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.)
(*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).
No comments:
Post a Comment