Osteomyelitis and discitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Bone infection reaches tissue through the bloodstream, direct inoculation or contiguous spread from an ulcer or soft-tissue focus. The route predicts organism spectrum and source-control requirements.

Necrotic bone has poor perfusion and can separate as a sequestrum, creating a protected bacterial reservoir. Chronic sinus formation and biofilm on fixation material explain relapse despite apparently active antibiotics.

Vertebral osteomyelitis often presents with persistent focal back pain rather than fever. Epidural extension can compress cord or cauda equina, making repeated neurological examination and urgent MRI central.

Antimicrobial courses are prolonged and must be planned from reliable microbiology, bone removed or retained, abscess drainage, stability and clinical response. A fixed empirical course without tissue diagnosis risks failure and unnecessary toxicity.

Key points

Osteomyelitis is infection of bone; discitis and vertebral osteomyelitis commonly overlap across the disc and adjacent vertebral endplates.
Blood cultures are essential before antibiotics in suspected haematogenous or vertebral disease and may establish the organism without biopsy.
MRI with appropriate contrast is the preferred imaging test for vertebral infection, marrow involvement, epidural abscess and neural compression.
In a stable patient with negative blood cultures, obtain image-guided or operative bone or disc tissue before antibiotics when the result will direct prolonged therapy.
Do not delay antibiotics for biopsy in sepsis, neurological compromise or rapidly progressive infection; obtain cultures and treat immediately.
Superficial wound swabs do not reliably identify the bone pathogen; deep bone tissue for histology and culture is the reference microbiological specimen.
Management combines organism-active therapy with drainage of abscess, removal of devitalised bone, implant decisions, perfusion and mechanical stability.
Staphylococcus aureus in blood with compatible spinal pain requires clearance cultures and assessment for endocarditis and other metastatic foci.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Haematogenous bone seeding

Bacteraemia deposits organisms in vertebral endplates or metaphyseal vascular beds, with Staphylococcus aureus the leading adult pathogen.

Contiguous ulcer spread

Pressure injury, diabetic ulcer and chronic soft-tissue infection extend directly through cortex into bone, often producing mixed flora.

Direct inoculation

Open fracture, operation, fixation material, injection and penetrating trauma introduce organisms into bone and create biofilm-prone surfaces.

Unusual host-associated organisms

Tuberculosis, fungi, Brucella and Gram-negative bacilli become relevant with epidemiological exposure, immune compromise or particular bloodstream sources.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Marrow inflammatory pressure
Bacterial growth and neutrophilic exudate raise intraosseous pressure, impair perfusion and produce pain, ischaemia and cortical extension.
2
Sequestrum formation
Infarcted bone separates from viable tissue, creating an avascular reservoir inaccessible to immune cells and poorly reached by antibiotics.
3
Involucrum and sinus
Chronic periosteal new bone forms around infected sequestra while drainage tracks through cortex and soft tissue to skin.
4
Vertebral epidural extension
Endplate and disc infection can spread posteriorly into the epidural space, compress neural structures and destabilise the spinal column.
5
Implant biofilm
Adherent organisms enter a metabolically protected community on metal or devitalised bone, allowing persistence despite apparently susceptible planktonic cultures.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Focal persistent bone pain

Deep local pain, tenderness and impaired function lasting beyond a simple soft-tissue injury suggests bone infection, especially after bacteraemia or surgery.

Vertebral infection patternRed flag

Constant focal spinal pain, night pain, painful movement and paraspinal spasm with inflammatory or bloodstream risk supports discitis or vertebral osteomyelitis.

Neurological extensionRed flag

Radicular pain, weakness, sensory loss, gait change, saddle symptoms or sphincter dysfunction suggests epidural abscess or vertebral collapse.

Contiguous ulcer disease

A chronic ulcer probing to bone, draining sinus, exposed bone or persistent wound over a pressure point supports contiguous osteomyelitis.

Haematogenous sourceRed flag

Current or recent Staphylococcus aureus bacteraemia, endocarditis, line infection, injection exposure or skin infection raises probability of metastatic bone seeding.

Chronic subtle infection

Low-grade drainage, non-union, implant loosening and intermittently raised inflammatory markers can represent indolent biofilm disease without fever.

