Spinal Infections

Spinal infections are a spectrum of infections affecting the vertebral column and associated structures. They comprise vertebral osteomyelitis, discitis and epidural abscess. Vertebral osteomyelitis and discitis frequently occur together as spondylodiscitis, given the shared blood supply and contiguous anatomy of the vertebral endplate and intervertebral disc.

They arise predominantly through haematogenous spread, though also through direct inoculation (spinal surgery, procedures) or contiguous extension from an adjacent infective source.

The central clinical priority is early recognition. Epidural extension that is not promptly identified and treated risks progressive neurological deficit from cord or cauda equina compression.

Pathophysiology and risk factors

• Haematogenous seeding of the vertebral body, typically via the arterial supply to the vertebral endplate, accounts for the majority of cases.
• Infection then frequently extends across the disc space to involve the adjacent vertebra. This explains the characteristic pattern of contiguous two level vertebral involvement with disc space narrowing seen on imaging.
• Staphylococcus aureus is the commonest causative organism overall.
• Mycobacterium tuberculosis is an important cause in endemic regions and specific risk groups. It produces the classically more indolent, chronic presentation historically termed Pott disease, addressed further under tuberculosis.
• Gram negative organisms are also recognised causes, including as a specific consideration following urinary tract instrumentation or infection, given venous drainage pathways.
• Risk factors include diabetes, intravenous drug use, immunocompromise, recent spinal surgery or procedure, and advanced age.
• Recent bacteraemia from any source is a risk factor, with a particular association with infective endocarditis. Every case of confirmed spinal infection should prompt consideration of screening for an occult endocarditis source, and vice versa.

• Back pain, typically insidious in onset and progressively worsening over weeks, is the dominant and most consistent presenting symptom.
• The pain is often disproportionately severe, unremitting, and notably present at rest and at night. This distinguishes it from the more typical mechanical back pain pattern that improves with rest.
• Fever is present in only a proportion of cases, and its absence should never be used to exclude the diagnosis, particularly given the frequently indolent, subacute nature of presentation.
• Constitutional symptoms including malaise and weight loss are also common, particularly with more chronic or tuberculous disease.
• Progressive neurological deficit, including limb weakness, sensory disturbance, and bladder or bowel dysfunction, reflects extension to the epidural space with cord or cauda equina compression. It is a neurosurgical emergency requiring immediate imaging and urgent intervention.
• Actively seek a relevant preceding history of bacteraemia, recent spinal instrumentation, intravenous drug use, or an identifiable source of infection elsewhere.
• Examine specifically for localised spinal tenderness, any neurological deficit, and evidence of a potential source or associated infective focus elsewhere, including cardiac auscultation for a murmur suggesting endocarditis.

• Magnetic resonance imaging with contrast is the investigation of choice. It has superior sensitivity for identifying vertebral osteomyelitis, discitis and, critically, any associated epidural or paraspinal abscess formation.
• Characteristic findings include vertebral endplate signal change, disc space narrowing and enhancement, and, where present, a defined epidural collection causing thecal sac or cord compression.
• Obtain blood cultures in every suspected case. A positive result in the appropriate clinical context is frequently sufficient to guide targeted antibiotic therapy without image guided biopsy.
• Image guided percutaneous biopsy of the affected disc or vertebral body is indicated where blood cultures are negative, given the importance of a definitive microbiological diagnosis to guide the required prolonged antibiotic course.
• Inflammatory markers, particularly C reactive protein and erythrocyte sedimentation rate, are typically elevated. They are non specific for diagnosis but useful for monitoring treatment response over the subsequent weeks of therapy.
• Consider echocardiography in patients with confirmed spinal infection and no other clear identifiable source, given the recognised association with infective endocarditis.
• Pursue specific mycobacterial testing (culture, molecular testing) of biopsy material where tuberculous infection is a relevant consideration, based on epidemiological context or a compatible, more indolent clinical and radiological picture.

• Targeted intravenous antibiotic therapy, guided wherever possible by blood culture or biopsy culture results, is the mainstay of treatment.
• Empirical therapy (where culture results are pending or a specific organism has not been identified) typically comprises flucloxacillin or vancomycin (where methicillin resistant Staphylococcus aureus is a concern) combined with a third generation cephalosporin for broader Gram negative cover. Adjust once susceptibility results are available.
• Total antibiotic duration is prolonged, typically a minimum of six weeks of therapy.
• An initial intravenous course (commonly two to six weeks depending on clinical response and the specific organism) is followed by transition to an appropriate oral agent to complete the full course. Guide this by clinical response and trending inflammatory markers rather than a rigid fixed schedule.
• Epidural abscess causing significant cord or cauda equina compression, or progressive neurological deficit of any degree, is a neurosurgical emergency requiring urgent surgical decompression alongside antibiotic therapy.
• The timing of intervention directly influences the likelihood of neurological recovery. Any suggestion of evolving neurological compromise mandates immediate imaging and neurosurgical involvement without delay.
• Surgical intervention beyond decompression is considered for cases with extensive bony destruction, failure of medical management, or significant spinal instability. It includes debridement or, for significant vertebral destruction with instability, spinal stabilisation. The decision is made through multidisciplinary discussion involving spinal surgery and infectious disease specialists.
• Adequate analgesia and, where required, temporary immobilisation or bracing support symptomatic management alongside definitive antimicrobial and, where indicated, surgical treatment.
• A structured, gradual mobilisation and rehabilitation programme is appropriate as the acute infection comes under control.
• Regular clinical review underpins management throughout the prolonged treatment course. Add serial inflammatory marker monitoring and, where there is any concern about inadequate response, repeat imaging.
• Premature curtailment of treatment risks relapse or inadequate source control.