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Microbiological and epidemiological investigation of cholera epidemic in Ukraine during 1994 and 1995

Published online by Cambridge University Press:  01 August 1998

C. G. CLARK ,
A. N. KRAVETZ ,
V. V. ALEKSEENKO ,
YU. D. KRENDELEV  and
W. M. JOHNSON
C. G. CLARK
Affiliation:
National Laboratory for Enteric Pathogens, Laboratory Centre for Disease Control, Health Canada, Ottawa, Canada
A. N. KRAVETZ
Affiliation:
National Laboratory for Enteric Pathogens, Laboratory Centre for Disease Control, Health Canada, Ottawa, Canada Laboratory of Biochemistry and Genetics of Micro-organisms, Kiev Research Institute of Epidemiology and Infectious Diseases, Kiev, Ukraine
V. V. ALEKSEENKO
Affiliation:
Laboratory of Cholera Infection, Kiev Research Institute of Epidemiology and Infectious Diseases, Ukraine
YU. D. KRENDELEV
Affiliation:
Laboratory of Biochemistry and Genetics of Micro-organisms, Kiev Research Institute of Epidemiology and Infectious Diseases, Kiev, Ukraine
W. M. JOHNSON
Affiliation:
National Laboratory for Enteric Pathogens, Laboratory Centre for Disease Control, Health Canada, Ottawa, Canada
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Abstract

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The Ukraine cholera epidemic of 1994 and 1995 was caused by Vibrio cholerae O1, serotype Ogawa, biotype El Tor. This epidemic was centred in the area around Respublika Krim (Crimea) and Mykolajiv, and spread to include parts of southern Ukraine. Cases of cholera occurred between September and November of 1994 and between June and October of 1995. The 32 fatalities among 1370 recorded cases (case fatality ratio, 2·3%) occurred throughout the course of the epidemic. V. cholerae from patients with cholera produced cholera toxin and were resistant to multiple antibiotics, though no resistance plasmids were found. Conjugation experiments suggested that resistance to multiple antibiotics may be present on a self-transmissible genetic element. Environmental sources of V. cholerae O1 El Tor included sewage, sea and surface water, and fresh water and marine fish. All but one of the environmental V. cholerae isolated during the epidemic were very similar to selected isolates from patients at the same time, supporting the role of these environmental sources in the spread of disease.

Type
Research Article
Information
Epidemiology & Infection , Volume 121 , Issue 1 , August 1998 , pp. 1 - 13
Copyright
© 1998 Cambridge University Press