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BII > L14: Osteomyelitis > Flashcards

L14: Osteomyelitis Flashcards

1
Q

Routes of infection

A

Osteomyelitis = infection and inflammation of bone/bone marrow

Trauma: joint replacement, root canal treatment
Spreading from local area of infection: SSTI, diabetic ulcer
Haematogenous route: bacteria

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2
Q

Pathogenesis of osteomyelitis

A
  1. Bacteria infect bone = colonise and proliferate
  2. Leukocytes infiltrate and fight bacteria
  3. Inflammation and formation of pus
  4. Devascularisation, dead bone, abscess formation
  5. Bacteria can invade bone cells and evade immune response and drugs -> chronic osteomyelitis
  6. Bacteria can spread to joint -> septic arthritis
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3
Q

What area of the body is affected by osteomyelitis?

A

Adults: can be vertebral (rare in children), prosthetic joint infection, diabetic foot infection or post-traumatic infection (anywhere)

Children: mostly long bones (tibia, femur) and less common (humerus, fibula, calcaneus)

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4
Q

Risk groups for osteomyelitis

A
  • Diabetics with foot ulcers
  • Patients with infections following trauma, bone surgery, joint replacement, root canal
  • IV drug user
  • Patients with skin and soft tissue infections
  • Children with chicken pox infection (infrequent)
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5
Q

Causative pathogens of osteomyelitis

A
  • S. aureus most common (>80% of cases)
  • S. pyogenes (group A strep)
  • Group B strep (mainly infants at delivery)
  • Coagulase-negative staph
  • Haemophilus influenzae
  • Enterobacter species
  • Fungi
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6
Q

Diagnosis of osteomyelitis

A

Specific symptoms: pain/weakness of specific bone, redness, fever
Radiology: xray, CT
Bone biopsy: invasive, avoided if possible
Blood sample: high WBC count, bacteria present when associated with bacteraemia
MRI: to confirm diagnosis

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7
Q

Lab diagnostics - gram staining

A
  • Differentiation of cell wall type (gram negative = thin peptidoglycan layer, gram positive = much thicker)
  • Crystal violet stained (water soluble) taken up by both gram neg and pos then iodine to crystalise dye (trapped in gram positive)
  • Decolourise
  • Gram positive = violet (staph grape-like, strep chains)
  • Gram negative = wash out then counter stain with safranin (pink)
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8
Q

Lab diagnostics - catalase test

A
  • Staph positive and strep negative
  • Bacteria on glass slide with drop of hydrogen peroxide = oxygen bubbles with staph (conversion to oxygen and water)
  • Staph has catalase enzyme
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9
Q

Lab diagnostics - haemolysis and coagulase test

A

Haemolysis: on blood agar to distinguish alpha, beta and gamma strep

Coagulase test:

  • For staphylococci
  • Positive for S. aureus (clot forms - converts fibrinogen to fibrin)
  • Negative for coagulase negative staphylococci (CONS)
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10
Q

Staphylococci aureus

A
  • Opportunistic pathogen
  • Colonises anterior nares (20% of people are asymptomatic carriers), transient carriage on skin
  • Transmitted human to human
  • Source of infection from community, hospital
  • Diseases: SSTIs, invasive disease, toxic shock
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11
Q

S. aureus virulence factors

A

Adhesions (e.g. MSCRAMMS)
Immune evasion factors (neutralise parts of immune response)
Spreading factors:
- Staphylokinase (fibrinolysin) causes fibrinolysis (dissolves clots)
- Lipases
- DNAases (decrease viscosity of purulent material)
- Cytolysins (destroy epithelial cells)

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12
Q

Immune evasion factors

A
  • Cytolysins: (haemolysis, leukocidin) kills RBCs, leukocytes, tissue cells
  • Capsule: prevents opsonisation by C3b or Ig
  • Slime layer (biofilm): microbial community with bacteria attached to substrate embedded in a matrix of EC polymeric substances, prevents antibiotics and immune components getting to bacteria (e.g. catheter)
  • Protein A: binds IgG via Fc region, prevents opsonisation and phagocytosis
  • Cell bound coagulase (clumping factor): binds prothrombin and induces fibrin polymerisation, fibrin surrounds bacteria preventing opsonisation and phagocytosis
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13
Q

