跳到主要內容

臺灣博碩士論文加值系統

(18.97.14.86) 您好!臺灣時間:2025/02/20 06:26
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果 :::

詳目顯示

我願授權國圖
: 
twitterline
研究生:吳竺晏
研究生(外文):Chu-Yen Wu
論文名稱:探討秀麗隱桿線蟲模式於困難梭狀芽孢桿菌毒力之評估
論文名稱(外文):Investigation of Caenorhabditis elegans Model in Evaluating the Toxicity of Clostridium difficile
指導教授:陳德勛
指導教授(外文):Ter-Hsin Chen
口試委員:陳志銘郭致榮
口試委員(外文):Chih-Ming ChenChih-Jung Kuo
口試日期:2017-06-21
學位類別:碩士
校院名稱:國立中興大學
系所名稱:獸醫病理生物學研究所
學門:獸醫學門
學類:獸醫學類
論文種類:學術論文
論文出版年:2017
畢業學年度:105
語文別:中文
論文頁數:58
中文關鍵詞:困難梭狀芽孢桿菌秀麗隱桿線蟲存活週期
外文關鍵詞:Clostridium difficileCaenorhabditis eleganssurvival lifespan
相關次數:
  • 被引用被引用:0
  • 點閱點閱:175
  • 評分評分:
  • 下載下載:0
  • 收藏至我的研究室書目清單書目收藏:0
困難梭狀芽孢桿菌(Clostridium difficile)為一厭氧性革蘭氏陽性菌,於環境中會形成芽孢並藉由醫療照護人員以及住院環境傳播,其感染症狀可見不等程度之下痢、偽膜性結腸炎與毒性巨結腸症等,嚴重可引發敗血症而導致死亡。秀麗隱桿線蟲(Caenorhabditis elegans)是一種身形小且透明的生物,生活於土壤中並以微生物如大腸桿菌為食,目前是研究宿主和病原菌之間交互關係的重要生物模式,本實驗室的研究則著重於以線蟲作為研究困難梭狀芽孢桿菌臨床株毒力的生物模式。選用的菌株包括困難梭狀芽孢桿菌臨床株ribotype 078 lineage、標準株ribotype 027、只產生toxin B的強毒株ribotype 017與不產生Clostridium difficile transferase (CDT)的菌株進行線蟲毒殺試驗。結果可見,相較於對照組,以ribotype 078 lineage、ribotype 027與ribotype 017攻毒之線蟲其平均壽命皆縮短,而在不產CDT的組別結果則較不顯著。從線蟲的外觀也可見受感染的個體其體型較小且腸腔蒼白,表示困難梭狀芽孢桿菌會對秀麗隱桿線蟲造成一定程度的傷害。
本實驗室也利用不具毒性之大腸桿菌與困難梭狀芽孢桿菌進行等比例混合之線蟲毒殺試驗,結果發現困難梭狀芽孢桿菌ribotype 078 lineage、ribotype 027與ribotype 017皆會造成線蟲平均壽命縮短,這代表著線蟲在大腸桿菌與具致病性的困難梭狀芽孢桿菌強毒株之間並無出現偏好行為。為了探討困難梭狀芽孢桿菌營養細胞與芽孢對於線蟲毒殺效果的差別,額外將梭菌經熱處理後再對線蟲進行毒殺試驗,結果可見困難梭菌ribotype 078 lineage, ribotype 027與ribotype 017組別一樣會造成線蟲大量死亡,顯示經加熱殺死營養細胞後之梭菌以芽孢型態存在時仍會造成線蟲平均壽命大幅縮短。
將線蟲毒殺試驗之結果與梭菌經熱處理後之毒殺試驗結果相比較,發現僅以芽孢進行攻毒時,ribotype 078 lineage毒殺線蟲所需花費時間相對縮短,而ribotype 027與ribotype017所需時間則相對延長。根據此結果額外進行困難梭狀芽孢桿菌之芽孢萌發試驗,結果顯示困難梭狀芽孢桿菌ribotype 078 lineage之芽孢在嚴苛的環境中較ribotype 027與ribotype017容易萌發,因此推測其對於線蟲造成傷害的時間較快速。
綜合以上,本研究證實了秀麗隱桿線蟲可作為評估困難梭狀芽孢桿菌毒力的新興生物模式,並發現困難梭狀芽孢桿菌之芽孢對於線蟲具有毒性,於未來或許可作為研究困難梭狀芽孢桿菌芽孢與宿主腸道間交互作用的研究模式。
Clostridium difficile is an anaerobic gram-positive bacterium. Caenorhabditis elegans is a small and transparent roundworm living in the soil and fed on microorganism. Nowadays, C. elegans has become an important animal model to investigate the relationship between host and pathogenic bacteria. In our laboratory, we focus on using C. elegans as a surrogate host to study the virulence of different clinical isolates of Clostridium difficile. The strains of C. difficile in C. elegans killing assay included clinical isolates ribotype 078 lineage, standard strain ribotype 027, hyervirulent strain ribotype 017, and