Clinical and molecular aspects of the pathogenesis of Staphylococcus aureus bone and joint infections

Abstract

Staphylococcus aureus is an important cause of bone and joint infections. In recent years, significant changes in the incidence of septic arthritis and osteomyelitis have occurred. Haematogenous osteomyelitis is now less common during childhood, but secondary spread of infection to bone or joint from a contiguous site in adults is increasing in incidence. Infection introduced at the time of surgery or arising by the haematogenous route is a significant complication of prosthetic joint implantation, and the effect of bone cement on local immune function may be important in this setting. Although S. epidermidis is a more common cause of prosthetic joint infection, S. aureus is more difficult to treat. S. aureus produces a number of extracellular and cellassociated factors, but it is unclear what role these have as virulence factors in vivo. Furthermore, it is difficult in animal models to simulate transient bacteraemia followed by non-fulminating septic arthritis or osteomyelitis, as occurs in the patient. Surface factors which may be important in pathogenesis include the cell wall (activates complement and stimulates cytokine release), capsular polysaccharide (promotes adhesion to host cell surfaces), collagen receptors and fibronectin-binding protein.Staphylococcal toxic shock syndrome toxin (TSST-1) and the enterotoxins are superantigens and have the potential to suppress plasma cell differentiation and antibody responsiveness. TSST-1-positive isolates have been shown to cause more severe joint infection in one animal model, but most other studies to date have focused on in-vitro rather than in-vivo effects. There is little evidence supporting a role for coagulase, lipase and the haemolysins in staphylococcal bone and joint infections. Despite the clinical importance of these infections, surprisingly little is known about pathogenesis at the cellular level. Future research should focus on the role of the host immune system in limiting spread of infection, and the expression of virulence factors in animal or other models incorporating isogenic mutant strains.

An Unusual Case Report of Two Bone Osteomyelitis With Long-Term Follow-up

“…An effusion of the subtalar joint may present with ankle joint swelling that is more prominent below the lateral malleolus, given the communicating lateral anatomy of the subtalar and ankle joints. 7 Computerized tomography of the foot and ankle further supports the hypothesis of subtalar sepsis by displaying adjacent boney lesions located in the inferior talus and superior calcaneus. Therefore, the original septic joint may have been the subtalar joint in isolation or in combination with the ankle joint.…”

“…This form is commonly monomicrobial, with staphylococcal organisms isolated most frequently. 7 The second type is direct extension osteomyelitis. It is usually polymicrobial in origin and seen more frequently in the general population.…”

Characterization of Staphylococcus caprae Clinical Isolates Involved in Human Bone and Joint Infections, Compared with Goat Mastitis Isolates

“…On the contrary, all S. caprae isolates except one had a lipase gene. The role of this enzyme in staphylococcal species pathogenicity remains unclear, but the lipase gene may be involved in pathogenesis, especially in S. aureus where reduction in biofilm formation is related to a deleted lipase-encoding gene (10,32).…”

Staphylococcus aureus expresses a cell surface protein that binds both IgG and β2-glycoprotein I

“…vitronectin and immunoglobulins (Cunningham et al, 1996). The binding of IgG is a common property among pathogenic Gram-positive cocci and the IgG-binding protein protein A (SpA; Uhlen et al, 1984) is one of the most studied surface proteins of S. aureus.…”

“…aureus strains export a number of potential virulence factors into the surroundings, e.g. alpha-, beta-, deltaand gamma-toxins, toxic shock syndrome toxin, enterotoxins, lipase, coagulase and proteases (Cunningham et al, 1996). The bacterium is also known to express adhesins which bind to host matrix and plasma proteins, e.g.…”