Do No Harm

The Scandinavian canine realm is often held in high esteem among other dog people around the world, from their breeding practices to the transparency of their kennel clubs. 

Unfortunately, I seem to have found out the hard way that they have the same chinks in their armor as everyone else. 

A few days ago I wrote on FB Mudi groups about a litter that was created in Finland with a sire we co-own but we did not agree could be used for this litter.  Actually, we were not even asked, it was all done covertly by the Finnish breeder and the other Czech co-owner of the stud.  I found out about the litter from the FKK website shortly after it was listed.

Yesterday I found a discussion on the Finnish Mudi FB forum about how the sire of a Finnish litter was not being named publicly and some forum members wondered why this was?  The discussion took place in March of this year.  Someone asked was this some new kind of fashion?  Others also asked what the reasons would be for doing this as it was rather unusual not to list both parents?  Why the secrecy some asked?

The discussion went on to cover the need for transparency in all things Mudi and surely the breeder had a good reason not to tell who the father of the litter was.   

Well the truth is, it was not for a good reason the sire was not named and not only the breeders, but many other people were involved in the secret keeping as well.  It was shocking to learn of the widespread deception. I thought something like this would not happen in Scandinavia.  I was pitifully naive.  People are people all over the world, none should be thought of as better than others as everyone is still a human underneath that proud exterior and our nature is to do what benefits us, even at the expense of others or doing what is right, even those we put on a pedestal.

The reason behind this conspiracy was to prevent us from contacting the FKK before the registration of the pups was complete, otherwise they could cancel it.  Not only did the two breeders involved falsify documents, but the FKK broke their own rule by not making sure all 3 co-owners of the sire signed the litter registration form, when they had the proof in their hands, on the back of the sire’s pedigree.  The FKK refuses to take responsibility for the falsified documents they failed to catch, even after the deception was brought to their attention.   Or was it purposely overlooked for a friend?  This is the damage that gets done by one little lie that snowballs into a sizable scandal.  People see collaborators in every corner.   

I was shocked that so many other people knew what was going on and did not tell me about it.  Why would so many become accomplices to something they surely knew was wrong. Even the breeders knew it was wrong as they worked so hard to keep it a secret.  How could so many people go along with this?  This is the biggest disappointment of all.  I am sure I counted some of these co-conspirators as friends.  This is perhaps the most hurtful part of this whole issue to be knowingly deceived by friends. I hope that at least some of the conspirators are ashamed to have participated in this plot to defraud other people.  

Finally, it became clear with this incident that the Scandinavian superiority is not reality, they are just like everyone else. I really hoped they were the light in the darkness we could all follow, but now I see they are also following a light at the end of a tunnel they also cannot reach, just like the rest of us.

So where is the world’s Mudi community to go from here…. we need to realize, now more than ever, that we are all equally good and bad and no one, absolutely no one, is doing a better job than anyone else and deserves to be put on a pedestal.  Perhaps we should all strive not to make things better, but just to not make things worse, then we can all move forward at the same pace via a shared path, not in separate directions.  ‘United we conquer, divided we fall’, ‘there is no ‘I’ in team’…. über corny sayings, but maybe it’s time to take them to heart and do the right things or at least do no harm.  Now that we are all standing on level ground, I think this is something we can all agree on.

"Practice two things in your dealings with disease: either help or do not harm the patient".
Thomas Inman

Facts, NOT Fiction

I came across 3 different Mudi breeder websites recently that have statements regarding epilepsy and COI.  Two of them have eerily similar statements.  Did one copy from the other or is there some internet site they are poaching these blanket declarations from?  In any case, the information they provide is largely incorrect.

The first breeder site issues I want to cover are probably due to misinformation or lack of knowledge about epilepsy and COI.  All site excerpts are italicized and in “ “ (although some spelling and grammar errors may have been corrected by me as well as important points made bold).

“Today there is no litter where both parents would be epilepsy-connection free! “  This is sadly true.

