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Saturday, June 27, 2009

[AlpacaTalk] more info



Here is a bit of information for those who haven't seen it yet. Everything I have read says to me, "Don't panic!" Research is underway. Yes, make careful breeding decisions. Ask question of sire owners. If you read this summary, you see that the actual reported cases of CA in alpacas is less than 1/2% of all births. How many more are not reported? I don't know how we could know. Just like when someone asked how many unregistered alpacas there were in the country. How can one know? 


And finally, there is nothing to suggest that CA and BEW are related in any way. No link has ever been suggested by any camelid researcher. BEW is a condition that occurs when the white spot gene is inherited by the cria, from one parent, and the grey/merle/roan gene is inherited from the other. It sort of makes a "double white" alpaca. It can happen from ANY grey alpaca, if bred to an alpaca that is white or is colored with white spots. It doesn't mean that either parent has defective genes, those color genes combined, has a chance of producing BEW. This is borne out by research and enumeration of BEW alpacas. No opinion here. Fact.

So, just be careful with your breeding decisions. I think we all generally are.


Heather



Proceedings of the 1st International 
Workshop on Camelid Genetic

Summary Report of Choanal Atresia and Wry Face in Camelids 
LaRue W. Johnson DVM, PhD 
Facial defects in camelids are relatively common as compared to other species. The now deceased 
Professor Horst Leipold of Kansas State University was a recognized "guru" of congenital and genetic 
conditions. He is quoted as saying that "If the incidence of a condition seems unusually high as compared 
to other species, chances are it is genetic".  

The two most commonly recognized congenital facial defects in both llamas and alpacas are Choanal 
Atresia (CA) and Wry Face (WF). While possible causes of these defects would include chromosomal 
aberrations, trauma, en utero positioning and Teratogenic effects, genetics appears to be involved. 
CA is defined as a failure of the internal nares (choanae) to develop the normal opening. It may be 
complete or partial, unilateral or bilateral as well as variable in structure ranging from membranous to 
boney. Consequently, affected individuals will likely have variable manifestations with the most severe 
being total inability to breathe through the nose at birth making it impossible to nurse without aspirating 
milk. The gold standard for making a diagnosis employs contrast media placed in the nose and diagnostic 
imaging to demonstrate blockage. 

While heroic but ill advised surgical efforts can be employed to correct the problem, generally affected 
individuals are euthanatized soon after birth. Researchers at Oregon State University (Smith, Timm et al.) 
conducted extensive necropsy and breeding studies with goals to establish mode of heritability and 
identification of carrier llamas. Many affected individuals were found to also have facial distortions like 
WF, cardiac and limb alterations as well as Arhinencephalia. Breeding trial results were erratic and 
planned DNA studies were not completed. They concluded that their research supports the presumption 
that the problem is passed by both the male and female and is not a sex linked problem. 

WF (Campylognathia) is by definition a maxillary jaw distortion that can occur in varying degrees and 
progress throughout life resulting in dental malocclusion. Most cases are present at birth and may have 
concomitant CA as well as cardiac abnormalities. Breeding trial research I performed at Colorado State 
University using "proven" carriers, presumed carriers as well as affected male and female llamas 
produced a 10% occurrence which is much greater than the natural occurrence of <1%. My conclusions 
from the study include that WF is a genetic problem, selective breeding will increase WF occurrence, the 
inheritance is to date not understood but likely involves multiple recessive genes with both parents 
contributing and that CA and WF have a genetic association.  

From a survey I conducted of 34 respected camelid veterinary colleagues, I received 18 responses to 
questions related to CA and WF. These individuals had and average of 17.6 years working with llamas 
and or alpacas upon which to base their opinions and recollections. Their averaged response to % 
prevalence of congenital defects in llamas was 3.4% with alpacas 4.0%. A total of 174 llama and 153 
alpaca cases of CA were recorded along with 46 llama and 69 alpaca WF cases. 18 examples of CA and 
WF occurring together were reported. Of all congenital defects, respondents expressed that CA 
represented approximately 15% and WF 5% in both llamas and alpacas. The prevalence of CA from all 
births was estimated to be .75% for llamas and .48% for alpacas while for WF, .48% for llamas and .35% 
for alpacas. When asked if camelid genetics are involved in the occurrence of CA, 16 responded yes and 2 
probably. For WF, 13 responded yes, 2 probably, 2 not clear and 1 no. 

There is no question that CA and WF need further research. With the reported progress of the alpaca 
genome research, it seems logical to utilize this tool to focus on these conditions. The camelid community 
will need to provide credibility, capital and cooperation to accomplish progress in the goal to further 
understand and hopefully eliminate these conditions.







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