Top > JDR > Activity of Collaborative Research Center of Okayama Universit ...

single-dr.php

JDR Vol.9 No.5 pp. 774-783
(2014)
doi: 10.20965/jdr.2014.p0774

Review:

Views over last 60 days: 673

Activity of Collaborative Research Center of Okayama University for Infectious Disease in India

Sumio Shinoda*, Daisuke Imamura*, Tamaki Mizuno*,
and Shin-ichi Miyoshi**

*Collaborative Research Center of Okayama University for Infectious Disease in India, NICED-JICA Building, Banerjee Road, Beliaghata, Kolkata 700010, India

**Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 1-1-1 Tsushima-naka, Kita-ku, Okayama, Okayama 700-8530, Japan

Received:
March 11, 2014
Accepted:
April 9, 2014
Published:
October 1, 2014
Creative Commons License
Keywords:
Vibrio cholerae, VBNC, EL Tor variant, NICED, Rotavirus
Abstract
The Collaborative Research Center for Infectious Disease of Okayama University in India (CRCOUI) is located at the NICED (National Institute of Cholera and Enteric Diseases) in Kolkata, India. The main CRCOUI research project involves measure against diarrheal diseases based on JICA project conducted at the NICED. Specifically, this involved four study themes: (1) Active surveillance of diarrheal patients, (2) Development of dysentery vaccine, (3) Viable but nonculturable (VBNC) Vibrio cholerae, (4) Pathogenic mechanism of various diarrhogenic microorganisms. Diarrheal diseases are a major health problem in developing countries, so our project confirmed the detection system of diarrhogenic microorganisms including bacteria, viruses and protozoa. Project have been applied the system at 2 hospitals in Kolkata. To spread system use to other countries, training courses were conducted for researchers and technicians from the Vietnam and Indonesia Research Center, then similar active surveillance was started in both countries.
Cite this article as:
S. Shinoda, D. Imamura, T. Mizuno, and S. Miyoshi, “Activity of Collaborative Research Center of Okayama University for Infectious Disease in India,” J. Disaster Res., Vol.9 No.5, pp. 774-783, 2014.
Data files:
References
  1. [1] R. Koch, “Die Conferenz zur Erorterrung der Cholerafrage,” Deutche Med. Wochenschr, 10, pp. 499-507, 1884.
  2. [2] G. B. Nair, T. Ramamurthy, M. K. Bhattacharya, T. Krishnan, S. Ganguly, D. R. Saha, K. Rajendran, B. Manna, M. Ghosh, K. Okamoto, and Y. Takeda, “Emerging trends in the etiology of enteric pathogens as evidenced from an active surveillance of hospitalized diarrhoeal patients in Kolkata, India,” Gut Pathog., Vol.2, No.4, doi: 10.1186, 2010.
  3. [3] S. Chakraborty, G. B. Nair, and S. Shinoda, “Pathogenic vibrios in the natural aquatic environment,” Rev. Environ. Health, Vol.12, pp. 63-80, 1997.
  4. [4] P. Mukherjee, T. Ramamurthy, M. K. Bhattacharya, K. Rajendran, and A. K. Mukhopadhyay, “Campylobacter jejuni in hospitalized patients with diarrhea, Kolkata, India,” Emerg. Infect. Dis., Vol.19, pp. 1155-1156, 2013.
  5. [5] A. Sumi, K. Rajendran, T. Ramamurthy, T. Krishnan, G. B. Nair, K. Harigane, and N. Kobayashi, “Effect of temperature, relative humidity and rainfall on rotavirus infections in Kolkata, India,” Epidemiol. Infect., Vol.141, pp. 1652-1661, 2013.