Red flags requiring action

New limb weakness, sensory level, saddle sensory change or bladder and bowel dysfunction requires emergency spinal imaging.
Severe spinal pain with fever, bacteraemia or injection exposure suggests discitis, vertebral osteomyelitis or epidural abscess.
Haemodynamic instability or persistent Staphylococcus aureus bacteraemia indicates invasive infection and metastatic-focus risk.
Sinus, exposed bone, chronic ulcer or implant may represent contiguous polymicrobial bone infection.
Spinal deformity, mechanical instability or progressive pain despite therapy requires surgical reassessment.
Immune compromise, diabetes, vascular insufficiency and previous antimicrobial treatment can blunt presentation and reduce culture yield.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Blood culturesFirst step
Why
Identify haematogenous organisms before antimicrobial exposure and guide the need for biopsy.
Interpretation and limitations
Take at least two sets in vertebral or systemic disease. Staphylococcus aureus or another credible pathogen with compatible MRI may establish aetiology.
02
MRI of the involved region
Why
Detect marrow oedema, endplate and disc infection, abscess, sinus and neural compression.
Interpretation and limitations
MRI is the preferred sensitive anatomical test, but postoperative and neuropathic change can mimic infection; interpret with time course and microbiology.
03
Plain radiography
Why
Assess alignment, fracture, implant, chronic destruction, sequestrum and a baseline for progression.
Interpretation and limitations
Early films can be normal because mineral loss is delayed; normal radiography does not exclude acute osteomyelitis or discitis.
04
Image-guided bone or disc biopsy
Why
Obtain deep tissue for histology and aerobic, anaerobic and exposure-directed culture when blood cultures are nondiagnostic.
Interpretation and limitations
In a stable patient, perform before antibiotics where feasible; prior antibiotics lower yield, and a negative biopsy may require repeat or operative sampling.
05
Deep operative tissue samples
Why
Define infection during debridement and distinguish viable from necrotic bone.
Interpretation and limitations
Send multiple separately labelled specimens with clean instruments; superficial sinus swabs are less reliable and histology helps resolve contamination.
06
Full blood count, CRP, ESR, renal and liver profile
Why
Assess inflammation, baseline organ function and treatment safety.
Interpretation and limitations
CRP and ESR are useful trends but cannot localise infection or prove cure; normal leukocytes and absent fever are common in vertebral disease.
07
CT and nuclear imaging
Why
Define cortical destruction, guide biopsy or investigate when MRI is contraindicated or equivocal.
Interpretation and limitations
CT is better for bony detail and procedural planning; radionuclide or PET techniques require specialist interpretation and do not replace culture.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Malignancy

Primary or metastatic tumour causes focal pain, marrow signal change and pathological fracture and may require biopsy alongside culture.

Degenerative spinal disease

Mechanical back pain and Modic endplate change can resemble discitis, but systemic risk, inflammatory trend and microbiology alter probability.

Neuropathic arthropathy

Charcot destruction produces warmth, deformity and marrow oedema without primary infection, particularly in an insensate diabetic foot.

Inflammatory spondyloarthritis

Morning stiffness, sacroiliitis and multisystem inflammation can mimic spinal infection while following a different distribution and chronic course.

Bone infarction or stress injury

Ischaemia and repetitive-load fracture cause marrow oedema and pain without microbial growth and need exposure and imaging correlation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01NEUROLOGICALProtect cord and cauda equinaFirst stepSpinal infection is possible and a neurological deficit, sphincter symptom, deformity or instability is present.

1Use ABCDE, document motor power, sensation, reflexes, gait if safe, perianal sensation and bladder findings and repeat after any change.
2Obtain blood cultures and urgent whole-region MRI with sequences adequate to detect epidural abscess and compression.
3Contact spinal surgery and infection specialists immediately and begin local intravenous treatment after cultures without waiting for biopsy.
4Arrange decompression, drainage and stabilisation according to neural compression, abscess, instability and operative risk.

02STABLESecure microbiology before prolonged therapyBone or disc infection is likely but the patient has no sepsis, neurological compromise or rapidly destructive progression.

1Take blood cultures, MRI the involved region and review prior antibiotics, procedures, ulcers, implants, exposures and endocarditis risk.
2If blood cultures do not establish a credible organism, arrange image-guided or operative tissue for culture and histology before antibiotics when feasible.
3Request bacterial culture and add mycobacterial, fungal or molecular testing only when host and epidemiology support it.
4Start directed treatment after sampling and record the organism, bone anatomy, source-control plan and intended review milestones.

03SOURCE CONTROLRemove pus and non-viable boneAbscess, sequestrum, sinus, infected non-union, instability or ongoing bacteraemia indicates uncontrolled anatomy.

1Involve orthopaedic, spinal, podiatric, vascular or plastics services according to site and arrange drainage and debridement.
2Obtain multiple deep samples at surgery and determine whether all infected bone and any implant can be removed safely.
3Restore perfusion, cover exposed bone, manage pressure and stabilise mechanically so viable tissue can receive antimicrobial therapy and heal.
4Use operative findings to set antimicrobial duration and avoid assuming a clean-looking surface proves complete infected-bone resection.

04FOLLOWConfirm response and detect relapseDirected therapy and any source-control procedure are underway.

1Review pain, function, wound or sinus, neurological examination and inflammatory markers at defined intervals and check medicine toxicity.
2Switch from intravenous to a high-bioavailability active oral regimen only with specialist agreement, reliable absorption, stable anatomy and improving disease.
3Do not repeat MRI routinely in an improving patient because marrow signal can lag; image new deficit, instability, worsening pain or failed response.
4After treatment, provide a relapse route for recurrent focal pain, drainage, fever or neurological symptoms and continue rehabilitation and pressure prevention.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Covers likely invasive organisms while deep microbiology, implant status and source-control anatomy are established.

