Woke up one morning to find that a post on a controversial subject, which many had taken a great deal of thought to write about, was gone. Also found I had been de-moderated. It was a cool hand Luke moment.
Many of you are aware that I have been intimately involved with the PHA gene hunt almost since it first reared its ugly head in a public way. This effort involved not only education and writing articles, but also obtaining samples, encouraging people to submit ears from PHA calves & pedigrees, talking with veterinarians across the US etc. This experience provided me with some of the best and the worst in our breed, as far as people and behavior goes, and what follows is my interpretation of the ride.
As you may be aware the first step in identifying the gene that carries the defect is developing an informed pedigree. An informed pedigree is developed by obtaining samples from many generations surrounding a known affected animal. Since Draft Pick had the best pedigree and was the most used of the 3 “original in recent history” identified PHA carriers, Draft Pick’s pedigree was used. The more members of the pedigree you have the easier it is to identify the gene (in theory) – so it was crucial to obtain as many DP daughters and sons as possible. Many people provided samples in an expeditious fashion – however, 2 AMAA board members failed to provide requested samples in a timely fashion, in some cases resulting in Dr B proceeding without the samples because the wait was already long. Now clearly only the people who were slow to provide samples can provide an explanation, and clearly people have reinvented themselves since the PHA test is now available, so maybe even they don’t know why, but my interpretation of their behavior does not suggest that at that moment they had the best interests of the breed at heart. If they did they would have provided those samples ASAP – after all how hard is it to send a straw of semen or ask someone to bleed the your cow that is at an ET facility?
However, many people at their own expense provided samples, raided their semen tanks, drove hundreds of miles to take PHA calves for necropsy and did whatever they could to provide Dr B with necessary information to create an informed pedigree. Many people spent countless hours looking for specific semen, on the phone, on the internet, contacting all sorts of people who might provide a clue – IMHO these people had the best interest of the breed in mind.
Griswold was the first person to publicly acknowledge that his bull Irish Whiskey was a PHA carrier – while I don’t much personally like his philosophy (at least he has one) and I applaud him for coming clean way way before anyone even thought about admitting publically that the bull they syndicated or the bull they were promoting was a carrier. At the time there was much concern from breeders about what bull to use and there was much denial from owners of now known carriers that they had ever had a PHA calf. Now of course if you only used your PHAC bull on Angus cows that actually could be true. But the number of people who told me they had a PHA calf and dumped it boggles the mind. As it became clear that the gene had been identified and a test was on the horizon other bull owners (IMHO) reluctantly identified their bulls as carriers.
Don Coover was the first person to publicly print in his catalog the TH and PHA results of bull he sold semen on. He took a lot of flack from bull owners and probably lost some money, but he did it because he thought it was the right thing to do. His decision was based on an incident where a child lost both her heifer and her heifer’s first calf to PHA. You can’t tell me one incident can’t have an impact.
Many people, Gypsy and Jay Crull to name a few, ended up with a bunch of high dollar carriers when all they wanted to do was improve their herd. Their experiences, and those of others, lead us to better understand the pathogenesis of PHA. We now know that PHA very often leads to early abortion, that the calves are often born weeks early and assumed to be AI sired, when in fact they are bull bred, that the fluid accumulation begins somewhere around 5 or 6 months gestation, and Gypsy’s recent experience suggests that fertility may indeed be affected. Unlike TH, where the affected gene is known to be involved in hind limb development (and probably hair) and there appears to be a TH carrier phenotype, there does not appear to be a PHA phenotype. The gene and it’s function are known but not yet public knowledge, and the relationship between PHA and the known function of the gene is not readily apparent. The complete pathogenesis of the defect is not yet understood, but there are wide and varied histopathological abnormalities.
There were of course many reports of many bulls siring PHA calves, and many people across the country provided calf samples and semen samples. Dr Coover provided many samples, including some from a highly promoted Angus bull said to have sired several PHA calves. Because the breeders and the vet cared enough to submit samples from the calf and the dam, and Don provided semen on the bull in question, Dr B was able to exonerate this Angus bull because he did not parentally verify. It was a concerted effort on the part of concerned breeders and their veterinarians that allowed Dr B to get the info he needed.
