© Therese Rodin
Background: Pug myelopathy (PM) is a disease that has similarities to DM (see the section “Degenerative Myelopathy (DM)”), with ataxia and paralysis of the hind legs, but it does not proceed to the front of the body and it is slower in its progression. Furthermore, whereas in DM the spinal cord itself degenerates, in PM the problems are a result of a local compression of the spinal cord. In PM the affected area is found somewhere in the region of T10 to L1 (Fisher et al. 2013: 224 (has the range T9 to L2); Smiler and Patterson 2013; Rohdin et al. 2018: 26 and table 1; Driver et al. 2019: 3).
Whereas DM is still uncommon in the Pug (see the section about DM here on the web page) PM “has become a widespread problem in Pugs” (Smiler 2019). Besides the symptoms of ataxia and paralysis, a characteristic of PM is that it is most often pain-free; usually the Pug does not have a history of pain in relation to the affected area and neither does it show pain when it is palpated there (Fisher et al. 2013: 223; Smiler 2019). In spite of this, the disease is traumatic for the owners since their dog is completely healthy mentally and aware just like before the illness but it loses its ability to walk. Furthermore, because of the paralysis the Pugs might develop both urinary and fecal incontinence. (In the study of Alisauskaite et al., two of 24 Pugs were incontinent (2019: 1377f.) and in the study of Driver et al. 50% of the Pugs were incontinent (2019: 1, 3)) (Read an article here written by Dr. Kathleen Smiler (2016) about the urination of Pugs with PM.)
There are no gene tests that identify PM, and a great difficulty with this disease for breeders is that it commonly debuts late in life. PM is currently being investigated e.g. by a team at Michigan State University (MSU) as well as by the Swedish veterinarian Cecilia Rohdin (see Rohdin’s website (in Swedish)). Most Pugs included in the MSU study fell ill at 9-12 years of age (Patterson 2016). This corresponds to a study of Driver et al. where the median age of onset was 9 years, the youngest being five and the oldest 12 years (2019: 1, 3). In a study of Fisher et al., the median age of onset was 7.7 years, with a range from two to 11 years (2013: 223). It takes one to four year from the onset of PM to complete paralysis (Smiler 2019).
In the study of Driver et al., of the 18 afflicted Pugs included in the study, 17 showed spinal cord compression (2019: 1, 3) and in general spinal cord compression is thought to be the cause of PM (Smiler 2019). There are several reasons why the spinal cord is compressed. Pugs often have defect or missing caudal articular processes (CAPs), degenerated discs (intervertebral disc disease, IVDD), or subarachnoid diverticula (SAD), which are commonly seen in the area of the spinal cord compression (Driver et al. 2019: 1, 3; Smiler and Patterson 2013). Furthermore, fibrous connective tissue and granulation tissue coming from the dura mater are also frequently seen in the affected area (Fisher et al. 2013: 225). Fisher et al. differentiated between spinal cord compressions in Pugs depending of the reason (IVDD, SAD or CAPs with fibrous connective tissue) (Fisher et al. 2013: 227). Nowadays instead, it is seen as one Pug disease, Pug Myelopathy, with the same symptoms, regardless of which of the mentioned reasons that are thought to have caused the PM (Smiler and Patterson 2013; Smiler 2019; Driver et al. 2019).
One main suspected causative of the conditions that lead to PM is the common hypo- or aplastic caudal articular processes in Pugs (Fisher et al. 2013; Driver et al. 2019). (I.e. the underdeveloped or lacking processes on the side of the vertebrae that is facing the “tail side” of the dog.) A theory presented by Fisher et al. is that the lack of normal caudal articular processes leads to “chronic instability of the vertebral column” (2013: 227), something that is also cited by Driver et al. (2019: 2). However, the defect caudal articular processes are seen in more or less all Pugs, both those who are neurologically healthy and those with neurological problems (Fisher et al. 2013: 223; Driver et al. 2019: 7, Smiler 2019).
