Conference noted::equitation

    
    
    Excuse my ignorance, but what is a "lethal white foal"?
    
    

    I too, have never heard that expression before??  I am just
    starting to get into breeding quarter horses, and would like
    to know more about this.
    
    Thanks
    Marianne
    

    
    Within the past 12 months, EQUUS has covered the subject of breeding
    with special attention given to the genetics of overo paints.  If
    you can get too these issues, you will find at least some of the
    information you want.  If you'd like, I'll find the issue the
    article was in and reply here.
    
    					Monty
    

    RE. 1 & 2   The problem is that I do not know all that much about
    the lethal white foal, except that my mare had one.  The only
    information that I have is that all overo paints carry this recessive
    gene.  The stallion that she had been bred to, had never had a lethal
    white foal before.  He has been bred to many overo mares and has
    been lucky in that the lethal white gene never showed up before.
    I guess what it amounts to is that if the gene is present in the
    egg as well as the sperm, then the baby is born totally white (maybe
    a small amount of brown, black or whatever) and totally blind. 
    But the real killer, is the malformed small intestine.  The baby
    starts out able to eat and seems O.K. but cannot pass the meconum
    (?) or anything else.  They start showing severe signs of colic
    and there is nothing that can be done to save the baby.  I had called
    the Paint Horse Assn. and they told me that there had been cases
    reported of lethal white foals when an overo mare had been bred
    to a quarter horse stallion, which means that the stallion carried
    the lethal white gene also.  It really seems to be just a chance
    type thing.  I have been told that I shouldn't breed my mare to
    the quarter stallion, but I feel that I need to know whether or
    not the mare will throw a normal foal.  The paint registry only
    registers paints with paint, quarter horse, and thoroughbred
    bloodlines.  I am not sure whether the thoroughbred carries this
    lethal white gene either.  The paint registry also told me that
    if I bred to the same stallion, that she had this foal by, then
    there would be a greater chance of having another lethal white.
    They told me that if I bred to a quarter stallion, that the chances
    would be less than 5%.  So, this is the only information that I
    have so far, but the registry is supposed to be sending me some
    more information.  If you would like to know what they say, I will
    be glad to put the information here.
    
    RE. 3  I have been receiving the Equus Mag. for the last 6 or 7
    months.  If you could tell me what issue that you saw these articles
    in, then I will see if I have them.   Thanks a lot

    
    It seems I'm getting old quickly...
    
    The issue with the article is number 62 ( December 1982 ).  So here,
    reprinted without permission, is the sidebar of interest:
    
    			Overo x Overo    Risky Business
    
    	The birth of a pure white foal is the sight most dreaded by
    Paint horse breeders.  Along with the chance of breeding striking,
    often symmetrical overo coat color patters comes an elemment of
    risk: most overo x overo matings are potential producers of a lethal
    white foal.
    	Such a foal is destined to die within hours of birth.  Although
    he appears normal, he is born with a nonfunctioning lower intesting
    incapable of nervous contraction.  How did it happen?  Early in
    the embryonic development of these foals there is a failure of the
    normal migration of pigment cells, which ultimately leave the horse
    without color.  Since the gut wall arises from the same original
    cell layer as the skin, it's logical to assume that an error in
    one wall could be duplicated in the other.  In the lethal white
    foal, nerve cells in the lower gut are never hooked up, and the
    baby is born incapable of intestinal movement.
    	No one is sure of the incidence of the lethal white factor in
    Paint horse breeding; it's tough to trace in registry records because
    few lethal foals are reported.  But California geneticist Ann Bowling,
    PhD, estimates that as many as '25 percent of all overo x overo
    matings may theoretically produce lethal white foals.  It's not
    a trivial number.'
    	Adds Bowling: 'I feel strongly that if you want to breed overo,
    you must financially and emothionally face the fact that you are
    going to lose some foals.'
    	Bowling welcomes correspondence from Paint breeders on the subject,
    as a strong data base is the best weapon in the battle to identify
    the enemy.  Bowling may be contacted at the Serology Laboratory,
    Department of Reproduction, School of Veterinary Medicine, University
    of California, Davis, CA  95616.

