Arko R J, Rasheed J K, Broome C V, Chandler F W, Paris A L
J Infect. 1984 May;8(3):205-11. doi: 10.1016/s0163-4453(84)93859-3.
The complete pathogenesis of toxic shock syndrome (TSS) has yet to be elucidated. Unmasking the complex interactions among bacterial products, host factors, and possibly tampon components requires a suitable in vivo model. For this purpose, subcutaneous chambers implanted in rabbits were inoculated with Staphylococcus aureus isolated from patients with TSS. Infected rabbits developed illness characterised by multisystem involvement that included periportal inflammation of the liver, erythrophagocytosis in the spleen and lymph nodes as well as extreme vascular dilatation and epithelial lesions similar to those described in patients with TSS. Concentrations of serum creatinine (P less than 0.03) and triglycerides (P less than 0.04) were significantly raised in rabbits infected with TSS strains compared with rabbits infected with non-TSS strains of S. aureus. Both TSS and non-TSS strains of S. aureus produced fever and diarrhoea, but TSS strains were significantly (P less than 0.05) more lethal and more likely to produce respiratory distress and lowered blood pressure. This model may help to prove or disprove proposed mechanisms for the development of TSS.
中毒性休克综合征（TSS）的完整发病机制尚未阐明。要揭示细菌产物、宿主因素以及可能的卫生棉条成分之间的复杂相互作用，需要合适的体内模型。为此，将植入兔皮下的小室接种从TSS患者分离出的金黄色葡萄球菌。受感染的兔子出现以多系统受累为特征的病症，包括肝脏门周炎症、脾脏和淋巴结中的红细胞吞噬现象，以及与TSS患者中所描述的类似的极度血管扩张和上皮病变。与感染非TSS菌株金黄色葡萄球菌的兔子相比，感染TSS菌株的兔子血清肌酐浓度（P<0.03）和甘油三酯浓度（P<0.04）显著升高。金黄色葡萄球菌的TSS菌株和非TSS菌株均引起发热和腹泻，但TSS菌株的致死性显著更高（P<0.05），且更有可能导致呼吸窘迫和血压降低。该模型可能有助于证实或反驳关于TSS发病机制的推测。
