Etiology
Osteomyelitis may be caused from hematogenous spread, direct inoculation of microorganisms into bone, or from a contiguous focus of infection.[9] A trivial skin infection may be the source of bacteremia, or it may have emerged as the result of a more serious infection such as acute or subacute bacterial endocarditis. Intravenous drug misuse has been linked to hematogenous osteomyelitis involving the long bones or vertebrae.[10][11]
Worldwide, childhood acute hematogenous osteomyelitis and septic arthritis are common, with chronic disease following inadequate initial management.[12] Pediatric spondylodiscitis (infection involving the intervertebral disk and adjacent vertebrae) is rare and accounts for 1% to 2% of osteomyelitis in children.[12] In the developed world, bone infection is now mostly seen after injury or surgery (contiguous focus osteomyelitis) and is often implant-related.[1] The rising number of patients living longer with multiple comorbidities, and the increasing incidence of bone and joint surgery, have led to a higher proportion of osteomyelitis cases associated with contiguous focus infection.
The commonest organism causing osteomyelitis remains Staphylococcus aureus.[1] Streptococci, Enterobacteriaceae, and anaerobic bacteria are also implicated in acute osteomyelitis.[13]
Different groups of patients are more susceptible to different organisms; common microorganisms in acute hematogenous osteomyelitis are listed below by patient age:
Neonates (especially those with indwelling venous catheters):[9]
Group B streptococcus (Streptococcus agalactiae)
Aerobic gram-negative bacteria, especially Escherichia coli
Infants:[12]
S aureus
Group B streptococcus
Aerobic gram-negative bacilli (e.g., Escherichia coli)
Candida albicans.
Children 3 months up to 5 years:[9][12][14][15]
S aureus
Kingella kingae (increased incidence in children under 4 years)
Streptococcus pyogenes
Streptococcus pneumoniae
Haemophilus influenzae (in those not immunized).
Children >5 years:[12]
S aureus
Group A Streptococcus.
Adults:[1]
S aureus
Coagulase-negative staphylococci
Aerobic gram-negative bacteria
Anaerobic gram-positive Peptostreptococcus species.
Older adults:
Gram-negative bacilli.
Patients with intravascular devices:
S aureus
Candida species.
Patients who misuse intravenous drugs:[9]
S aureus
Pseudomonas aeruginosa
Candidaspecies
Patients with sickle cell disease; patients from developing countries:
S aureus
Salmonella species.
In endemic areas, Brucella, Burkholderia pseudomallei (melioidosis), and dimorphic fungal infections should be considered.[13]
Mycetoma is a chronic soft tissue infection of the extremities which can extend into contiguous bone and connective tissue.[9] It occurs most often in tropical and subtropical climates and may be characterized by the development of draining sinuses. Etiologic agents are derived from the soil and include Nocardia species, other aerobic actinomycetes and soil filamentous fungi.[9]
Pathophysiology
Bacteria that enter the bloodstream exist in a free-floating planktonic state. Most infections in orthopedics, including osteomyelitis, are caused by biofilm-forming bacteria. A biofilm is a highly structured community of bacterial cells that adopt a distinct phenotype, communicate through cell-to-cell signals, and adhere to an inert or living surface.
Planktonic bacteria express surface components called adhesins that bind to proteins found in the host tissues. Once attached, the bacteria produce a polysaccharide extracellular matrix. This forms a substrate in which colonies may develop, forming a biofilm.[16][17][18][19][20] Once sufficient numbers of organisms are present in the biofilm, a complex system of cell-to-cell signaling develops, known as quorum sensing. This controls the maturation and further development of the mature biofilm. It may also propagate the spread of infection by controlling separation of fragments of this biofilm and seeding to local sites. A proportion of the organisms in biofilm are able to enter a dormant state with minimal cellular division. In this state, antibiotics that act on cell division are ineffective.[21][22] Similarly the organisms are also protected to a degree from the host immune system within the glycocalyx. The sensitivity of a culture in the laboratory on an agar plate (in vitro) may bear no relationship to the ability of the same antibiotic to kill bacteria in a biofilm in dead tissue or in an implant (in vivo). In vitro biofilm models may be more representative. Staphylococcus aureus has been shown to express a number of virulence factors, and can invade living cells and survive inside osteoblasts.
Hematogenous osteomyelitis usually involves the metaphysis of long bones in children or the vertebral bodies in adults. In acute hematogenous osteomyelitis, the joint is usually spared, unless the metaphysis is intracapsular, as is found at the proximal radius, humerus, or femur. Septic arthritis of an adjacent joint may be an early complication of acute osteomyelitis in children.[23]
Classification
Cierny-Mader classification[2]
Three physiologic groups of patients (A, B, C):
A: people with no comorbidities that compromise outcome; able to withstand the stresses associated with surgery and antibiotic therapies
B: those with comorbidities that directly reduce the likelihood of wound healing, reduce the efficacy of drug treatment, or increase the risks of surgery
C: people who are so severely compromised that treatment has an unacceptable risk-benefit ratio, and therefore the treatment of their infection can be more harmful than the condition.
Four anatomic types (I to IV) based on the degree of bone involvement:
I: involves medullary and endosteal bone; mostly associated with hematogenous infection
II: superficial osteomyelitis from contiguous focus infection; often arises in the base of a varicose ulcer or from external trauma or a pressure sore
III: both medullary and cortical involvement; the osteomyelitis is limited to part of the circumference of the bone, leaving a healthy portion of the bone to maintain stability across the zone of infection
IV: diffuse involvement of the entire circumference of the bone.
Waldvogel classification system[3]
Acute: typically presents with symptoms that have a duration of a few days to weeks.
Chronic: more indolent and characterized by longstanding infection that occurs over months to years; sequestra or dead bone is usually present.
Nonhematogenous: may occur as a result of contiguous spread of infection to bone from adjacent soft tissues and joints or from a direct inoculation of infection into the bone as a result of trauma, bite wounds, or surgery; further classified by presence or absence of associated vascular insufficiency.
Hematogenous: caused by microorganisms that infect the bone in the setting of bacteremia.
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