    
    
    While searching, I found some other references you may be interested
    in:  "Practical Horseman" of October 1985 has a brief article
    discussing color genetics.  While this is a light coverage and doesn't
    talk about overo genetics explicitly, they did give several references.
    Might be interesting.  ( If you read any of these, how about a
    review? )
    
	I'd guess that with simple Mendelian genetics, 25% of the foals
    would be lethal white, 25% solid, and 50% overo but the Equus article
    led me to believe that overo genetics is rather complicated.

    					Monty
    

    Thankyou for putting the article in.  I have never heard of such
    a case before.  Do you know if this only pertains to the breeding
    of Paints, or could it happen when breeding Quarter horses also?
    
    Thanks,
    Marianne
    

    
    The article mentions that the overo is sometimes a product of two
    Quarter horses.  The genetics of overo are not strictly
    dominant/recessive: overo x overo breeding won't necessarily
    produce overos while two solid-colored parents may produce an
    overo.  It seems VERY unpredictable.  ( There is a photograph of
    a crazyquilt with overo characteristics resulting from Appaloosa
    x Appaloosa breeding in the Equus article. )  It is more of a
    birth defect than a true color gene.
    
    				Monty
    

    

             LETHAL WHITES:  The problem that won't go away.
         
    Reprinted without permission from Paint Horse Journal, Jan. 1985
    
       In Feb. 1982,  The Journal of the American Veterinary Association,
    volume 180, published and article entitled "Ileocolonic Aganglionosis
    in white progeny of overo spotted horses" by Dr. Bruce D. Hultgren.
    For the first time this article documented the cause of illness
    and death in white foals produced by overo spotted horses.  The
    syndrome is commonly called "lethal white foals" bye the spotted
    horse industry.  Because thies abnormality appears to be directly
    connected with the cause of white spots in the overo horse, the
    spotted horse industry has a problem that won't go away.
       It is now known that lethal white foals become ill and die because
    of ileocolonoic aganglionosis.  That is a medical term designating
    a total lack of submucosal and myenteric ganglia (large cells) in
    the ileum (the end part of the small intestine and parts of the
    colon (large intestine.
       Submucosal and myenteric ganglia are large cells that can be
    seen with a light microscope by trained scientists.  These cells
    partially control the normal action of the intestine in passing
    food through the horse's intestinal system.  They act like fuse
    boxed in the electrical circuit of a house.  They must function
    in order for all of the appliances to work.  In the lethal white
    foal the ileum and colon do not work. 
       Ileocolonic aganglionosis explains the illness and death of lethal
    white foals.  The foals show signs of colic including restlessness,
    anxiety, kicking at their sides, and constantly lying down and getting
    up just as other horses with colic do.  These signs of colic appear
    from 5 to 24 hours (average, 13 hours) after birth.  The life span
    of foals dying of natural causes averaged 46 hours and ranged from
    23 to 132 hours. The foals usually were normal at birth; that is
    they stood, nursed and generally behaved as normal foals prior to
    colic signs.  However, none of the foals were abserved to defecate
    (pass meconium or manure).  All of the observations can be explained
    scientifically as caused by the aganglionosis.
       Necropsy (autopsy) findings also corresond to those from other
    autopsies where deaths were caused by ileocolonic aganglionosis.
    Milk was found in the stomach and beginning of the small intestine
    in the foals that had suckled.  The beginning part of the foals
    intestines have ganglia and thus move the milk into the first part
    of the small intestine.  Meconium was retained in the ileum (end
    of the small intestine) and colons.  Meconium is the thick, sticky,
    green-yellow-brown material normally present in the intestine of
    newborn foals.  It is pased within a few hours as manure.  The 
    meconium cannot be passed in lethal white foals because the end
    of the intestines which lacks submucosal and myenteric ganglia cannot
    putsh it along and out.  Parts of the colon also appeared small.
    This is explained by the lack of nervous control due to the
    aganglionosis and not due to that part of intestine being incompletely
    developed.
       The white spotting seen in overo horses and the ileocolonic 
    aganglionosis of the associated lethal white foal are probably related.
    Both melanocytes (cells that produce color in skin) and the ganglia
    cells in the intstine come from an area of the developing fetus
    called the neural crest.  It is probable that whatever causes white
    spots on overo horses also causes the lethal white foal.  This has
    been shown to be true in the piebald-lethal and lethal spotting
    strains of mice.  These are white spotted mice that also have
    intestinal aganglionosis.  A similar association has been noted
    in Heischsprungs disease in man in which intestinal aganglionosis
    is again present.  
       The inheritance (genetics) of the overo horse and the associated
    lethal white foal is not understood.  Both males and females are
    known to be overo spotted and affected by the lethal white foal
    syndrome.  This indicates an autosomal pattern of inheritance (that
    is, the inheritance is not sex-linked).  Parents of lethal whites
    range from less than 24% - more than 75% white.  Apparently excessive
    white or confluent white spotting is not necessarily related to
    the production of lethal white foals.  Also it has been known that
    solid (registered as broodstock) colored horses can produce affected
    foals.
       Because so much of the lethal white foal's intestinal system
    is affected with the aganglionosis, no treatment or surgery is
    available.Humane euthanasia is recommended.  Caution is necessary
    in diagnosing primarily white foals with dark spotting around the
    head, hooves, and base of tail because other causes of intestinal
    obstruction in newbon foals could be the cause and note ileocolonic
    aganglionosis.
       It is not known if normal white foals can result from overo matings.
    For the spotted horse industry, future research concerning the genetics
    and cytogenetics of spotted horses and the overo lethal white foal
    is very important.  Prevention of the birth of the lethal white
    foal is desirable.  Until the genetics and cytogenetics is know,
    the spotted horse industry has a problem that won't go away.

