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从无症状携带者中分离出的持续性A群链球菌菌株内化相关基因prtF1的流行情况。

Prevalence of internalisation-associated gene, prtF1, among persisting group-A streptococcus strains isolated from asymptomatic carriers.

作者信息

Neeman R, Keller N, Barzilai A, Korenman Z, Sela S

机构信息

Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Israel.

出版信息

Lancet. 1998;352(9145):1974-7. doi: 10.1016/S0140-6736(97)12452-7.

DOI:10.1016/S0140-6736(97)12452-7
PMID:9872247
Abstract

BACKGROUND

The failure of antibiotic treatment to eradicate group-A streptococci in up to 30% of patients with pharyngotonsillitis is unexplained. Some strains of group-A streptococci can enter respiratory epithelial cells, where they would be inaccessible to antibiotics unable to penetrate the cell membrane, such as penicillins. The fibronectin-binding proteins, F1 and SfbI, are needed for this process. We hypothesised, therefore, that an intracellular reservoir of group-A streptococci could account, at least partly, for failure to eradicate throat carriage, and that the presence of the gene for fibronectin-binding protein (F1) might be linked to the ability of a strain to persist in the throat after therapy.

METHODS

We investigated the frequency of prtF1-containing strains among 67 patients with pharyngotonsillitis. All patients were clinically cured, although 13 of them continued to carry group-A streptococci in the throat during or after therapy. To distinguish between persisting and recolonising strains, isolates from the 13 patients were serologically tested and compared by polymorphic DNA-amplification technique.

FINDINGS

12 (92%) of the 13 patients with symptomless carriage had prtF1-containing strains in the throat, compared with 16 (30%) of the 54 patients with successful eradication (p=0.0001). Three of the 13 eradication-failure patients were recolonised with strains that differed from the pretreatment strains. Nine of the ten (90%) persisting strains carried prtF1 (p=0.0009).

INTERPRETATION

Our findings suggest that protein-F1-mediated entry to cells is involved in the causative process of the carriage state.

摘要

背景

在高达30%的咽扁桃体炎患者中,抗生素治疗未能根除A组链球菌的原因尚不清楚。一些A组链球菌菌株可进入呼吸道上皮细胞,在那里它们对抗生素来说是无法触及的,因为抗生素无法穿透细胞膜,如青霉素。这个过程需要纤连蛋白结合蛋白F1和SfbI。因此,我们推测,A组链球菌的细胞内储存库可能至少部分地解释了未能根除咽部携带菌的原因,并且纤连蛋白结合蛋白(F1)基因的存在可能与菌株在治疗后在咽部持续存在的能力有关。

方法

我们调查了67例咽扁桃体炎患者中含prtF1菌株的频率。所有患者临床均已治愈,尽管其中13例在治疗期间或治疗后咽部仍携带A组链球菌。为了区分持续存在的菌株和重新定植的菌株,对这13例患者的分离株进行了血清学检测,并通过多态性DNA扩增技术进行了比较。

结果

13例无症状携带患者中有12例(92%)咽部有含prtF1的菌株,而54例成功根除的患者中有16例(30%)(p=0.0001)。13例根除失败的患者中有3例被与治疗前菌株不同的菌株重新定植。10株持续存在的菌株中有9株(90%)携带prtF1(p=0.0009)。

解读

我们的研究结果表明,蛋白F1介导的细胞进入参与了携带状态的致病过程。

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