I have to applaud Lautner for his latest catalog – not only is it nicely designed but he has included both PHA and TH results. Do I think he should/could have done it sooner – sure, but he has made the effort and the information is available. I also have to applaud Jirl Buck – he is castrating all his carrier bulls – this is a step in the right direction (again IMHO).
I must take issue with the Rowe sale catalog opinion that “it is undeniably also true….the percentage of carrier calves among the best calves – the most desirable ….is consistently higher than the percentage of carriers in the general population”. They are certainly entitled to their opinion, but in my opinion that is a self-serving statement by a group that has a high percentage of carrier genetics. It is unclear to me how carrying a recessive gene for a lethal defect makes you the best.
Many of us went thru many agonizing times prior to identification of the gene and developing the test. After a little research (where I discovered that a cow taken to a major U for a c-section a mere 4 years ago had a fetal monster that we now know as PHA) I found that the “free semen” I had used on the cows with the last chance had a 50% chance of being a PHA carrier – I had to do a lot of soul searching and decided I couldn’t sell the fabulous heifer I was sure was a carrier to the kid who was willing to pay me more than I had ever gotten for a heifer. It didn’t seem right. It was my decision so I could sleep at night. Once the test was available turns out the fabulous heifer is clean but her ugly duckling relative is a carrier. After again much soul searching I realized that I couldn’t sell her either and made her a recip – she is currently carrying an egg. If and when she no longer takes an egg she will go directly to the kill floor. I will not sell carriers to other breeders or to kids. I couldn’t sleep at night if I did. You can chose to do what you want, but I have made my decision.
With the exception of the recip, I have the luxury of having a totally clean herd of both PHA and TH – therefore my approach is likely different than others. I will not use carrier genetics – I think it is bad for the breed. I think the fastest way to clean up the mess is to not use carrier genetics – this is not feasible for many with carrier cows. But using and selling carrier bulls is certainly a great way to propagate the defect. I doubt that breeders are interested in that, multipliers might be, but not breeders.
I think testing and reporting the results is certainly one step in the right direction, but I also think a large number of people don’t get it and end up buying problems they didn’t expect. Many people still don’t understand – one of my favorite examples of not getting it is the question of how could this animal have a PHA calf her sire is clean (well how about her crossbred dam??) or the recent question is Draft Pick a known carrier of PHA? Although we have done a lot to educate people, there are many who are unaware. As a breeder and a veterinarian I feel compelled not to propagate genetic defects – it is my approach, what you do is your business.
I did not begin posting to make friends or have a substitute for life – I did find some interesting perspectives and some interesting people. As with all controversial topics if people felt uncomfortable or thought about a different view then we were successful.
I have ultimately enjoyed the ride – recently I received an email about a potential PHA calf in a totally other breed – this resulted from my interaction with a vet in another state who had a student when he c-sectioned their first PHA calf. The student was doing a rotation in another state when they c-sectioned a registered cow carring a registerable (if it had lived) calf. The word is getting out. It would be genetically fascinating if this calf proves to have the defect and there is a third PHA mutation.
I have lost a job over this issue (is it a job if you aren't paid?), I have been threatened, intimidated (well they tried), and lost some acquaintances - but I have not lost a single friend, in fact I have gained a few. I have helped 4Hers with projects, 4H dads with breeding, breeders with breeding, and people too numerous to count with information on testing, sires etc. I have no regrets and I believe that eventually honest breeders with the best interests of the breed will prevail - one only has to look historically at dwarfism in cattle - My email is [email protected]
DL
PS 1: RE the Red Angus post - red is a mutant gene but not a defect. Polled is a mutant gene but not a defect – there is a big difference between mutations that are good or neutral and those that are lethal.
