Enterotoxic, neurotoxic and cytotoxice demonstrated by shiga toxin (2d) producing escherichia coli in experimental models

Authors

  • Chowdhury Rafiqul Ahsan Departemnt of Microbiology, University of Dhaka, Dhaka, Bangaldesh. https://orcid.org/0000-0001-5024-6293
  • Kohinur Begum Department of Pharmacy, ASA University, Dhaka, Bangladesh.
  • Enamul Kabir Department of Pathology, Sir Salimullah Medical College, Dhaka, Bangladesh.
  • Alam Nur-E- Kamal Department of Biology, Medgar Evers College of the City University of New York, Brollklyn, N.Y. 11225, USA
  • Kaisar Ali Talukder Department of Biotechnology and Genetic Engineering, Mawlana Bhashani Science and Technology University, Tangail, Bangladesh.

DOI:

https://doi.org/10.3329/bmrcb.v46i1.47468

Keywords:

Stx2d, cytotoxic effect, enterotoxic effect, neurotoxic effect

Abstract

Background: Shiga toxin (Stx) producing Escherichia coli (STEC) colonize human intestinal tract and their infections have asymptomatic clinical manifestations which cause local and systemic pathological changes.

Objectives: This study intended to establish the role of Shiga toxin (Stx2d) in developing clinical manifestations in STEC infections using experimental models.

Methods: A total 300 stool samples were screened from hospitalised diarrhoeal patients enrolled in 2% surveillance system at International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b). The stx gene profile including their variants was identified byPCR.stx2d gene positive STEC PT187 was selected for toxin (s) preparation.Toxin was prepared by centrifugation of culture supernatant. Enterotoxicand paralytic-lethal activities were tested in rabbit ileal loops and mice, respectively.  Histopathological study of the rabbit ileal loop segments and different tissues of mice  by paraffin embedded method and stained by H & E staining. Cytotoxic effect was performed on  HeLa cells.

Results: Nine STEC strains were identified for stx2 gene positive.  Among them STEC PT187 was found stx2d gene positive strain and selected for toxic activities. Toxin (s) responsible for causing accumulation of fluid in rabbit ileal loops and its segments showed inflammation and enterocytenecrosis. In mouse model, toxin(s) was found to cause hind limbs paralysis and death. Brain, spinal cord and kidney tissue of mice showed histopathological changes. Toxin (s) also showed positive cytotoxic activity in HeLa cell.

Conclusion: In this study, results indicated that Stx2d producing E. coli exhibit not only enterotoxic activity, but also cause impaired neurological functions and cytotoxic effect.

Bangladesh Med Res Counc Bull 2020; 46(1): 41-47

Downloads

Download data is not yet available.
Abstract
28
PDF
40 Online View
0

Downloads

Published

2020-06-10

How to Cite

Ahsan, C. R., Begum, K., Kabir, E., Kamal, A. N.-E.-., & Talukder, K. A. (2020). Enterotoxic, neurotoxic and cytotoxice demonstrated by shiga toxin (2d) producing escherichia coli in experimental models. Bangladesh Medical Research Council Bulletin, 46(1), 41–47. https://doi.org/10.3329/bmrcb.v46i1.47468

Issue

Vol. 46 No. 1 (2020)

Section

Research Papers

License

Authors who publish with this journal agree to the following terms.

Authors retain copyright and grant the journal right of first publication.

Creative Commons Licence
Articles in the Bangladesh Medical Research Council Bulletin are licensed under a Creative Commons Attribution 4.0 International License (CC-BY) that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.

Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.

Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).