bone infections Flashcards
Mechanisms of infection of osteomyelitis
how do the organisms spread
haematogenous eg staph aureus endocarditis-> vertebral osteomyelitis (Adults)
children -> metaphysis of long bones affected
contiguous ; organism directly on bone via trauma or from adjacent focus of infection
USUALLY monomicrobial
Causative agents in children of acute osteomyelitis
Children Metaphysis of long bones • Staphylococcus aureus (commonest) • Streptococcus species – e.g. Strep. pyogenes (“group A strep”) or Strep. pneumoniae • Kingella kingae (children <5) • In sickle cell disease: nontyphoidal Salmonella
Causative agent in adults of acute osteomyelitis
Adults Mostly vertebrae • Staphylococcus aureus (commonest) • Mycobacterium tuberculosis endemic areas & immunocompromised neurological features, systemic upset infrequent • Brucella spp. (uncommon in Ireland/ UK)
What is the mech of action for contiguous method of spread for organisms in osteomyelitis
• Trauma
– Penetrating injury/ bites
– Contaminated open fracture
• Surgery
– Reconstruction of bone
– Prosthetic material e.g. intra-medullary nail
– Traumatic dental procedure
• Spread from adjacent skin/ soft tissue focus
– e.g. acute, from ear, sinus infection
– e.g. chronic, from pressure sore/ diabetic foot ulcer
Causative agents for contiguous osteomyelitis
May be monomicrobial or polymicrobial
• Staphylococcus aureus (commonest) e.g.
from adjacent cellulitis/ soft tissue infection
• Streptococci (Str. pneumoniae, group A strep)- more
common in children e.g. from ear or sinus infection
• Coagulase negative staphylococci e.g. after
insertion of metal to stabilise a fracture
• Polymicrobial with Gram negatives/anaerobes, e.g.
contaminated wound due to trauma
What are the causative agents of acute osteomyelitis in relation to age groups?
newborns <4 months= Staph aureus, group B strep , E coli
children (4 months to 4 years) = Staph aureus, Group A strep , strep pneumo, kingella kingae, H influenzae , Enterobacteriaceae
children, adolescents (>4 years to adult) - Staph aureus, Group A strep , H influenzae, Enterobacteriaceae
adults - staph aureus and occassionally enterobacteriaceae/strep
Pathogenesis of acute OM
• Bacteria invade bone
• Pressure within bone
increases due to
inflammation & pus
Pathogenesis of chronic OM
• Fluid reaches periosteum, elevates it & bone dies (dead necrotic bone= sequestrum) • Separated periosteum produces new bone = involucrum • Sinus tract forms
Mechanism of chronic OM
• Usually due to contiguous spread from pressure
sore/ diabetic foot ulcer
• Patients with poor mobility, multiple comorbidities
• Diabetes mellitus, peripheral vascular disease
• Non-acute presentation, usually present for some
time at diagnosis
Define chronic OM
• Usually polymicrobial (> 1 organism), e.g. S. aureus
plus Gram negative bacilli plus anaerobes- organisms
that colonise ulcers
• Staphylococcus aureus (>50% cases)
• Anaerobes (10-20%) including Bacteroides/
Actinomyces
• Gram negative bacilli, i.e. Pseudomonas aeruginosa,
E. coli, Klebsiella spp.
– Nosocomial infection
– Open wound/fracture
– May complicate trauma or surgery
– IVDU
Clinical features of OM
• General – fever – malaise – anorexia – myalgia more often seen in acute OM • Local – pain – tender – hot – swollen – restricted motion – pseudoparalysis – fistula – deformity more common in chronic OM
Differentiate acute vs chronic OM clinical features
Acute • Evolves over days/weeks • Fever, rigors, high WCC • Painful tender bone • No necrosis/ fistulae • In previously well patients • If untreated for ≥10 days (may be reflected by ongoing clinical features), get necrotic bone & chronic osteomyelitis can occur
Chronic • Evolves over months/years with lowgrade inflammation, dead bone (sequestrum) & fistulous tracts • Chronic pain • Patient systemically well • Usually co-morbidities • Often relapses despite apparently appropriate treatment
dx of OM non micro
• History & examination • Probe-to-bone test (chronic osteomyelitis associated with an ulcer) • Imaging, plain X-ray, may be normal, MRI, see bone oedema early, bone scan (nuclear) if MRI not possible • Blood tests (non-specific) –White cell count (elevated, neutrophilia) – Inflammatory markers • ESR, CRP • Histology on bone biopsy (in formalin) –Pathological (not microbiological) diagnosis
dx of OM micro
finding the causative agent
• Bone biopsy for culture & histology is the
gold standard
• In suspected chronic OM, hold antibiotics until
after biopsy being taken
• Biopsy of affected bone (not in formalin)
– Gram stain, culture & susceptibility testing
– Consider TB culture if chronic
• Molecular, 16S ribosomal RNA
• Blood cultures if acute OM +/- systemic
symptoms, e.g. fever
– Diagnose if the patient is bacteraemic
what is chronic osteomyelitis a./w
non healing ulcer w chronic discharge
