Journal
BONE
Volume 30, Issue 1, Pages 275-280Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S8756-3282(01)00632-9
Keywords
Staphylococcus aureus; collagen adhesin; osteomyelitis; septic arthritis; mouse model; cna
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Funding
- NIAID NIH HHS [R29-AI37729] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R29AI037729] Funding Source: NIH RePORTER
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To evaluate the role of the Staphylococcus aureus collagen-binding adhesin (Cna) in bone and joint infection, we generated a cna mutant in S. aureus UAMS-1, a strain that was originally isolated from the bone of a patient suffering from osteomyelitis. The mutant (UAMS-237) was unable to bind collagen but bound fibronectin at levels comparable to UAMS-1. The relative virulence of UAMS-1 and UAMS-237 was assessed using a murine model of acute hematogenous osteomyelitis. Specifically, 10(8) colony-forming units (cfu) Were Introduced into the bloodstream of NIH-Swiss mice via tail-vein injection. After 2 weeks, the left hind limb was harvested and examined histologically for evidence of osteomyelitis and septic arthritis. Osteomyelitis developed in 14 of 20 mice (70%) infected with UAMS-1, but only 1 of 20 (5%) infected with UAMS-237 (p < 0.001). In contrast, septic arthritis was observed in 12 of 20 mice (60%) infected with UAMS-1 and 14 of 20 (70%) infected with UAMS-237 (p < 0.75). These results indicate that Cna is not required to establish joint infection, but does make an important contribution to the ability of S. aureus to establish infection in bone through hematogenous spread. (C) 2002 by Elsevier Science Inc. All rights reserved.
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