“You just need to check pedigrees carefully and wider than only till 4th generation.”  You need to go back 5 generations, not 4, but maybe this is a misunderstanding or typo.  It is very hard, if not impossible, to check a pedigree if you don’t know all the epilepsy affected Mudis and their parents and grandparents.

“This list* can help you.”  Um no it can’t because this list doesn’t exist anymore, but that is actually a good thing as not all the Mudis we need to be concerned with were on that list, which can lead to false hope that your Mudi or litter is not closely connected to an epileptic, when in actuality it is.

“More "critical" dogs are in the pedigree of the parents, lower COI of the litter has to be.”  This is not correct, and what do they mean by “critical”?  The COI and epi risk are not connected in ANY way.  I have seen high epi risk with low COI and low epi risk with high COI, these two factors are not related.  You cannot estimate the epi risk (or any other health issue risk) based on the COI.

“We´ll choose an appropriate male with low COI…” This is regarding a male for their next litter.  A low COI male is not important.  What is important is the COI of the litter the male will make with your female.  You want to make a litter that has a low COI.  You can put together a low COI male and a low COI female and get a litter with a very high COI.  It is not about the COI of the parents, it is about the COI of the litter.

“We count COI (Coefficient Of Inbreeding) for every combination of parents we plan. Our "limit" is about 8% for 10 generations - the lower the better.”  You need to use every generation you have in your database for the correct COI calculation, not just 10. Currently, most Mudis have on average 26-28 generations behind them. Many official websites (such as the FKK) use less than 10 gens and as they do not have the database to back up the COI’s, this means the COI’s they give for even 5-10 gens is incorrect for most every pedigree I have looked at on their site.  You need to be aware of things like this, all COI’s are not created equally.

COI calculation is not a game and incorrect COI’s and incorrect COI information is harmful.

When considering the next litter you want to produce, you must balance many things.  In order to get a low epi risk, you might have to compromise on a higher than you would prefer COI.

On to the next two Mudi breeder websites, these are the pair that have quite similar and very lengthy, epilepsy statements.

 “In our dogs' lineal relatives and among their descendants there is no suspected epilepsy”

“IN OUR DOG'S LINEAL RELATIVES THERE IS NO SUSPECTED EPILEPSY”

Is it purely coincidence they say almost the exact same thing and use a rather rare term - lineal? Are they the only two breeders that give a similar disclaimer?  No. If there is a conspiracy, as suggested by one of these breeders, it’s the smokescreen being deployed by these incorrect statements.    

There is almost no Mudi alive today (which has a mostly complete pedigree) that does not have some connections to an epileptic in the first 5 generations.  And you must go back 5 generations.

These two websites both claim (again coincidentally?) that:

“In the Mudi breed (as it is in people) there is a risk of 1 to 3%. What does this mean? It means that in a population (where there is no inbreeding) there is a small possibility that 1 Mudi will develop Epilepsy in every 100 puppies born. This is a very low risk and should not be looked at with fear or over thinking. Even though there are no Mudis with Epilepsy in our breeding dogs, a famous and popular stud dog with no history of Epilepsy in the bloodline may in 100 puppies (bred to many different females) produce 1 to 3 puppies with a Seizure disorder. That is still a very low risk, especially when considering that not all seizures are Epilepsy.”

” In the human population in Hungary it is said that the occurrence of epilepsy is 1-3%. What does this mean? In a population, where there is no inbreeding, as it is extremely rare that people marry their relatives, there will be at least 1 ill person from 100.” “So going back to dogs and taking a famous stud who had more than 50 offspring, having 1 ill dog among them is considered "normal", even if there is no genetical problem in the population.”

"All in all, we have a much bigger chance to have dementia at the age of 60 than to have a mudi with epilepsy (statistically)."

Where are they getting these statistics? They list no source for any of their claims. Wherever they conjured up this data, it is wrong on so many levels.

-Humans and dogs are not comparable as humans pick their own mates, purebred dogs mates are chosen for them. 

-Purebred dog breeds ARE inbred, people are not.  You cannot compare apples to oranges.