In a study of Rohdin et al. that included 57 Pugs, 30 of them had neurological problems related to gait and of these 90% had defect caudal articular processes. Of the 27 Pugs with no neurological problems, 88.9% had defect caudal articular processes. All defect CAPs were located to T10-T11, in both neurologically affected and unaffected Pugs (Rohdin et al. 2018: 26 and table 1). In Rohdin et al:s study 27 of the 30 Pugs with neurological symptoms had vertebral defects in the region of spinal cord compression; 22 of them had a caudal articular process dysplasia, four had a hemivertebra, and one had a damaged disc in that region. In the three remaining Pugs with PM, no vertebral anomalies adjacent to the myelopathy were detected (Rohdin et al. 2018: 26 and table 2).
Thus, what the scientists see is that nearly all Pugs with PM have some vertebral defect in the region from where the PM originates but at the same time, also neurologically healthy Pugs have such defects. Rodin et al. write that “the demonstrated lack of association between multiple types of CVMs [congenital vertebral malformations] and chronic T3-L3 myelopathies is of great importance, as it shows the urgent need to look for other/additional factors for the development of FSCP [focal spinal cord pathology] in pugs” (Rohdin et al. 2018: 28). They also conclude with the statement that it cannot be excluded that some of the Pugs in the group without neurological symptoms will develop such later in life (Rohdin et al. 2018: 29).
Then, how is PM treated? There are some things you can do for your PM-Pug that can give it a better and more mobile life for a longer time with the illness. One thing that helps is physical therapy. Read more about that on Dr. Kathleen Smiler’s website: Pug Rear Leg Ataxia – Paralysis (Smiler is a member of the MSU team). There are also several tips on the Facebook group Wheelie Pugs that is likewise administered by Smiler.
Surgery is a strategy that has been applied to PM with varying success. In the study of Fisher et al., eight of the affected Pugs got surgery. It was only possible to follow up four of those eight dogs. One of the follow-ups got a normal neurological status within three months after surgery. The other three dogs did not improve but they did not get worse during the following 1.5 to 2.5 years either (Fisher et al. 2013: 226).
Alisauskaite et al. studied the short- and long-term outcome of surgery of 25 Pugs that had surgery because of a spinal arachnoid diverticulum causing PM. In the short-term (after six months), surgery was successful in 80% of the cases. However, in the long-term (after 12+ months), 86% of the Pugs showed deterioration. Thus, the authors conclude that surgery was successful in the short-term but poor in the long-term (Alisauskaite et al. 2019).
An example of a successfully operated Pug is Wellington who was operated by Dr. Wong. Here you can see two videos showing the Pug Wellington before and after surgery. However, as we saw, in the long run, surgery is seldom a solution. We have to work towards healthy Pugs that do not need surgery. Thus, the solution must be found in breeding strategies.
Goal: No Pug shall experience PM.
Strategy: We suggest three strategies to come to terms with PM: all Pugs intended for breeding should have their spine CT-scanned and only those with normal spines should be used in breeding. We should also breed towards a normal length of the back and we should introduce new genes from a donor breed to reduce homozygosity.
We recommend all breeders to have their dogs intended for breeding thoroughly examined with a CT-scan, through which both soft tissue and bones can be seen. An X-ray image is not enough since you see neither soft tissue, nor the caudal articular processes. The CT-scan should be made when the Pug is fully grown, from about 15 months old. Preferably, only Pugs with no vertebral defects should be used in breeding. Since it is still uncommon to have the spine examined with a CT-scan (and the Old German Pug (altdeutscher Mops) and Retro Pug breeders are the only ones who examine it at all), we hope that more breeders will do that so that we get a better picture of the state of the spines of altdeutsche Möpse and Retro Pugs.
