Bone and Joint Infections — Osteomyelitis, Septic Arthritis and Pott Spine (Tuberculous Spondylitis)

Written & medically reviewed by the Kinase Medical Team · Last reviewed

Quick Answer

Osteomyelitis is bone infection, usually Staphylococcus aureus, seeded in the metaphysis in children by blood-borne spread; MRI detects it earliest. Septic arthritis is an orthopaedic emergency: aspirate the joint (synovial fluid WBC above 50,000 with 90% neutrophils), then drain and give antibiotics. Pott spine is tuberculous spondylitis, commonest at the thoracolumbar junction.

What are the main bone and joint infections and how do they differ?

Three conditions dominate exam questions: osteomyelitis (infection of bone), septic arthritis (infection of a joint) and tuberculous spondylitis (Pott disease) (TB of the spine). All three can spread into each other — osteomyelitis can break into a joint, and a vertebral infection can produce paraspinal and psoas abscesses — so recognise the typical site, organism and imaging pattern of each.

Quick comparison
FeatureOsteomyelitisSeptic arthritisPott spine
SiteMetaphysis of long bones in children; vertebrae in adultsKnee most common, then hip, shoulder, ankleThoracolumbar junction most commonly
Commonest organism*Staphylococcus aureus**Staphylococcus aureus**Mycobacterium tuberculosis*
First testPlain X-ray (late), then MRIArthrocentesis with synovial fluid analysisX-ray, then MRI; tissue biopsy for diagnosis
Emergency?Acute: needs urgent antibioticsYes — orthopaedic emergencySlow; neurological deficit is the urgent problem
Treatment mainstayDebridement plus prolonged antibioticsJoint drainage plus antibioticsAnti-TB drugs; surgery for deformity, deficit or abscess
Osteomyelitis Bone Infection - Everything You Need To Know - Dr. Nabil EbraheimOrthopaedic professor's overview of osteomyelitis — causes, classification, imaging and treatment.Video: nabil ebraheim · 10:19 · Watch on YouTube · Loads from YouTube (privacy-enhanced mode) only when you press play.

How does osteomyelitis develop and how is it classified?

Healthy intact bone resists infection. It becomes vulnerable after a large inoculum from trauma, ischaemia or a foreign body, because exposed bone sites let bacteria bind. S. aureus expresses adhesins for bone matrix components (laminin, collagen, fibronectin, bone sialoglycoprotein) and can survive inside cells.

Routes of infection
RouteWhoNotes
HaematogenousMore frequent in children; long bonesIn adults it most often affects the vertebrae
Contiguous spreadYoung adults after trauma and surgery; older adults with pressure ulcers or infected joint prosthesesDiabetic foot: poor blood supply plus neuropathy; sacral, heel and buttock pressure ulcers (often polymicrobial)
Direct inoculationOpen fractures, bone surgery, orthopaedic hardwarePolymicrobial or monomicrobial

In long bones the metaphysis is the usual site of haematogenous infection: it is well perfused, has few functioning phagocytes, and slowing of blood flow in the vascular loops of the metaphysis lets microbes lodge. Phagocytes release enzymes that lyse bone, forming pus and raising intramedullary pressure; the exudate can then burst through the cortex into the subperiosteal space.

Acute vs chronic osteomyelitis (histological definition)
AcuteChronic
Defining featureBefore sequestrum forms (usually within 2 weeks)Necrotic bone and sequestra present
HistologyOrganisms, congested or thrombosed vessels, neutrophilsNecrotic bone, mononuclear cells, granulation and fibrous tissue, sinus tracts
SymptomsLocal erythema, warmth, swelling, feverLonger than 2 weeks; fever less common; non-healing ulcer or discharging sinus
Historic photograph on yellowed card of five long, jagged pieces of dead bone standing upright against a dark background; the handwriting beneath reads 'Sequestra, osteomyelitis'. The bone fragments have rough, pitted, irregular surfaces.
Sequestra — fragments of dead bone separated from living bone — from chronic osteomyelitis. Necrotic bone is the histological hallmark of the chronic form.Image: Otis Historical Archives, National Museum of Health & Medicine, CC BY 2.0
  • Lew and Waldvogel classification: acute vs chronic, and haematogenous vs contiguous (contiguous further divided by presence of vascular insufficiency).
  • Cierny and Mader classification guides management: anatomic stage — 1 medullary, 2 superficial, 3 localised, 4 diffuse — plus host class (A normal, B compromised systemically or locally, C when treatment is worse than the disease).
  • Vertebral osteomyelitis is usually haematogenous and involves two adjacent vertebral endplates because segmental arteries supply adjacent endplates; Batson's venous plexus explains spread from a urinary focus in older men.