-The % rate they give (1-3%) is not accurate for either humans, dogs in general, or the Mudi breed.  In order to compare statistics on the same level, their 1-3 per 100 = 10-30 per 1000.

The WHO states that epilepsy occurs in humans “between 4 and 10 per 1000 people. However, some studies in low- and middle-income countries suggest that the proportion is much higher, between 7 and 14 per 1000 people.” (2)  The Epilepsy Foundation states that:  “The estimate currently thought to be most accurate is 2.2 million people or 7.1 for every 1,000 people in the USA.” (3)

This means that the affected human population is between 4 and 14% (per 1000) in the whole world and about 7.1% (per 1000) in the USA, which is obviously far less than the 10-30% (per 1000) these Mudi website authors give.

Using these breeders occurrence rate, based on the estimated 3800 Mudis alive today, that would be 38-114 epileptic Mudis born since 2006.  Remember that these breeders consider this “very low risk” and “normal”.

According to the article my last Mudi Directions post was about (For Whom the Bell Tolls), .6% of the general canine population is affected with epilepsy (1).  In the Mudi, my statistics indicate epilepsy affects about .34 -.54% (13-22 epileptics) of the current population of 3800 estimated living Mudis.

If you are the owner of one of those 1-3 expected epileptic puppies, it is a terrible tragedy and there is nothing normal about it.  I had a seriously epileptic Aussie so I speak from experience.  To devalue producing a puppy with a serious illness as “normal” is incredibly insensitive and ignorant of their responsibility and the suffering of the dog and its family.  Yes it can happen that any Mudi will produce a serious health issue, but the moment it does, you should immediately stop breeding the dog and their immediate family that produced the ill puppy at the very least, and that is not what happens when you consider it “normal”.  Regardless of whose statistics you want to believe, even one seizing Mudi is too many, especially if that Mudi is yours and it could have been prevented had Mudi breeders taken responsibility decades ago, as epilepsy was first seen in the Mudi breed in the mid 1980’s.

Please watch this video and tell me this is anything even close to “normal”, and yes that is a Mudi having a grand mal seizure from idiopathic epilepsy (which is considered by vets to be genetic epilepsy, see my previous post).  If this video does not deeply affect you, then nothing will.  How could anyone explain this as “normal” and “very low risk” which is acceptable in the breeding of Mudis. Epilepsy is not an acceptable outcome of breeding for any animal and anyone that chooses to downplay it as such has no business breeding animals.

https://www.youtube.com/watch?v=zbhyw2X2JCI

We need to convert their claim that a male with 50-100 pups that produces 1-3 pups with epilepsy is “low risk” and considered “normal” to percentages to properly compare their data to reality.

50 pups produced with 1 being epileptic = 2%

50 with 3 epileptics = 6%

100 pups produced with 1 epileptic = 1%

100 pups with 3 epileptics = 3%

This can be rounded off to an occurrence between 1% and 6%, that does not agree with their claim that it is around 1-3%.  They rounded it downward by half.  If they can’t do simple math or check that the data they poached is correct before using it on a public website, is this someone you want to get a puppy or breed advice from?

I checked on the number of pups the sires of the epileptics had and as expected, the numbers are not anywhere near to what they suggest (1-3 epileptics born to males that have 50-100 pups).

No Mudi males in my database have had 100 puppies, 90 is the most pups any Mudi male has sired that I am aware of.

34 Mudi males sired 39 epileptic pups, most had only 1 known epileptic puppy, three males had 2 and one has produced 3 known epileptics.

The male that produced 3 known epileptics has only sired 22 puppies, that is 13.6%, which is significantly higher than their claim of 1-3%.

These 34 males had 798 pups between them, of which 39 are epileptics.  That is a 4.9% occurrence rate, which is also higher than their 1-3%.  The males sired between 1-65 pups, with the average being 24, not anywhere close to the 50-100 they write about.

Any way you look at it, these figures are not “normal” or “low risk” or indicative of not-genetic epilepsy, especially as most epi producer males are very closely related to each other, which clearly indicates genetic epilepsy as the cause.