     re. 57.8
    
     I just reread the article that I just typed in and saw quite a
    few spelling errors.  Please excuse my poor typing.
                                                        
     I also omitted the author who is Bruce D. hultgren. DVM. PhD

    
         Thankyou for printing that article.  I, too, had never heard
    of a "lethal white foal" befor.  I guess I'm lucky I own a Paint
    gelding.
    
    			Wishing You Better Luck Next Time,
    							A Paint Lover
    
    
    

    First of all let me say Howdy ya'll from Colorado
    
    Just found this notesfile and your note on "lethal white"  I breed
    Pintos out here so I do try and keep abreast of the color issues.
    
    If you want some more reading the "Pinto Horse Magazine" has published
    a couple of articles on the subject.  Their number is (619)286-1570
    I'm sure that you could get re-prints(talk to Carrie).
    
    From what I remember they had "lethal white foals" from two solid
    parents.  I take this to mean that both parents were carrying the
    overo pattern as a recessive.  The "lethal white" seems to be a
    fault that is linked to the overo pattern.  This is not limited
    to the quarter horse lines but you do tend to see it more in that
    breed.
    
    What I try to do is to breed the tobiano to the overo.  The tobiano
    pattern is a dominant gene type since you always have one tobiano
    parent if you have a tobiano foal.  The overo is a recessive since
    you can have a overo foal from two solid parents.  I have not so
    far heard of a "lethal white foal" linked to the tobiano pattern.
    
    So far doing this I have not had the problem occur although I do
    know of farms that have had problems breeding overo to overo.
    
    I hope this helps instead of confuses you
    
    -John-

    RE: 11
    
    Hi John,
       You said that you try to breed tobiano to overo.  In the long
    run, want the tobiano then carry the lethal white gene?  I had been
    told that there was a possibility of this, since overos are bred
    to tobiano's quite a bit.  If this is the case, then essentially
    there are no safe color patterns, in which an overo paint could bred
    to.  Am I correct or incorrect in believing this?  I did have my
    mare rebred to a quarter stallion, but since there is a possibility
    that she could have another lethal white, I am really holding my
    breath.  Needless to say, I am rather worried, and will be until
    the foal is on the ground.  I pray that it is a healthy foal, but
    if it is another lethal white, I will never breed my mare  again.
    I will also have the vet out immediately to have the foal put down,
    because I do not think that I could bear to watch it go through
    the colic pains, that this 1st foal went through.  The vet schools
    want to do reserch on this, but they want the foal alive, and they
    want to watch it until the foal dies to get data (I guess) to see
    how long it will survive if it has this affliction.   I don't think
    that I could stand to do this either, even in the name of RESEARCH!
    

