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耐甲氧西林金黄色葡萄球菌引起的小肠结肠炎:呼吸道和消化道分离株的分子特征

Enterocolitis caused by methicillin-resistant Staphylococcus aureus: molecular characterization of respiratory and digestive tract isolates.

作者信息

Watanabe H, Masaki H, Asoh N, Watanabe K, Oishi K, Kobayashi S, Sato A, Nagatake T

机构信息

Department of Internal Medicine, Institute of Tropical Medicine, Nagasaki University, Nagasaki, Japan.

出版信息

Microbiol Immunol. 2001;45(9):629-34. doi: 10.1111/j.1348-0421.2001.tb01295.x.

Abstract

We investigated the mechanism of outbreak of enterocolitis caused by methicillin-resistant Staphylococcus aureus (MRSA). Five epidemiological markers [coagulase type, enterotoxin type, toxic shock syndrome toxin-1 (TSST-1) production, beta-lactamase production and pulsed-field gel electrophoresis (PFGE)] of 45 strains of MRSA isolated simultaneously from the respiratory tract (nasal cavity and/or pharynx and/or sputum) and stool (plus one sample of gastric juice) in 13 patients (8 males and 5 females, mean age, 77.1 years) were compared retrospectively. Forty-four of the 45 isolates of MRSA were positive for enterotoxin C and TSST-1 production, and the remaining isolate was positive for enterotoxin A and negative for TSST-1 production. All isolates were coagulase type II, and 27 showed beta-lactamase production. The patterns of coagulase type, enterotoxin type, TSST-1 and beta-lactamase production of MRSA isolated from the respiratory tract were similar to those of MRSA isolated from the intestine in 12 of 13 patients. Molecular typing by PFGE demonstrated that the pattern of respiratory tract isolates was identical to those of stool isolates in 9 (69.2%), similar in 3 (23.1 %), and different in 1 (7.7%). The data suggested that enterocolitis might be caused by the MRSA colonized in the respiratory tract and incorporated into the digestive tracts. Therefore, we propose that early eradication of MRSA in the respiratory tract is important for protection of patients against the development of enterocolitis, particularly in susceptible patients, e.g., immunocompromised or pre-operated patients with digestive diseases, especially malignant disease.

摘要

我们研究了耐甲氧西林金黄色葡萄球菌(MRSA)引起小肠结肠炎暴发的机制。回顾性比较了从13例患者(8例男性和5例女性,平均年龄77.1岁)的呼吸道(鼻腔和/或咽部和/或痰液)和粪便(加一份胃液样本)中同时分离出的45株MRSA的五个流行病学标志物[凝固酶类型、肠毒素类型、毒性休克综合征毒素-1(TSST-1)产生、β-内酰胺酶产生和脉冲场凝胶电泳(PFGE)]。45株MRSA分离株中有44株肠毒素C和TSST-1产生呈阳性,其余分离株肠毒素A呈阳性,TSST-1产生呈阴性。所有分离株均为凝固酶II型,27株显示β-内酰胺酶产生。在13例患者中的12例中,从呼吸道分离出的MRSA的凝固酶类型、肠毒素类型、TSST-1和β-内酰胺酶产生模式与从肠道分离出的MRSA相似。通过PFGE进行的分子分型表明,呼吸道分离株的模式与粪便分离株的模式在9例(69.2%)中相同,在3例(23.1%)中相似,在1例(7.7%)中不同。数据表明,小肠结肠炎可能由定植于呼吸道并进入消化道的MRSA引起。因此,我们建议早期根除呼吸道中的MRSA对于保护患者免受小肠结肠炎的发生至关重要,特别是在易感患者中,例如免疫功能低下或患有消化系统疾病(尤其是恶性疾病)的术前患者。

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