Suppr超能文献

艰难梭菌的营养体在潮湿表面的室内空气中以及酸度降低的胃内容物中存活:这是解释质子泵抑制剂与艰难梭菌相关性腹泻之间关联的潜在机制吗?

Vegetative Clostridium difficile survives in room air on moist surfaces and in gastric contents with reduced acidity: a potential mechanism to explain the association between proton pump inhibitors and C. difficile-associated diarrhea?

作者信息

Jump Robin L P, Pultz Michael J, Donskey Curtis J

机构信息

Louis Stokes Cleveland Veterans Affairs Medical Center, Infectious Diseases Section, Cleveland, OH 44106, USA.

出版信息

Antimicrob Agents Chemother. 2007 Aug;51(8):2883-7. doi: 10.1128/AAC.01443-06. Epub 2007 Jun 11.

Abstract

Proton pump inhibitors (PPIs) have been identified as a risk factor for Clostridium difficile-associated diarrhea (CDAD), though the mechanism is unclear because gastric acid does not kill C. difficile spores. We hypothesized that the vegetative form of C. difficile, which is killed by acid, could contribute to disease pathogenesis if it survives in room air and in gastric contents with elevated pH. We compared the numbers of C. difficile spores and vegetative cells in stools of patients prior to and during the treatment of CDAD. We assessed the survival of vegetative cells on moist or dry surfaces in room air versus anaerobic conditions and in human gastric contents, in pH-adjusted gastric contents, and in gastric contents from individuals receiving PPI therapy. Stool samples obtained from patients prior to the initiation of antibiotic treatment for C. difficile contained approximately 10-fold more vegetative cells than spores. On dry surfaces, vegetative C. difficile cells died rapidly, whereas they remained viable for up to 6 h on moist surfaces in room air. Vegetative C. difficile cells had only marginal survival in gastric contents at low pH; adjustment to a pH of >5 resulted in survival similar to that in the phosphate-buffered saline control. The survival of vegetative C. difficile in gastric contents obtained from patients receiving PPIs was also increased at a pH of >5. The ability of the vegetative form of C. difficile to survive on moist surfaces and in gastric contents with an elevated pH suggests a potential mechanism by which PPI therapy could increase the risk of acquiring C. difficile.

摘要

质子泵抑制剂(PPIs)已被确定为艰难梭菌相关性腹泻(CDAD)的一个风险因素,尽管其机制尚不清楚,因为胃酸并不能杀死艰难梭菌孢子。我们推测,虽能被酸杀死,但如果在室内空气和pH值升高的胃内容物中存活,艰难梭菌的营养体形式可能会导致疾病发病。我们比较了CDAD患者治疗前和治疗期间粪便中艰难梭菌孢子和营养体细胞的数量。我们评估了营养体细胞在室内空气与厌氧条件下以及在人类胃内容物、pH值调整后的胃内容物和接受PPI治疗个体的胃内容物中在潮湿或干燥表面上的存活情况。在开始针对艰难梭菌的抗生素治疗之前从患者获得的粪便样本中,营养体细胞的数量比孢子多大约10倍。在干燥表面上,艰难梭菌营养体细胞迅速死亡,而在室内空气中的潮湿表面上它们可存活长达6小时。艰难梭菌营养体细胞在低pH值的胃内容物中仅能勉强存活;将pH值调整至>5会导致其存活情况与磷酸盐缓冲盐水对照相似。从接受PPI治疗的患者获得的胃内容物中,艰难梭菌营养体在pH值>5时的存活能力也有所增强。艰难梭菌营养体形式在潮湿表面和pH值升高的胃内容物中存活的能力提示了一种潜在机制,通过该机制PPI治疗可能会增加获得艰难梭菌的风险。