    RE:12
    
    Sorry it tool me so long to respond but this company I work for
    thinks that I am supposed to work for a living.
    
    I have been doing some more checking around with breeders out here
    and in the article I quoted.  The article does infer that the 'lethal
    white' is linked to the overo pattern.  And since any horse breed
    can/does carry the gene all colors/patterns are possible carriers.
    
    The reason that I try and breed the tobiano to the overo is that
    I don't feel comfortable with the overo to overo cross unless I
    am sure that neither of the parents have every had a lethal white.
    And with some breeders this is very hard to determine.
    
    One of the paint breeders I know out here claims that the problem
    lies with the mare and not the stallion.  I have a hard time with
    this since according to genetics it does take two to tangle.  This
    rancher though has been breeding paints for over 30 years.  He said
    that he finally came to the point that if a mare had a lethal white
    the mare went down the road.
    
    I know this is not good news for you.  You didn't mention if you
    had bred you mare back to the same stallion.
    
    When is the foal due?  I hope that you will keep us all up on the
    situation.  I'm sure that others would also be interested in the
    pedigrees of both the mares and stallion.

    My mare is bred to a quarter horse this time.  The stallion is by
    Speculator, and the mare is by Ratchett.   She is due the 12th of
    April, and I am a little worried about it because I have a feeling
    that she may be the cause, since the overo stallion that she had
    been bred to has been bred to numerous overo mares and has never
    sired a "lethal white" before.  Of course that isn't to say that
    the possibility isn't there.  I have also been given some new
    information, (source not necessary reliable), that only one horse
    needs to carry the gene, be it stallion or the mare.   I will be
    glad to keep everyone informed about the outcome of this foal. 
    I do pray that it will be normal.

    I read in a book on genetics that the lethal white gene is dominant
    and is represented by W ( as opposed to w).  Perhaps the dominance
    can more easily explain the numbers of white foals.
    
    Perhaps the best way is to check the history of each mare and stallion
    in a prospective breeding.  If either produced a lethal white foal,
    don't breed it/to it.  In the Arabian industry, horses that produce
    CID (combined immunodeficiency) foals -- which usually die shortly
    after weaning -- are not supposed to be re-bred.  The Arabian Horse
    Registry encourages breeders who discover carriers in their herd
    to file a report about each one.  That way prospective breeders
    can contact the Registry about the stallion/mare they want to breed.
    It takes two carriers to produce a CID foal.
    
    Perhaps the spotted horse industry could do the same.  While the
    impact of such action could hurt individual breeders, who can no
    longer breed those animals, in the long run CID could be eliminated.

    Hello !
    
    Just got finished reading this whole list of responses and was
    wondering if anyone out there knows what happened to this mare.
    
    Did she have a normal healthy foal ?  What happened ?
    
    Very Interested !
    Hoping for the very best in news !
    Lorna Caribo
    

    Well,   I have some good news to report about this mare, and some
    bad news.   When the foal was born, it was a beautiful paint filly.
    But, she had some problems after birth.  She seem to have a severe
    allergic reaction to the mares' milk.  She almost did not make it
    during the 1st week after birth.  The foal had to be given daily
    shots of antibiotics and after a couple of weeks started doing well.
    
    Since the first foal died of the lethal white gene, I felt like
    the people that had leased her for breeding should have another
    chance with this foal, so I gave them the option of keeping her
    and I would get a breed-back this coming year.
    
    So, they decided they would keep the filly for sale.  They found
    someone to buy her and the person that wanted to buy her wanted
    to get her weaned so she could get her ready for a futurity.  One
    week after she was weaned, they found her dead in the stall.  The
    vet did an autopsy and could find nothing physically wrong with
    the liver, heart, and intestines.  This being the case, I was advised
    not to ever re-breed my mare, because it was believed to be a
    congenital problem.  I am not totally convinced that this is the
    case.  They weaned this baby at 3 months, and I feel this is way
    too early to wean a foal under such bad circumstances when this
    foal was born.  I have been told that babies are weaned at 3 months
    only under the best of circumstances or when there was a problem
    with the mare.
    