I also made a list of 15 Mudi males that have between 40-90 pups that have not produced any known epileptics. So if their claim is correct, that sires with 50-100 pups have between 1-3% of seizing pups which is considered “normal”, then why don’t these 15 males have at least one known epileptic?  There are several reasons, all of which can be easily employed to lessen the incidence of epilepsy in future litters.  These males were either not closely related to the other males, or they had low risk mates (the females they were bred with were not closely related to the epi producer males), or only one of their parents was closely related.

There’s no need to beat this section any further, as it is clear their claims are totally without evidence to back them up.  One of these breeders has a database, but as I have seen the incorrect COI’s they give on their website and also the incorrect dogs on one of their pedigrees provided, their data cannot be trusted even if they had any to use for research like this.

Let’s move on to their other claims.

“In our dogs' lineal relatives and among their descendants there is no suspected epilepsy.” Unfortunately, their dogs are close relatives to the some of the 34 Mudi males that produced epileptic puppies.  They are also related to some of the females that have also created epileptic pups.  Genetic epilepsy comes from both parents, pointing fingers at only the sire or only the dam is not correct.  Genetic epilepsy is not a dominant gene, it is recessive which means both parents must each contribute some of the genes that cause it.

“Seizures can be caused by many things: complications during labour at birth. Premature newborns with hypoxia which can lead to neurological problems and seizures. True Eplilepsy can actually be aquired by an extremely high fever as is in the case of contracting Distemper, causing brain injury.

Any dog can have a seizure brought on by hypoglicemia, ataxia, reaction to medications (such as Ivermectin), ingestion of toxic plants or poisons, severe pain, shock from a trauma, head or brain injury, tumours, vascular abnormalities, liver shunts, kidney problems, metobolic or digestive disorders, hemagiocarcomas and cancers. These do not mean the dog has epilepsy, it only means the dog had a seizure reaction to an underlying condition.”

It is true not all seizures are due to genetic epilepsy, but the majority of seizures in both dogs and humans are due to idiopathic epilepsy which is considered to be genetic (read my last post).  Seizures from other causes typically stop once the cause has been found and treated.  Seizures from birth trauma are present from birth.  Seizures from poisoning or accident can be determined by blood and urine tests and visible injuries.  Any bodily injury that would cause seizures would not go unnoticed.

If a puppy is so oxygen compromised at birth, seizures are not the only symptoms that puppy will have, if it even survives.  Seizures before the age of 6 months are usually not from genetic epilepsy and any puppy that had birth trauma would typically have seizures starting shortly after birth.

One seizure does not make genetic epilepsy, but a pattern of seizures without any health issues prior to the first seizure, or in between the seizures and for which there are no other explanations, is in most cases genetic epilepsy. If the Mudi is not ailing before, shortly after the seizure or before the next seizure occurs, then you are almost surely facing genetic epilepsy.  But only your vet can determine this for sure and any dog that has a seizure must be taken to the vet immediately, because seizures are NOT “normal”.

Once again, these breeders are making much more of this than is relevant. Dogs with seizures from idiopathic/genetic epilepsy are typically healthy before, shortly after and in between seizures. When the dog is seizing from most any other cause, it is otherwise unwell before, after and in between seizures. It’s that simple.

If the genetic epilepsy deniers would put as much effort into breeding less epi risk litters as they do the misinformation on their websites, the Mudi breed would be dealing with far less seizing Mudis.  

If they cannot be honest about epilepsy in the Mudi, what can they be honest about in other areas?  If they cannot provide factual data to back up their claims, can you trust any of their data?  If the care to post factual data is not taken at even basic levels….it is highly unlikely to be there for more important issues.

If these breeders want to pass the blame everywhere but on themselves for the important issues that occur in the breed, you can be sure they will put the blame for anything that goes wrong with a puppy onto the owners.

As for your chance to be demented being higher than having an epileptic Mudi….not quite, they are making great strides in lowering the incidence of dementia by getting people to lower their risk factors with campaigns to alter your life choices.  Now that’s great news that can also be applied to epilepsy risk in the Mudi!  Lower the epi risk in the litters produced and a few years from now, even these breeders might finally be right about something.