CDT-non-producing clinical isolates. Our results showed that ribotype 078 lineage, ribotype 027 and ribotype 017 shortened the median lifespan of C. elegans compared to control group, and the results in CDT-non-producing C. difficile strains were less significant. The appearances of C. elegans infected with hypervirulent C. difficile strains showed smaller size and paler intestine structure, indicating that C. difficile can cause a certain degree of damage towards C. elegans.
Our laboratory further mixed target bacterium with avirulent E. coli strain OP50. The results showed that C. difficile ribotype 078 lineage, ribotype 027 and ribotype 017 could shortened the median lifespan of C. elegans, indicating that the death of C. elegans towards hypervirulent C. difficile strains was not due to avoidance of feeding. To figure out the differences of killing C. elegans between vegetative cells and spores of C. difficile, we fed C. elegans on heat-killed C. difficile. The results showed that C. difficile ribotype 078 lineage, ribotype 027 and ribotype 017 could still killed C. elegans massively, indicating that spores of C. difficile ingested by C. elegans could shortened the lifespan of nematode.
Compared the results of C. elegans killing assay to heat-killed C. elegans killing assay, we found that when C. elegans fed only with spores, the median lifespan of C. elegans killed by ribotype 078 lineage was relatively shortened, while ribotype 027 and ribotype 017 relatively prolonged. We further conducted C. difficile spore germination ability test. The results showed that spores of C. difficile ribotype 078 lineage were more easily germinated in tough environment than ribotype 027 and ribotype 017, therefore caused damage to C. elegasn much quickly.
Overall, our research indicated the possibility of C. elegans as a new animal model used in evaluating the toxicity of C. difficile. We also discovered the toxicity of C. difficile spores towards C. elegans, making it become a research model for investigating the cross-reaction between C. difficile spores and host intestine environment.
摘要 i
Abstract ii
目次 iii
表次 v
圖次 vi
第一章 文獻探討 1
第一節 困難梭狀芽孢桿菌之介紹 1
一、歷史背景 1
二、生長特性 1
第二節 困難梭狀芽孢桿菌感染症 1
一、人類流行病學 1
二、傳染途徑 2
三、腸道菌叢失衡 3
四、診斷、症狀、治療及預防 3
五、動物之困難梭狀芽孢桿菌感染 4
第三節 困難梭狀芽孢桿菌之毒力及其相關因子 4
一、Toxin A與Toxin B 4
二、Clostridium difficile transferase (CDT) 6
三、芽孢(Spore) 7
四、黏附相關因子 8
第四節 困難梭狀芽孢桿菌分子分型 9
一、限制性內切酶分析法 9
二、脈衝場凝膠電泳法 9
三、毒素分型法 9
四、PCR-核醣分型法 10
