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"Choanal atresia is probably the most well known of all camelid defects.
This involves the failure of the rostral and caudal nasopharynx to unite
into one continuous pathway for air movement through the nose. Camelids are
semi-obligate nasal breathers and many of these crias die soon after birth.
However, surgical correction of the defect is possible. Research at Oregon
State University (The Alpaca Registry Journal, Vol V, No 1, 2000) has shown
that choanal atresia is a heritable defect; however, the participation of
the dam and sire in propagation of the trait is unclear."
Dr. David Anderson, DVM; Ohio State University
"Defects that are thought to be hereditary, can be very complex. Then throw in some random or environmental cases and it becomes extremely difficult to pin down. At this time, although CA is thought to be a hereditary defect, it is still unknown exactly how CA is passed on. Is it a recessive gene in both parents involved? Or is it a recessive gene in only one parent and when paired with just that specific partner, the defect is triggered to surface? Perhaps all of the animals carry the marker that will trigger it but it takes a special set of circumstances to have it develop and we don't know what those are yet. Although everyone agrees that the affected offspring definitely should not ever be bred, the question remains whether both parents should immediately be withdrawn from the breeding pool or not. Or how about the grandparents? Perhaps it skips a generation ...... or even two or three. Or how far back should you go to remove related blood lines from the breeding pool? What about full siblings that appear OK? Is it possible they should also be removed from breeding? Should the parents be given another chance at breeding with a different sire and dam? However, if CA would occur
repeatably from the same line, although with different pairings, it would be unquestionably agreed that this particular animal be culled from the herd."
"As I understand it, CA is not a dominant trait that makes its presence known every time the same 2 animals that
produced a CA cria are bred (if my memory is correct, this is what the Oregon research showed). Therefore,
repeating the breeding does not guarantee that your dam or sire is not a carrier, it just proves that the resulting
cria does not have CA, but... and this is a big hitch, it might be a carrier.
In other words, you really can't extrapolate any information from the breeding of two animals that previously
created a CA cria unless they have another CA cria. For example, if both parents are recessive for CA and
you have a CA free cria, what do you conclude? Because you can only look at the phenotype (outward
expression or what you see), you can't conclude anything about genotype (the actual genetic makeup).
Now if they do have a CA cria, you are still at square one, cause you really don't know who is responsible. Is
Mom the carrier, and Dad just has the switch that turns that gene on to express itself? Or is it the opposite?
Or is it a simpler inheritance, and both parents are equally responsible? We simply do not know enough about
the inheritance of CA to draw definite conclusions.
So the question then becomes, how safe do you want to play the game? It is very easy for those of us who
have not had the horrible misfortune of a CA cria or other genetic defect, to say cull both, but in all honesty, I
don't know that I could. While there is no doubt in some cases that it is a straight genetic inheritance, there is
some question that there may also be environmental stimuli that can cause defects. This could explain the CA
cria occurring out of a dam and sire that have had many CA free cria before when crossed with other animals."
"One example: IHSS is an autosomal dominant human heart defect. SO every adult who has this defect has a 50% chance of
giving it to each child. However half of the cases found each year have occurred RANDOMLY as neither parent has the trait.
The person who developed it randomly has the same 50% chance of giving it to their children, but both parents of the randomly
affected person are NOT affected.
So if we were talking alpacas, you would cull an affected animal and it's offspring, but you would be wrong to cull any parents
of the randomly occurring defective animal. You would be correct to cull parents in a family line where it has occurred multiple
times. In addition, this dominant heart defect doesn't always manifest itself if present, so can appear to skip a generation, in a
family where pictures of the heart have not been taken to see the defect. Because this dominant trait is so bad for the heart, it
is NOT increasing in the population even though the statistics suggest it would. The affected individuals don't usually do well,
dying suddenly anywhere from teen years up. If we didn't have the ability to take heart pictures, it would be difficult to figure
out this was an autosomal dominant trait."
Allie Angott, MD
"However, remember in the case of choanal atresia (CA), one female produced it five
consecutive times when bred to five different males and two corrected CA animals did not produce a CA cria. The defect did
however occur more frequently in certain familial lines. The researchers concluded, without a doubt, that it is an inherited
defect, just as in humans, and that the manifestation is random and sometimes skips a generation. Some folks only have to live
with CA briefly, until the cria is euthanized, as most CA are a complete blockage. I live am reminded of it daily when I'm in
the pasture and hear Primo gasping for air. He requires no special care and is playful with his pasturemates, but I know he gets
real uncomfortable sometimes. If a CA cria is born, I would strongly suggest taking the time to research the sire's and dam's
lines thoroughly (try to go back four generations) to find out if a CA cira has been born in the past."
Quoted from a camelid breeder who owns a living partial CA cria and is trying to raise awareness
of defects in order to help reduce their occurrence.
"We really don't know what is going on with this.
I think that if a I have a cria with CA I will try breeding the male to
another female to see if it happens again then I will know it is not the
male, at the same time breed the dam to a different male looking for the same
result. That should pin the problem down to one or the other of the parents.
Records should be kept to see if this problem crops up again later with other
pairings. But to cull a bunch of animals without knowing which one is really
at fault would be foolish in my opinion. And until we have a genetic marker
that we can say for sure this is the animal that is the carrier we will have
to go with our best guess. I may go way out on a limb with a saw here but
would hazard a guess that all and I mean ALL of our animals carry this faulty
gene and that it is just the particular pairing of male and female and the
right conditions that all play a part in this. Until we know for sure we are
all wasting a lot of energy getting worked up about something we have very
little control over."
Jim Morton, JSC Alpacas
"I am certainly not slinging mud here, but once again, I want to state that
we know too little about most defects to be able to make these decisions.
We need research, and I mean multiple research projects, before we can ask
people to make such sacrifices. So, let's put the horse before the cart
here and support those projects that are underway. Let's give money to ARF
or the Morris Animal Foundation to support other projects relating to
genetic defects. Once we have a handle on the carriers, and preferably have
a gene marker to identify them, then we would be in a strong position to
implement a plan such as you propose. Until then, I ,for one, would scream
loud and long if I were so arbitrarily put out of business.
Now, please don't misunderstand me. I have never had a case of CA to date,
and am not defending any position or action. I would voluntarily remove my
male and/or female from the breeding pool, after finding out as much about
what we know in terms of carriers as possible. I would also inform any one
who had purchased from this line. That is all that we can do right now, it
seems to me. And we do need to try and encourage people to do this. But
how far we can go with that...Do we try to notify everyone who has bred to
him? How about the sire and dam of the offending pair? How far back do you
go for common ancestors, and which ones would you point to? You can see
what a can of worms we could be opening. CA is a terrible thing to
experience, and I would love to think that we could eliminate it from our
national herd. But, I simply think we know too little to get hard nosed
about this, yet."
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