Which organisms cause osteomyelitis in different settings?

*Staphylococcus aureus* is the most common cause of acute and chronic haematogenous osteomyelitis in both adults and children, and MRSA now accounts for over one-third of staphylococcal isolates in some studies. Other organisms depend on the setting.

Organism by clinical setting
SettingOrganism
Sickle cell disease*Salmonella* and S. aureus
Spinal infectionMycobacterium tuberculosis; Brucella and Salmonella
Bite woundsPasteurella multocida (animal) or Eikenella corrodens (human)
HIV-relatedBartonella henselae
Traumatic inoculationActinomyces, Sporothrix; Pseudomonas is typical of puncture wounds
ImmunocompromisedCandida, Aspergillus, Cryptococcus, nontuberculous mycobacteria
Diabetic foot / pressure ulcerPolymicrobial: skin and gut flora, gram-negative bacilli, anaerobes

How is osteomyelitis diagnosed and treated?

ESR and CRP are usually raised but non-specific; CRP is useful for monitoring response. Blood cultures may be positive, especially in haematogenous vertebral, clavicular or pubic disease. Bone biopsy (open preferred) gives the histological diagnosis, the organism and its sensitivities; superficial wound or sinus-tract cultures correlate poorly with bone cultures.

Imaging in osteomyelitis
ModalityRole / timing
Plain X-rayFirst test, but changes lag by about 14 days; lytic lesions show only after 50–75% of bone matrix is lost; shows soft-tissue swelling, osteolysis, periosteal reaction
MRIHighest combined sensitivity (78–90%) and specificity (60–90%); detects early infection within 3–5 days; high negative predictive value
CTBetter for cortical destruction, gas, sinus tracts; superior to MRI for necrotic bone fragments (sequestra)
Bone scintigraphyHigh sensitivity, poor specificity; useful when metal hardware limits MRI

Treatment has two pillars: surgical containment (debridement of all diseased bone, because antibiotics penetrate poorly into abscesses and dead bone) and prolonged antibiotics. Adults usually receive 4 to 6 weeks of parenteral therapy; a shorter course is acceptable when infected bone is completely removed with clean margins. Revascularise an ischaemic limb and control diabetes where relevant; hyperbaric oxygen is not routine.

Antibiotic choices quoted by StatPearls (adult doses)
SituationRegimen
Empiric (broad, covers MRSA)Vancomycin 15 mg/kg IV every 12 h plus ceftriaxone 2 g IV daily, or a beta-lactam/beta-lactamase inhibitor such as piperacillin-tazobactam
Penicillin-sensitive *S. aureus*Penicillin G 4 million units every 6 h
Penicillin-resistant (MSSA)Nafcillin 2 g IV every 4 h; alternatives include cefazolin, clindamycin or vancomycin

What is septic arthritis and which organisms cause it?

Septic arthritis is joint inflammation from infection, usually bacterial. It is classically monoarticular in a large joint, presents with acute pain, swelling, fever and refusal to move the joint, and is an orthopaedic emergency because inflammatory cytokines and proteases can rapidly destroy the joint. The knee is the commonest joint in adults, followed by hip, shoulder and ankle. The synovium is highly vascular and has no limiting basement membrane, so it is easily seeded by blood-borne bacteria; contiguous spread from adjacent osteomyelitis is also possible.

Organisms by age and risk group
GroupOrganism
Any age (overall)*Staphylococcus aureus* is the commonest bacterial pathogen in children and adults
Children under 2–3 years*Kingella kingae* — commonest gram-negative cause
NeonatesGroup B Streptococcus, S. aureus, Neisseria gonorrhoeae, gram-negative bacilli
Sexually active young adults*Neisseria gonorrhoeae* — often involves several joints; culture other sites as synovial fluid grows it poorly
Sickle cell diseaseSalmonella species
Injection drug useSternoclavicular and sacroiliac joints; Serratia, Pseudomonas
Puncture wound / traumaPseudomonas aeruginosa
Prosthetic jointEarly (<3 months): staphylococci; delayed (3–24 months): gram-negatives and coagulase-negative staphylococci; late: haematogenous
Understanding Septic ArthritisShort explainer on septic arthritis — causes, presentation, synovial fluid analysis and treatment.Video: Zero To Finals · 7:21 · Watch on YouTube · Loads from YouTube (privacy-enhanced mode) only when you press play.

