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Septic, pyogenic, and suppurative arthritis are the terms describing inflammation of the joint space caused by bacteria or fungi. Septic arthritis is more common in childhood than in any other period of life, and more than half of all cases are diagnosed in individuals younger than 20 years of age. Since pediatric septic arthritis usually has a hematogenous origin, the age distribution of patients with joint infection is markedly skewed, reflecting the increased attack rate of bacteremia in early childhood. In a series of 725 pediatric patients with joint infections, 52% of the children were younger than 2 years, 25% were aged 2–5 years, 15% were 6–10 years old, and the remaining 6% were aged 11–15 years.1

The estimated annual incidence among children in Western countries ranges between 2 and 10 cases per 100,000, whereas in the developing world the attack rate may be one order of magnitude higher.2,3 Since a significant fraction of suspected cases of septic arthritis remains bacteriologically unconfirmed, the true incidence of the disease is uncertain. Septic arthritis in childhood exhibits a clear male predominance, with a male-to-female ratio of 1.7:1.4 Several pediatric subpopulations are at increased risk for septic arthritis, as summarized in Table 51-1.

TABLE 51-1Conditions Associated with Increased Risk for Pediatric Septic Arthritis


The highly vascular synovial tissue lacks a limiting basement membrane, enabling easy access of circulating bacteria to the joint space during an episode of bacteremia. Occasionally, septic arthritis results by direct inoculation of bacteria into the joint by penetrating trauma, bites, intra-articular injections (particularly corticosteroids) or a surgical procedure. In neonates and young infants, bacteria may migrate from an adjacent focus of osteomyelitis into the joint, traversing capillaries that cross the metaphyseal growth plate. This capillary network recedes between 6 and 9 months of age, and in the older child only the metaphyses of the hip, shoulder, and ankle bones remain intracapsular.5

Once organisms have penetrated into the joint, the low fluid shear conditions facilitate microbial adherence. A variety of bacterial adhesins have been implicated in anchoring organisms to the synovial layer, which explains the virulence and tropism exhibited by bacteria such as Staphylococcus aureus, Streptococcus agalactiae (group B Streptococcus), and Nesisseria gonorrhoeae. These adherence-promoting molecules, termed microbial surface components recognizing adhesive matrix molecules, have been best studied in S. aureus and include, among others, fibrinogen-, fibronectin-, and elastin-binding proteins, a collagen receptor, and an adhesin with wide specificity. Mutations in the genes encoding for these proteins markedly reduce or abolish the capability of the organism to cause septic arthritis in ...

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