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骨髓炎的动物模型。知识、假说与推测。

Animal models of osteomyelitis. Knowledge, hypothesis, and speculation.

作者信息

Rissing J P

机构信息

Infectious Disease Section, Medical College of Georgia, Augusta.

出版信息

Infect Dis Clin North Am. 1990 Sep;4(3):377-90.

PMID:2212595
Abstract

Each animal model has provided insights. Particularly important was the considerable resistance of bone to infection without manipulation (no morrhuate, fracture, rod, wax, or prosthesis). Such perturbations allow bone infection with much smaller inocula. Typical inocula decreases are 1000 to 10,000 fold. Staphylococci may have a selective advantage in bone because of specialized or tropic binding, perhaps to cartilage or collagen. Osteoclast-induced resorption of hydroxyapatite might explain the distribution of some osteomyelitis. Increased osteoclast activity could link the susceptible metaphyseal regions, the repetitively traumatized diabetic foot, a history of blunt bone trauma, fracture, and perhaps even nearby soft tissue infection. Diagnosis remains difficult; gallium-67 and indium111 labeled WBC probably deserve additional investigation. Therapeutic failures in the rabbit and rat models mirror clinical experience. Clindamycin, rifampin, and quinolones are promising. Neither systemic nor local antimicrobial prophylaxis is well studied yet.

摘要

每种动物模型都提供了一些见解。特别重要的是,在未进行操作(无鱼肝油酸钠、骨折、髓内钉、骨蜡或假体)的情况下,骨骼对感染具有相当强的抵抗力。这些干扰因素会使骨骼在接种量小得多的情况下发生感染。典型的接种量减少为1000至10000倍。葡萄球菌可能由于与软骨或胶原蛋白的特异性或嗜性结合而在骨骼中具有选择性优势。破骨细胞诱导的羟基磷灰石吸收可能解释了一些骨髓炎的分布情况。破骨细胞活性增加可能与易感染的干骺端区域、反复受创伤的糖尿病足、钝性骨创伤史、骨折,甚至可能与附近的软组织感染有关。诊断仍然困难;镓67和铟111标记的白细胞可能值得进一步研究。兔和大鼠模型中的治疗失败反映了临床经验。克林霉素、利福平和喹诺酮类药物前景乐观。全身或局部抗菌预防措施尚未得到充分研究。

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