Discussion Of
Coanal Atresia

Thoughts, comments, and experiences of camelid owners.

"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affected offspring definitely should not ever be bred, the question remains whether both parents should immediately be withdrawn from the breeding pool or not.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 doesnt 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 occurance.

"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."

If you have comments that you would like to contribute to this discussion, please send them to us at CA Discussion and we'll be happy to post your opinions and/or experiences here for others to consider - with or without your signature .... your choice.
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