Lecture 15: Osteomyletitis Flashcards
Pathogenesis of osteomyletitis?
- Bacteria infect bone
- Leukocytes infiltrate 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
Risk groups for osteomyletitis?
- Diabetics with foot ulcers
- Patients with infections following trauma, bone surgery, joint replacement
- Root canal treatment
- Patients with skin and soft tissue infections
- Children with chicken pox infection (infrequent)
Pathogens causing osteomyletitis?
- Staph aureus (most common cause 80%)
- Strep pyogenes
- group B strep
- Coagulase negative staphlococci
- Hemophilus influenzae
- Enterobacter spp.
Diagnosis?
- Radiology
- Bone biopsy
- Blood sample
Staph aureus
- Oppoturnistic (doesnt always cause infection) 20% asymptomatic carriers with it in anterior nares
- Human - human transmission
- Causes SSTI, toxic shock, invasive disease and more
- major hospital aquired infection
How can S. areus cause infection?
- Break in skin
- Hair follicles
3 general types of virulence factors?
- Adhesins
- Immune evasion factors
- Spreading factors
Staph spreading factors?
- Staphlokinase: causes fibrinolysis
- Lipases
- DNases
- Cytolysins: destroy epithelial cells
Immune evasion factors? (5)
- Cytolysins
- Capsule (prevents opsonisation with C3b or Ig and phagocytosis
- Slime laye, Extracellular polysacharide
- Protein A: binds IgG in wrong orientation
- Cell bound coagulase: clumping factor (camo)
What are superantigens?
- Family of heat-resistant proteins that are highly potent T cell mitogens
- This triggers massive ammounts of pro-inflam cytokines which creates “noise”
- Synergustic effect with endotoxin
- systemic inflammation with tissue destruction, vascular leakage, multiorgan failure, toxic shock
Therapy for staph aureus infection?
- Methicillin however 30% MRSA
- Vancomycin last option for MRSA
- possible surgical debridement
How is staph aureus resistant to penicillin (beta-lactam antibiotics)?
-Beta-lactamases that break down the antibiotics e.g penicillinase, cephlasporinase, carbapenemase
What to do about beta-lactamases?
- Methicillin (derivitive from penicillin) not really used though as toxic
- Clinical use Oxacillin, flucloxacillin … these cant be destroyed
- OR can combine penicillin with beta -lactamase inhibitor OR a penicllin with b-lactamase inhibitor e.g amoxycillin + clavulanic acid= AUGMENTIN
Other common staph aureus infections?
- Impetigo/pyoderma: prevent with good hygiene, treat with soap water, topical antibiotics/ointments (mupirocin)
- Folliculitis, can lead to a boil (furuncle) leading to a carbuncle which ca leads to systemic spread. Treat with antibiotic creams , flucloxacillin, augmentin
- Cellulitis: dermis/subcutaneous tissue. Area tender warm, eryhtematous, no sharp demarcation
- Septic arthitis, IV antibiotics, analgesia, aspiration
- Acute infectious endocarditis. Chronic or subacute streptococci
- Bacterial pneumonia called necrotizing, staph pnemuoniae more common
Staphyloccal scalded skin syndrome
Affects neonates, formation of large cutaneous blisters due to exfoliative toxins.
Toxic shock syndrome
Caused by superantigen producing strains
Menstrual TSS: TSST (only one that can penetrate mucosal barrier) due to prolonged use of expandable tampon
Non-menstrual: Growth of TSS strain in wound. Toxins are released in blood causing systemic disease with fever, hypotension etc
