Hypotrichosis and Dwarfism ??? and pics

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Alan

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I have a couple of questions about a cow I have. I have an older cow who in about 2004 dropped a heifer who had Hypotrichsis. I never had it verified, but the heifer had a very thin coat of hair and it was very curly (kinky) hair. Now approx. 5 or 6 years later the same cow drops a (maybe) dwarf heifer. I say maybe because at first the head looked bigger than it should have been, but today maybe not. The main thing was the calf was very small (short, height wise) maybe 50 or 60 pounds and the two front legs looked like the shoulders are very wide and she was very 'bull legged" in both front legs. Also all the joints in all 4 legs are very much over size.... I feel she was deformed. She took a full day to stand and today she could stand on her own but when she tried to take a step on her front legs she would fall down. I put her down tonight and the cow goes to the next sale on Tuesday. My 3 question are;

1. I assume these genetics defects are a reccessive (sp) gene, maybe not (?) but if the gene is reccessive, would it mean that both the sire and the dam have to be carriers to pass it on?

2. The same cow has thrown two calves with genetic defects, if it is drawfism, is dwarfism and hypotrichosis connected? or is it more likely the latest calf is just deformed rather than the same cow throwing 2 different genetic defects?

3. Could this be the result of a noxious weed?

Thanks,
Alan


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From your description and the pictures included in your post, it is My Opinion that the calf is expressing "Dwarfism" traits! Your were wise to "put it down">

I think that you will be making a mistake to "pass it's dam off" at the sale barn! I would be enraged if I purchased that cow and then discovered that it carried the Dwarf gene, with the seller being aware of that fact!!

Not good stockmanship on your part!

DOC HARRIS
 
DOC HARRIS":3mg0x0gd said:
From your description and the pictures included in your post, it is My Opinion that the calf is expressing "Dwarfism" traits! Your were wise to "put it down">

I think that you will be making a mistake to "pass it's dam off" at the sale barn! I would be enraged if I purchased that cow and then discovered that it carried the Dwarf gene, with the seller being aware of that fact!!

Not good stockmanship on your part!


DOC HARRIS


Relax Doc! It will go as a slaughter cow. I'm a little put off about your opinion of me, I have more ethics then that. When I unload cattle at the sale they ask if it's for slaughter to be preg'd ck or ???????

With luck I can get some answers to my questions without this post getting lost on other thoughts.

Alan
 
I still believe you need to get to the cause before sweeping her under the carpet.
 
KNERSIE":1xwl6srh said:
I still believe you need to get to the cause before sweeping her under the carpet.


Thanks again Harley, my concern is that she has thrown 2 genitic defects during her time with me (I bought her as a heifer). She is still one of my better cows. BTW the 2 defects were results of matings with 2 different bull. I guess your response begs a different question, can she have thrown this calf without being a carrier?

Thanks,
Alan
 
Alan":ynrsoykx said:
KNERSIE":ynrsoykx said:
I still believe you need to get to the cause before sweeping her under the carpet.


Thanks again Harley, my concern is that she has thrown 2 genitic defects during her time with me (I bought her as a heifer). She is still one of my better cows. BTW the 2 defects were results of matings with 2 different bull. I guess your response begs a different question, can she have thrown this calf without being a carrier?
Thanks,
Alan

if it is indeed a dwarf, no, as far as my knowledge goes you need a recessive dwarf gene from each parent for it to be expressed, but don't quote me on that. I'm still not absolutely convinced it is a dwarf and given the repercussions it could have I'd rather make sure it is a dwarf before deciding how to handle the situation.
 
I am confused. What happened to the calf? You for sure should have had a sample taken before getting rid of it to determine any genetic problems. I am no Vet but am not sure it is a dwarf. Could be or maybe not. Could be environmental as you alluded to.
 
Some of these genetic defects seem to trace back to one animal, if you needed a gene from both parents, the defect would only show in relatives bred to relatives of the first known carrier, which I don't think is always the case.
 
I grew up with a straightbred Polled Hereford herd where Dwarfism was definitely a problem. That looks vaguely like a dwarf. I won't say it is not, but it is not what I remember as typical. I don't ever remember one with the shoulders swung waay out like that, and the head was usually bigger in proportion to the body. Could be what the oldtimers used to call a "bulldog" calf, which is a different recessive, though I thought most bulldogs didn't live that long. Some sort of toxicity problem would be my biggest fear. I would have kept the both of them (and that would mean bottle feeding the calf) and call a vet to get this resolved to my satisfaction.
 
Alan":3034xe4s said:
She is still one of my better cows. BTW the 2 defects were results of matings with 2 different bull.