  6. [6] S. Dutta, K. Rajendran, S. Roy, A. Chatterjee, P. Dutta, G. B. Nair, S. K. Bhattacharya, and S. I. Yoshida, “Shifting serotypes, plasmid profile analysis and antimicrobial resistance pattern of Shigellae strains isolated from Kolkata, India during 1995-2000,” Epidemiol. Infect., Vol.129, pp. 235-243, 2002.
  7. [7] S. Ghosh, G. P. Pazhani, G. Chowdhury, S. Guin, S. Dutta, K. Rajendran, M. K. Bhattacharya, Y. Takeda, S. K. Niyogi, G. B. Nair, and T. Ramamurthy, “Genetic characteristics and changing antimicrobial resistance among Shigella spp. Isolated from hospitalized diarrhoeal patients in Kolkata, India,” J. Med. Microbiol., Vol.60, pp. 1460-1466, 2011.
  8. [8] S. K. Niyogi, “Shigellosis,” J. Microbiol., Vol.43, pp. 133-143, 2005.
  9. [9] A. Phalipon, L. A. Mulard, and P. J. Sansonetti, “Vaccination against shigellosis: is it the path that is dif?cult or is it the difficult that is the path?” Microb. Infect., Vol.10, pp. 1057-1062, 2008.
  10. [10] M. M. Levine, K. L. Kotloff, E. M. Barry, M. F. Pasetti, and M. B. Sztein, “Clinical trials of Shigella vaccines: two steps forward and one step back on a long, hard road,” Nat. Rev. Microbiol., Vol.5, pp. 540-553, 2010.
  11. [11] S. Barman, R. Kumar, G. G. Choudhury, D. R. Saha, T. Wajima, T. Hamabata, T. Ramamurthy, G. B. Nair, Y. Takeda, and H. Koley, “Live noninvasive Shigella dysenteriae 1 strain induces homologous protective immunity in a guinea pig colitis model,” Microbiol. Immunol., Vol.55, pp. 683-693, 2011.
  12. [12] S. Barman, H. Koley, T. Ramamurthy, M. K. Chakrabarti, S. Shinoda, G. B. Nair, and Y. Takeda, “Protective immunity by oral immunization with heat-killed Shigella strains in a guinea pig colitis model,” Microbiol. Immunol., Vol.57, pp. 762-771, 2013.
  13. [13] A. Huq, R. R. Colwell, R. Rahman, A. Ali, M. A. Chowdhury, S. Parveen, D. A. Sack, and E. Russek-Cohen, “Detection of Vibrio cholerae O1 in the aquatic environment by fluorescent-monoclonal antibody and culture methods,” Appl. Environ. Microbiol., Vol.56, pp. 2370-2373, 1990.
  14. [14] M. S. Islam, M. K. Hasan, M. A. Miah, M. Yunus, K. Zaman, and M. J. Albert, “Isolation of Vibrio cholerae O139 synonym Bengal from the aquatic environment in Bangladesh: implications for disease transmission,” Appl. Environ. Microbiol., Vol.60, pp. 1684-1686, 1994.
  15. [15] M. M. Levine, J. B. Kaper, D. Herrington, G. Losonsky, J. G. Morris, M. L. Clements, R. E. Black, B. Tall, and R. Hall, “Volunteer studies of deletion mutants of Vibrio cholerae O1 prepared by recombinant techniques,” Infect. Immun., Vol.56, pp. 161-167, 1988.
  16. [16] D. B. Roszak and R. R. Colwell, “Survival strategies of bacteria in the natural environment,” Microbiol. Rev., Vol.51, pp. 365-379, 1987.
  17. [17] M. Alam, M. Sultana, G. B. Nair, R. B. Sack, D. A. Sack, A. K. Siddique, A. Ali, A. Huq, and R. R. Colwell, “Toxigenic Vibrio cholerae in the aquatic environment of Mathbaria, Bangladesh,” Appl. Environ. Microbiol., Vol.72, pp. 2849-2855, 2006.
  18. [18] S. M. Faruque, K. Biswas, S. M. Udden, Q. S. Ahmad, D. A. Sack, G. B. Nair, and J. J. Mekalanos, “Transmissibility of cholera: In vivo-formed biofilms and their relationship to infectivity and persistence in the environment,” Proc. Natl. Acad. Sci. USA, Vol.103, pp. 6350-6355, 2006.