相似文献

2
Is over-use of proton pump inhibitors fuelling the current epidemic of Clostridium difficile-associated diarrhoea?
J Hosp Infect. 2008 Sep;70(1):1-6. doi: 10.1016/j.jhin.2008.04.023. Epub 2008 Jul 3.
4
Gastric acid suppression by proton pump inhibitors as a risk factor for clostridium difficile-associated diarrhea in hospitalized patients.
Am J Gastroenterol. 2008 Sep;103(9):2308-13. doi: 10.1111/j.1572-0241.2008.01975.x. Epub 2008 Aug 12.
7
Laboratory maintenance of Clostridium difficile.
Curr Protoc Microbiol. 2009 Feb;Chapter 9:Unit9A.1. doi: 10.1002/9780471729259.mc09a01s12.
8
Proton pump inhibitors as a risk factor for paediatric Clostridium difficile infection.
Aliment Pharmacol Ther. 2010 Apr;31(7):754-9. doi: 10.1111/j.1365-2036.2009.04229.x. Epub 2009 Dec 29.
9
Clostridium difficile infection and proton pump inhibitors.
Curr Opin Pediatr. 2012 Oct;24(5):627-31. doi: 10.1097/MOP.0b013e328355a3e1.
10
Clostridium difficile-associated diarrhea and proton pump inhibitor therapy: a meta-analysis.
Am J Gastroenterol. 2012 Jul;107(7):1001-10. doi: 10.1038/ajg.2012.179. Epub 2012 Jun 19.

引用本文的文献

2
Exploring the etiology of colitis: insights from gut microbiota research.
Gut Microbes. 2025 Dec;17(1):2512010. doi: 10.1080/19490976.2025.2512010. Epub 2025 Jun 2.
5
The small acid-soluble proteins of Clostridioides difficile regulate sporulation in a SpoIVB2-dependent manner.
PLoS Pathog. 2024 Aug 30;20(8):e1012507. doi: 10.1371/journal.ppat.1012507. eCollection 2024 Aug.
6
Effects of proton pump inhibitors on inflammatory bowel disease: An updated review.
World J Gastroenterol. 2024 Jun 7;30(21):2751-2762. doi: 10.3748/wjg.v30.i21.2751.
7
The pH-responsive SmrR-SmrT system modulates antimicrobial resistance, spore formation, and toxin production.
Infect Immun. 2024 Mar 12;92(3):e0046123. doi: 10.1128/iai.00461-23. Epub 2024 Feb 12.
8
Correlating Antibiotic-Induced Dysbiosis to Spore Germination and Host Susceptibility to Infection Using an Assay.
ACS Infect Dis. 2023 Oct 13;9(10):1878-1888. doi: 10.1021/acsinfecdis.3c00192. Epub 2023 Sep 27.
9
The small acid-soluble proteins of regulate sporulation in a SpoIVB2-dependent manner.
bioRxiv. 2024 Jun 25:2023.05.17.541253. doi: 10.1101/2023.05.17.541253.
10
Proton Pump Inhibitors, Kidney Damage, and Mortality: An Updated Narrative Review.
Adv Ther. 2023 Jun;40(6):2693-2709. doi: 10.1007/s12325-023-02476-3. Epub 2023 May 4.

本文引用的文献

1
In vitro killing of nosocomial pathogens by acid and acidified nitrite.
Antimicrob Agents Chemother. 2006 Nov;50(11):3901-4. doi: 10.1128/AAC.01506-05.
2
Proton pump inhibitors and hospitalization for Clostridium difficile-associated disease: a population-based study.
Clin Infect Dis. 2006 Nov 15;43(10):1272-6. doi: 10.1086/508453. Epub 2006 Oct 13.
4
Proton pump inhibitor therapy is a risk factor for Clostridium difficile-associated diarrhoea.
Aliment Pharmacol Ther. 2006 Aug 15;24(4):613-9. doi: 10.1111/j.1365-2036.2006.03015.x.
5
Clostridium difficile infection in patients discharged from US short-stay hospitals, 1996-2003.
Emerg Infect Dis. 2006 Mar;12(3):409-15. doi: 10.3201/eid1205.051064.
7
An epidemic, toxin gene-variant strain of Clostridium difficile.
N Engl J Med. 2005 Dec 8;353(23):2433-41. doi: 10.1056/NEJMoa051590. Epub 2005 Dec 1.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验