第五節 秀麗隱桿線蟲感染模式 10
一、歷史背景 10
二、秀麗隱桿線蟲模式之運用 10
三、秀麗隱桿線蟲生長特性 11
第六節 研究目的 11
第二章 材料與方法 13
第一節 細菌來源與培養 13
一、困難梭狀芽孢桿菌菌株來源 13
二、大腸桿菌菌株來源 13
三、細菌培養基與培養液 13
第二節 困難梭狀芽孢桿菌之分型 14
一、困難梭菌Toxinotyping 14
二、困難梭菌Riboyping 15
第三節 秀麗隱桿線蟲之培養 16
一、秀麗隱桿線蟲專用培養基 16
二、秀麗隱桿線蟲之培養 17
第四節 秀麗隱桿線蟲存活曲線測定 18
一、困難梭狀芽孢桿菌感染線蟲後之存活曲線評估 18
二、困難梭狀芽孢桿菌與大腸桿菌之混合線蟲攻毒試驗 19
三、困難梭狀芽孢桿菌之熱處理線蟲毒殺試驗 19
第五節 困難梭狀芽孢桿菌之芽孢萌發能力試驗 20
一、困難梭狀芽孢桿菌芽孢製備 20
二、困難梭狀芽孢桿菌芽孢萌發能力試驗 20
第六節 統計分析 20
第三章 結果 21
第一節 困難梭狀芽孢桿菌分型結果 21
一、毒素鑑定結果 21
二、PCR-核醣分型結果 21
第二節 困難梭狀芽孢桿菌之秀麗隱桿線蟲毒殺試驗 22
一、具Clostridium difficile transfearse分泌能力之困難梭狀芽孢桿菌組別 22
二、不具Clostridium difficile transfearse分泌能力之困難梭狀芽孢桿菌組別 22
第三節 細菌混合感染之秀麗隱桿線蟲毒殺試驗 23
第四節 困難梭狀芽孢桿菌熱處理之秀麗隱桿線蟲毒殺試驗 23
第五節 困難梭狀芽孢桿菌毒殺試驗與熱處理之毒殺試驗結果比較 23
第六節 困難梭狀芽孢桿菌對線蟲外觀之傷害 24
第七節 困難梭狀芽孢桿菌芽孢萌發能力之結果 24
第四章 討論 26
第一節 困難梭狀芽孢桿菌毒力基因以及核醣分型比較結果 26
第二節 秀麗隱桿線蟲毒殺試驗之結果比較 26
第三節 細菌混合感染之秀麗隱桿線蟲毒殺試驗結果比較 27
第四節 困難梭狀芽孢桿菌熱處理之秀麗隱桿線蟲毒殺試驗結果比較 27
第五節 困難梭狀芽孢桿菌熱處理與否於毒殺線蟲之結果比較 28
第六節 困難梭狀芽孢桿菌芽孢萌發能力試驗結果比較 29
第七節 總結 30
參考文獻 53
參考文獻
郭承儒、陳怡偉、陳昌熙。 蟲蟲危機–以線蟲做為模式生物。科學發展 487:48-52,2013。
Barbut F, Corthier G, Charpak Y, 1996. Prevalence pathogenicity of Clostridium difficile in hospitalized patients. Arch Intern Med 156: 1449-56.
Barbut F, Mastrantonio P, Delmee M, Brazier J, Kuijper E, Poxton I, 2007. Europeaned Study Group on Clostridium. Prospective study of Clostridium difficile infections in Europe with phenotypic and genotypic characterisation of the isolates. Clin Microbiol Infect 13: 1048-1057.
Barth H, Pfeifer G, Hofmann F, Maier E, Benz R, Aktories K, 2001. Low pH-induced formation of ion channels by Clostridium difficile toxin B in target cells. J Biol Chem 276(14): 10670-6.
Bartlett JG, Chang TW, Moon N, Onderdonk AB, 1978. Antibiotic-induced lethal enterocolitis in hamsters: studies with eleven agents and evidence to support the pathogenic role of toxin-producing Clostridia. Am J Vet Res 39: 1525-1530.
Bartlett JG, 1994. Clostridium difficile: history of its role as an enteric pathogen the current state of knowledge about the organism. Clin Infect Dis 18(4): 265-72.
Bauer MP, Notermans DW, van Benthem BH, Brazier JS, Wilcox MH, Rupnik M, Monnet DL, van Dissel JT, Kuijper EJ, 2011. Clostridium difficile infection in Europe: a hospital-based survey. Lancet 377(9759): 63-73.
Bidet P, Barbut F, Lalande V, Burghoffer B, Petit JC, 1999. Development of a new PCR-ribotyping method for Clostridium difficile based on ribosomal RNA gene sequencing. FEMS Microbiol Lett 175(2): 261-6.