  19. [19] M. Alam, M. Sultan, G. B. Nair, A. K. Siddique, N. A. Hasan, R. B. Sack, D. A. Sack, K. U. Ahmed, A. Sadique, H. Watanabe, C. J. Grim, A. Huq, and R. R. Colwell, “Viable but nonculturable Vibrio cholerae O1 in biofilms in the aquatic environment and their role in cholera transmission,” Proc. Natl. Acad. Sci. USA, Vol.104, pp. 17801-17806, 2007.
  20. [20] R. R. Colwell, P. Brayton, D. J. Grimes, D. B. Roszak, S. A. Huq, and L. M. Palmer, “Viable but non-culturable Vibrio cholerae and related pathogens in the environment: implications for release of genetically engineered microorganisms,” Biotechnology, Vol.3, pp. 817-820, 1985.
  21. [21] M. Halpern, O. Landsberg, D. Raats, and E. Rosenberg, “Culturable and VBNC Vibrio cholerae: interactions with chironomid egg masses and their bacterial population,” Microb. Ecol., Vol.53, pp. 285-293. 2007.
  22. [22] R. R. Colwell, P. Brayton, D. Henrington, B. D. Tall, A. Huq, and M. M. Levine, “Viable but nonculturable Vibrio cholerae O1 revert to a culturable state in the human intestine,” World J. Microb. Biotechnol., Vol.12, pp. 28-31, 1996.
  23. [23] S. Chaiyanan, S. Chaiyanan, C. Grim, T.Maugel, A. Huq, and R. R. Colwell, “Ultrastructure of coccoid viable but non-culturable Vibrio cholerae,” Environ. Microbiol., Vol.9, pp. 393-402, 2007.
  24. [24] M. Senoh, J. Ghosh-Banerjee, T. Ramamurthy, T. Hamabata, T. Kurakawa, M. Takeda, R. R. Colwell, G. B. Nair, and Y. Takeda, “Conversion of viable but nonculturable Vibrio cholerae to the culturable state by co-culture with eukaryotic cells,” Microbiol. Immunol., Vol.54, pp. 502-507, 2010.
  25. [25] M. Senoh, J. Ghosh-Banerjee, T. Ramamurthy, R. R. Colwell, S. Miyoshi, G. B. Nair, and Y. Takeda, “Conversion of viable but nonculturable enteric bacteria to the culturable state by co-culture with eukaryotic cells,” Microbiol. Immunol., Vol.56, pp. 342-345, 2012.
  26. [26] M. Senoh, J. Ghosh-Banerjee, T. Mizuno, S. Shinoda, S. Miyoshi, T. Hamabata, G. B. Nair, and Y. Takeda, “Isolation of viable but nonculturable Vibrio cholerae O1 from environmental water samples in Kolkata, India, in a culturable state,” Microbiol Open 2014 doi: 10.1002/mbo3.164.
  27. [27] J. B. Kaper, J. J. Morris, Jr., and M. M. Levine, “Cholera,” Clin. Microbiol. Rev., Vol.8, pp. 48-86, 1995.
  28. [28] G. B. Nair, S. M. Faruque, N. A. Bhuiyan, M. Kamruzzaman, A. K. Siddique, and D. A. Sack, “New variants of Vibrio cholerae O1 biotype El Tor with attributes of the classical biotype from hospitalized patients with acute diarrhea in Bangladesh,” J. Clin.Microbiol., Vol.40, pp. 3296-3299, 2002.
  29. [29] G. B. Nair, F. Qadri, J. Holmgren, A. M. Svennerholm, A. Safa, N. A. Bhuiyan, Q. S. Ahmed, S. M. Faruque, A. S. G. Faruque, Y. Takeda, and D. A. Sack, “Cholera due to altered El Tor strains of Vibrio cholerae O1 in Bangladesh,” J. Clin. Microbiol., Vol.44, pp. 4211-4213, 2006.
  30. [30] A. Safa, G. B. Nair, and R. Y. C. Kong, “Evolution of new variants of Vibrio cholerae O1,” Trends Microbiol., Vol.18, pp. 46-54, 2010.
  31. [31] A. Naha, G. P. Pazhani, M. Ganguly, S. Ghosh, T. Ramamurthy, R. K. Nandy, G. B. Nair, Y. Takeda, and A. K. Mukhopadhyay, “Development and evaluation of a PCR assay for tracking the emergence and dissemination of Haitian variant ctxB in Vibrio cholerae O1 strains isolated from Kolkata, India,” J. Clin. Microbiol., Vol.50, pp. 733-736, 2012.