PS 2: # of vets CA- 7691; TX – 5783; NY- 3878; KS – 1500;DE –200; AK – 219; RI – 239; Hawaii – 268; WY – 288
Many of you are aware that I have been intimately involved with the PHA gene hunt almost since it first reared its ugly head in a public way. This effort involved not only education and writing articles, but also obtaining samples, encouraging people to submit ears from PHA calves & pedigrees, talking with veterinarians across the US etc. This experience provided me with some of the best and the worst in our breed, as far as people and behavior goes, and what follows is my interpretation of the ride.
As you may be aware the first step in identifying the gene that carries the defect is developing an informed pedigree. An informed pedigree is developed by obtaining samples from many generations surrounding a known affected animal. Since Draft Pick had the best pedigree and was the most used of the 3 “original in recent history” identified PHA carriers, Draft Pick’s pedigree was used. The more members of the pedigree you have the easier it is to identify the gene (in theory) – so it was crucial to obtain as many DP daughters and sons as possible. Many people provided samples in an expeditious fashion – however, 2 AMAA board members failed to provide requested samples in a timely fashion, in some cases resulting in Dr B proceeding without the samples because the wait was already long. Now clearly only the people who were slow to provide samples can provide an explanation, and clearly people have reinvented themselves since the PHA test is now available, so maybe even they don’t know why, but my interpretation of their behavior does not suggest that at that moment they had the best interests of the breed at heart. If they did they would have provided those samples ASAP – after all how hard is it to send a straw of semen or ask someone to bleed the your cow that is at an ET facility?
However, many people at their own expense provided samples, raided their semen tanks, drove hundreds of miles to take PHA calves for necropsy and did whatever they could to provide Dr B with necessary information to create an informed pedigree. Many people spent countless hours looking for specific semen, on the phone, on the internet, contacting all sorts of people who might provide a clue – IMHO these people had the best interest of the breed in mind.
Griswold was the first person to publicly acknowledge that his bull Irish Whiskey was a PHA carrier – while I don’t much personally like his philosophy (at least he has one) and I applaud him for coming clean way way before anyone even thought about admitting publically that the bull they syndicated or the bull they were promoting was a carrier. At the time there was much concern from breeders about what bull to use and there was much denial from owners of now known carriers that they had ever had a PHA calf. Now of course if you only used your PHAC bull on Angus cows that actually could be true. But the number of people who told me they had a PHA calf and dumped it boggles the mind. As it became clear that the gene had been identified and a test was on the horizon other bull owners (IMHO) reluctantly identified their bulls as carriers.
Don Coover was the first person to publicly print in his catalog the TH and PHA results of bull he sold semen on. He took a lot of flack from bull owners and probably lost some money, but he did it because he thought it was the right thing to do. His decision was based on an incident where a child lost both her heifer and her heifer’s first calf to PHA. You can’t tell me one incident can’t have an impact.
Many people, Gypsy and Jay Crull to name a few, ended up with a bunch of high dollar carriers when all they wanted to do was improve their herd. Their experiences, and those of others, lead us to better understand the pathogenesis of PHA. We now know that PHA very often leads to early abortion, that the calves are often born weeks early and assumed to be AI sired, when in fact they are bull bred, that the fluid accumulation begins somewhere around 5 or 6 months gestation, and Gypsy’s recent experience suggests that fertility may indeed be affected. Unlike TH, where the affected gene is known to be involved in hind limb development (and probably hair) and there appears to be a TH carrier phenotype, there does not appear to be a PHA phenotype. The gene and it’s function are known but not yet public knowledge, and the relationship between PHA and the known function of the gene is not readily apparent. The complete pathogenesis of the defect is not yet understood, but there are wide and varied histopathological abnormalities.
There were of course many reports of many bulls siring PHA calves, and many people across the country provided calf samples and semen samples. Dr Coover provided many samples, including some from a highly promoted Angus bull said to have sired several PHA calves. Because the breeders and the vet cared enough to submit samples from the calf and the dam, and Don provided semen on the bull in question, Dr B was able to exonerate this Angus bull because he did not parentally verify. It was a concerted effort on the part of concerned breeders and their veterinarians that allowed Dr B to get the info he needed.
