Osteomyelitis Flashcards
What could be the possible causes of a 2 day history of limp in a 10yr old who recently had chicken pox?
- Rheumatic fever: migratory polyarthritis, often carditis, associated with group A streptococcus infection X because don’t usually have pain at just one joint with this
- Septic arthritis: extremely painful with movement, purulent synovial fluid X guessing he didn’t have this upon joint aspiration
- Osteomyelitis: skin and soft tissue infections are common complications of chicken pox. Skeletal complication rare but very serious
What is osteomyelitis?
Infection and inflammation of the bone or the bone marrow
Route of infection
Trauma: joint replacement, root canal etc Spreading from local area of infection e.g. STI, diabetic ulcer Haematogenous routs (bacteria)
Pathogenesis
Bacteria infect bone (colonise and proliferate)
Leukocytes infiltrate infected site and fight bacteria
Inflammation and formation of pus
Devascularisation, dead bone, accesses
Bacteria might invade mine cells and evade response and drugs (possible chronic osteomyelitis)
Bacteria might spread to joint (septic arthritis)
Risk groups
diabetics with foot ulcers
Patients with infections following trauma, surgery, joint replacement
Root canal treatment
Patients with skin and soft tissue infections
Children with chicken pox (infrequent)
Pathogens
S. aureus most common, ~80% of osteomyelitis cases in children and young adults Strep. Pyogenes (group A) Group B strep Coagulase negative staplococci etc
Which parts of the body are more susceptible in older vs younger people?
Slightly higher risk factor for prosthetic joints whereas in children long bones are more susceptible
Diagnosis
Radiology (X-ray, MRI, CT)
Bone biopsy
Blood sample
Lab diagnosis
gram staining
Describe staphylococcus aureus
grape like
habitat = anterior nares (20% people asymptomatic carriers), transient carriage on skin
Transmission = human to human
Source of infection = community to hospital (one of the most common noscominal infections)
Diseases: skin and soft tissue infections, invasive disease, toxic shock and more
What makes bacteria virulent?
Virulent means “full of poison”
virulence factors
- Adhesions: for binding to host tissue (colonisation)
- Immune evasion factors: neutralise certain parts of the immune response
- Spreading factors: allow bacteria to spread form local infection into deeper tissue or blood (bacteria) e.g. proteases
What are some spreading factors viruses use?
Staphlokinase (fibrinolysis) causes fibrinolysis, dissolves fibrin clots
Lipases: hydrolyse lipids
DNAses: hydrolyse DNA (released from dead leukocytes), decreases viscosity of purulent material
Cytolysis: destroy epithelial cells
Immune evasion factors
Cytolysis (hemolysin, leukcydin = kill RBC’s, leukocytes, tissue cells)
Capsule: thick layer outside the cell wall prevents opsonisation with C3b or Ig and phagocytosis (immune evasion)
Slime layer, extracellular polysacchires (EPS) = microbial community with bacteria attached to a substrate or interface or to each other embedded in a extracellular polymeric substance. Prevents antibiotics and immune components reaching bacteria
e.g. biofilm sometimes found on indwelling catheter
What is protein A?
binds IgG (not Ig3) in wrong orientation (via Fc region) prevents opsonisation and phagocytosis (Fc receptors on phagocytes are unable to recognise IgG)
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 Tcell mitogens
trigger strong pro inflammatory immune responses (IL-1beta, TNFalphs etc
Synergistic effect with endotoxin (LPS)
Systemic inflammation with tissue destruction, vascular leakage, multi organ failure, toxic shock
Treatment
Prolonged antibiotics (weeks to months) e.g. PIC line, empirical treatment till organism known
relative percentages of resistant bacteria
90% of S. aureus resistant to penicillin
~30% of S.aureus are resistant to methicillin (MRSA)
Increasing resistance to other antibiotics
Vancomycin often used as last resort for MRSA (not for MSSA to avoid rise in vancomycin resistance)
Possible surgical debridement
Beta lactam antibiotics
penicillins, cephalosporins, carbapenenms
Penicillin works only against gram positives
extended spectrum penicillins (e.g. amoxicliins)
Irreversible inhibition of transpeptidase (PBP)
Resistance to betalactam antibiotics
beta lactamses are plasma encoded enzymes that can be transferred between bacterial strains and species
beta lactam reistant penicillins
beta lactamses are plasma encoded enzymes that can be transferred between bacterial strains and species
Beta lactam resistant peniciliins
prototype: methicliin
clinical use: oxacillin, flucloxacillin cannot be destroyed by beta lactase
OR
Penicillin combined with beta lactase inhibitor: amoxicillin + clavulanic acid = augmentin
Resistance to beta lactamase resistant penicillins
New PBP with low affinity for beta lactams
MRSA
* emergence of vancomycin resistant strains are still rare
Other important diseases caused by S. aureus
Impetigo Folliculitis Furuncle Carbuncle Cellulitis Staphlococcyl scalded skin syndrome (Ritters disease) Bacterial pneumonia Toxic shock syndrome Septic arthritis
