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Case report: Disseminated Discospondylitis in a two-year-old Crossbred Dog


A two-year-old, female, neutered crossbred (body weight 14kg) was referred for assessment of diffuse spinal pain. The patient had been rescued six weeks previously from Romania. On arrival into the U.K., she was presented to the referring veterinarian with neck pain. There had been an initial response to NSAIDs and diazepam, but four days prior to presentation at the Downs signs progressed to lumbar spinal pain and spontaneous vocalisation at rest. The patient had also been bitten by another dog in the right axilla the night prior to presentation and had subsequently received a single parenteral dose of amoxiclav.


On presentation, the patient was bright, alert and responsive. Gait analysis revealed a tentative, shuffling gait with the hindquarters tucked under-neath. The patient was reluctant to rise and consistently cried out when doing so. General physical examination revealed guarding of the cervical and thoracolumbar spine, but was otherwise unremarkable. Neurological examination revealed no deficits.


C-reactive protein levels were elevated; 121 (<20) mg/L. Survey radiology of the spine (figs. 3.1 & 3.2) revealed extensive, bridging spondylosis along the thoracolumbar spine. In addition, there was evidence of end-plate lysis at several disc spaces, throughout the cervical, thoracic and lumbar spinal segments, consistent with disseminated discospondylitis. Blood and urine samples were submitted for bacteriology.

fig. 3.1 – Lateral, plain radiograph of cervicothoracic spine; there is evidence of disc space widening, due to lysis of endplate bone at disc-spaces Ce2, 4, 5, 6, and T4, 5, 6, 7, 8, 9, 11, & 12. There is also evidence of facet-joint arthropathy at Ce2-6


fig 3.2 – Lateral view of the lumbar spine again revealed bridging ventral spondylosis L1-7, widening of disc spaces due to lysis of end plates at T12-L1, L2-6 and facet joint arthropathy at L2-3 & L3-4.

The patient was hospitalised for supportive care and started on a course of cefuroxime 25mg/kg q12h I.V. She subsequently developed gastritis which was managed with ranitidine 2mg/kg q12h P.O. and maropitant 1mg/kg q24h S.C. After 72 hours, there was resolution of vomiting, reduced spinal pain and improved mobility. The patient was discharged with a course of cephalexin 250mg q12h P.O. cimetidine 50mg q8h P.O. and a transdermal fentanyl (Durogesic 50) patch, which was removed three days later. NSAIDs were with-held for a further 24h.

Extended cultures of both blood and urine samples failed to yield any microorganism growth.

At the time of writing, the patient is currently continuing to receive oral cephalexin as above, and remains free of discomfort, eight weeks after starting treatment.


Where there are financial constraints, choice of imaging modality for assessment of spinal pain is controversial: Ordinarily, the diagnostic yield for plain radiology is low. However, with a history of trauma, patients having been rescued on welfare grounds, or in young patients/ those with comorbidities, obtaining survey radiographs prior to advanced imaging may be helpful.

Discospondylitis is usually seen as a single-site lesion, and may be secondary to bacterial cystitis, periodontal disease, septicaemia or other nidus of infection. The case presented here is unusual as no primary source of infection was reported or found clinically. However, multiple discs were affected, suggestive of bacteraemia overwhelming a naïve/ compromised immune response.

The absence of microorganisms, in both the urine and blood samples may possibly be explained by the dose of antimicrobials given prior to referral. Where patients fail to respond to treatment, it is possible to aspirate/ surgically debride affected discs so as to obtain samples for bacteriology, as isolation of the causative organism and sensitivity testing are important steps towards effective therapy. Further intervention was not performed in this case due to a good response to initial therapy and financial constraints.

Guidelines for management of discospondylitis include prolonged courses of appropriate anti-microbials, selected on the basis of sensitivity testing. Accepted length of treatment varies from six weeks to as much as a year.

Lack of response to medical treatment may prompt recourse to surgical intervention to debride the affected discs, with possible use of omental pedicles to augment the local immune response (see previous article, Downs Diary Issue No. 13).