Characterization of the importance of Staphylococcus epidermidis autolysin and polysaccharide intercellular adhesin in the pathogenesis of intravascular catheter-associated infection in a rat model
Characterization of the importance of Staphylococcus epidermidis autolysin and polysaccharide intercellular adhesin in the pathogenesis of intravascular catheter-associated infection in a rat model
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DOI：
10.1086/319279
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发表时间：
2001-04-01
影响因子：
6.4
通讯作者：
Götz, F
中科院分区：
文献类型：
--
作者：
Rupp, ME;Fey, PD;Götz, F
采用大鼠中心静脉导管（CVC）感染模型，研究表皮葡萄球菌（Staphylococcus epidermidis，CVC）相关感染中蛋白质自溶素（Proteinacian autolysin，CVC）和多糖细胞间粘附素（polysaccharide intercellular adhesin，PIA）的表达。野生型（wt）S.表皮葡萄球菌0 - 47比同基因突变株（β-内酰胺酶阴性[0 - 47mut1]或PIA阴性[0 - 47mut2]）中的任一种显著更可能引起CVC感染。87.5%的大鼠从接种S. epidermidis O-47感染的大鼠中，25%感染了S. O-47mut1和O-47mut2的表达差异有统计学意义（P = 0.007）。75%的大鼠感染S.与O-47mut1和O-47mut2攻击的12.5%和25%相比，表皮O-47攻击的12.5%和25%（P =.009）。转移性疾病在接种wt S的大鼠中更常见。epidermidis，相比，与ESTE或PIA缺陷型突变体。这些结果证实了在S.表皮实验性CVC感染。
A rat central venous catheter (CVC) infection model was used to assess the importance of the proteinacious autolysin (AtlE) and the polysaccharide intercellular adhesin (PIA) in the pathogenesis of Staphylococcus epidermidis CVC-associated infection. Wild-type (wt) S. epidermidis O-47 was significantly more likely to cause a CVC infection than was either of the isogenic mutant strains (AtlE- negative [O-47mut1] or PIA-negative [O-47mut2]). Bacteria were retrieved from the explanted catheters of 87.5% of rats inoculated with S. epidermidis O-47, compared with 25% of rats challenged with either S. epidermidis O-47mut1 or O-47mut2 (P = .007). Peripheral bacteremia was documented in 75% of rats challenged with S. epidermidis O-47, compared with 12.5% and 25% challenged with O-47mut1 and O-47mut2, respectively (P = .009). Metastatic disease was more common in rats inoculated with wt S. epidermidis, compared with AtlE- or PIA-deficient mutants. These results confirm the importance of initial adherence, associated with AtlE, and biofilm production, mediated by PIA, in the pathogenesis of S. epidermidis experimental CVC infection.