Lecture 14: Osteomyelitis Flashcards
What is osteomyelitis? Route of infection?
Infection and inflammation of the bone or bone marrow
- Trauma (joint replacement, root canal treatment etc)
- Spreading from local area of infection (eg SSTI, Diabetic ulcer)
- Hematogenous route (bacteremia)
Pathogenesis of osteomyelitis?
- Bacteria infect bone (colonise and proliferate)
- Leukocytes infiltrate infected site and fight bacteria
- Inflammation and formation of pus
- Devascularisation, dead bone, abscess (pus filled vesicles)
- Bacteria might invade bone cells and evade the immune response and drugs (possible chronic osteomyelitis)
- Bacteria might spread to joint as it normally occurs at the end of long bones (septic arthritis)
Risk groups for Osteomyelitis?
- Diabetics with foot ulcers
- Patients with infections following trauma, bone surgery, joint replacement
- IV drug users
- Root canal treatment
- Patients with SSTIs
- Children with chicken pox (very uncommon)
Pathogens causing Osteomyelitis?
Staphyloccus aureus: most common cause in upto 80% of childhood cases
- Streptococcus pyogenes* (group A streptococcus)
- Group B Streptococcus* (mainly in infants)
- Coagulase-negative staphylococci*
- Hemophilius influenzae*
- Enterobacter spp*
- Some fungi (far less common)*
Diagnosis of osteoyelitis?
Diagnosis is complex but:
- Symptoms like pain/weakness of specific bones, redness, fever
- Blood samples: high WBC, bacteria present (if associated with bacteremia)
- Radiology (X-ray or CT) not overly sensitive and moderately specific
- MRI used to confirm diagnosis or Bone biospsy (highly invasive)
Gram staining?
Staphylococcus aureus habitat, transmission, source of infection, diseases?
Habitat: Anterior nares (≈20% of people are asymptomatic carriers), transient carriage on skin
Transmission: Human-to-human
Source of Infection: Community and hospital (one of the most common sosocomial infections)
Diseases: skin and soft tissue infection, invasive disease, toxic shock and more…
What makes Staphylococcus aureus virulent? A?
Adhesins: for binding to host tissue
- MSCRAMMS = microbial surface components recognising adhesive matrix molecules
What makes S aureus virulent? I?
Immune evasion factors: Neutralise certain parts of the immune response
- cytolysins/hemolysins/leukocidin lyse WBC/RBC, Capsule outside the cell wall prevents opsonisation with C3b or Ig,
- Slime layer- extracellular polysaccharide (EPS) form a biofilm where the inner bacteria can’t be reached,
- Protein A binds IgG in wrong orientation preventing opsonisation and phagocytosis
- Cell bound Coagulase binds prothrombin and induces fibrin polymerisation, fibrin deposition on cell surface prevents opsonisation and phagocytosis
What makes S aureus virulent? S?
Spreading Factors: allow bacteria to spread from local infection into deeper tissue or blood.
- Staphylokinase causes fibrinolysis dissolving clots,
- lipases,
- DNAses hydrolyse DNA decreasing viscosity of purulent material,
- Cytolysins destroy epithelail cells)
What are superantigens?
- A family of heat-resistant secreted proteins that are non-specific, highly potent T cell mitogens
- They trigger strong pro-inflammatory immun responses
- Synergistically effect with endotoxins
- systemic inflammation with tissue destruction, vascular leakage, multiorgan failure, toxic shock
Therapy options?
Prolonged antibiotic treatment (weeks to months)
(NB: 90% of staph aureus are resistant to penicillin and 30% are MRSA with increasing resistance to others)
Vancomycin often used as last option for MRSA and if in rare cases the bacteria are resisitant then surgical removal of tissue can be used.
B-lactamase resistance?
Some bacteria are able to produce B-lactamase toxins that render some (B-lactam antibiotics) antibiotics useless. They can be specific such as (Penicillinase, cephalosporinase or carbapenemase) or more general broad spectrum B-lactamases.
BUT
We now have B-lactam resistant penicillins:
- Oxacillin and Flucloxacillin that can’t be destroyed by B-lactamase
- or penicillin combined with B-lactamase inhibitor (amoxicillin + clavulanic acid = augmentin)
Other diseases caused by S. aureus?
Impetigo - infection of the skin via direct contact, mostly young children in tropical climates. Rupture of pus-filled vesicles. (often a hygene issue) - also seen with GAS
Folliculitis - pyogenic infection of hair follicle
Furuncle (boil) - Extension of folliculitis, large reaised cutaneous nodules (pus-filled)
Carbuncle - coalescence of furuncles as they progress deeper into the skin. Possible systemic symptoms treated with antibiotic cream and oral fluoxacillin or augmentin
Cellulitis - pyogenic inflammation of dermis/subcutaneous tissue treated with oral or IV antibiotics (augmentin or fluoxacillin)
Septic arthritis - infection of the joint by hematogenous route or nearby soft tissue infection or osteomyelitis trauma. IV antibiotics, analgesia and aspiration of the joint required.
Necrotising fasciitis
Toxic shock syndrome - both menstrual and non-menstrual