(1) Negative effects of epilepsy and antiepileptic drugs on the trainability of dogs with naturally occurring idiopathic epilepsy (Rowena M.A. Packer, Paul McGreevy, Amy Pergande, Holger Volk; Applied Animal Behaviour Science Volume 200, March 2018)

(2) http://www.who.int/mediacentre/factsheets/fs999/en/

(3) https://www.epilepsy.com/learn/about-epilepsy-basics/epilepsy-statistics

* link is for http://www.mudi-epilepsy-project.estranky.cz/ which is no longer available

For Whom The Bell Tolls: Epilepsy in the Mudi

Magyarul - Blogbejegyzések Magyarul Blog Oldal

Mudi owners and breeders have struggled with several questions relating to canine epilepsy. How do we know the epilepsy we have in the Mudi is genetic epilepsy (versus a non-genetic cause)? How can we be sure genetic epilepsy is the cause of a Mudi’s seizures? Why are we so concerned with epilepsy? 

Epilepsy in the Mudi is a welfare issue. Hip dysplasia (HD) can also be a welfare issue in some breeds, however in the Mudi HD is usually only detected on x-rays, it is quite rare a Mudi shows any suffering from painful hip joints, while epilepsy is experienced because of true symptoms – seizures, and seizures occur more often than symptomatic HD. Therefore, epilepsy in the Mudi represents an acute problem that needs to be dealt with immediately. 

“Idiopathic Epilepsy (IE) is the most common chronic neurologic condition in dogs. It affects on average between .6 and .75% of the general canine population (that is 6 to 7 dogs per thousand). It is characterized by an enduring predisposition to epileptic seizures.” “Most canine epilepsy cases are diagnosed as ‘idiopathic’ (IE) in that there are no gross neuroanatomical or neuropathological abnormalities nor other relevant underlying diseases causing seizure activity, and a predominantly genetic or purely genetic origin is presumed.” (cited from *1,*3) Simply, if there is no other reason found (such as, brain injury caused by accident, poisoning, infectious disease, etc.) for a dog to be having seizures, then Idiopathic Epilepsy is the diagnosis and IE is caused by inherited genes. 

With the help of a new study (*1) just published in a well-known science journal (Applied Animal Behaviour Science), the criteria for identifying dogs with Idiopathic Epilepsy (IE) became available as a simple set of four yes/no questions, which we can also use to determine if a Mudi has IE. These questions were used to determine which dogs would be participants in the study (in this study, the researchers are also veterinarians and veterinary professors from Australia and the UK). Of course, you will also need the assistance of a veterinarian, but a vet should be the first person you contact when your Mudi shows seizure activity anyway. 

The questions they used to determine if the dogs they needed for the current study had IE were developed by the International Veterinary Epilepsy Task Force (*3). The four questions require only a yes or no answer. 

1) Has your dog ever had a seizure? 

2) Has your dog had at least two or more seizures that were at least 24 hours apart? 

3) Did your dog’s first seizure occur between the ages of 6 months and 6 years? 

4) Did your veterinarian perform blood and urine tests on the dog from which no identifiable cause for the seizures was found? 

If the answer is yes to all 4 of these questions, the dog is diagnosed as having Idiopathic Epilepsy. 

The majority of dogs which met the criteria for IE diagnosis in this study were purebred (70.3%). Purebred dogs are members of isolated populations which are useful for creating a similar outlook and purpose among all the individuals, but looks and purpose are not the only things shared in a closed gene pool, unwanted genes which cause health disorders are also circulated. This is why purebred dogs have so many inherited diseases. This doesn’t mean that mongrels do not also suffer from IE, they do, however according to an article about a study (*2) done in 2013, purebreds are significantly more likely to have epilepsy than mongrels (as well as nine other inherited diseases (*2)). 

