Lecture 15: Osteomyletitis

Question 1

Pathogenesis of osteomyletitis?

Answer 1

• 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

Question 2

Risk groups for osteomyletitis?

Answer 2

• 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)

Question 3

Pathogens causing osteomyletitis?

Answer 3

• Staph aureus (most common cause 80%)
• Strep pyogenes
• group B strep
• Coagulase negative staphlococci
• Hemophilus influenzae
• Enterobacter spp.

Question 4

Diagnosis?

Answer 4

• Radiology
• Bone biopsy
• Blood sample

Question 5

Staph aureus

Answer 5

• 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

Question 6

How can S. areus cause infection?

Answer 6

• Break in skin

- Hair follicles

Question 7

3 general types of virulence factors?

Answer 7

• Adhesins
• Immune evasion factors
• Spreading factors

Question 8

Staph spreading factors?

Answer 8

• Staphlokinase: causes fibrinolysis
• Lipases
• DNases
• Cytolysins: destroy epithelial cells

Question 9

Immune evasion factors? (5)

Answer 9

• 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)

Question 10

What are superantigens?

Answer 10

• 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

Question 11

Therapy for staph aureus infection?

Answer 11

• Methicillin however 30% MRSA
• Vancomycin last option for MRSA
• possible surgical debridement

Question 12

How is staph aureus resistant to penicillin (beta-lactam antibiotics)?

Answer 12

-Beta-lactamases that break down the antibiotics e.g penicillinase, cephlasporinase, carbapenemase

Question 13

What to do about beta-lactamases?

Answer 13

• 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

Question 14

Other common staph aureus infections?

Answer 14

• 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

Question 15

Staphyloccal scalded skin syndrome

Answer 15

Affects neonates, formation of large cutaneous blisters due to exfoliative toxins.

Question 16

Toxic shock syndrome

Answer 16

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