The Challenges of Bacterial Diskospondylitis Diagnosis and Treatment

Meet Lars…

a 6 ½ year old MN German Shepherd Dog who acts like a real toughy, but when he is with his dad, he is a big teddy bear. His case shows some of the challenges of treating bacterial diskospondylitis, an infection of the intervertebral discs and adjacent vertebrae that primarily affects large, middle-aged to older dogs, causing pain, stiffness, and lethargy. Early and aggressive treatment generally leads to a good prognosis, as we saw with Lars, although relapses can occur.

Lars was referred to Veterinary Neurology and Imaging of the Chesapeake due to pain and difficulty rising. One month prior to this visit, he had been seen by his primary care veterinarian as he was having difficulty jumping into the car, and was experiencing pain, decreased appetite, and an inability to sit up straight. On examination at his primary care veterinarian, he was noted to have back pain, a hunched posture, diarrhea, and bloody urine. 

Radiographs, a complete blood count (CBC), and serum chemistry analysis were performed. The radiographs showed early signs of lumbosacral spondylosis and a collapsed disk space at the lumbosacral junction. The blood work indicated mild anemia and an elevated count of mature neutrophils. 

Lars was presumptively diagnosed with intervertebral disk disease and was started on a treatment regimen that included rest, methocarbamol, gabapentin, and prednisone. 

Over the course of the following month, Lars initially showed improvement in his attitude, appetite, and mobility. However, in the week leading up to his initial appointment at VNIOC, he became weaker, was unable to go for long walks, and ultimately could not stand independently. 

Upon our examination, Lars was found to be febrile with a temperature of 103.5°F and was tachycardic at 126 beats per minute. He was experiencing significant generalized pain and appeared irritable but oriented. Since his initial examination at the primary care veterinarian, he had lost 5 kg from his initial weight of 42 kg. He looked thin and in poor condition. 

The neurological examination revealed non-ambulatory flaccid paraparesis with severe localized pain in the lumbar region. While his tail was weak, he was still able to elevate it, and both his anal tone and anal reflexes remained weak but intact.

Lars' issues were determined to be localized to the lumbar-lumbosacral spine. A plan was made to further evaluate his condition through imaging and laboratory tests. Baseline labwork showed non-regenerative anemia, neutrophilia with a left shift, elevated alkaline phosphatase, hyper-globulinemia, hematuria, and bacturia. A urine culture was negative. 

The significant imaging findings are displayed below.

Figure 1: Lateral radiograph of Lars’ lumbar spine (LS). At the LS junction,
there is collapse and subluxation of the disk space with profound sclerosis and lysis.

Figure 2: Magnetic resonance imaging (MRI) study of Lars.
(A) Sagittal STIR sequence of lumbar-lumbosacral spine and
(B) sagittal post-contrast T1 sequence both show abnormal signal in the LS disk.
There is advanced sclerosis surrounding the intervertebral disc space
at the level of caudal vertebral body of L7 and of cranial vertebral body of S1
with erosions within the ventral intervertebral disc space and protrusion of the intervertebral disks.
The yellow line marks the site and orientation of the axial images (C and D). (C) Axial T2 sequence and
(D) axial post-contrast T1 sequence of the lumbosacral disk show extradural compression of the overlying nerve roots at the LS junction with contrast enhancement within the intervertebral disk space.

A radiographically-guided needle aspirate of the LS disk was performed immediately after the MRI, which revealed chronic neutrophilic inflammation without any evidence of infectious or neoplastic agents. The aspirate yielded negative cultures under both aerobic and anaerobic conditions.

Lars was discharged with strict rest instructions and prescribed Tylenol 3, pregabalin, and amoxicillin-clavulanic acid. After a five-day washout period for the steroids, he was started on carprofen.

Lars improved slowly but steadily. Within three weeks, he was ambulatory and showed significantly improved proprioception. At this point, Tylenol 3 and carprofen were discontinued. 

However, after eight weeks of continuous antibiotics, he still exhibited pain and mild spinal ataxia. Repeat radiographs showed incomplete healing of the LS diskospondylitis. His LS space showed spondylosis and subluxation. Consequently, the decision was made to continue amoxicillin-clavulanic acid and to restart carprofen.

After four months of antibiotic treatment, Lars’ examination was normal, and his radiographs indicated healing at the LS joint.

Discussion

This case highlights several important aspects of diskospondylitis. The initial symptoms were quite nonspecific, suggesting a systemic issue, particularly with the presence of diarrhea and blood in the urine. While hematuria (blood in urine) can occur with intervertebral disk disease (IVDD) due to urine retention, it can also indicate systemic conditions like diskospondylitis. Diarrhea is not typically associated with IVDD. 

The complete blood count revealed nonregenerative anemia, which is characteristic of anemia of chronic disease and not a common finding in IVDD. A review of the radiographs showed collapse of the lumbar spine (LS) disk space, along with endplate sclerosis and a slight periosteal reaction around the disk space. Often, it is only in retrospect that we recognize early signs of diskospondylitis that mimic intervertebral disk disease. In this instance, diskospondylitis presented as if it were intervertebral disk disease.

During our examination, it became clear that this was a systemic disease characterized by weight loss, fever, and a poor overall condition. The neurological symptoms were localized to the lumbar or lumbosacral spinal segments. Radiographs and MRI revealed severe changes in the lumbosacral (LS) disk, including subluxation and collapse of the LS region, sclerosis and lysis at the LS endplates, as well as contrast enhancement of the disc space and surrounding tissue.

The prognosis for Lars to walk again was uncertain, even with appropriate antibiotic therapy. Severe diskospondylitis caused pudendal nerve dysfunction and paraparesis and suggests a guarded to poor prognosis.

Often, the causative bacteria are not identified, even after extensive investigations. We submitted samples of urine and disk aspirates for both aerobic and anaerobic cultures, but the results were negative. We selected the antibiotic Clavamox due to its broad spectrum of activity and its effective penetration in bone, blood, urine, and infected tissue.

We were delighted with Lars' response and grateful that he quickly regained his ability to walk. Often, prolonged treatment with antibiotics is necessary and may continue for one month after all clinical signs have resolved. Follow-up radiographs indicated that the lesions from diskospondylitis were healing, but there was still evidence of subluxation and collapse of the lumbosacral space, which likely contributed to his discomfort at the lumbosacral junction.

Lars continues to do well without any medications. He was very happy to share his progress with us at his 18-month recheck.