In the cow business, beauty is what beauty does. She has thrown two useless calves so she is definitely NOT one of your better cows. Some podunk ugly cow that weans a 450 lb but sound calf every year; beats a show winner that throws a deformed calf every third year but weans 700 lbers the rest of the time no matter how you do the math.
 
Alan,

I don't know enough about dwarfism to tell you one way or the other. It could be environment too as I have seem caves born with rickets that looked similar. Dr Beever @ the University of Illinois does a lot of work on genetic defects and I think would be interested in your case. Before you do anything drastic like shoot the calf or dispose of the cow, it may make sense to get his take on it. If it is environment, wouldn't it be nice to know if you can prevent it in future calves?

If the cow and calf are dwarf carriers, it would be valuable information in having a DNA profile of these animals and a 100% DNA pedigree of the animals. It may save years on developing a DNA test for them. Also, in order to identify a true dwarf, I think they would want to do an autopsy and look at the skeleton of the calf.

Here is his address. I know he would love to hear from you and see your pictures.

Jonathan E. Beever, Ph.D.
Associate Professor of Molecular Genetics
Department of Animal Sciences
University of Illinois at Urbana-Champaign
220 Edward R. Madigan Laboratory, MC-051
1201 West Gregory Drive
Urbana, IL 61801 USA
Phone: 217-333-4194
Fax: 217-244-5617
email:[email protected]



Brian
 
DOC HARRIS":1h7f8tqo said:
I think that you will be making a mistake to "pass it's dam off" at the sale barn! I would be enraged if I purchased that cow and then discovered that it carried the Dwarf gene, with the seller being aware of that fact!!

Not good stockmanship on your part!

pretty judgemental there Doc.

nobody takes their best cows to the sale barn; buy one there and you better know the risks. breed her to a clean bull and the new owner should have no problems. the sire of this calf hopefully gets just as much blame and the same outcome.
 
KNERSIE":316ex0hg said:
I still believe you need to get to the cause before sweeping her under the carpet.


Alan I agree with Knersie. You need to find out the cause before you ship her, especially if it is a toxicity problem. Get some blood work done on her, I wish you would have had the calf posted too.
 
From CT


BVD IS THE MOST COSTLY VIRAL DISEASE IN CATTLE

by: Heather Smith Thomas

Bovine viral diarrhea virus (BVDV) is widespread in cattle, with a high number of animals testing positive to this disease. It has been estimated that 80 percent of cattle in this country have been exposed to BVD, and that 70 to 90 percent of infections go undetected, without visible symptoms. It is the most costly viral disease in cattle, inhibiting conception, causing abortion and birth defects, and hindering the immune system -- making the animals more susceptible to other diseases. In the U.S. cattle industry BVD is costing producers an estimated $2 billion per year.
The first descriptions of BVD in North America (outbreaks of diarrhea in some herds, and erosive lesions in the digestive tract -- sometimes with nasal discharge, drooling, diarrhea and abortion) were reported more than 60 years ago. It got its name from the profuse, watery diarrhea shown by weanling/yearling age cattle, but we later learned that this was only one of many forms of disease caused by this virus. The first attempts to isolate the cause of these various problems were not successful; medical technology was not advanced enough to detect and identify the virus. Eventually researchers found that all these symptoms were caused by one virus.

TYPE I AND TYPE II VIRUS, STRAINS AND CYTOPATHIC/NON-CYTOPATHIC -- The BVD virus is an elusive villian because it comes in two forms that have different effects within the body cells (cytopathic and non-cytopathic). There are also two basic genetic types of the virus (and several strains within each type), and each of these types or strains may fall into either one of these categories regarding how they affect the cells.

When scientists were trying to isolate the virus, they used certain body tissue cells to culture it, and discovered that the cultures didn't respond the same way. Some cells became infected but were not changed. In other cultures, the virus caused obvious changes in the shape of the cells and killed them. This version of BVD virus was termed cytopathic, meaning that it killed the cells. The other version of BVD virus was called non-cytopathic, meaning that it did not destroy or change the shape of the cells.

The two basic genetic types of the virus (Type I and Type II) are about 70 percent similar in genetic make-up and can both be present in the same animal. They can also change their genetic composition during the process of multiplication. This explains why there can be such a variation in disease symptoms and in how the animal's immune system deals with the virus. Each type also has both cytopathic and non-cytopathic characteristics.

Thus there are several forms of BVD, ranging from subclinical infections (in which the animal shows no obvious signs) to a severe and highly fatal form called mucosal disease. BVD can affect the digestive, respiratory, immune, nervous and reproductive systems. It can cause abortion in cows, stillborn calves, calves born with birth defects or with immune deficiencies or persistent infection.