  32. [32] D. Lantagne, G. B. Nair, F. Claudio, C. F. Lanata, and F. A. Cravioto, “The origin of cholera in Haiti,” J. Disast. Res., Vol.7, pp. 759-767, 2012.
  33. [33] C. S. Chin, J. Sorenson, J. B. Harris, W. P. Robins, R. P. Charles, R. R. Jean-Charles, J. Bullard, D. R. Webster, A. Kasarskis, P. Peluso, E. E. Paxinos, Y. Yamaichi, S. B. Calderwood, J. J. Mekalanos, E. E. Schadt, and M. K. Waldor, “The origin of the Haitian cholera outbreak strain,” N. Engl. J. Med., Vol.364, pp. 33-42, 2011.
  34. [34] G. Y. Ang, Y. Y. Choo, B. Kamarudin, H. T. Elina, A. Hussin, M. H. Hani, and C. Y. Yean, “Molecular evidence of cholera outbreak caused by a toxigenic Vibrio cholerae O1 El Tor variant strain in Kelantan, Malaysia,” J. Clin. Microbiol., Vol.48, pp. 3963-3969, 2010.
  35. [35] A. Naha, G. Chowdhury, J. Ghosh-Banerjee, M. Senoh, T. Takahashi, B. Ley, K. Thriemer, J. Deen, L. V. Seidlein, S. M. Ali, A. Khatib, T. Ramamurthy, R. K. Nandy, G. B. Nair, Y. Takeda, and A. K. Mukhopadhyyay, “Molecular characterization of highlevel-cholera-toxin-producing El Tor variant Vibrio cholerae strains in Zanzibar Archipelago of Tanzania,” J. Clin. Microbiol., Vol.51, pp. 1040-1045, 2013.
  36. [36] P. Ghosh, A. Naha, S. Basak, S. Ghosh, T. Ramamurthy, H. Koley, R. K. Nandy, S. Shinoda, H. Watanabe, and A. K. Mukhopadhyay, “Haitian variant tcpA in Vibrio cholerae O1 El Tor strains in Kolkata, India,” J. Clin. Microbiol., Vol.52, pp. 1020-1021, 2014.
  37. [37] D. Dutta, S. Chattopadhyay, P. Bagchi, U. C. Halder, S. Nandi, A. Mukherjee, A. Kobayashi, K. Taniguchi, and M. Chawla-Sarkar, “Active Participation of Cellular Chaperone Hsp90 in Regulating the Function of Rotavirus Nonstructural Protein 3 (NSP3),” J. Biol. Chem., Vol.286, pp. 20065-20077, 2011,
  38. [38] S. Chattopadhyay, T. Basak, M. K. Nayak, G. Bhardwaj, A. Mukherjee, R. Bhowmick, S. Sengupta, O. Chakrabarti, N. S. Chatterjee, and M. Chawla-Sarkar, “Identification of cellular calcium binding protein calmodulin as a regulator of rotavirus A infection during comparative proteomic study,” PLoS One., Vol.8, No.2, 2013. e56655.
  39. [39] P. Bagchi, R. Bhowmick, S. Nandi, M. Kant Nayak, andM. Chawla-Sarkar, “Rotavirus NSP1 inhibits interferon induced non-canonical NFκB activation by interacting with TNF receptor associated factor 2,” Virology, Vol.444, pp. 41-44, 2013.
  40. [40] E. Ghosh, A. Ghosh, A. N. Ghosh, T. Nozaki, and S. Ganguly, “Oxidative stress-induced cell cycle blockage and a proteaseindependent programmed cell death in microaerophilic Giardia lamblia,” Drug. Des. Devel. Ther., Vol.21, pp. 103-110, 2009.
  41. [41] D. Raj, E. Ghosh, A. K. Mukherjee, T. Nozaki, and S. Ganguly, “Differential gene expression in Giardia lamblia under oxidative stress: significance in eukaryotic evolution,” Gene, Vol.535, pp. 131-139, 2014.
  42. [42] T. Wajima, S. Sabui, S. Kano, T. Ramamurthy, N. S. Chatterjee, and T. Hamabata, “Entire sequence of the colonization factor coli surface antigen 6-encoding plasmid pCss165 from an enterotoxigenic Escherichia coli clinical isolate,” Plasmid, Vol.70, pp. 343-752, 2013.

Creative Commons License  This article is published under a Creative Commons Attribution-NoDerivatives 4.0 Internationa License.

*This site is desgined based on HTML5 and CSS3 for modern browsers, e.g. Chrome, Firefox, Safari, Edge, Opera.

Last updated on Apr. 19, 2024