Staphylococcus aureus collagen adhesin contributes to the pathogenesis of osteomyelitis

Staphylococcus aureus collagen adhesin contributes to the pathogenesis of osteomyelitis
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DOI:
10.1016/s8756-3282(01)00632-9
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发表时间:
2002-01-01
期刊:
影响因子:
4.1
通讯作者:
Smeltzer, MS
Smeltzer, MS
中科院分区:
医学2区
文献类型:
--
作者:
Elasri, MO;Thomas, JR;Smeltzer, MS

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为了评估金黄色葡萄球菌胶原结合粘附素(Cna)在骨和关节感染中的作用,我们在S。aureus UAMS-1,一种最初从患有骨髓炎的患者的骨中分离的菌株。突变体(UAMS-237)不能结合胶原蛋白,但结合纤连蛋白的水平与UAMS-1相当。使用急性血源性骨髓炎的小鼠模型评估UAMS-1和UAMS-237的相对毒力。具体地,通过尾静脉注射将10(8)个集落形成单位(cfu)引入NIH-瑞士小鼠的血流中。2周后,收获左后肢,并进行组织学检查以确定骨髓炎和脓毒性关节炎的证据。感染UAMS-1的20只小鼠中有14只(70%)发生骨髓炎,但感染UAMS-237的20只小鼠中只有1只(5%)发生骨髓炎(p < 0.001)。相比之下,在感染UAMS-1的20只小鼠中的12只(60%)和感染UAMS-237的20只小鼠中的14只(70%)中观察到脓毒性关节炎(p < 0.75)。这些结果表明,Cna并不是建立关节感染所必需的,但确实对S.金黄色葡萄球菌通过血行播散在骨中建立感染。(C)2002年,Elsevier Science Inc. All rights reserved.
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.