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Comparison of antibiogram, virulence genes, ribotypes and DNA fingerprints of Vibrio cholerae of matching serogroups isolated from hospitalised diarrhoea cases and from the environment during 1997–1998 in Calcutta, India

S. CHAKRABORTY, P. GARG, T. RAMAMURTHY, M. THUNGAPATHRA^*, J.K. GAUTAM^*, C. KUMAR^*, S. MAITI^*, S. YAMASAKI, T. SHIMADA, Y. TAKEDA, A. GHOSH^* and G.B. NAIR

National Institute of Cholera and Enteric Diseases, Beliaghata, Calcutta - 700 010, *Institute of Microbial Technology, Chandigarh, India, Research Institute, International Medical Center of Japan, Shinjuku-ku, Tokyo 162 and National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162, Japan

Corresponding author: Dr G. B Nair (e-mail: gbnair{at}vsnl.com).

Received 16 Oct. 2000; revised version received 23 March 2001; accepted 3 April 2001.

Abstract

This study identified 17 matching serogroups of Vibrio cholerae belonging to serogroups other than O1 and O139 isolated from human cases and from the environment during a concurrent clinical and environmental study conducted in Calcutta, a cholera endemic area. Isolates within these matching serogroups were compared by various phenotypic and genotypic traits to determine if the environment was the source of the organisms associated with the disease. Clinical strains of V. cholerae were resistant to a greater number of drugs and exhibited multi-drug resistance compared with their environmental counterparts. Except for the presence of the genes for the El Tor haemolysin and the regulatory element ToxR in most of the strains of V. cholerae examined, non-O1, non-O139 V. cholerae strains lacked most of the other known virulence traits associated with toxigenic V. cholerae O1 or O139. Restriction fragment-length polymorphism of virulence-associated genes, ribotypes and DNA fingerprints of strains of matched serogroups showed considerable diversity, although some gene polymorphisms and ribotypes of a few strains of different serogroups were similar. It is concluded that despite sharing the same serogroup, environmental and clinical isolates were genetically heterogeneous and were of different lineages.

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