    Since, the foal wasn't under my care at the time, and I wasn't able
    to spend much time with them (I just had a baby myself 14 days before
    the filly was born) I really can't say if I am correct about everything
    that I was told about the baby.  I was talking with a vet recently
    and he told me that it sounded like neo-natal erythr---- something.
    That for some reason factors in the mare and the stallions blood
    caused the foal's body to actually fight the antibodies available
    in the mares first milk. He said that it would probably happen again,
    but that I could avoid the same allergic reaction to the mares milk
    by muzzleing the baby and not allowing the baby to drink the mares
    first milk, but that the antibodies would have to be supplied from
    another mare or by plasma.  Another method would be to do blood
    tests on the mare and stallion prior to breeding to check for these
    factors that would cause this problem.
    
    Well, this is the status.  Any  comments and information about any
    of this would be appreciated.
    
    Thanks a lot,
    
    Sarah

    In the June 1989 Animal Health Newsletter, I found some more info of
    lethal white foals produced by overo-overo matings in paint/pinto
    horses. Actually, there have been some cases of lethal white in foals
    sired by overo stallions and out of a mare w/another pattern when the
    mare was sired by an overo stallion...read on if you breed
    paints/pintos.
    
    "Unanswered Questions about White Foal Syndrome
    
    Much is known about White Foal Syndrome but many mysteries still remain
    about this hereditary condition which is so lethal that there is
    literally no evidence of any affected foal surviving, nor of any
    surgical or medical treatment staying its fatal course. The syndrome
    occurs in a completely white foal born from mating an overo mare with
    an overo stallion. The foal usually appears normal at birth but signs
    of colic appear within 24 hours and reach their tragic end within
    8[more] hours.
    
    Contrary to the widespread misconception that white foals are likely to
    be born to overo parents that have a lot of white in their pattern,
    they have been found to be the offspring of [arents that are anywhere
    from 25 to 75 percent white. To complicate matters further, foals with
    the syndrome have even been the product of mating overo stallions with
    non-overo mares that had been sired by overo stallions. There is one
    small consolation however - only true or completely white foals are in
    danger, and these inevitably have pink skin and pale blue eyes, and may
    have only a trace of pigment on the body or a few black tail hairs.
    
    The colic that proves fatal to the white foal can develop as quickly as
    the fifth hour after birth with a telltale sign being the foal's
    failure to pass meconium, the first intestinal discharges after birth.
    Studies have shown that the colic is actually due to retained meconium
    and ingested milk(these foals can stand and nurse at first). The
    retention itself results from the root cause of the syndrome: failure
    of the normal muscular activity in the gut(peristalsis) that moves the
    food and feces along. The most recent studies at Cornell have
    demonstrated that foals with the syndrome lacked the motor nerves
    responsible for peristalsis in the rectum, in the small and large colon
    and in most of the small intestine.
    
    In addition, the small colon was tightly contracted. This is an
    important new finding indicating that the problem is in the inherent
    flaw in the gut wall which prohibits the gut from being supplied with
    the normal nerve endings needed for propoer muscle motion. This finding
    answers the question of why white foals appear to have normally
    developed nervous systems. In fact, they do have them except,
    unfortunately, for the nerves necessary for the functioning of the
    intestines. Thus, even though the foals appear alert with normal
    reflexes(witness the avid nursing right after birth) they cannot
    survive.
    
    There is a comprable condition in humans called Hirschsprung's disease
    that can be successfully treated by surgical removal of the affected
    parts of the colon, but in foals, too much of the bowel is affected.
    Hence the best course of action is prevention. But for that to be
    effective, more must be known about the mode of inheritance of the
    disease. When that is clear, breeding recommendation can be established
    and the potential carriers of the disease can be identified and
    excluded from breeding programs."

    Keeping in mind that I am not in the least bit technically educated on
    this subject, I'm responding with a couple of reactions to patterns in
    the preceding replies.
    
    1. Since the syndrome is the result of genetics, I am curious if
    research has isolated the DNA gene(s) involved.  If so, then I would
    imagine Overo x Overo breedings might be preceded by DNA testing of the
    animals to be mated (remember, pardon my ignorance - I love horses,
    used to have a couple, miss them greatly - they were the best things in
    my life!).
    