Epidemiology: incidence 2–6 per 100,000 population. In children the peak is at 2–3 years with a male predominance (2:1). Adult risk factors include age over 80, diabetes, rheumatoid arthritis, recent joint surgery, joint prosthesis and previous intra-articular injections. In-hospital mortality is quoted at 7–15%, and about one-third of patients have lasting morbidity.

How is septic arthritis diagnosed and treated?

The most useful test is arthrocentesis with synovial fluid analysis (Gram stain, culture, crystals, cell count and differential). A synovial fluid WBC count above 50,000 with 90% neutrophils suggests a bacterial cause, and identifying an organism confirms the diagnosis. Take blood cultures (two sets) before antibiotics. A normal plain X-ray does not exclude septic arthritis; ultrasound identifies effusions and guides aspiration, and MRI detects early fluid and soft-tissue or bone involvement.

Management of septic arthritis
StepDetail
Aspirate firstObtain joint fluid and cultures before starting antibiotics
Empiric antibioticsAnti-staphylococcal cover for all groups (nafcillin, oxacillin or vancomycin if MRSA suspected)
Drain the jointArthrotomy, arthroscopy or repeated daily needle aspiration
DurationNon-gonococcal: IV for about 2 weeks then oral for 1–2 weeks (3–4 weeks total); 4–6 weeks for Pseudomonas
GonococcalCeftriaxone, continued 24–48 h after improvement, then oral
No improvement in 5–6 daysRe-aspirate; consider Lyme disease, fungi, reactive arthritis, and image for osteomyelitis
Prosthetic jointOften needs aggressive debridement or removal of the prosthesis

What is Pott spine (tuberculous spondylitis)?

Pott disease, named after Percivall Pott (1779), is tuberculosis of the spine. TB spondylitis is the most common form of osteoarticular tuberculosis (about 50–70% of osteoarticular TB) and children account for about half of cases. The organism reaches the vertebrae from a lung focus through the rich vertebral blood supply, through paraaortic lymphatics, or via the paravertebral venous plexus from genitourinary TB.

  • Site: the thoracolumbar junction most commonly, then lumbar, and less often cervical vertebrae.
  • Pathology: the paradiscal subchondral bone is involved first; the bony cortex and later the intervertebral disc are destroyed, producing anterior column collapse, wedging and a gibbus (sharp angular kyphosis).
  • Spread: subligamentous, with a paravertebral, psoas or lumbar paraspinous abscess that may point in the groin, thigh or gluteal region; cervical disease may form a retropharyngeal abscess.
  • Presentation: chronic local back pain and tenderness for months to years; fever and weight loss are uncommon (20–30%); paraplegia is present at presentation in 20–75% of patients.
Photograph of a bony specimen of the thoracic spine against a blue cloth. Several vertebral bodies at the top of the specimen have collapsed and fused into a sharply angled forward curve, while the lower vertebrae remain normal with a visible intervertebral disc space.
Thoracic spine specimen with collapsed vertebrae from tuberculosis: destruction of the vertebral bodies produces the forward angulation (kyphosis or gibbus) of Pott disease.Image: Otis Historical Archives, National Museum of Health & Medicine, CC BY 2.0

How is Pott spine diagnosed and treated, and how is it told from pyogenic spondylitis?

Imaging features of TB spondylitis
ModalityFindings
X-rayOften normal early; later reduced endplate density, loss of vertebral height, disc-space narrowing, bone destruction; fusiform prevertebral abscess
CTEarlier detection; calcification within a paraspinous abscess suggests TB; CT-guided biopsy
MRI (most sensitive)Two or more vertebral bodies, skip lesions, epidural extension, paravertebral collection, subligamentous spread with initial disc preservation, thin-walled paraspinous abscess, collapse and kyphosis
TB vs pyogenic spondylitis (differential noted in the source)
FeatureTB spondylitisPyogenic spondylitis
DiscDisc often preserved early (subligamentous spread)Disc abnormalities seen more often on MRI
Abscess wallThin-walledThick-walled abscesses common

A definitive diagnosis needs tissue: culture or a molecular probe positive for the organism. Histology may show epithelioid granulomas, lymphocytes and multinucleated giant cells; acid-fast smears are positive in fewer than 50%, so the diagnosis often rests on imaging, histology and high clinical suspicion.