The International Veterinary Epilepsy Task Force (*3) study also has this to say about the cause of IE: “Idiopathic epilepsy (suspected genetic epilepsy)—a genetic influence supported by a high breed prevalence (>2 %), genealogical analysis and/or familial accumulation of epileptic individuals (*6), (*7).” This means that a breed that has greater than 2% of the living population having seizures of unknown cause, tracing of family lineage to affected individuals, and/or there are numerous family ties between affected individuals, supports genetic influence as the cause of the seizures. 

From the 2015 Hülsmeyer study (*4), it was told that breeds which are small in number (population), have increased risk of hereditary disorders as well. 

Now that we have collected the evidence, it’s time for the Mudi breed statistics. 

I have more than 8000 Mudis in my pedigree database. 

I know of 28 confirmed epileptics and 11 suspect epileptics. 

The percentage rates for epilepsy in the general population apply to the current living population, not the total amount of Mudis that ever existed. I assume that 12 years is a realistic life expectancy for the average Mudi. I sorted out the Mudis that were born on/after 1/1/2006 and this was equal to 3800. 

Since 1/1/2006, 13 confirmed epileptics are known, with 9 suspected. 

According to the new study (*1), theoretically the following numbers of epileptics should occur in the existing Mudi population: 

.6 % of 3800 = 22.8 

.75 % of 3800 = 28.5 

This means on average, there should be about 22-29 epileptics occurring in the time period between 1/1/2006 to today. I know of a minimum 13, and as many as 22 if the suspected Mudis did indeed have IE. 

According to the International Veterinary Epilepsy Task Force study (*3), a high breed prevalence would be greater than 2% and/or would have pedigrees showing accumulation of affected individuals among family lines. 

2% would be 76 epileptic Mudis, which is significantly more than we currently know about. However, it is more important to note that my database does show an overwhelming familial connection between the 28 confirmed and 11 suspected epileptics we do know about. (In the case of familial-pedigree relationships, all epileptics apply, not just those occurring from 2006.) 

We must bear in mind that I certainly do not know about every epileptic Mudi that ever existed. Most were probably not disclosed to me, the breeder, or any other Mudi person. Some probably died before they had seizures or died before they were observed to be having seizures and others may have only had focal seizures which are called petite mal in humans, and easily missed, especially if they mainly occur when you are away from the dog or when you are sleeping. If we could get data from Hungarian veterinarians as to how many Mudis they have treated for IE in the last 10-15 years, it would be an even more accurate evaluation of the occurrence of IE in the Mudi, but this is currently not available data. 

You also need to recall that the most common neurological disease in dogs is idiopathic epilepsy, which means, the epilepsy that occurs in any breed is most likely to be a genetic type. The next point is that purebred dogs are more likely to have epilepsy than mongrels, the Mudi is a purebred dog. And dog breeds with small populations are more likely to have hereditary disorders, the Mudi is not a populous breed by any measure. 

While we may not be overwhelmed with epileptics at this point, the criteria and numbers are more than enough, along with the substantial familial connection, to conclude the epilepsy seen in these 28 confirmed Mudis is a genetic type of epilepsy. 

If we are to at least keep the occurrence of IE in the Mudi to a minimum level, rather than the high level it is in many other dog breeds, then it will take EVERY Mudi breeder and Mudi owner’s cooperation. 

We need to make a future where we don’t have to ask for whom the epilepsy bell tolls in the Mudi. There are things that can be done now to lower the occurrence of affected Mudis. Ask for an epilepsy risk score before you plan a mating. Choose mates that give a low epi risk score for the planned litter. Ask the breeder for the epilepsy risk score and COI, before you commit to buy a puppy. Report any Mudi that is having seizures which answer yes to all four of the above questions. 

The bell is tolling for thee, the time for epilepsy denial is over. 

(I would like to thank Dr. Péter Pongrácz and Michelle Murvai for their review and comments on this article, as well as the Hungarian translation was done by Dr. Péter Pongrácz.)