Burns DA, Heap JT, Minton NP, 2010. The diverse sporulation characteristics of Clostridium difficile clinical isolates are not associated with type. Anaerobe 16(6): 618-22.
Burns DA, Minton NP, 2011. Sporulation studies in Clostridium difficile. J Microbiol Methods. 87(2): 133-8.
Centers for Disease Control and Prevention (CDC), 2013. Antibiotic Resistance Threats in the United States.
Cerquetti M, Serafino A, Sebastianelli A, Mastrantonio P, 2002. Binding of Clostridium difficile to Caco-2 epithelial cell line and to extracellular matrix proteins. FEMS Immunol Med Microbiol 32(3): 211-8.
Chen S, Sun C, Wang H, Wang J, 2015. The Role of Rho GTPases in Toxicity of Clostridium difficile Toxins. Toxins (Basel) 7(12): 5254-67.
Chen X, Katchar K, Goldsmith JD, Nanthakumar N, Cheknis A, Gerding DN, Kelly CP, 2008. A mouse model of Clostridium difficile-associated disease. Gastroenterology 135(6): 1984-92.
Chou TC, Chiu HC, Kuo CJ, Wu CM, Syu WJ, Chiu WT, Chen CS, 2013. Enterohaemorrhagic Escherichia coli O157:H7 Shiga-like toxin 1 is required for full pathogenicity and activation of the p38 mitogen-activated protein kinase pathway in Caenorhabditis elegans. Cell Microbiol 15(1): 82-97.
Chung CH, Wu CJ, Lee HC, Yan JJ, Chang CM, Lee NY, Chen PL, Lee CC, Hung YP, Ko WC, 2010. Clostridium difficile infection at a medical center in southern Taiwan: incidence, clinical features and prognosis. J Microbiol Immunol Infect 43(2): 119-25.
Cohen SH, Gerding DN, Johnson S, Kelly CP, Loo VG, McDonald LC, Pepin J, Wilcox MH, 2010. Clinical practice guidelines for Clostridium difficile infection in adults: 2010 update by the society for healthcare epidemiology of America (SHEA) and the infectious diseases society of America. Infect Control Hosp Epidemiol 31(5): 431-55.
Collins DA, Hawkey PM, Riley TV, 2013. Epidemiology of Clostridium difficile infection in Asia. Antimicrob Resist Infect Control 2(1): 21.
Dubberke ER, Haslam DB, Lanzas C, Bobo LD, Burnham CA, Gröhn YT, Tarr PI, 2011. The Ecology and Pathobiology of Clostridium difficile Infections: An Interdisciplinary Challenge. Zoonoses Public Health 58(1): 4-20.
Dubberke ER, Olsen MA, 2012. Burden of Clostridium difficile on the healthcare system. Clin Infect Dis. 55(2): 88-92.
Félix MA, Braendle C, 2010. The natural history of Caenorhabditis elegans. Curr Biol 20(22): R965-9.
Fire A, Xu S, Montgomery MK, Kostas SA, Driver SE, Mello CC, 1998. Potent and specific genetic interference by double-stranded RNA in Caenorhabditis elegans. Nature 391(6669): 806-11.
Frisch C, Gerhard R, Aktories K, Hofmann F, Just I, 2003. The complete receptor-binding domain of Clostridium difficile toxin A is required for endocytosis. Biochem Biophys Res Commun 300(3): 706-11.
Gerding DN, Johnson S, Peterson LR, Mulligan ME, Silva J Jr, 1995. Clostridium difficile-associated diarrhea and colitis. Infect Control Hosp Epidemiol 16(8): 459-77.
Gerding DN, Johnson S, Rupnik M, Aktories K, 2014. Clostridium difficile binary toxin CDT: mechanism, epidemiology, and potential clinical importance. Gut Microbes 5(1): 15-27.
Gough E, Shaikh H, Manges AR, 2011. Systematic review of intestinal microbiota transplantation (fecal bacteriotherapy) for recurrent Clostridium difficile infection. Clin Infect Dis 53(10): 994-1002.
