Journals / Türk Mikrobiyoloji Cemiyeti Dergisi / 2007 / Cilt: 37 - Sayı: 4

The pathogenesis of noninflammatory diarrhea

Noninflamatuvar ishallerin patogenezi

Pages
234–241
Publication Date
2022-11-04
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

In this review article, the roles of bacteria, such as enterotoxigenic Escherichia coli, Vibrio cholerae, Clostridium perfringens; viruses, such as Rotavirus; and protozoa, such as Giardia and Cryptosporidium in the pathogenesis of noninflammatory diarrhea have been discussed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Acute diarrhea defined as an increased frequency of defecation (more than 200 g of stool per day).
📊
Key Findings & Data:Noninflammatory diarrhea is characterized by watery stools.
💡
Conclusion & Impact:In this review article, the roles of bacteria, such as enterotoxigenic Escherichia coli, Vibrio cholerae, Clostridium perfringens; viruses, such as Rotavirus; and protozoa, such as Giardia and Cryptosporidium in the pathogenesis of noninflammatory diarrhea have been discussed.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Acute diarrhea defined as an increased frequency of defecation (more than 200 g of stool per day). Noninflammatory diarrhea is characterized by watery stools. Because of the morphology of the intestinal mucosa is normal or only minimally altered, stools do not contain leukocytes and blood or only a few leucocytes and occult blood. Noninflammatory diarrhea is caused various bacteria, viruses, and protozoa. In this review article, the roles of bacteria, such as enterotoxigenic Escherichia coli, Vibrio cholerae, Clostridium perfringens; viruses, such as Rotavirus; and protozoa, such as Giardia and Cryptosporidium in the pathogenesis of noninflammatory diarrhea have been discussed.

Özet

Akut ishal, dışkılama sıklığında (günde 200 gr.'dan fazla dışkı) artış olarak tanımlanır. Noninflamatuvar ishal, sulu dışkı ile karakterizedir. Bu tip diarede, barsak mukoza morfolojisi normal veya çok az değiştiği için, dışkıda lökosit ve kan bulunmaz veya çok az miktarda lökosit ve gizli kan vardır. Noninflamatuvar diare değişik bakteri, virus ve parazitlerle oluşur. Bu derleme yazıda, enterotoksijenik Escherichia coli, Vibrio cholerae, Clostridium perfringens gibi bakterilerin, Rotavirus gibi virusların, Giardia ve Cryptosporidium gibi protozoonların noninflamatuvar ishal patogenezindeki rolleri tartışılmıştır.

🔖

Cite This Article

ROTA, S., FİDAN, I. (2022). The pathogenesis of noninflammatory diarrhea. Türk Mikrobiyoloji Cemiyeti Dergisi, Cilt: 37 - Sayı: 4, 234–241. https://ajindex.com/articles/636004

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (9)

  1. Qadir A, Hussain N. GI Consult: Acute Diarrhea. Emerg Med 2004; 36:19-25. 2. http://www.cdc.ubc.ca/Publications/Presentations/Steiner_BEI_ Mar06.pdf 3. Aranda-Michel J, Giannella RA. Acute Diarrhea: A practical review. Am J Med 1999; 106: 670-676
  2. Brown T. Commentary. Ann Emergen Med 2003; 2:420-422 5.http://www.emedicine.com/med/byname/food-poisoning.htm 6.
  3. Satchell KJF. Activation and supression of the proinflammatory immune response by V. cholerae toxins. Microb Infect 2003; 5: 1241-1247 8. Haan L, Hirst TR. Cholera toxin: a paradigm for multifunctional engagement of cellular mechanisms (Review). Mol Memb Biol 2004; 21: 77-92
  4. Sanchez J, Holmgren J. Virulence factors, pathogenesis and vaccine protection in cholera and ETEC diarrhea. Curr Opin Immunol 2005; 17: 388-398 10. http://www.textbookofbacteriology.net/. Todar's Online Textbook of Bacteriology. Vibrio cholerae and Asiatic Cholera 11. Simmons CP, Clare S, Dougan G. Understanding mucosal responsiveness: lessons from enteric bacterial pathogens. Sem Immunol 2001; 13: 201-209 12. Fernandez Mlyakawa ME, Brero ML, Mateo NA. Cholera toxin modulates tne systemic immune responses against Vibrio choleraesurface antigens after repeated inoculations. Microbiol Immunol 2006; 50 607-619 13. Reidl J, Klose KE. Vibrio cholerae and cholera: out of the water and into the host. FEMS Microbiol Rev 2002; 26:125-139
  5. Murray PR, Rosenthal KS, Pfaller MA. Bacteriology pp: 191. In: Schmitt W ed, Medical Microbiology. 5 th ed. Philadelphia: Elsevier, 2005
  6. Sack DA, Sack RB, GB Nair, Siddique AK. Cholera. Lancet 2004; 363: 223-33 16. Paulovicova E, Machova E, Hostacka A, Bystricky S. Immunological properties of complex conjugates based on V. cholerae O1 Ogawa lipolysaccharide antigen. Clin Exp Immunol 2006; 144: 521-527
  7. Chatterjee SN, Chaudhuri K. Lypopolysaccharides of Vibrio cholerae: III: Biological functions. Biochi Biophy Acta 2006; 1762: 1-16 18. Girard MP, Steele D, Chaignat CL, Kieny MP. A review of vaccine research and development: human enteric infections. Vaccine 2006; 24: 2732-2750
  8. Qadri F, Ahmed F, Ahmed T, Svennerholm AM. Homologous and cross-reactive immune responses to enterotoxigenic Escherichia coli colonization factors in Bangladeshi children. Infect Immun 2006; 74: 4512-4518
  9. Byrd W, Cassels FJ. Long-term systemic and mucosal antibody responses measured in BALB/c mice following intranasal challenge with viable Enterotoxigenic Esch