We see in Old German Pugs and Retro Pugs that they do not have defects in the spine as the Standard Pugs do. (Read more under “Hemivertebrae and other vertebral anomalies”.) We believe that this has to do with the fact that the Old German Pugs and Retro Pugs have been given a normal length of the back, not being too compact. The Pug must be rectangular, not square in form. In this way, the vertebral anomalies will probably disappear by themselves.
There is presumably also a genetic component in PM although we do not know the genetic background of it. However, we do know that this type of disease has increased in many breeds because purebred dogs are very homozygous, i.e. there is very little genetic variation. Carol Beuchat writes in a text in her course “Managing genetics for the future”:
“The most efficient way to produce puppies that will be homozygous for a recessive allele is by breeding related dogs. In a population of registered, purebred dogs, ALL the dogs are related if you go back far enough. […] So genetic disorders are a predictable – even guaranteed – consequence of inbreeding in dogs […].” (Beuchat 2018).
In the end, the problems cannot be handled with further genetic tests or even primarily with research on the diseases. Essential to breed healthier Pugs besides working towards a less extreme conformation, is to have an inflow of new genes that break up the homozygosity, i.e. crossbreeding. Read more about this under “Genetic diversity”.
Sources and further reading:
Alisauskaite, Neringa et al. 2019. “Short- and long-term outcome and magnetic resonance imaging findings after surgical treatment of thoracolumbar spinal arachnoid diverticula in 25 Pugs”. Journal of Veterinary Internal Medicine 33, 1376–1383. doi: 10.1111/jvim.15470
Beuchat, Carol. 2018. “Managing genetics for the future”. Course at the Institute of Canine Biology.
Driver, Colin J. et al. 2019. “Magnetic resonance image findings in pug dogs with thoracolumbar myelopathy and concurrent caudal articular process dysplasia”. BMC Veterinary Research 15:182. https://doi.org/10.1186/s12917-019-1866-0
Fisher, Stephen C. et al. 2013. “Constrictive Myelopathy secondary to hypoplasia or aplasia of the thoracolumbar caudal articular processes in Pugs: 11 cases (1993–2009)”. Journal of the American Veterinary Medical Association 242: 223–229.
Patterson, Jon. 2016. “Pathogenesis of Pug Myelopathy: For Veterinarians” Home page: Pug Rear Leg Ataxia – Paralysis. Downloaded 170119.
Rohdin, Cecilia, et al. 2018. “Presence of thoracic and lumbar vertebral malformations in pugs with and without chronic neurological deficits”. The Veterinary Journal 24, 24–30.
Rohdin, Cecilia. “Mops, ‘Vingelmopsar’, progressiv icke-smärtsam myelopati på mops, PMP”. Home page: NeuroVet. Downloaded 120419.
Smiler, Kathleen and Jon Patterson. 2013. “Constrictive Myelopathy: a cause of hind limb ataxia unique to Pug dogs?”. Poster. Downloaded 170119.
Smiler, Kathleen. 2016. “Is your ataxic pug still urinating normally?”. Home page: Pug Rear Leg Ataxia – Paralysis. Downloaded 170119.
Smiler, Kathleen. 2019. “Pug Myelopathy: a new understanding of a ‘weak rear’”. ShowSight Magazine 19:3. Downloaded 100919.
Wong, Michael. “Wellington – Subarachnoid diverticulum” Home page: Southeast Veterinary Neurology. Downloaded 040419.
Chapters in Strategies for the breeding of Healthy Pugs
- Hips, Elbows and Patella
- Hemivertebrae and other vertebral anomalies
- Spinal Arachnoid Diverticulum (SAD)
- Pug Myelopathy (PM)
- Degenerative Myelopathy (DM)
- PDE/NME and other non-viral induced encephalitides
- Brachycephalic Obstructive Airway Syndrom (BOAS)
- Dentition and mouth health in the Pug
- Eyes (Brachycephalic Ocular Syndrome)
- Mating and Fertility
- Mentality (work in progress)
- Genetic diversity