple days ago), which was born to a cow sold by a member of leadership? The bull that bred that cow was sold to a woman in Missouri, and was NOT advised by ADCA leadership/genetic committee the bull was a carrier, and she bred him across her entire herd. Judy |
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