Osteomyelitis TP Flashcards
Route of infection
- Trauma (joint replacement, root canal treatment, etc)
- Spreading from local area of infection (e.g. SSTI, diabetic ulcer)
- Hematogenous route (bacteremia)
Risk factors
• Diabetics with foot ulcers
• Patients with infections following trauma, bone
surgery, joint replacement
• Root canal treatment
Pathogenesis
- Bacteria infect bone (colonise and proliferate)
- Leukocytes infiltrate infected site and fight
bacteria - Inflammation and formation of pus
- Devascularisation, dead bone, abscess
- Bacteria might invade bone cells and evade
immune response and drugs (possible chronic
osteomyelitis) - Bacteria might spread to joint (septic arthritis)
Pathogens
- Staphylococcus aureus (most common cause, ~80% of osteomyelitis cases in children and young adults )
- Streptococcus pyogenes (Group A Streptococcus)
- Group B Streptococcus (mainly in infants)
- Hemophilus influenzae
- Enterobacter spp.
Diagnosis (3)
- Radiology (X-ray, MRI, CT)
- Bone biopsy
- Blood sample (if associated with bacteremia)
Staph aureus
• 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 nosocomial infections)
• Diseases: skin and soft tissue infections,
invasive disease, toxic shock, etc
How does SA cause an infection
- crack in skin
- splinter
- hair
Virulent factors (3)
- Adhesins - binding/colonisation
- Immune evasion factors - neutralisation of immune response
- Spreading factors - proteases, DNAses, HAse
Spreading factors (4)
- Staphylokinase (fibrinolysin): causes fibrinolysis, dissolves fibrin clots
- Lipases: hydrolyse lipids
- DNases: hydrolyse DNA (released from dead leukocytes), decreases viscosity of purulent material
- Cytolysins: destroy epithelial cells!
Immune evasion factors (5)
- Cytolysins
e.g. hemolysin, leukocidin
kill erys, leukocytes, tissue cells - Capsule
thick layer outside the cell wall, prevents opsonisation and phagocytosis (=immune evasion) - Slime layer, extracellular polysaccharide (EPS)
• microbial community with bacteria attached to a substrate or interface or to each other, embedded in a matrix of extracellular polymeric substance!
• Immune evasion, antibiotic tolerance - Protein A:
binds IgG (except IgG3) in “wrong orientation” (via Fc region), prevents opsonisation and phagocytosis. - Cell bound coagulase (clumping factor)
binds prothrombin and induces fibrin polymerisation, fibrin deposition on cell surface prevents opsonisation and phagocytosis
Superantigens
- family of heat-resistant secreted proteins (>20 members)! - non-specific, highly potent T cell mitogens!
- trigger strong pro-inflammatory immune response (IL-1”, TNF-!,!
IFN-#)! - synergistic effect with endotoxin (LPS) !
- systemic inflammation with tissue destruction, vascular leakage, !
multiorgan failure, toxic shock!
Treatment/therapy
• Prolonged antibiotic treatment (weeks to months),e.g. PIC line, empirical treatment until organism is known
! Note: ~90% of S. aureus are resistant to penicillin
! ~30% of S. aureus are methicillin-resistant (MRSA)
! Increasing resistance to other antibiotics
! Vancomycin often used as last option for MRSA (not
for MSSA to avoid rise of vancomycin-resistance)
• possibly surgical debridement
beta lactam resistant penicillins
- oxacillin
- flucloxacillin
- methicillin (prototype)
OR
penicillin with betalactamase inhibitor
ie amoxicillin + clavulanic acid = augmentin
Other disease caused by SA (11)
- impetigo
- Folliculitis
- Furuncle
- Carbuncle
- Staphylococcal Scalded Skin Syndrome (Ritter’s disease)
- Cellulitis
- Septic arthritis
- Acute infectious endocarditis
- Bacterial Pneumonia
- Necrotising fasciitis (flesh-eating disease)
- Toxic Shock Syndrome!