Treatment: all patients receive anti-TB chemotherapy — an intensive phase of 2 months with isoniazid, rifampicin, pyrazinamide and ethambutol, then a continuation phase of isoniazid and rifampicin for 4 to 16 months (duration varies because large trials are lacking). Surgery is used for intractable pain, nerve compression, kyphosis correction, spinal instability, large abscesses or failure of medical therapy. Prognosis is excellent when treatment starts before vertebral collapse or severe neurological deficit. See also anti-tubercular drugs and the NTEP regimens.

What are the high-yield exam points for bone and joint infections?

  • *S. aureus* is the commonest cause of osteomyelitis and septic arthritis; Salmonella in sickle cell disease; *Kingella kingae* in children under 2–3 years; gonococcus in sexually active young adults.
  • Haematogenous osteomyelitis begins in the metaphysis of long bones in children; in adults the vertebrae are most often affected.
  • Sequestrum (dead bone), involucrum and cloaca are the imaging features of chronic osteomyelitis; necrotic bone and sinus tracts are its histological hallmark.
  • X-ray changes lag by ~14 days; MRI detects disease in 3–5 days; CT best shows sequestra.
  • Septic arthritis: aspirate, then drain and treat; synovial WBC >50,000, 90% neutrophils.
  • Pott spine: thoracolumbar junction, paradiscal, anterior collapse, gibbus, thin-walled abscess, 2 months HRZE then HR.
  • Late-onset paraplegia of Pott disease results from severe deformity long after infection has healed.

Frequently asked questions

What is the most common organism in osteomyelitis?
Staphylococcus aureus is the most common cause of acute and chronic haematogenous osteomyelitis in both adults and children, and MRSA is increasingly isolated. Salmonella is associated with sickle cell disease, Pseudomonas with puncture wounds, and Mycobacterium tuberculosis, Brucella and Salmonella with spinal infection.
Why does haematogenous osteomyelitis affect the metaphysis in children?
The metaphysis is well perfused but has few functioning phagocytes, and blood flow slows in its vascular loops, which encourages bacteria to lodge. Phagocyte enzymes lyse bone, pus forms, and intramedullary pressure rises; the exudate can then rupture through the cortex into the subperiosteal space.
Which investigation detects osteomyelitis earliest?
MRI. It detects early bone infection within three to five days of onset and has the highest combined sensitivity and specificity, while plain X-ray changes lag by about two weeks. A negative MRI after at least a week of symptoms effectively excludes osteomyelitis. CT is better for sequestra and cortical destruction.
What synovial fluid findings suggest septic arthritis?
A synovial fluid white cell count above 50,000 per microlitre with about 90 percent neutrophils suggests a bacterial cause, and a positive Gram stain or culture confirms the diagnosis. Fluid is also examined for crystals. Blood cultures should be sent, and aspiration must precede antibiotic therapy whenever possible.
How is septic arthritis treated?
It needs both joint drainage (arthrotomy, arthroscopy or repeated aspiration) and antibiotics, started after aspiration with anti-staphylococcal cover and vancomycin if MRSA is likely. Non-gonococcal infection usually needs three to four weeks in total; gonococcal arthritis responds to ceftriaxone. Failure to improve in five to six days calls for re-aspiration and imaging.
Which part of the spine does Pott disease most often involve?
The thoracolumbar junction is most commonly involved, followed by the lumbar and then the cervical spine. Infection starts in the paradiscal bone, destroys the anterior column and disc, and produces collapse, gibbus deformity and paravertebral or psoas abscesses. Neurological deficit can occur early or years later because of kyphosis.
What is the drug regimen for tuberculous spondylitis?
All patients receive anti-TB chemotherapy: an intensive phase of two months with isoniazid, rifampicin, pyrazinamide and ethambutol, followed by a continuation phase of isoniazid and rifampicin for four to sixteen months. The exact duration varies because there are few randomised trials. Surgery is added for deformity, instability, large abscesses or neurological compromise.
How do you tell tuberculous from pyogenic spondylitis on MRI?
Tuberculous disease tends to involve two or more vertebrae with skip lesions, subligamentous spread with early disc preservation, and thin-walled paraspinous abscesses with calcification possible on CT. Pyogenic infection shows disc abnormalities more often on MRI and thick-walled abscesses. Tissue biopsy with culture is needed for a definitive diagnosis.

Sources

  1. StatPearls — Osteomyelitis (NCBI Bookshelf)
  2. StatPearls — Septic Arthritis (NCBI Bookshelf)
  3. StatPearls — Tuberculous Spondylitis (Pott Disease) (NCBI Bookshelf)

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