Etiology and Pathogenesis

Bacterial or fungal infection of the intervertebral disks and adjacent vertebral bodies (diskospondylitis), or of only the vertebral bodies (spondylitis), may result in extradural spinal cord or cauda equina compression due to granulation tissue, bony proliferation, or pathologic fracture or luxation. Less commonly, diskospondylitis may lead to diffuse or focal meningitis and myelitis.

Diskospondylitis and spondylitis result from implantation of bacteria or fungi introduced by migrating plant awns (grass seeds, foxtails), hematogenous spread, extension of a paravertebral infection, a penetrating wound, or previous disk or vertebral surgery.

Diskospondylitis and spondylitis occur more commonly in dogs in areas where grass awn infections are a problem. Several theories exist to explain migration of grass awns to the vertebral column. Awns may be swallowed and migrate through the bowel wall (possibly at the caudal duodenal flexure), through the mesentery to the attachment to ventral epaxial muscles, and to the vertebral column. Evidence of scarring, however, has not been found in the gut or abdomen of dogs with diskospondylitis. As dogs with diskospondylitis thought to be due to plant awn migration have lesions most commonly in the cranial lumbar spine (L2-L4) it has been suggested that awns may be inhaled and migrate through the lungs to the diaphragm, and lodge at the crural insertion on the lumbar vertebrae. Plant awns may also migrate through skin and paravertebral or abdominal muscles to the vertebral column. Grass seeds are able to travel long distances owing to the direction of the barbs. Forward progress may be aided by muscle movements.

Hematogenous spread of bacteria or fungi is probably the most common cause of diskospondylitis. Sources of infection include bacterial endocarditis, sites of dental extraction, and urinary tract infections. Retrograde flow in the vertebral veins has been suggested as a possible route of infection to the vertebral column. Many dogs with diskospondylitis have concurrent urinary tract infection. Diskospondylitis due to Brucella cants infection most likely results from bacteremic spread from a genital infection.

Affected intervertebral disks may have evidence of degeneration (collapsed disk space, spondylosis deformans) or trauma (traumatic disk protrusion, vertebral luxation). Prior disease or injury to the disk has been suggested as a factor in the pathogenesis of diskospondylitis.

Diskospondylitis may occur with increased frequency in immunocompromised animals. Diskospondylitis and vertebral osteomyelitis also have been reported associated with Mycobacterium avium infection in basset hounds in which an inherited immunodeficiency was suggested as a predisposing factor German shepherd dogs may be predisposed to fungal diskospondylitis.

Organisms most commonly isolated from blood, affected vertebrae, and urine of dogs with diskospondylitis are coagulase-positive Staphylococcus spp (aureus, intermedius). Other organisms isolated include Bacteroides capillosus, Brucella canis, Nocardia sp, Streptococcus canis, Corynebacterium sp, Escherichia coli, Proteus sp, Pasteurella sp, Paecilomyces sp, Aspergillus sp, and Mycobacterium sp. Coccidioides immitis may cause vertebral body osteomyelitis. Hepatozoon canis infection has been associated with periosteal bone proliferation of the vertebrae as well as other bones of the body. Spirocerca lupi infection may cause productive bony changes on the ventral aspect of thoracic vertebrae where the aorta and the esophagus run in parallel course.

Clinical Findings

Diskospondylitis may occur in dogs or cats of any age, however it is most commonly seen in giant and large breeds of dog. Any level of the vertebral column may be affected by diskospondylitis, and multiple lesions may be seen, in either adjacent vertebrae or nonadjacent vertebrae. Diskospondylitis occurs more commonly in thoracic and lumbar spine than in cervical spine. The lumbosacral disk space frequently is involved.

Clinical findings depend on the location of the affected vertebra or vertebrae. The most common clinical signs are weight loss, anorexia, depression, fever, reluctance to run or jump, and apparent spinal pain (which may be severe). Hyperesthesia may be present only over the site of the lesion or may be poorly localized, especially with involvement of multiple sites.

Diagnosis

Diagnosis may be difficult, as clinical signs often are nonspecific. Diskospondylitis should always be considered in an animal with fever of unknown origin. If the lumbosacral intervertebral disk is involved, dogs often show a stilted, short-strided pelvic limb gait and shifting pelvic limb lameness. Clinical signs commonly are present for several weeks or months before a diagnosis of diskospondylitis is made.

Neurologic deficits associated with spinal cord or cauda equine compression may be present, and may reflect either a transverse or a multifocal myelopathy. Cervical lesions most commonly cause only apparent cervical pain, and lumbosacral lesions may cause neurologic deficits due to compression of nerves of the cauda equine. Rarely, animals may demonstrate clinical signs of diffuse suppurative meningitis associated with extension of infection to involve the spinal meninges. Dogs may have a history of draining tracts in the paravertebral area associated with grass seed migration.

