Basic bacterial structure
A typical bacterium may contain:
- cell membrane
- cell wall
- cytoplasm
- ribosomes
- chromosomal DNA
- plasmids
- surface structures such as pili or flagella in some species
Bacteria lack a membrane-bound nucleus.
Gram stain
The Gram stain differentiates bacteria according to cell-wall structure.
Sequence:
- crystal violet
- iodine
- decolourisation
- counterstain
Gram-positive organisms
- thick peptidoglycan layer
- retain the primary stain
Gram-negative organisms
- thinner peptidoglycan
- outer membrane containing lipopolysaccharide
- become counterstained after decolourisation
Antibiotic targets
Major mechanisms include:
- inhibition of cell-wall synthesis
- inhibition of protein synthesis
- disruption of nucleic-acid synthesis
- interference with metabolic pathways
- disruption of cell membrane function
Resistance mechanisms
Bacteria can resist antibiotics through:
- drug-inactivating enzymes
- altered drug targets
- reduced permeability
- active efflux
- bypass pathways
- biofilm formation
- acquisition of resistance genes on mobile genetic elements
MRSA
Methicillin-resistant Staphylococcus aureus commonly carries mecA or related resistance determinants encoding an altered penicillin-binding protein with reduced affinity for many beta-lactam antibiotics.
Biofilm
Biofilm is a structured community of microorganisms attached to a surface and embedded within an extracellular matrix.
Clinical importance in orthopaedics:
- reduced antibiotic penetration or susceptibility
- low metabolic activity of some organisms
- protection from host immune response
- persistence on implants
This is a major reason implant-associated infection behaves differently from uncomplicated soft-tissue infection.
Bacteria on an implant can adhere to the surface and form a biofilm. Within the biofilm, organisms exist in a protected community with altered metabolic activity and reduced susceptibility to host defence and antibiotics.
This explains why an antimicrobial that appears active against planktonic organisms may not eradicate an established implant-associated infection without adequate surgery.
Specimen principles in suspected orthopaedic infection
- obtain appropriate deep samples
- avoid relying on superficial swabs for deep implant infection
- collect multiple tissue specimens when indicated
- obtain cultures before antibiotics when clinically safe to do so
- interpret culture results in the clinical context
Antibiotic stewardship
Antibiotic choice should consider:
- likely organism
- local resistance pattern
- allergy
- renal and hepatic function
- tissue penetration
- culture results
- presence of an implant or biofilm
- need for surgical source control
Clinical principle
Antibiotics cannot compensate for inadequate debridement, retained necrotic tissue or an unstable infected construct. Orthopaedic infection treatment is a combined surgical and microbiological problem.
Organisms and orthopaedic infection
Orthopaedic infection ranges from acute soft-tissue infection to chronic biofilm-associated implant infection. Common organisms include staphylococci, but microbiology varies with:
- host
- anatomical site
- mechanism of contamination
- healthcare exposure
- open injury
- previous antibiotics
- local resistance patterns
Culture results must be interpreted in the clinical context rather than treated as isolated laboratory facts.
Specimen strategy
When deep infection is suspected:
- obtain multiple separate deep tissue samples
- use clean instruments for each sample where practical
- sample representative tissue rather than superficial drainage
- avoid swabs when better tissue specimens are available
- coordinate with microbiology for unusual organisms or prolonged culture where relevant
Antibiotics may be withheld before planned sampling in a stable patient if clinically appropriate, but sepsis or rapidly progressive infection requires prompt treatment.
Antimicrobial principles
Selection depends on:
- likely organism
- culture and sensitivity
- tissue penetration
- renal and hepatic function
- allergy
- drug interactions
- local resistance
- presence of implant or biofilm
- planned surgical strategy
Empirical therapy should be revised once reliable microbiology is available.
Surgical source control
Antibiotics do not substitute for:
- debridement of necrotic tissue
- drainage of pus
- removal of sequestra where necessary
- restoration of viable soft-tissue cover
- management of unstable or infected implants
In implant-associated infection, the feasibility of retention depends on factors including timing, implant stability, soft tissues, organism, host and ability to achieve a thorough debridement.
Prophylaxis
Surgical prophylaxis aims to achieve effective tissue concentrations at the time contamination is most likely. Timing relative to incision and repeat dosing in long procedures or major blood loss are therefore important.
Prophylaxis should complement, not replace:
- sterile technique
- skin preparation
- careful tissue handling
- appropriate operating environment
Resistance and stewardship
Excessive or poorly targeted antibiotic use promotes resistance and exposes patients to toxicity and complications. Orthopaedic surgeons should understand the indication, planned duration and review point for every antimicrobial course.
FRCS synthesis
When faced with infection, frame the answer around four questions:
- Is the diagnosis secure?
- What organism is present?
- What surgical source control is required?
- What targeted antimicrobial strategy supports that surgery?
That is stronger than simply naming a broad-spectrum antibiotic.