Greco A, Ho JG, Lin SJ, Palcic MM, Rupnik M, Ng KK, 2006. Carbohydrate recognition by Clostridium difficile toxin A. Nat Struct Mol Biol 13(5): 460-1.
Guinane CM, Cotter PD, 2013. Role of the gut microbiota in health and chronic gastrointestinal disease: understanding a hidden metabolic organ. Therap Adv Gastroenterol. 6(4): 295-308.
Hall AJ, Curns AT, McDonald LC, Parashar UD, Lopman BA, 2012. The roles of Clostridium difficile and norovirus among gastroenteritis-associated deaths in the United States, 1999-2007. Clin Infect Dis 55: 216-223.
Hall I, O'Toole E, 1935. Intestinal flora in newborn infants. Am J Dis Child 49: 390.
Hecht G, Koutsouris A, Pothoulakis C, LaMont JT, Madara JL, 1992. Clostridium difficile toxin B disrupts the barrier function of T84 monolayers. Gastroenterology 102(2): 416-23.
Hennequin C, Janoir C, Barc MC, Collignon A, Karjalainen T, 2003. Identification and characterization of a fibronectin-binding protein from Clostridium difficile. Microbiology 149(10): 2779-87.
Hennequin C, Porcheray F, Waligora-Dupriet A, Collignon A, Barc M, Bourlioux P, Karjalainen T, 2001. GroEL (Hsp60) of Clostridium difficile is involved in cell adherence. Microbiology 147(1): 87-96.
Hensgens MPM, Keessen EC, Squire MM, Riley TV, Koene MG, de Boer E, Lipman LJ, Kuijper EJ, 2012. Clostridium difficile infection in the community: a zoonotic disease. Clin Microbiol Infect 18: 635-645.
Higgins D and Dworkin J, 2012. Recent progress in Bacillus subtilis sporulation. FEMS Microbiol Rev 36(1): 131-148.
Honda H, Dubberke ER, 2014. The changing epidemiology of Clostridium difficile infection. Curr Opin Gastroenterol 30: 54-62.
Huber CA, Foster NF, Riley TV, Paterson DL, 2013. Challenges for Standardization of Clostridium difficile Typing Methods. J Clin Microbiol 51(9): 2810-4.
Jank T, Aktories K, 2008. Structure and mode of action of clostridial glucosylating toxins: The ABCD model. Trends Microbiol 16(5): 222-9.
Janoir C, Péchiné S, Grosdidier C, Collignon A, 2007. Cwp84, a surface-associated protein of Clostridium difficile, is a cysteine protease with degrading activity on extracellular matrix proteins. J Bacteriol 189(20): 7174-80.
Joshi LT, Phillips DS, Williams CF, Alyousef A, Baillie L, 2012. The contribution of the spore to the ability of Clostridium difficile to adhere to surfaces. Appl. Environ Microbiol 78(21): 7671-9.
Just I, Selzer J, Wilm M, von Eichel-Streiber C, Mann M, Aktories K, 1995. Glucosylation of Rho proteins by Clostridium difficile toxin B. Nature 375(6531): 500-3.
Kato H, Kita H, Karasawa T, Maegawa T, Koino Y, Takakuwa H, Saikai T, Kobayashi K, Yamagishi T, Nakamura S, 2001. Colonisation and transmission of Clostridium difficile in healthy individuals examined by PCR ribotyping and pulsed-field gel electrophoresis. J Med Microbiol 50(8): 720-7.
Keel K, Brazier JS, Post KW, Weese S, Songer JG, 2007. Prevalence of PCR ribotypes among Clostridium difficile isolates from pigs, calves, and other species. J Clin Microbiol 45(6): 1963-1964.
Khanna S, Pardi DS, Aronson SL, Kammer PP, Orenstein R, St Sauver JL, Harmsen WS, Zinsmeister AR, 2012. The Epidemiology of Community-Acquired Clostridium difficile Infection: A Population-Based Study. Am J Gastroenterol 107(1): 89-95.
Kuehne SA, Collery MM, Kelly ML, Cartman ST, Cockayne A, Minton NP, 2014. Importance of toxin A, toxin B, and CDT in virulence of an epidemic Clostridium difficile strain. J Infect Dis 209(1): 83-6.
