Volume 16, Number 4—April 2010
Cholera Outbreak, Laos, 2007
To the Editor: Cholera is a major public health problem in countries where access to safe water and adequate sanitation cannot be guaranteed for all. Vibrio cholerae serogroups O1 and O139 are the causative agents of cholera (1). One of the most powerful virulence factors in this organism is cholera toxin encoded by the ctxAB gene, located on the CTX prophage. V. cholerae O1 is classified into 2 biotypes, classical and El Tor. The El Tor type of V. cholerae O1 is responsible for the ongoing seventh worldwide pandemic of cholera (2). The sequence of ctxB of a certain strain has been believed to correspond to its biotype; that is, a biotype classical strain has classical type ctxB, and a biotype El Tor strain has El Tor type ctxB. However, recent research studies suggest that novel types of V. cholerae O1, hybrid strains, and altered El Tor or El Tor variant strains (1,3) are emerging. Altered El Tor or El Tor variant strains are biotype El Tor but produce classical cholera toxin (3,4). Recent reports suggest that this type of V. cholerae O1 is spreading to many areas of the world (5).
In December 2007–January 2008, a cholera outbreak occurred in Xekong Province in southeastern Laos, in the Mekong Basin. The first case of the outbreak was detected on December 23, 2007. The outbreak spread to 10 villages and lasted through January 2008. Specifically, in the Thateng District, 117 cases occurred and 2 deaths were reported. The sources of the outbreak were suspected to be regularly used water. In October 2007, 2 months before the outbreak, 3 sporadic cases of V. cholerae infection had been identified in Vientiane (the capital city) and Xaignabouri Province in north-central and northwestern Laos, respectively. The outbreak investigation in the Xekong Province identified no linkage between these sporadic cases and the outbreak cases.
In this study, we analyzed 18 V. cholerae isolates obtained in 2007: 3 were from patients with sporadic cases, and 15 were from the Xekong outbreak (13 from patients and 2 from water samples). All the isolates were serotype O1 Ogawa and biotype El Tor, but their ctxB types were classical, according to the method previously described (6). This finding indicates that they were the type of altered El Tor.
We used pulsed-field gel electrophoresis (PFGE) to investigate relationships between the isolates according to the PulseNet protocol (7). All 18 isolates from the sporadic cases and the outbreak in 2007 displayed profiles indistinguishable from each other (Figure). We also compared 2 additional V. cholerae O1 isolates, 1 from a patient in Vientiane in 1998 and another from a patient in Louangphabang in 2000 (Figure). The profiles of the isolates obtained in 1998 and 2000 clearly differed from those obtained in 2007. These results indicate that all isolates from sporadic and outbreak cases in 2007 were likely from the same source of contamination, although extensive epidemiologic investigation did not identify any common source.
Nguyen et al. characterized the isolates from a cholera outbreak in Vietnam from late 2007 to early 2008 (8). Their report suggests that the isolates from the outbreaks in Vietnam and Laos shared the same elements of the CTX prophage. Our study suggests a common source for the strains of sporadic cases in Vientiane and Xaignabouri Province in October 2007 and those of the outbreak in Xekong Province in December 2007. Molecular typing suggests that a novel clone of V. cholerae O1 is being disseminated along the Mekong Basin. However, no epidemiologic association has been identified so far. Thus, a more extensive regionwide surveillance system is needed to identify and control V. cholerae infection in Laos and neighboring countries.
We thank Khambien Yanphichit, the Xekong Province team, and the epidemiologic team of the National Center for Laboratory and Epidemology, Vientiane, Laos.
This study was partly supported by grants-in-aid from the Ministry of Health, Labour and Welfare of Japan (H18-Shokuhin-Ippan-003, H20-Shinko-Ippan-013, H20-Shinko-Ippan-015, and International Health Cooperation Research 18C-5), and from Reiko Tsuyuoka and her team, CSR, World Health Organization, Laos.
- World Health Organization. Cholera 2007. Wkly Epidemiol Rec. 2008;83:269–83.PubMedGoogle Scholar
- Sack DA, Sack RB, Nair GB, Siddique AK. Cholera. Lancet. 2004;363:223–33. DOIPubMedGoogle Scholar
- Raychoudhuri A, Mukhopadhyay AK, Ramamurthy T, Nandy RK, Takeda Y, Nair GB. Biotyping of Vibrio cholerae O1: time to redefine the scheme. Indian J Med Res. 2008;128:695–8.PubMedGoogle Scholar
- Nair GB, Qadri F, Holmgren J, Svennerholm AM, Safa A, Bhuiyan NA, Cholera due to altered El Tor strains of Vibrio cholerae O1 in Bangladesh. J Clin Microbiol. 2006;44:4211–3. DOIPubMedGoogle Scholar
- Safa A, Sultana J, Dac Cam P, Mwansa JC, Kong RY. Vibrio cholerae O1 hybrid El Tor strains, Asia and Africa. Emerg Infect Dis. 2008;14:987–8. DOIPubMedGoogle Scholar
- Morita M, Ohnishi M, Arakawa E, Bhuiyan NA, Nusrin S, Alam M, Development and validation of a mismatch amplification mutation PCR assay to monitor the dissemination of an emerging variant of Vibrio cholerae O1 biotype El Tor. Microbiol Immunol. 2008;52:314–7. DOIPubMedGoogle Scholar
- Cooper KL, Luey CK, Bird M, Terajima J, Nair GB, Kam KM, Development and validation of a PulseNet standardized pulsed-field gel electrophoresis protocol for subtyping of Vibrio cholerae. Foodborne Pathog Dis. 2006;3:51–8. DOIPubMedGoogle Scholar
- Nguyen BM, Lee JH, Cuong NT, Choi SY, Hien NT, Anh DD, Cholera outbreaks caused by an altered Vibrio cholerae O1 El Tor biotype strain producing classical cholera toxin B in Vietnam in 2007 to 2008. J Clin Microbiol. 2009;47:1568–71. DOIPubMedGoogle Scholar
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Table of Contents – Volume 16, Number 4—April 2010
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Hidemasa Izumiya, Department of Bacteriology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 162-8640, Japan