REFERENCES
(*1) Negative effects of epilepsy and antiepileptic drugs on the trainability of dogs with naturally occurring idiopathic epilepsy (Rowena M.A. Packer, Paul McGreevy, Amy Pergande, Holger Volk; Applied Animal Behaviour Science Volume 200, March 2018

(*2) Health of purebred vs mixed breed dogs: the actual data, 2015, The Institute of Canine Biology, Carol Beuchat PhD
http://www.instituteofcaninebiology.org/blog/health-of-purebred-vs-mixed-breed-dogs-the-data

(*3) Berendt, M., Farquhar, R. G., Mandigers, P. J., Pakozdy, A., Bhatti, S. F., De Risio, L., ... & Patterson, E. E. (2015). International veterinary epilepsy task force consensus report on epilepsy definition, classification and terminology in companion animals. BMC veterinary research, 11(1), 182.
https://bmcvetres.biomedcentral.com/articles/10.1186/s12917-015-0461-2

(*4) Hülsmeyer, V. I., Fischer, A., Mandigers, P. J., DeRisio, L., Berendt, M., Rusbridge, C., ... & Packer, R. M. (2015). International Veterinary Epilepsy Task Force’s current understanding of idiopathic epilepsy of genetic or suspected genetic origin in purebred dogs. BMC veterinary research, 11(1), 175.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4552344/ (Hülsmeyer et al.)

(*5) Shorvon S. The concept of symptomatic epilepsy and the complexities of assigning cause in epilepsy. Epilepsy Behav. 2014;32C:1–8.
http://www.epilepsybehavior.com/article/S1525-5050(13)00656-2/fulltext

(*6) Shorvon stated in 2014 [5]: “It seems very likely that the genetic influences in idiopathic epilepsies probably are complex involving multiple genes and interactions between genes (epistatic) and between genes and the environment (epigenetic)”.

(*7) A list of breeds with a high epilepsy incidence or prevalence compared to the general background population can be found in Hülsmeyer et al. [26]. Please note that the epilepsy status within breeds may fluctuate over time and furthermore be influenced by differences between countries (e.g. due to preferences with respect to currently popular breeding lines).

FAKE NEWS

I’ve been lurking in the background for a while, watching where things are going.  I’m still trying to figure out if there is any hope for the Mudi breed or not, “hope dies last” is a rather famous Hun saying and quite aptly applies these days.  I decided to dust off my database and bring it fully up to speed, not a monumental task, but indeed there have been a few jaw dropping moments.

It’s nearly impossible to sort out the real from the fabricated these days.  As I look around Mudi-dom I see so much incorrect information being posted on every type of media.  COI’s that are far lower than reality, health and performance data offered without any accompanying documentation, lines that are professed to be clear of epilepsy risk, if in fact the author even acknowledges there is any epilepsy in the breed. How is anyone able to verify any of it without tempting the fates? 

First, the Mudi needs to get on board with some uniformity, across all nations and languages.  I see colors called by all sorts of names, there are more name variations than actual colors and patterns, how did this happen?  COI’s based on only 5 or 10 gens, what’s the reason behind this?  I read breeders claiming they have no connection to epilepsy in their lines since they started breeding, how is that possible?  Are their Mudis somehow different from the rest of the world’s Mudis?

What is the best way to get much needed information and data out to the Mudi interested public?  How do we make it uniform and standardized in all languages and countries, as well as equally and easily accessible?

Perhaps it is best to start with standardizing the basic information. I am fluent in English and semi-fluent in Hungarian, other languages will need someone native to their own language and English to play along.

Breed = Mudi, plural in English is Mudi’s, or Mudis, not Mudik.  If you are not speaking Hungarian, then please do not use mudik.  But if you must use mudik, then learn to speak Hungarian.

COI = You have to use all gens to arrive at the correct COI, as many as can be found for the breed, any other calculation is incorrect, but you can google it if you don’t believe me.

I have 26 or more generations behind many litters now, if your database does not go back that far, then you are not going to get a correct COI. If you don't have the correct parents for all of the dogs in the pedigree, your COI will not be correct. Using incorrect COI’s is misleading. I give COI’s for free, you can do comparisons between the source you were using and mine, I don’t have a problem with that, as long as you use the correct COI.  Why do I think my COI's are correct?  I’ll save that for another time, you will just have to trust me on this one for now.

