Pyogenic Discitis & Osteomyelitis

Pyogenic spondylodiscitis is infection of the intervertebral disc and the adjacent vertebral bodies. In the adult it begins in the vertebral endplate and spreads into the disc.

Who. The distribution is bimodal, with one peak under 20 years and another over 50 years. The adult at risk carries one or more of these:

• Diabetes, as an immunocompromised host
• Intravenous drug use, which carries a Pseudomonas risk
• Chronic steroid use
• Cancer, metastatic or primary
• A recent infection such as a UTI or pneumonia
• Trauma, or surgery with post-operative infection
• Immunosuppression from HIV or chemotherapy

Where. The lumbar spine is affected more often than the thoracic, and the thoracic more often than the cervical. Tuberculosis of the spine, by contrast, prefers the thoracic region.

Which organism. Staphylococcus aureus is the most common, accounting for over 50%. The others follow the source:

• E. coli from a urinary infection
• Cutibacterium after surgery, slow growing
• Pseudomonas in intravenous drug users

The adult disc is avascular. It is nourished by diffusion from the endplates. The endplate is the "metaphysis" of the spine: a rich vascular loop system with slow flow, which predisposes to bacteria lodging in its end-arterioles.

How it crosses the segment. The infection sets up an osteomyelitis in the endplate, then breaks through into the disc and destroys it rapidly with proteolytic enzymes. From the disc it spreads to the adjacent vertebra. The child is different, because vascular channels persist across the endplate into the disc (see Childhood Discitis below).

Routes into the spine. Spread is haematogenous, by one of two routes:

• Arterial, through the nutrient arteries
• Venous, through Batson's plexus

Batson's plexus. A valveless system of vertebral veins that communicates freely with the pelvic, abdominal and thoracic venous systems. A rise in intra-abdominal or intra-thoracic pressure, from coughing, straining or lifting, can reverse the flow. That retrograde flow lets bacteria from the pelvis (UTI, prostatitis) or abdomen bypass the liver and lung filters and lodge directly in the spine, which explains the strong association between urinary tract infection and vertebral osteomyelitis.

The mechanical consequence. Infection weakens the anterior column, the body and the disc, and leads to kyphosis (gibbus deformity). Destruction of more than 50% of the vertebral body means mechanical instability.

Paediatric discitis behaves so differently from adult vertebral osteomyelitis that it deserves separate treatment.

Why it differs. In young children the disc still has a direct vascular supply, so infection, or a low-grade inflammatory process, can settle in the disc itself rather than starting in the endplate. It is usually a single lumbar level, commonly L3-4 or L4-5, low-virulence, and frequently culture-negative and even blood-culture-negative.

How it presents. The classic picture is a young child, often 1 to 5 years old, who refuses to walk, sit or bear weight, or who is irritable with back, abdominal or hip pain, rather than the toxic septic adult. Fever and inflammatory markers are often only mildly raised. Loss of the normal lumbar lordosis and reluctance to flex the spine are typical.

How it is managed. Much less aggressively than in the adult. It is largely a clinical and MRI diagnosis, and routine biopsy is not required in the typical case. Management is usually immobilisation or rest and a course of anti-staphylococcal antibiotics, with biopsy reserved for atypical, non-responding or destructive disease.

Prognosis. Good: most children recover fully, in contrast to the high residual-morbidity, deformity and mortality figures quoted for adult pyogenic vertebral osteomyelitis.

Pola's classification is treatment-oriented; Homma's grades bone destruction on MRI.

The pain. Constant and non-mechanical, present at night and progressively worsening. Back pain is about 90% sensitive, and back pain with a raised CRP is discitis until proven otherwise.

Fever is unreliable. Fever, rigors and weight loss may occur but are often absent. Only 50% of patients are febrile, so do not rule out infection because the patient is afebrile.

The neurology. Weakness or numbness suggests an epidural abscess, the most feared complication because of cord compression. Examine the myotomes and dermatomes in detail. Any new neurology mandates urgent MRI to rule out compression.

Examination of the spine. Percussion tenderness is highly sensitive. Paravertebral muscle spasm is "board-like".

The trap. Degenerative Modic type 1 endplate change produces endplate marrow oedema that looks like early infection, dark on T1 and bright on T2/STIR. It is the commonest false positive, and distinguishing the two is a classic examiner trap.

Look at the disc, not just the endplate. The single most useful discriminator is the disc itself. A T2-bright disc with endplate destruction and paradiscal or epidural enhancement points to infection; a T2-dark degenerate disc with intact endplates and no soft-tissue enhancement is Modic type 1 degeneration. The same caveat explains why a routine post-operative MRI mimics infection.

Organism before antibiotics. Do not start antibiotics before biopsy unless the patient is septic or has neurological compromise. Starting them before deep cultures sterilises the field and makes targeted treatment impossible.

The pathway. Suspicion starts with back pain and a raised CRP; where suspicion is low, monitor. Suspected discitis gets an MRI and blood cultures, and an assessment of the neurology. From there:

1. Neurological deficit or sepsis is an emergency: surgery, with empirical antibiotics after cultures
2. Stable: hold antibiotics and proceed to CT-guided biopsy
3. Biopsy positive: targeted IV or oral antibiotics for 6 weeks
4. Biopsy negative: repeat biopsy, or open biopsy

Algorithm

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Antibiotics. Empirical cover is vancomycin with ceftriaxone, for MRSA and Gram-negative organisms. Once sensitivities are known, narrow the spectrum to match them.

