Orthopaedic Antibiotic Therapy

This topic is about using antibiotics to treat established orthopaedic infection - osteomyelitis, septic arthritis, and prosthetic joint or other implant infection. It is the opposite side of the coin to surgical prophylaxis: prophylaxis prevents infection in clean tissue before contamination, whereas here the infection is already present and the goal is to eradicate it.

Three ideas run through everything that follows and are the threads examiners pull on. First, antibiotics are an adjunct to surgery - dead bone and infected implants must be dealt with surgically, because no drug penetrates a sequestrum or a mature biofilm. Second, the right drug means an agent that covers the likely organism (usually Staphylococcus aureus) and actually reaches bone. Third, biofilm on implants changes the rules: it is the reason implant infection is so hard to clear, the reason rifampicin is added for susceptible staphylococci, and the reason an implant sometimes has to be removed.

To clear a bone or joint infection an antibiotic has to do three things: reach the infected tissue at an adequate concentration, remain active against the organism, and keep working in the hostile environment of infected bone (low oxygen, dead tissue, biofilm).

Why bone is a difficult place to treat:

• Poor blood supply: chronically infected, sclerotic bone and any dead fragment (a sequestrum) have little or no blood flow, so the drug simply cannot get there. This is the single biggest reason chronic osteomyelitis needs surgery.
• Biofilm: bacteria on implant surfaces and dead bone secrete a protective matrix. Inside it they grow slowly and tolerate antibiotic concentrations many times higher than would kill free-floating bacteria.
• Intracellular survival: Staphylococcus aureus can survive inside osteoblasts and other cells, providing a reservoir that ordinary antibiotics reach poorly.

Bone penetration of common agents:

Biofilm is the central concept in implant-associated infection. Within hours of contamination, bacteria attach to the implant surface and to dead bone and begin to secrete an extracellular matrix. The bacteria inside this biofilm are metabolically slow, physically shielded from antibiotics and immune cells, and can tolerate drug concentrations that would easily kill the same organism floating free. This is why a biofilm-coated implant usually cannot be sterilised by antibiotics alone and often has to be removed.

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Rifampicin is special because it penetrates biofilm and kills slow-growing, adherent staphylococci that other drugs miss. The catch is that staphylococci develop resistance to rifampicin very quickly if it is used on its own, so it is always combined with a partner drug (commonly a fluoroquinolone such as ciprofloxacin or levofloxacin). The classic indication is a stable, susceptible staphylococcal implant infection of short duration that is being managed with debridement and implant retention (DAIR).

Antibiotic therapy for infection touches every part of orthopaedic practice and the exam. In trauma, early antibiotics plus debridement halve the early infection rate after open fractures. In arthroplasty, prosthetic joint infection is a feared complication, and the decision to retain (with rifampicin) or remove the implant is a core viva. In paediatrics, acute haematogenous osteomyelitis and septic arthritis are emergencies where prompt, correctly chosen antibiotics after cultures can avoid surgery or growth disturbance. In the basic-science viva, the biofilm concept, bone penetration, and the rifampicin rule are classic asks. Across all of these the same principles apply: culture, source control, the right drug into bone, narrow to the organism, and a defined duration.

• Staphylococcus aureus is consistently reported as the commonest organism in osteomyelitis, septic arthritis, and prosthetic joint infection across global series, so empirical regimens everywhere are built around reliable anti-staphylococcal cover.
• Local resistance patterns drive empirical choice: where MRSA prevalence is high, empirical regimens add a glycopeptide (such as vancomycin) or another MRSA-active agent until cultures return, then narrow.
• The OVIVA trial has shifted international practice towards earlier oral switch for stable bone and joint infection, reducing prolonged intravenous lines and hospital stay while preserving cure rates.
• The rifampicin combination for stable staphylococcal implant infection, established by the Zimmerli foreign-body infection trial, is embedded in major prosthetic-joint-infection guidance (for example IDSA and European consensus statements) as the basis for the DAIR strategy.
• For open fractures, society guidance worldwide pairs early antibiotics with prompt irrigation, debridement and stabilisation, keeping antibiotic courses short and grade-appropriate rather than open-ended.