Interaction of staphylococci with bone

被引:205
作者
Wright, John A. [1 ]
Nair, Sean P. [1 ]
机构
[1] UCL, UCL Eastman Dent Inst, Div Microbial Dis, London WC1X 8LD, England
关键词
Staphylococcus aureus; Small colony variants; Bone infection; Osteoblasts; Osteoclasts; Signalling; TUMOR-NECROSIS-FACTOR; SMALL-COLONY VARIANTS; NF-KAPPA-B; ACUTE HEMATOGENOUS OSTEOMYELITIS; FIBRONECTIN-BINDING PROTEINS; RESISTANT ACID-PHOSPHATASE; ALPHA-INDUCED OSTEOCLASTOGENESIS; PANTON-VALENTINE LEUKOCIDIN; AUREUS COLLAGEN ADHESIN; MURINE SEPTIC ARTHRITIS;
D O I
10.1016/j.ijmm.2009.10.003
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
Staphylococci, in Particular Staphylococcus aureus, are the predominant cause of bone infections worldwide. These infections are painful, debilitating and with the rise in anti biotic-resistant forms. increasingly difficult to treat. The growth in the number of prosthetic joint replacement Procedures also provides new opportunities for these infections to take hold. Comprehending the mechanisms by which staphylococci interact with and damage bone is critical to the development of new approaches to meet this challenge. This review summarises current understanding of the mechanisms by which staphylococci infect and damage bone. We address the role of the inflammatory response to staphylococcal infection in disrupting the homeostatic balance of bone matrix deposition and resorption and thereby mediating bone destruction. A number Of Virulence factors that have been shown to contribute to bone infection and pathology are discussed, however no single factor has been defined as being specific to bone infections. Although traditionally considered an extracellular pathogen, there is increasing evidence that staphylococci are able to invade host cells, and that an intracellular lifestyle may facilitate long-term persistence in bone tissue, enabling evasion of antimicrobials and host immune responses. 'Small colony variant' strains, with mutations disabling the electron transport pathway appear Particularly adept at invading and persisting within host cells, and exhibit enhanced antimicrobial resistance, and may represent a further complication in the treatment and management of staphylococcal bone disease. (C) 2009 Elsevier GmbH. All rights reserved.
引用
收藏
页码:193 / 204
页数:12
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