Color and pattern names = how did it get so disorganized and whimsical?  Why do kennel clubs that are not the originating country for the breed have any right to change the names used in the country of origin, albeit properly translated (and with some guidance from color genetic terms; https://www.pawprintgenetics.com/products/traits/)?  For example:

Hungarian = English

Fekete       = Black   

Fehér         = White  

Fakó          = Yellow (Fakó translates to pale, which has no color meaning in English, yellow is the genetic term and the color that you see on the Mudi; fawn is not correct as fawn is a color term used on the A locus with Sable.)

Barna          = Brown

Hamvas      = Ash (While Dilute is the genetic term, it is not recognizable by most people, and blue has been used for decades to describe this color and could be an alternative, ash is the perfect term for this color as it is not gray or silver which is another color gene which the Mudi does not have. There is no reason English speaking Kennel Clubs cannot add ash to their already long lists of color terms.)

Hamvasbarna         = Ashbrown

Cifra                        = Black Merle (Cifra actually translates to flashy or gaudy which has no color meaning in English; historically the cifra Mudi was black merled; the common English and genetic term is merle; however as the Mudi comes in many merled colors, merle needs to be used in conjunction with the correct base color term: black merle, brown merle, etc.)

Hamvas Cifra          = Ash Merle (This solves the blue merle problem best.)

Barna Cifra              = Brown Merle

Hamvasbarna Cifra = Ashbrown Merle

And yes White Merle and Yellow Merle can occur, DNA testing needs to be done to verify, you cannot rely on blue or merled eyes as an indicator.

Colors that are not standard also happen from time to time, although lately they seem to be almost viral in appearance:

Albínó      = Albino (Snow white coat, pink nose, lips, eye rims and paw pads, eyes can be blue or red; albino is thankfully quite rare but it does happen.)

Cirkás, Tigris, Csíkos   = Brindle (This striped pattern is seen on Boxers, Great Dane, etc., Csíkos translates to striped, Tigris is tiger, cirkás is used for the brindle Sinka; brindle can also have a black mask.)

Fekete-cser or Mézeslábú = Black & Tan (Mézeslábú translates to honey feet as the tan color is mostly seen on the lower legs in the Mudi.)

Barna-cser = Brown & Tan

Maszkos fakó = Masked Yellow (As seen on a Malinois, there are no stripes, unfortunately most Mudi breeders call brindle by this name.)

Ordas = Wolf (The exact translation is wolf, but it is also known as sable or fawn.)
Fekete-fehér = Black & White (Like a Border Collie, again this is a rather rare pattern in the Mudi.)

I do not see the reason that these color names cannot be used in every English speaking country and properly translated into other languages, so we are all talking about the same colors and patterns when we visit Mudi websites, talk on FB or other forums about the breed or meet at events.  No one should have to guess the color of a Mudi, this is an unnecessary problem that is easy to fix.

Epilepsy…what can I say that I have not already.  If you do not want to believe the owners of the 25+ Mudis that suffer from seizures, then there is nothing I can say to you to make you believe it occurs in the breed now either.  It is generally acknowledged by Veterinarians worldwide, that when there are no known causes for a dog to have repetitive seizures, the cause is most likely genetic – inherited.  Some Mudi breeders claim they have no epilepsy in their lines, my database which tracks inheritance patterns disagrees with them.  Other breeders claim that problems at birth (such as lack of oxygen) cause these seizures, a lack of oxygen that would be serious enough to cause seizures would most probably cause other visible problems in the puppy such as cerebral palsy, not only seizures, if the puppy would even survive such a catastrophic event.  And the seizures would be present from the time of birth, not many months or years later.

It amazes me that any breeder would still be in denial of the existence of genetic epilepsy in the Mudi today.  Whether it is out of ignorance, refusal to face the facts, or fear, the essential point is they are not helping the Mudi breed.  Every choice that is made, whether it is where to get a puppy or which Mudis to breed with, matters. The future of the Mudi is everyone’s responsibility, every decision you make is a step in the right or wrong direction.  Where are your steps taking you?