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.
| Feature | Osteomyelitis | Septic arthritis | Pott spine |
|---|---|---|---|
| Site | Metaphysis of long bones in children; vertebrae in adults | Knee most common, then hip, shoulder, ankle | Thoracolumbar junction most commonly |
| Commonest organism | *Staphylococcus aureus* | *Staphylococcus aureus* | *Mycobacterium tuberculosis* |
| First test | Plain X-ray (late), then MRI | Arthrocentesis with synovial fluid analysis | X-ray, then MRI; tissue biopsy for diagnosis |
| Emergency? | Acute: needs urgent antibiotics | Yes — orthopaedic emergency | Slow; neurological deficit is the urgent problem |
| Treatment mainstay | Debridement plus prolonged antibiotics | Joint drainage plus antibiotics | Anti-TB drugs; surgery for deformity, deficit or abscess |
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.
| Route | Who | Notes |
|---|---|---|
| Haematogenous | More frequent in children; long bones | In adults it most often affects the vertebrae |
| Contiguous spread | Young adults after trauma and surgery; older adults with pressure ulcers or infected joint prostheses | Diabetic foot: poor blood supply plus neuropathy; sacral, heel and buttock pressure ulcers (often polymicrobial) |
| Direct inoculation | Open fractures, bone surgery, orthopaedic hardware | Polymicrobial 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 | Chronic | |
|---|---|---|
| Defining feature | Before sequestrum forms (usually within 2 weeks) | Necrotic bone and sequestra present |
| Histology | Organisms, congested or thrombosed vessels, neutrophils | Necrotic bone, mononuclear cells, granulation and fibrous tissue, sinus tracts |
| Symptoms | Local erythema, warmth, swelling, fever | Longer than 2 weeks; fever less common; non-healing ulcer or discharging sinus |

- 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.
| Setting | Organism |
|---|---|
| Sickle cell disease | *Salmonella* and S. aureus |
| Spinal infection | Mycobacterium tuberculosis; Brucella and Salmonella |
| Bite wounds | Pasteurella multocida (animal) or Eikenella corrodens (human) |
| HIV-related | Bartonella henselae |
| Traumatic inoculation | Actinomyces, Sporothrix; Pseudomonas is typical of puncture wounds |
| Immunocompromised | Candida, Aspergillus, Cryptococcus, nontuberculous mycobacteria |
| Diabetic foot / pressure ulcer | Polymicrobial: 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.
| Modality | Role / timing |
|---|---|
| Plain X-ray | First 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 |
| MRI | Highest combined sensitivity (78–90%) and specificity (60–90%); detects early infection within 3–5 days; high negative predictive value |
| CT | Better for cortical destruction, gas, sinus tracts; superior to MRI for necrotic bone fragments (sequestra) |
| Bone scintigraphy | High 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.
| Situation | Regimen |
|---|---|
| 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.
| Group | Organism |
|---|---|
| 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 |
| Neonates | Group 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 disease | Salmonella species |
| Injection drug use | Sternoclavicular and sacroiliac joints; Serratia, Pseudomonas |
| Puncture wound / trauma | Pseudomonas aeruginosa |
| Prosthetic joint | Early (<3 months): staphylococci; delayed (3–24 months): gram-negatives and coagulase-negative staphylococci; late: haematogenous |
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.
| Step | Detail |
|---|---|
| Aspirate first | Obtain joint fluid and cultures before starting antibiotics |
| Empiric antibiotics | Anti-staphylococcal cover for all groups (nafcillin, oxacillin or vancomycin if MRSA suspected) |
| Drain the joint | Arthrotomy, arthroscopy or repeated daily needle aspiration |
| Duration | Non-gonococcal: IV for about 2 weeks then oral for 1–2 weeks (3–4 weeks total); 4–6 weeks for Pseudomonas |
| Gonococcal | Ceftriaxone, continued 24–48 h after improvement, then oral |
| No improvement in 5–6 days | Re-aspirate; consider Lyme disease, fungi, reactive arthritis, and image for osteomyelitis |
| Prosthetic joint | Often 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.

How is Pott spine diagnosed and treated, and how is it told from pyogenic spondylitis?
| Modality | Findings |
|---|---|
| X-ray | Often normal early; later reduced endplate density, loss of vertebral height, disc-space narrowing, bone destruction; fusiform prevertebral abscess |
| CT | Earlier 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 |
| Feature | TB spondylitis | Pyogenic spondylitis |
|---|---|---|
| Disc | Disc often preserved early (subligamentous spread) | Disc abnormalities seen more often on MRI |
| Abscess wall | Thin-walled | Thick-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.