I have to applaud Lautner for his latest catalog – not only is it nicely designed but he has included both PHA and TH results. Do I think he should/could have done it sooner – sure, but he has made the effort and the information is available. I also have to applaud Jirl Buck – he is castrating all his carrier bulls – this is a step in the right direction (again IMHO).
I must take issue with the Rowe sale catalog opinion that “it is undeniably also true….the percentage of carrier calves among the best calves – the most desirable ….is consistently higher than the percentage of carriers in the general population”. They are certainly entitled to their opinion, but in my opinion that is a self-serving statement by a group that has a high percentage of carrier genetics. It is unclear to me how carrying a recessive gene for a lethal defect makes you the best.
Many of us went thru many agonizing times prior to identification of the gene and developing the test. After a little research (where I discovered that a cow taken to a major U for a c-section a mere 4 years ago had a fetal monster that we now know as PHA) I found that the “free semen” I had used on the cows with the last chance had a 50% chance of being a PHA carrier – I had to do a lot of soul searching and decided I couldn’t sell the fabulous heifer I was sure was a carrier to the kid who was willing to pay me more than I had ever gotten for a heifer. It didn’t seem right. It was my decision so I could sleep at night. Once the test was available turns out the fabulous heifer is clean but her ugly duckling relative is a carrier. After again much soul searching I realized that I couldn’t sell her either and made her a recip – she is currently carrying an egg. If and when she no longer takes an egg she will go directly to the kill floor. I will not sell carriers to other breeders or to kids. I couldn’t sleep at night if I did. You can chose to do what you want, but I have made my decision.
With the exception of the recip, I have the luxury of having a totally clean herd of both PHA and TH – therefore my approach is likely different than others. I will not use carrier genetics – I think it is bad for the breed. I think the fastest way to clean up the mess is to not use carrier genetics – this is not feasible for many with carrier cows. But using and selling carrier bulls is certainly a great way to propagate the defect. I doubt that breeders are interested in that, multipliers might be, but not breeders.
I think testing and reporting the results is certainly one step in the right direction, but I also think a large number of people don’t get it and end up buying problems they didn’t expect. Many people still don’t understand – one of my favorite examples of not getting it is the question of how could this animal have a PHA calf her sire is clean (well how about her crossbred dam??) or the recent question is Draft Pick a known carrier of PHA? Although we have done a lot to educate people, there are many who are unaware. As a breeder and a veterinarian I feel compelled not to propagate genetic defects – it is my approach, what you do is your business.
I did not begin posting to make friends or have a substitute for life – I did find some interesting perspectives and some interesting people. As with all controversial topics if people felt uncomfortable or thought about a different view then we were successful.
I have ultimately enjoyed the ride – recently I received an email about a potential PHA calf in a totally other breed – this resulted from my interaction with a vet in another state who had a student when he c-sectioned their first PHA calf. The student was doing a rotation in another state when they c-sectioned a registered cow carring a registerable (if it had lived) calf. The word is getting out. It would be genetically fascinating if this calf proves to have the defect and there is a third PHA mutation.
I have lost a job over this issue (is it a job if you aren't paid?), I have been threatened, intimidated (well they tried), and lost some acquaintances - but I have not lost a single friend, in fact I have gained a few. I have helped 4Hers with projects, 4H dads with breeding, breeders with breeding, and people too numerous to count with information on testing, sires etc. I have no regrets and I believe that eventually honest breeders with the best interests of the breed will prevail - one only has to look historically at dwarfism in cattle - My email is [email protected]
DL
PS 1: RE the Red Angus post - red is a mutant gene but not a defect. Polled is a mutant gene but not a defect – there is a big difference between mutations that are good or neutral and those that are lethal.
PS 2: # of vets CA- 7691; TX – 5783; NY- 3878; KS – 1500;DE –200; AK – 219; RI – 239; Hawaii – 268; WY – 288
;D 