Route and duration. The traditional course is six weeks intravenously. OVIVA shows oral therapy is non-inferior once a bioavailable agent can be chosen against a known organism, which presupposes an organism. Bernard's trial established six weeks as non-inferior to twelve, but every patient in it had a microbiologically confirmed infection:

• Continue for 6 weeks minimum from the start of targeted therapy
• Stop when the CRP normalises and radiographic healing is seen
• In culture-negative disease, which is roughly half of biopsied patients, six weeks is an extrapolation, and a longer course with closer surveillance is defensible

Bracing. A TLSO is often used for pain control and to prevent kyphosis, worn for 6-12 weeks while the bone heals.

When to operate. Surgical source control, decompression with or without debridement and instrumentation if the spine is unstable or kyphotic, is for failure of medical treatment, abscess, deformity or instability.

Surveillance. Check the CRP weekly. Radiographs at 6 weeks and 3 months check fusion and alignment. MRI is only for worsening symptoms, because post-operative change mimics infection.

Mortality. High, at 2-20% depending on comorbidities such as age and diabetes, and higher in MRSA infection.

Recurrence. About 5-10%. The risk factors are an inadequate duration of antibiotics, an undrained abscess and retained hardware if it is loose.

Function. The majority, greater than 70%, have significant residual back pain, and functional impairment is worse than after standard degenerative spine surgery. Quality-of-life scores in studies such as Carragee et al are similar to those in chronic heart failure.

Long-term sequelae. Chronic pain is due to facet joint destruction and the altered biomechanics of kyphosis. Degenerative spondylolisthesis may develop years later above or below the fused level, as adjacent segment disease.

Poor prognostic factors. These predict a worse outcome:

• Age greater than 60
• Concurrent endocarditis
• Disseminated S. aureus infection
• Delay in diagnosis greater than 3 months
• Neurological deficit at presentation, which is often permanent

Global epidemiology

• Incidence is rising worldwide (ageing populations, IV drug use, more spinal instrumentation and intravascular devices). Reported population incidence is roughly 1 to 7 per 100,000 person-years in high-income settings.
• Strong male predominance and a peak in patients over 50 years. Staphylococcus aureus is the dominant pathogen globally; Gram-negative organisms cluster with urinary sources and IV drug use.
• In TB-endemic regions (much of South Asia, sub-Saharan Africa), Mycobacterium tuberculosis (Pott disease) is a major differential and may outnumber pyogenic cases; Brucella spondylitis is important around the Mediterranean, Middle East and Central Asia.

Registry and practice variation

• No dedicated international spondylodiscitis registry exists; arthroplasty/implant registries (NJR, AJRR, AOANJRR, SHAR) inform biofilm and revision principles that carry over to instrumented spinal infection.
• High-resource settings: routine MRI, CT-guided biopsy, prolonged targeted therapy, single-stage instrumented debridement, OPAT or early oral switch.
• Limited-resource settings: empirical therapy is often started before biopsy due to limited imaging/microbiology; high TB prevalence lowers the threshold for empirical anti-tuberculous treatment; surgical capacity for instrumented reconstruction may be constrained.

Related pages: Tuberculosis of the Spine (Pott's Disease) is the mimic that must be excluded before any culture-negative case is treated as pyogenic - it spares the disc early, crosses levels beneath the anterior longitudinal ligament and produces a paraspinal abscess out of proportion to the pain, and it is also the disease the instrumentation-safety paper carded above actually studied; Spinal Epidural Abscess for the complication that turns this from a medical problem into an emergency, and for the deficit-duration rule that governs the timing of decompression; Fungal Osteomyelitis for the other reason a biopsy grows nothing; Osteomyelitis Pathophysiology for the biofilm and sequestrum biology that explains why source control matters more than antibiotic duration; Pediatric Acute Osteomyelitis for the haematogenous disease in the child whose vascular anatomy differs; and Chronic Recurrent Multifocal Osteomyelitis for the sterile inflammatory condition that images like infection and must not be given six weeks of antibiotics.

• Empirical antibiotics before biopsy: Guidelines advise holding antibiotics in stable patients to maximise culture yield, yet real-world practice often starts therapy early. The optimal antibiotic-free window before biopsy (commonly quoted as 48 to 72 hours) is not firmly evidence-based.
• Total duration: The Bernard RCT supports 6 weeks for uncomplicated disease, but undrained abscess, implant-associated infection, endocarditis or persistently raised CRP frequently prompt longer courses; the right duration for these subgroups is unresolved.
• Oral versus IV: OVIVA supports early oral switch, but uptake varies and selection of a reliably bioavailable oral agent (and adherence) remains the practical limitation.
• Single-stage instrumentation in active infection: Increasingly accepted with radical debridement, but the threshold for instrumenting, choice of anterior versus posterior approach, and use of titanium versus PEEK cages are debated.
• Role of nuclear imaging: FDG-PET/CT is useful when MRI is contraindicated or equivocal and for monitoring, but is not universally available and its role in defining cure is not standardised.