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What is  (Pug Dog Encephalitis)PDE?

PDE is an inflammation of the brain.

There is no cure for PDE. 

Unfortunately, very little is known about the disease. It tends to strike pugs between 9 months and 3 years of age but not limited to. It is believed to be more common in females than in males.

It is believed to be a genetic condition; often litter mates and closely related dogs are susceptible.

A seizure is caused by abnormal activity taking place in the brain. Seizures can be from a few seconds to a few minutes. Seizures cannot be maintained using medications. Some dogs may have temporary remissions. Seizures are the main symptom of PDE.

It is important to note that conditions other than PDE can cause encephalitis and or seizures. Encephalitis can be caused by a virus. There are also other forms of encephalitis, such as GME.

Seizures can be caused by:

  • head trauma
  • poisoning
  • tumors
  • epilepsy
  • hypoglycemia
  • worm infestation
  • gasses
  • and for unknown and unexplained reasons.

A seizuring pug does not necessarily mean a PDE diagnosis

PDE can ONLY be positively diagnosed by a necropsy on the brain stem.

What to watch for:

  • Seizures
  • Walking in circles before or in between seizures (is a common symptom of PDE. The Pug will pace in a circular motion over and over again for a prolonged period.
  • Pressing their heads against the wall or furniture and or people 
     
  • A staggering walk
  • Apparent Blindness
  • Neck pain
  • Agitation or Aggression (the Pug appears to be disturbed for no apparent reason)
  • Sudden Death

Lethargy/Listlessness (Lethargy is a symptom to nearly all illnesses that can strike a dog ranging from a common infection to something more serious)

Loss of muscle coordination (this can also indicate other problems such as neurological issues and a side effective to convulsive activity brought out by inner ear disturbances such as Vestibular Disease or ruptured ear drums

Your vet may do blood work, urinalysis, chest x-rays, abdominal ultrasound to check for abnormalities. Your vet may even want to do a spinal tap. At one time it was believed this was a diagnosis for PDE it is no longer believed to be true. The only way for a positive diagnosis is a necropsy.

Two Classifications of PDE:

Slow Progressive: This classification of PDE features seizure activity and sometimes the additional symptoms preceding the seizure activity. The seizures will strike, last anywhere from just a few seconds to a few minutes and then recur in a matter of days or weeks. In between these seizures, the Pug will return to normal and demonstrate no symptomatic characteristics associated with PDE.

Rapid Progression: This classification of PDE features seizure activity that is often more frequent, but not always. In between the seizure activity however, the Pug does not return to normal but instead does demonstrate symptomatic characteristics associated with PDE. These characteristics between seizures are commonly depression, bewilderment, disorientation and signs of lacking muscular coordination such as having difficulty walking.

Either classification of PDE unfortunately is the same. Whether it strikes in the slow progressive or the rapid progressive form, PDE will eventually kill the Pug. Those Pugs that have been diagnosed with PDE and said to have survived are widely believed to have been misdiagnosed, or not diagnosed conclusively.

Necropsy and tissue donation to veterinary research helps to provide some means of examination into PDE, however the speed at which PDE strikes and results in death surely makes researching the disease more difficult.

Idiopathic Encephalitis:

A term used when an infectious cause can’t be found. In many cases of idiopathic encephalitis, an underlying immune-mediated cause is suspected because these animals improve after suppression of the immune system. Immune-mediated diseases occur when the body’s white blood cells mistakenly attacks normal tissue, in this case brain or spinal cord. There have been a number of different types of idiopathic encephalitis described in dogs


Susceptibility to Pug Dog Encephalitis (PDE)

Approximately 1.2% of Pug dogs die of necrotizing meningoencephalitis (NME), also known as Pug dog encephalitis (PDE).  NME is an inflammatory disease of the central nervous system that is usually progressive and fatal. Symptoms of NME include seizures, depression, ataxia, abnormal gait and blindness (1).   Female, fawn-colored Pug Dogs younger than 7 years of age are more apt to develop NME than older, male and non-fawn colored individuals (2). Recent research has revealed that susceptibility to NME is associated with the dog leukocyte antigen (DLA) region of dog chromosome 12 (3).  The association is at or near the region containing the DLA class II genes. Dogs that  have two identical copies of the NME associated markers in this region, have an observed risk (OR) of 12.75 for NME in their lifetime over Pugs that have only one or no copies of these markers (OR 0-1.08).

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Results reported as:

N/NNo copies of the NME associated markers (homozygous for normal). These dogs have a low risk of developing NME.
N/S1 copy of the NME associated markers (heterozygous for susceptibility). These dogs have a low risk of developing NME.  
S/S2 copies of the NME susceptibility associated markers.  These dogs are 12.75 times more likely to develop NME in their lifetime.

Outcomes of matings based on NME test results:

Detailed Information

1.  N/N x N/N = all puppies will have two copies of the low NME risk markers (N/N) and will have a significantly reduced risk of developing NME during their lifetime.

2.  N/N x N/S = One half of the puppies will have two copies of the low NME risk markers (N/N), and have a significantly reduced risk of developing NME during their lifetimes. One half of the puppies will carry one copy of the susceptibility markers (N/S), but will also be at low risk for developing NME.

3.  N/S x N/S = One fourth of puppies will be N/N and at low risk for NME; one half will be N/S, carry the susceptibility marker, but will also be at low risk for NME;  one fourth will be S/S and will be at high risk for NME.

4.  N/S x S/S = One half of the puppies will carry the susceptibility marker (N/S), but will not be at increased risk of NME; one half of the puppies will have two copies (S/S) of the susceptibility marker and be at high risk of NME.

5. N/N x S/S = All of the puppies will carry one copy of the susceptibility markers (N/S), and be at low risk for developing NME.

6. S/S x S/S = All of the puppies will carry two copies of the susceptibility marker (S/S) and be at high risk for NME.

Notes: This is not a diagnostic test for NME in Pug Dogs or for NME disease or risk in other breeds.  The test is only to determine risk for developing NME in Pug Dogs and for selecting matings that will produce puppies that are at decreased risk (N/N, N/S).  Although a significant proportion (11%) of Pug Dogs is S/S, only about 1 in 8 of this group will develop NME during their lifetime.

Also, breeders are advised against breeding out the S genotype, because 40% of Pug Dogs have the S genotype in a heterozygous (N/S = 29%) or homozygous state (S/S = 11%).  Eliminating the S genotype will lead to a considerable loss of genetic diversity.  Therefore, breeders should carefully select matings that do not produce S/S puppies. 

The NME report includes DNA types for a panel of 8 markers selected from the International Society of Animal Genetics (ISAG) canine parentage panel.  These markers provide individual identification for each sample tested.

References:

1. Talarico LR, Schatzberg SJ. Idiopathic granulomatous and necrotising inflammatory disorders of the canine central nervous system: a review and future perspectives. J Small Anim Pract 2010: 51: 138–149.

2. Levine JM, Fosgate GT, Porter B et al. Epidemiology of necrotizing meningoencephalitis in Pug dogs. J Vet Intern Med 2008: 22: 961–968.

3. Greer KA, AK Wong, H Liu, TR Famula, NC Pedersen, A Ruhe, M Wallace and MW Neff. Necrotizing meningoencephalitis of Pug Dogs associates with dog leukocyte antigen class II and resembles acute variant forms of multiple sclerosis. Tissue Antigens 2010: 76:110-118.

Information provided by http://www.vgl.ucdavis/edu/services/PDE.php