Kuntz JL, Chrischilles EA, Pendergast JF, Herwaldt LA, Polgreen PM, 2011. Incidence of and risk factors for community-associated Clostridium difficile infection: a nested case-control study. BMC Infect Dis 11: 194.
Kurti Z, Lovasz BD, Mandel MD, Csima Z, Golovics PA, Csako BD, Mohas A, Gönczi L, Gecse KB, Kiss LS, Szathmari M, Lakatos PL, 2015. Burden of Clostridium difficile infection between 2010 and 2013: Trends and outcomes from an academic center in Eastern Europe. World J Gastroenterol 21(21): 6728-35.
Kurz CL, Tan MW, 2004. Regulation of aging and innate immunity in C. elegans. Aging Cell 3(4): 185-93.
Laaberki MH, Dworkin J, 2008. Death and survival of spore-forming bacteria in the Caenorhabditis elegans intestine. Symbiosis 46: 95-100.
Labrousse A, Chauvet S, Couillault C, Kurz CL, Ewbank JJ, 2000. Caenorhabditis elegans is a model host for Salmonella typhimurium. Curr Bio 10(23): 1543-5.
Lawley TD, Clare S, Walker AW, Stares MD, Connor TR, Raisen C, Goulding D, Rad R, Schreiber F, Brandt C, Deakin LJ, Pickard DJ, Duncan SH, Flint HJ, Clark TG, Parkhill J, Dougan G, 2012. Targeted restoration of the intestinal microbiota with a simple, defined bacteriotherapy resolves relapsing Clostridium difficile disease in mice. PLoS Pathog 8(10): e1002995.
Lawley TD, Clare S, Walker AW, Goulding D, Stabler RA, Croucher N, Mastroeni P, Scott P, Raisen C, Mottram L, Fairweather NF, Wren BW, Parkhill J, Dougan G, 2009. Antibiotic treatment of Clostridium difficile carrier mice triggers a supershedder state, spore-mediated transmission, and severe disease in immunocompromised hosts. Infect Immun 77(9): 3661-9.
Lemee L, Dhalluin A, Testelin S, Mattrat MA, Maillard K, Lemeland JF, Pons JL, 2004. Multiplex PCR targeting tpi (triose phosphate isomerase), tcdA (Toxin A), and tcdB (Toxin B) genes for toxigenic culture of Clostridium difficile. J Clin Microbiol (12): 5710-4.
Lessa FC, Mu Y, Bamberg WM, Beldavs ZG, Dumyati GK, Dunn JR, Farley MM, Holzbauer SM, Meek JI, Phipps EC, Wilson LE, Winston LG, Cohen JA, Limbago BM, Fridkin SK, Gerding DN, McDonald LC, 2015. Burden of Clostridium difficile infection in the United States. N Engl J Med 372(24): 825-834.
Loo VG, Poirier L, Miller MA, Oughton M, Libman MD, Michaud S, Bourgault AM, Nguyen T, Frenette C, Kelly M, Vibien A, Brassard P, Fenn S, Dewar K, Hudson TJ, Horn R, René P, Monczak Y, Dascal A, 2005. A predominantly clonal multi-institutional outbreak of Clostridium difficile-associated diarrhea with high morbidity and mortality. N Engl J Med 353(23): 2442-9.
McGee MD, Weber D, Day N, Vitelli C, Crippen D, Herndon LA, Hall DH, Melov S, 2011. Loss of intestinal nuclei and intestinal integrity inaging C. elegans. Aging Cell 10(4): 699-710.
Mello CC, Kramer JM, Stinchcomb D, Ambros V, 1991. Efficient gene transfer in C.elegans: extrachromosomal maintenance and integration of transforming sequences. EMBO J 10(12): 3959-70.
Merrigan MM, Venugopal A, Roxas JL, Anwar F, Mallozzi MJ, Roxas BA, Gerding DN, Viswanathan VK, Vedantam G, 2013. Surface-layer protein A (SlpA) is a major contributor to host-cell adherence of Clostridium difficile. PLoS One 8(11): e78404.
McDonald LC, Owings M, Jernigan DB. Clostridium difficile infection in patients discharged from US short-stay hospitals, 1996-2003, 2006. Emerg Infect Dis 12: 409-415.