Empirical osteomyelitis intravenous regimen

Give the exact local site-, exposure-, allergy-, renal- and resistance-adjusted intravenous regimen after blood and deep cultures when the patient is stable enough for sampling.

Avoid empirical treatment before biopsy in stable culture-negative disease; seek microbiology advice for implants, ulcers, bites, water exposure, immune compromise or previous resistant isolates.

Provides high-dose bactericidal beta-lactam treatment for susceptible staphylococcal osteomyelitis after reliable cultures.

Flucloxacillin for susceptible staphylococci

Give 2 g intravenously every four to six hours when directed for methicillin-susceptible Staphylococcus aureus, using the exact local severe bone-infection interval.

Clarify immediate penicillin allergy, review hepatic and renal function and sodium exposure, and investigate persistent bacteraemia or undrained necrotic bone rather than only extending therapy.

Treats methicillin-resistant Gram-positive bone infection when culture or strong risk makes glycopeptide therapy necessary.

Vancomycin for MRSA bone infection

For MRSA osteomyelitis, use the local intravenous loading and maintenance schedule calculated from actual body weight, kidney function and serial measured serum exposure.

Monitor concentrations and kidney injury, document target exposure, avoid nephrotoxic combinations where possible and consider specialist alternatives when penetration, toxicity or susceptibility is problematic.

Allows completion of prolonged treatment outside hospital when source control, adherence and an active oral option are secure.

High-bioavailability oral step-down

Use an organism-active oral regimen and exact dose selected by infection specialists from susceptibility, bone penetration, interactions and patient absorption after initial stabilisation.

Do not substitute an arbitrary oral antibiotic; check food and cation interactions, QT risk, blood counts, liver and renal function and arrange laboratory and adherence monitoring.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Epidural abscess and paralysis

Purulent spinal extension compresses cord or cauda equina and can cause permanent weakness, sensory loss and sphincter dysfunction.

Pathological fracture and instability

Infected bone destruction weakens vertebra or long bone, producing deformity, mechanical pain and need for fixation.

Chronic draining sinus

Retained bone sequestrum or microbial biofilm sustains relapsing sinus drainage, secondary skin injury and repeated episodes of bloodstream infection.

Metastatic and systemic infection

Bacteraemia can seed endocardium, joints and other bones or progress to septic shock and multiorgan failure.

Treatment toxicity and relapse

Prolonged multi-drug therapy causes renal, hepatic, marrow and interaction harm, while incomplete source control permits recurrence.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat neurological examination promptly for any change in spinal pain, radicular symptoms, gait, sensation or bladder and bowel function.
Trend CRP or ESR with pain, wound healing and function rather than using a numerical target as proof of cure.
Review every blood, biopsy and operative culture and document contaminant judgments and directed antimicrobial changes.
Monitor renal, hepatic and haematological toxicity and drug concentrations or ECG where the selected prolonged regimen requires them.
Assess wound closure, sinus drainage, perfusion, pressure offloading, implant stability and fracture or spinal alignment.
Obtain clearance blood cultures in Staphylococcus aureus bacteraemia and complete endocarditis and metastatic-focus assessment.
Plan physiotherapy, mobility, analgesia, osteoporosis or fracture care and a clear route for suspected relapse after treatment ends.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Blood may replace biopsy

A credible bloodstream pathogen such as Staphylococcus aureus plus anatomically compatible MRI can establish cause without exposing a patient to unnecessary biopsy.

Stable patients offer a sampling window

Withholding antibiotics briefly before image-guided tissue sampling can materially improve yield when there is no sepsis or neurological threat.

MRI lags behind recovery

Bone marrow and endplate abnormalities may persist despite clinical cure, so routine early repeat imaging can falsely imply failure.

A sinus suggests chronic bone disease

Persistent drainage to skin often reflects sequestrum or implant biofilm that antibiotics alone are unlikely to eradicate.

Disc and vertebra behave together

Adult haematogenous spinal infection often crosses the endplate into the disc and adjacent vertebral body rather than remaining isolated.

S aureus is a systemic clue

Bone pain during Staphylococcus aureus bacteraemia should prompt metastatic-infection imaging and clearance cultures, not just local analgesia.

11Common pitfallsFrequent interpretation and management errors.

01
Do not start prolonged empirical antibiotics before deep sampling in a stable culture-negative patient when biopsy is feasible.
02
Do not delay treatment or decompression for biopsy when sepsis or neurological compromise is present.
03
Do not use a superficial sinus swab as the definitive bone culture.
04
Do not interpret a normal early radiograph or absence of fever as exclusion of vertebral osteomyelitis.
05
Do not repeat MRI solely because CRP remains mildly raised in a patient who is clinically improving.
06
Do not treat infected necrotic bone, epidural abscess or unstable spine with antibiotics alone when source control or stabilisation is required.