The BVD virus can mutate or change somewhat as it multiplies, and there are several strains of the virus, which means that the infected animal may or may not be able to mount a protective immune response or be protected from the virus by vaccination. This is why Type I and Type II viruses can produce different disease signs even though they are both BVD viruses. Since they can also both be present in the same animal this complicates the disease picture.

Some scientists subdivide the two types into more strains, with further subtle changes in genetic composition of each type. Because the BVD virus can be so varied, this is the reason some infections do not cause obvious disease, while others affect the animal's ability to develop an immune response to fight off the disease, and why BVD can appear in different systems (digestive, respiratory, reproductive, etc.) in different situations.

MUCOSAL DISEASE -- The most serious form of BVD was first called mucosal disease -- a sporadically occurring, highly fatal disease of the small intestine, in which the virus has a cytopathic effect (changing and destroying the cells). Researchers eventually discovered that mucusal disease only occurs in cattle that are infected before birth with a non-cytopathic version of the virus (they seem normal, but are persistently infected and have no immunity to the virus) and then encounter a cytopathic type of BVD virus. Since these animals cannot develop immunity (even if vaccinated), they are vulnerable to the severe effects of the cell- killing version of the virus, if that virus is a strain that is closely related to the persistently infecting virus. Not every combination of non-cytopathic and cytopathic BVD virus in a PI (persistently infected) animal results in mucosal disease however.

Mucosal disease has several forms. There is an acute form with a very high mortality rate and a chronic form that also has high mortality rate but a much longer course. Cattle most likely to develop mucosal disease are usually six months to two years old, and though only a small percentage of the herd may be affected, nearly all of the affected animals die. Often these young animals were persistently infected with the same strain of non-cytopathic virus and were then exposed to an animal with a cytopathic virus.

Mucosal disease is often characterized by profuse, watery diarrhea (which may contain blood and gut lining), which generally develops two to three days after the animal exhibits fever, weakness, depression and lack of appetite. There are usually lesions in the mouth that may involve the lips and tongue, or even the nasal cavity. The animal becomes emaciated and dehydrated. Acute cases usually die within a few days or weeks. A few become chronic and may survive for up to 18 months, becoming progressively emaciated. Diarrhea in these cases may be continuous or intermittent and some animals may develop chronic bloat. Lesions in the mouth and skin are slow to heal and the animal may become lame. Treatment is not recommended because even if there is a slight chance for recovery, the animal will be infected for life and should be culled.

INFECTIONS SPREAD VIA BREEDING -- Semen from bulls that are infected may contain the virus. Reduced conception rates have been reported in otherwise healthy cows that were bred to (or inseminated with semen from) persistently infected bulls. Bulls affected with acute BVD may shed the virus in their semen for awhile after being infected. BVD infection at the time of breeding can result in reduced pregnancy rates due to significant embryo or fetal loss.



SIDEBAR: BIRTH DEFECTS CAUSED BY BVD -- Infection of the fetus any time between 100 to 150 days of gestation can result in a variety of congenital defects, since this stage is when the nervous system is in its final stages of development and the fetal immune system is developing. BVD infection at any stage of gestation may retard fetal growth, resulting in lower birth weight and poor bone growth. Lung development may be incomplete. Skeletal defects may include a jaw too short, or fused joints. Another defect sometimes seen is less than normal amount of hair, curly hair, or hairlessness.

Defects involving the nervous system include inadequate brain development, incomplete development of the cerebellum (the portion of the brain involved with coordination of movements —affected calves have trouble standing up), water on the brain and other brain problems. Congenital defects involving the eyes may include cataracts, opaque cornea, inflammation of the optic nerve, atrophy or abnormality of the retina, and varying degrees of blindness.



SIDEBAR: BVD CAN BE THE UNDERLYING CAUSE OF OTHER DISEASE OUTBREAKS Since BVD infection suppresses the immune system, infected cattle (especially young calves) may have a higher incidence of other diseases, including pnuemonia, scours, pinkeye, footrot, diptheria, etc. Pregnant cattle may abort--with outbreaks of lepto, IBR and other diseases -- simply because they were not able to develop immunity to those diseases. BVD infection can be difficult to diagnose because it shows up in so many different ways. If a rancher has problems with several types of calf scours and a high incidence of respiratory diseases, this may be a clue that BVD is part of the problem. And besides affecting the immune system, BVD by itself can cause illness in calves.

A herd health program may be ineffective because BVD infected cattle don't mount a very good response to vaccinations. So even if a rancher diligently vaccinates against lepto, IBR, pinkeye and other common diseases, some of the vaccinated cattle may develop those diseases. The rancher may think the vaccine didn't work, when in reality the animal was unable to develop a good response.