Norman KN, Harvey RB, Scott HM, Hume ME, Andrews K, Brawley AD, 2009. Varied prevalence of Clostridium difficile in an integrated swine operation. Anaerobe 15(6): 256-60.
O'Neill G, Adams JE, Bowman RA, Riley TV, 1993. A molecular characterization of Clostridium difficile isolates from humans, animals and their environments. Epidemiol Infect 111(2): 257-264.
Ozaki E, Kato H, Kita H, Karasawa T, Maegawa T, Koino Y, Matsumoto K, Takada T, Nomoto K, Tanaka R, Nakamura S, 2004. Clostridium difficile colonization in healthy adults: transient colonization and correlation with enterococcal colonization. J Med Microbiol 53(2): 167-72.
Paredes-Sabja D, Bond C, Carman RJ, Setlow P, Sarker MR, 2008. Germination of spores of Clostridium difficile strains, including isolates from a hospital outbreak of Clostridium difficile-associated disease (CDAD). Microbiology 154(8): 2241-50.
Paredes-Sabja D, Shen A, Sorg JA, 2014. Clostridium difficile spore biology: sporulation, germination, and spore structural proteins. Trends Microbiol 22(7): 406-16.
Persson S, Torpdahl M, Olsen KE, 2008. New multiplex PCR method for the detection of Clostridium difficile toxin A (tcdA) and toxin B (tcdB) and the binary toxin (cdtA/cdtB) genes applied to a Danish strain collection. Clin Microbiol Infect (11): 1057-64.
Pothoulakis C, Lamont JT, 2001. Microbes and microbial toxins: paradigms for microbial-mucosal interactions II. The integrated response of the intestine to Clostridium difficile toxins. Am J Physiol Gastrointest Liver Physiol 280: G178-183.
Prohaska JV, 1959. Pseudomembranous enterocolitis; the experimental induction of the disease with Staphylococcus aureus and its enterotoxin. AMA Arch Surg 79: 197-206.
Pruitt RN, Chambers MG, Ng KK, Ohi MD, Lacy DB, 2010. Structural organization of the functional domains of Clostridium difficile toxins A and B. Proc Natl Acad Sci U S A 107(30): 13467-72.
Qin J., Li R, Raes J, Arumugam M, Burgdorf K, Manichanh C, Nielsen T, Pons N, Levenez F, Yamada T, Mende DR, Li J, Xu J, Li S, Li D, Cao J, Wang B, Liang H, Zheng H, Xie Y, Tap J, Lepage P, Bertalan M, Batto JM, Hansen T, Le Paslier D, Linneberg A, Nielsen HB, Pelletier E, Renault P, Sicheritz-Ponten T, Turner K, Zhu H, Yu C, Li S, Jian M, Zhou Y, Li Y, Zhang X, Li S, Qin N, Yang H, Wang J, Brunak S, Doré J, Guarner F, Kristiansen K, Pedersen O, Parkhill J, Weissenbach J, Bork P, Ehrlich SD, Wang J, 2010. A human gut microbial gene catalogue established by metagenomic sequencing. Nature 464(7285): 59-65.
Riegler M, Sedivy R, Pothoulakis C, Hamilton G, Zacherl J, Bischof G, Cosentini E, Feil W, Schiessel R, LaMont JT, 1995. Clostridium difficile Toxin B Is More Potent than Toxin A in Damaging Human Colonic Epithelium In Vitro. J Clin Invest 95(5): 2004-11.
Rodriguez C, Van Broeck J, Taminiau B, Delmée M, Daube G, 2016. Clostridium difficile infection: Early history, diagnosis and molecular strain typing methods. Microb Pathog 97: 59-78.
Rupnik M, Janezic S, 2016. An Update on Clostridium difficile Toxinotyping. J Clin Microbiol 54(1): 13-8.
Schwan C, Kruppke AS, Nölke T, Schumacher L, Koch-Nolte F, Kudryashev M, Stahlberg H, Aktories K, 2014. Clostridium difficile toxin CDT hijacks microtubule organization and reroutes vesicle traffic to increase pathogen adherence. Proc Natl Acad Sci U S A 111(6): 2313-8.
