Background: The purpose of the study was to compare radiographic and histopathologic findings with regard to number and extent of calcified discs in the dachshund.

The first cases of early-onset progressive polyneuropathy appeared in the Alaskan Malamute population in Norway in the late 1970s. Affected dogs were of both sexes and were ambulatory paraparetic, progressing to non-ambulatory tetraparesis. On neurologic examination, affected dogs displayed predominantly laryngeal paresis, decreased postural reactions, decreased spinal reflexes and muscle atrophy. The disease was considered eradicated through breeding programmes but recently new cases have occurred in the Nordic countries and the USA. The N-myc downstream-regulated gene (NDRG1) is implicated in neuropathies with comparable symptoms or clinical signs both in humans and in Greyhound dogs. This gene was therefore considered a candidate gene for the polyneuropathy in Alaskan Malamutes. The coding sequence of the NDRG1 gene derived from one healthy and one affected Alaskan Malamute revealed a non-synonymous G>T mutation in exon 4 in the affected dog that causes a Gly98Val amino acid substitution. This substitution was categorized to be “probably damaging” to the protein function by PolyPhen2 (score: 1.000). Subsequently, 102 Alaskan Malamutes from the Nordic countries and the USA known to be either affected (n = 22), obligate carriers (n = 7) or healthy (n = 73) were genotyped for the SNP using TaqMan. All affected dogs had the T/T genotype, the obligate carriers had the G/T genotype and the healthy dogs had the G/G genotype except for 13 who had the G/T genotype. A protein alignment showed that residue 98 is conserved in mammals and also that the entire NDRG1 protein is highly conserved (94.7%) in mammals. We conclude that the G>T substitution is most likely the mutation that causes polyneuropathy in Alaskan Malamutes. Our characterization of a novel candidate causative mutation for polyneuropathy offers a new canine model that can provide further insight into pathobiology and therapy of human polyneuropathy. Furthermore, selection against this mutation can now be used to eliminate the disease in Alaskan Malamutes.

Background Three Nordic countries have national breeding programs to reduce the frequency of intervertebral disc disease in dachshunds. The programs include a radiographic examination of the vertebral column and dachshunds with more than four calcified discs visible on radiographs (CDVR) are discouraged from use in breeding. However, disc extrusion is also diagnosed in dachshunds without CDVR. The utility of the breeding programs is therefore questioned. Results A prospective study of 25 dachshunds surgically treated for disc extrusion was conducted. For all the dogs, preoperative radiographs were evaluated for detectable disc calcifications and preoperative computed tomography (CT) scans were evaluated for presence of calcified material in the vertebral canal. Postoperatively, extruded disc material was examined for degeneration and calcification by histology. Diagnostic imaging and histology were done independently. Radiographically visible calcification was identified in 17 (68.0%) of 25 extruded discs. Calcification was seen in the disc space for all these 17 discs, and for eight of the 17, there was also calcified material visible in the vertebral canal. Extruded material from all the 25 discs was found to be calcified, both by CT and histopathology. Conclusions In dachshunds with acute disc extrusion, radiographically visible calcification will frequently be found in the affected disc space, but not all affected disc spaces contain radiographically visible calcification. Using histopathology as the gold standard, a sensitivity of 0.3 (8/25) for radiography and 1.0 (25/25) for CT was found for detecting calcified disc material in the vertebral canal. Further, a sensitivity of 0.7 (17/25) was found for radiography for detecting remaining calcified material in the disc space. Thus, extruded disc material should be considered to be calcified, even in the absence of radiographically visible calcification.

Thoracolumbar disc extrusions were diagnosed in three chondrodystrophic dogs with paraparesis of up to three days duration. All cases were managed by hemilaminectomy and removal of extruded disc material. In one dog, fenestration of the herniated disc space was also performed. Initially neurological function improved or was unchanged, but from two to ten days postoperatively clinical signs of deterioration became apparent. In all the dogs, recurrence of disc extrusion at the same location as the initial extrusion was diagnosed by computer tomography and at a second surgery abundant disc material was found at the hemilaminectomy site between the dura and an implanted graft of autogenous fat.

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