    2. With regards to a comment I recall where the originator of this
    conference feared the problem was all with his mare, not the stud
    because the stud had bred other Ovaro mares with no ill results.  That
    still doesn't make sense to me to blame the mare.  The Deadly White
    results from "Deadly" x "Deadly" parents, which is what happened in
    your case.  Therefore that stallion was "Deadly".  It also indicates to
    me that all the other mares he bred were "Non-Deadly", which is why no
    tragedies occured, and not because your mare was the only problem.  
    
    If I were you, I, too, would hesitate to breed my mare again, simply
    because you're playing a "Deadly" roulette game, ie: will the next stud
    be "Deadly" or not???
    
    Anyway, I'm glad to see this equine notesfile.  There's nothing like a
    half ton of horse to gladden the heart.
    
    Good luck!
    
    Chris
    

    To the best of my knowledge, the DNA that is directly responsible has
    not been identified. This syndrome has been known for more than 20
    years but it is not well researched due to the cost ratios involved(i.e.
    high costs and benefits a relatively small portion of the horse
    population).
    
    However, there are some statistical progeny testing approaches one
    could take to determine whether or not a stallion is "deadly" but you have 
    to do some test breedings to use them. Since it is known that the "deadly" 
    gene is recessive, a stallion and mare which are both recessive "deadly" 
    will produce 1 WFS foal out of every 4 matings on average with 3 out of
    4 producing foals which do not have the syndrome. Unfortunately, 2 out
    of the 3 live foals would be carriers of the syndrome since they had
    the recessive gene.
    
    To find out whether or not the stallion is a carrier, one could breed a 
    stallion to 5 mares known to have produced a WFS foal. If none of the 
    mares produces a WFS foal by this stallion, there is a strong
    probability (77% if I remember my probability theory correctly) that
    the stallion IS NOT a carrier. If the stallion does not produce a WFS
    foal in 10 matings with mares known to be carriers, the probability
    jumps to 95% that the stallion is not a carrier.
    
    Clearly, this approach could be used with mares too but it would take
    5-10 years to get the answer! 
    
    So, if you're a big breeder and want to minimize the number of WFS
    foals you produce, you could use this technique to find a few stallions
    that are non-carriers and breed them like crazy for a couple generations.

    Over the weekend, I checked out what I said in the previous note about
    progeny tests. I find that I remembered the theory correctly but was a
    bit sloppy with the arithmetic. It should be a 76.3% probability that
    the stallion is not a WFS carrier if 5 breedings to mares which are known 
    to be WFS carriers produce no WFS foal and 94.4% for 10 such breedings.
    
    In "Genetics of the Horse", Jones and Bogart state that the overo gene
    is recessive to the solid color gene and that the White Foal Syndrome
    gene is recessive to both. Therefore, they claim a solid color horse could 
    also be a carrier of WFS.
    
    In "Genetic Principles of Horse Breeding", Lasley describes the progeny
    test procedure I discussed in the previous note. He uses an example of
    a black stallion bred to chestnut mares producing black foals. That 
    procedure can be used to test whether or not an overo stallion carries the 
    WFS recessive. Lasley concludes his discussion with a table showing the 
    probability that a stallion does not a carry the recessive gene. I have 
    extended his table to 30 breedings being careful with the arithmetic this 
    time!
    
    Number of breedings with no WFS foal              Probability stallion
                                                 does not have recessive gene
    
    		1					25%
    		2					43.7%
    		3					57.8%
    		4					68.4%
    		5					76.3%
    		6					82.2%
    		7					86.7%
    		8					90.0%
    		9					92.5%
    		10					94.4%
    		11					95.8%
    		12					96.8%
    		13					97.6%
    		14					98.2%
    		15					98.7%
    		16					99.0%
    		20					99.7%
    		25					99.9%
    		30					99.98%
    
    After 16 to 30 breedings to mares known to carry the WFS recessive, it
    is practically impossible for the stallion to be a carrier. There's
    only 1 chance in 100 after 16 breedings and only 2 chances in 10,000
    after 30! The probability that he is a carrier but hasn't produced any
    WFS foals becomes even tinier if his career at stud goes on with no WFS
    foals.