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Septic, pyogenic, and suppurative arthritis are the names given to the inflammation of the joint space caused by the presence of bacteria or fungi. Septic arthritis is more common in childhood than in any other period of human life and more than half of cases are diagnosed in individuals younger than 20 years of age. Since septic arthritis usually has a hematogenous origin, the age distribution of pediatric patients with joint infection is markedly skewed, reflecting the increased attack rate of bacteremia in early childhood. In a large series of 725 pediatric patients with joint infections compiled by Trujillo and Nelson, 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 Since a significant fraction of suspected cases of septic arthritis remains bacteriologically unconfirmed, the true incidence of the disease is uncertain. The estimate annual incidence of the disease in the general population ranges between 2 and 10 cases per 100,000.2 Several pediatric subpopulations are at increased risk for septic arthritis, as summarized in Table 48–1.
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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. Once organisms have penetrated into the joint, the low fluid shear conditions facilitate microbial adherence. Occasionally, septic arthritis results by direct inoculation of bacteria in 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 through 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.3
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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), Nesisseria gonorrhoeae, and Borrelia burgdorferi. 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 animal models.3
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Trauma may facilitate the entrance of circulating bacteria into the joint space caused by increased local vascularization, whereas high concentration of a diversity of protein fibers in the synovial fluid after ...