Superantigens

A
  • Family of heat-resistant secreted proteins (>20 members)
  • Non-specific, highly potent T cell mitogens
  • Trigger strong pro-inflammatory immune responses (binds to T cells and stimulates mitosis)
  • Synergistic effect with endotoxin
  • Systemic inflammation with tissue destruction, vascular leakage, multi-organ failure, toxic shock
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14
Q

Therapy for osteomyelitis

A

Prolonged antibiotic treatment (weeks-months)
90% of S. aureus resistant to penicillin, 30% resistant to methicillin (MRSA)
Vancomycin often last option for MRSA
Possibly surgical debridement

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15
Q

Beta-lactam antibiotics

A
  • Penicillins, cephalosporins, carbapenems
  • Only work against gram positive
  • Extended spectrum penicillins e.g. amoxycillin
  • Irreversible inhibition of transpeptidase (=penicillin binding protein)

Resistance:

  • By beta-lactamases e.g. penicillinase
  • Plasmid-encode enzymes transferred between bacterial strains and species
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16
Q

Beta-lactamase-resistant penicillin

A
  • Cannot be destroyed by beta-lactamase
  • e.g. oxacillin, flucloxacillin (not methicillin)
  • Or use penicillin with beta-lactamase inhibitor e.g. amoxycillin + clavulanic acid (gentamicin)
17
Q

Impetigo

A
  • Purulent infection of skin
  • Affects mostly young children (tropical climate, low hygiene)
  • Pus-filled vesicles on face and limbs
  • Rupture and drying out causing crusting
  • Prevent with good hygiene
  • Treat with washing with soap water, topical antibiotics e.g. mupirocin
18
Q

Folliculitis

A
  • Pyogenic infection of hair follicles
  • Base of follicle is raised, reddened, pus beneath epithelial surface
  • Furuncle = extension of folliculitis, boil (large painful, pus-filled, raised cutaneous nodules)
  • Carbuncles = progress of infection into deeper tissues, sometimes systemic symptoms
  • Treatment with antibiotic cream, drainage, oral antibiotics (flucloxacillin, augmentin)
19
Q

Ritter’s disease

A

= staphylococcal scalded skin syndrome

  • Abrupt onset of localised perioral erythema over entire body
  • Formation of large bullae, cutaneous blisters
  • Desquamation of epithelium
  • No leukocytes in blisters (toxigenic disease, exfoliative toxins - ET)
  • ET are proteases which cleave cell connecting proteins
  • Primarily neonates, young children
20
Q

Cellulitis

A
  • Rapidly spreading pyogenic inflammation of dermis/subcutaneous tissue
  • Often after mild traumas, burns, surgical incisions
  • Area tender, warm, erythematous, swollen, no sharp demarcation
  • Risk factors = old age, immunodeficiency, diabetes
  • Treatment by oral or IV antibiotics (augmentin, flucloxacillin)
21
Q

Acute infectious endocarditis

A
  • Infection of inner tissue of heart including valves
  • S. aureus most common cause for acute IE
  • Sub-acute IE can be caused by other organisms (e.g. streptococci)
22
Q

Bacterial pneumonia

A
  • Inflammation of lung by colonisation of alveoli
  • Aspiration of oral secretion or by hematogenous spread
  • Consolidation and abscess formation in lung
  • Necrotising pneumonia is severe and caused by S. aureus
  • S. aureus common cause but most common is strep pneumoniae
23
Q

Necrotising fasciitis

A
  • Infection in subcutaneous tissue and fascia, extensive and rapid spreading necrosis
  • Can develop after wound infection
  • Deep tissue infection supported by spreading factors, often linked with bacteraemia and toxic shock syndrome
  • Treatment: IV antibiotic (flucloxacillin, clindamycin), surgical debridement
24
Q

Toxic shock syndrome

A

Menstrual TSS from S. aureus only
Non-menstrual TSS from superantigens, bacteria enter through wounds/small cuts, systemic inflammation, high mortality

Therapy: IV antibiotics, supportive

BII (41 decks)

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