In one study, BVD virus was the virus most often found in the lungs of feedlot cattle with pneumonia, and was usually found in conjunction with Pasteurella. Infection with the BVD virus has been associated with In outbreaks of respiratory disease complexes in feedlots, and on the ranch. In young calves with multiple viral infections, BVD virus is the most frequently found pathogen. Infection with BVD virus has been shown to impair the ability of calves to fight lung infections caused by bovine herpesvirus 1 (infectious bovine rhinotracheitis or IBR). Many vaccines combine IBR and BVD, to give protection against both of these viruses.
 
Whatever. There could be several causes.

As the calf grows older it will develop more dwarf symptoms if that is what it is. Those symptoms usually include the rest of the body growing but the heart and flank girths both staying tight and small. The belly gets pretty pronounced in its' bloated look. I think that the tight heart girth is what eventually kills some dwarfs as the heart is just compressed enough to cause death.

One time I saw a bull that had had a bad mid section hernia and to alleviate that CSU had branded three bands around his girth to hold the hernia in. I always felt that they might have gotten that idea from the tight girths that the dwarfs had. He was a great old CK ranch bull that we fell in love with and that love headed us to CK ranch.
 
Yeah, I agree with BVD as a differential especially since this cow has had two basically deformed calves with different issues. It is unlikely in my opinion that she would be both a dwarfism and a hypotrichosis carrier, but stranger things have happened. I would recommend testing your entire calf crop including this one's BVD PI (carrier) status. We usually do this with an ear notch using either an ELISA or a immunohistochemistry test. Your state veterinary diagnostic lab should offer this. Our clinic uses a lab out of Sublette, KS to run ours for about $3.50 per head. If a calf is positive, we ear notch the mother because if a cow is a carrier, she is so for life and will always produce a carrier calf. However this is unlikely because most (90%) of carriers die before they reach 2 yrs of age. That would be my recommendation #1. This calf does not have to be a BVD carrier, but may have just been exposed to BVD at the proper time of pregnancy to cause its birth defects. If you have BVD you need to know it!!! It will be an insidious cause of reproductive problems, health problems in the calves due to immunosuppression, poor rates of gain, and not to mention upset customers when they purchase cattle from you and get them tested to find PI animals in the group or have increased health issues/death loss with the purchased cattle. If you have any calves that test positive BVD PI, they need to be euthanized and removed from your cows at least 30 days before bull turn-out so we can prevent this problem for next year!! Exposure to such carrier calves during pregnancy (45-120days gestation - time frame is arguable) will make PI calves more likely to occur.
Another recommendation I have would be to euthanize this calf and send him to Dr. David Steffen at Univ. of Nebraska. He is involved in several studies on genetic defects in cattle and has done the majority of necropsy work for Dr. Beever. He was the go-to-pathologist on all the Angus Association genetic defect related necropsies. His ph. is (402) 472-1434. Address: 137 VDC, University of Nebraska at Lincoln, Lincoln, NE 68583-0907. He will be able to tell you if this is a dwarf, a nutritional problem like ricketts, or BVD associated. Good luck! Hope you get it figured out!
 
Alan said:
I have a couple of questions about a cow I have. I have an older cow who in about 2004 dropped a heifer who had Hypotrichsis. I never had it verified, but the heifer had a very thin coat of hair and it was very curly (kinky) hair. Now approx. 5 or 6 years later the same cow drops a (maybe) dwarf heifer. I say maybe because at first the head looked bigger than it should have been, but today maybe not. The main thing was the calf was very small (short, height wise) maybe 50 or 60 pounds and the two front legs looked like the shoulders are very wide and she was very 'bull legged" in both front legs. Also all the joints in all 4 legs are very much over size.... I feel she was deformed. She took a full day to stand and today she could stand on her own but when she tried to take a step on her front legs she would fall down. I put her down tonight and the cow goes to the next sale on Tuesday. My 3 question are;

1. I assume these genetics defects are a reccessive (sp) gene, maybe not (?) but if the gene is reccessive, would it mean that both the sire and the dam have to be carriers to pass it on?

2. The same cow has thrown two calves with genetic defects, if it is drawfism, is dwarfism and hypotrichosis connected? or is it more likely the latest calf is just deformed rather than the same cow throwing 2 different genetic defects?

3. Could this be the result of a noxious weed?

Thanks,
Alan



Alan,
You need to send the dead calf to the University of Nebraska, Dr Dave Steffen for analysis. Call the AHA for Dr Steffen's contact info and call him for instructions on how to send it to him. Another option would be sending it to a local animal science department that could work with Dr Steffen on a determination as to what the cause of the defects are. It may not be dwarfism and no one can responsibly say it is with the information you have given. There are definative tests that can be done.
 
Alan, the calf is typical of the dwarfs I've seen recently in Angus sired calves, did you take any dna samples? BTW. the sire of the calf would also be a carrier of the defect. Don't buy the BVD theory at all.
 

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