Affected animals may have a normal or elevated peripheral white blood cell count. Typical radiographic findings are destruction of the bony end-plates adjacent to an infected disk, collapse of the intervertebral disk, and varying degrees of new bone production. Early lesions may consist only of lytic areas in affected vertebral end-plates. More advanced lesions show a mixture of bone lysis and extensive new bone production, with osteophytes bridging adjacent vertebrae containing a central destructive focus. Affected vertebral bodies may be shortened, and bony proliferation may result in fusion of one or more vertebrae.

Infection may be difficult to distinguish from a healing fracture, unstable fracture, congenital malformation, or postoperative changes. Diskospondylitis usually can be distinguished from a neoplastic lesion, as neoplasms rarely cross intervertebral disk spaces.

Diskospondylitis may be present in more than one site in the vertebral column, therefore, it is important to radiograph the entire spine in animals suspected to have diskospondylitis. Occasionally, clinical signs may occur before characteristic radiographic changes are evident. If diskospondylitis is suspected, and characteristic lesions cannot be found, a dog should be radiographed again in 2 to 4 weeks. Advanced imaging (CT or MRI) may be useful in identification of subtle vertebral lesions.

Collection of CSF is indicated in animals with neurologic deficits. The CSF white blood cell count may be normal, or may be elevated, with an increase in PMN neutrophils in CSF from animals with meningitis or myelitis.

Myelography is indicated in animals with neurologic deficits indicative of spinal cord compression and is mandatory in cases in which decompressive surgery is considered.

Aerobic, anaerobic, and fungal cultures of blood and urine should be done prior to treatment in an attempt to isolate causative organisms. Cultures of CSF are indicated if the WBC count is elevated. Cultures of fluid from draining sinuses may also be done. Efforts should be made to diagnose B. Canis infection in all dogs with diskospondylitis.

Surgical biopsy may be indicated in affected dogs in which a causative organism is not isolated from blood or urine, and/or animals that are unresponsive to treatment with broad spectrum antibiotics. Fluoroscopy-guided needle aspiration of lesions is possible in some animals. However, cultures of samples collected in this way are often negative, especially if animals have been treated with antibiotics prior to completion of a biopsy.

Treatment

Treatment consists of long-term use of an antimicrobial that is effective against the causative organism(s) determined by results of blood and/or urine cultures. If an organism is not cultured, dogs without severe neurologic deficits may be treated empirically, assuming infection with the most common organism isolated from animals with diskospondylitis (coagulase-positive Staphylococcus sp). Antibiotics that are most effective for this purpose are cephalosporins, or beta-lactamase resistant penicillins such as oxacillin and cloxacillin. A trimethoprim/sulfonamide combination or chloramphenicol is less effective but is less expensive, and may be effective in some cases.

Clinical signs may recur if the infection is not completely eliminated prior to cessation of antibiotic therapy, and repeated cultures of blood and urine and ongoing treatment with an appropriate antibiotic may be necessary. Treatment is continued for at least 6 weeks, and vertebral radiographs are done every 4-6 weeks to monitor progression/ regression of a lesion, and to monitor for development of new lesions. Antibiotic administration may be necessary for up to 6 months before radiographic evidence of resolution of lesions is seen.

A combination of minocycline or tetracycline and streptomycin is recommended for treatment of B. canis infections. Infected dogs should be neutered to eliminate risk of transmission. B. canis infections have public health significance, as people may become infected.

Clinical improvement in animals with diskospondylitis (resolution of fever, improved appetite, reduction of apparent spinal pain) should be seen within 2 weeks of starting antibiotic therapy. If clinical improvement is not seen, treatment should be reevaluated. Fungal infection should be considered in animals non responsive to antibiotic therapy. Use of analgesics and restriction of exercise during the first weeks of treatment may be helpful.

Surgical exploration of a lesion should be considered in animals that are unresponsive to treatment or have persistent draining tracts suggestive of grass seed migration. Objectives of surgery are curettage of lesions and harvesting of material for bacterial and fungal culture. Decompressive surgery is indicated if evidence of spinal cord compression is found on myelography and if animals show severe or progressive neurologic deficits. Surgical stabilization of the vertebrae may be necessary following decompression.

Prognosis for animals with diskospondylitis depends on the ability to eliminate the causative organism(s) and on the degree of neurologic dysfunction. Animals with severe neurologic deficits and fungal infections have a guarded to poor prognosis.