Songer JG, Post KW, Larson DJ, Jost BH, Glock RD, 2000. Infection of neonatal swine with Clostridium difficile. Swine Health Prod 8(4): 185-189.
Songer JG, 2004. The emergence of Clostridium difficile as a pathogen of food animals. Anim Health Res Rev 5(2): 321-6.
Spigaglia P, Barketi-Klai A, Collignon A, Mastrantonio P, Barbanti F, Rupnik M, Janezic S, Kansau I, 2013. Surface-layer (S-layer) of human and animal Clostridium difficile strains and their behaviour in adherence to epithelial cells and intestinal colonization. J Med Microbiol 62(9): 1386-93.
Stein LD, Bao Z, Blasiar D, Blumenthal T, Brent MR, Chen N, Chinwalla A, Clarke L, Clee C, Coghlan A, Coulson A, D'Eustachio P, Fitch DH, Fulton LA, Fulton RE, Griffiths-Jones S, Harris TW, Hillier LW, Kamath R, Kuwabara PE, Mardis ER, Marra MA, Miner TL, Minx P, Mullikin JC, Plumb RW, Rogers J, Schein JE, Sohrmann M, Spieth J, Stajich JE, Wei C, Willey D, Wilson RK, Durbin R, Waterston RH, 2003. The genome sequence of Caenorhabditis briggsae: a platform for comparative genomics. PLoS Biol 1(2): E45.
Sunenshine RH, McDonald LC, 2006. Clostridium difficile-associated disease: new challenges from an established pathogen. Cleve Clin J Med 3(2): 187-97.
Tan MW, Rahme LG, Sternberg JA, Tompkins RG, Ausubel FM, 1999. Pseudomonas aeruginosa killing of Caenorhabditis elegans used to identify P. aeruginosa virulence factors. Proc Natl Acad Sci U S A 96(5): 2408-13.
Tasteyre A, Barc MC, Collignon A, Boureau H, Karjalainen T, 2001. Role of FliC and FliD Flagellar Proteins of Clostridium difficile in Adherence and Gut Colonization. Infect Immun 69(12): 7937-40.
van Nood E, Vrieze A, Nieuwdorp M, Fuentes S, Zoetendal EG, de Vos WM, Visser CE, Kuijper EJ, Bartelsman JF, Tijssen JG, Speelman P, Dijkgraaf MG, Keller JJ, 2013. Duodenal infusion of donor feces for recurrent Clostridium difficile. N Engl J Med Jan 368(5): 407-15.
von Eichel-Streiber C, Boquet P, Sauerborn M, Thelestam M, 1996. Large clostridial cytotoxins-a family of glycosyltransferases modifying small GTP-binding proteins. Trends Microbiol 4(10): 375-82.
Voth DE, Ballard JD, 2005. Clostridium difficile Toxins: Mechanism of Action and Role in Disease. Clin Microbiol Rev 18(2): 247-63.
Walker AS, Eyre DW, Wyllie DH, Dingle KE, Griffiths D, Shine B, Oakley S, O'Connor L, Finney J, Vaughan A, Crook DW, Wilcox MH, Peto TE, 2013. Relationship between bacterial strain type, host biomarkers, and mortality in Clostridium difficile infection. Clin Infect Dis 56(11): 1589-600.
Yun B, Oh S, Song M, Hong YS, Park S, Park DJ, Griffiths MW, Oh S, 2015. Inhibitory Effect of Epigallocatechin Gallate on the Virulence of Clostridium difficile PCR Ribotype 027. J Food Sci 80(12): M2925-31.
Zhang Y, Lu H, Bargmann CI, 2005. Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans. Nature 438(7065): 179-84.
Zilberberg MD, Shorr AF, Kollef MH, 2008. Increase in adult Clostridium difficile-related hospitalizations and case-fatality rate, United States, 2000-2005. Emerg Infect Dis 14: 929-931.
連結至畢業學校之論文網頁點我開啟連結
註: 此連結為研究生畢業學校所提供,不一定有電子全文可供下載,若連結有誤,請點選上方之〝勘誤回報〞功能,我們會盡快修正,謝謝!
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top