Volume 17, Number 1—January 2011
Vibrio cholerae O1 in 2 Coastal Villages, Papua New Guinea
To the Editor: Cholera outbreak reports are of international public health interest, especially in areas that were previously cholera free (1). Although many recent cholera outbreaks have originated in coastal areas (2), identifying the source of cholera introduction has been challenging (1). The detection of Vibrio cholerae in coastal, brackish and riverine waters in cholera-endemic and cholera-free areas supports the view that autochtonous V. cholerae is involved in the introduction of cholera (3,4). To our knowledge, cholera has not been reported in Papua New Guinea, despite social and environmental conditions likely to facilitate transmission and the nation's close proximity to cholera-endemic countries (5,6).
On August 6, 2009, a physician who visited the coastal village of Lambutina reported an outbreak of acute watery diarrhea that was associated with the death of his father and 4 other persons from this and a neighboring village. The outbreak began in the village of Nambariwa and spread to neighboring Lambutina, Morobe Province. From August 13, multidisciplinary teams worked with the community to reduce the number of deaths through early identification and treatment of case-patients. The teams also worked to limit transmission through improvements to the water and sanitation infrastructure and by encouraging better hygiene practices among the villagers. A suspected case of cholera was defined as acute watery diarrhea or vomiting in a resident of Lambutina or Nambariwa villages since July 22, 2009. In the 2 villages, 77 cases were identified; attack rates were 14% in Lambutina (48/343) and 5.5% in Nambariwa (29/532). The overall case-fatality ratio was 6.5% (5/77); 2 patients died after they were discharged from the referral hospital.
A retrospective frequency-matched case–control study was conducted in Lambutina to identify the risk factors associated with suspected cholera. Neighborhood controls (± 5 years of age) were selected from unaffected households. Univariate and multivariate analyses were conducted with STATA version 10 (StataCorp., College Station, TX, USA).
Of the 48 case-patients in Lambutina, 43 participated in the study with 43 age-matched controls. In addition to having close contact with patients who had cholera, univariate analysis showed that case-patients were more likely to have had several exposures related to the death of other patients (Table). However, having close contact with a patient was the only independent risk factor (adjusted odds ratio 4.8, 95% confidence interval 1.7–13.4) (Table). Close contact included providing nursing care for patients or carrying patients onto boats for transport to health care facilities.
From the 10 collected samples, 4 isolates were confirmed as V. cholerae O1, biotype El Tor, serotype Ogawa, by PCR detection of an O1-specific region of the rfb gene using established methods and PCR amplification of the tcpA gene polymorphism specific for the El Tor biotype (7). The ctxAB, vct genes (present in toxigenic strains) and the hemolysin gene hlyA (present in all V. cholerae strains) were detected by PCR in all 4 isolates.
Although health authorities promptly identified and responded to the outbreak, they could not determine its origin. The El Niño weather phenomenon generates increased rainfall and elevated sea surface temperatures and is a predictor of cholera outbreaks (8), which puts more coastal areas at risk for such outbreaks (9). During this outbreak, Papua New Guinea reported above-average rainfall (10) and warmer sea surface temperatures. Although cholera may have been introduced to Papua New Guinea through an infectious traveler or by other means, climatic factors may have initiated plankton blooms, the abundance of which have also been associated with increased presence of V. cholerae O1. Sea and estuarine waters of these villages are plausible sources of introduction.
In Lambutina, the age-specific attack rates were lowest among young children and increased among persons of middle age and among the elderly. Those providing patient care and lifting during transportation as well as those washing the bodies of the deceased may have been more represented in the >40 years age group; however, this situation may not explain the high attack rates among the elderly.
Generally, after a cholera outbreak is detected, interventions aim to reduce the proportion of deaths to <1%. The overall case-fatality ratio in the outbreak discussed here was 6.5%, which reflects the challenges to accessing adequate health care in remote settings. This difficulty is exacerbated when the disease occurs for the first time because cholera awareness and preparedness will be weak, as can be seen in the early management of cases during this outbreak. Villagers who have close contact with cholera patients are at greater risk for disease and should be a focus of interventions to limit transmission (e.g., eliminating ingestion of contaminated water, improving hygiene and sanitation). Education to increase awareness of the disease and enhanced access to low-osmolarity oral rehydration solution, Hartmann solution, and zinc supplements are essential.
Cholera-endemic and cholera–nonendemic countries with coastal populations are at an increasing risk for cholera outbreaks. Adequate preparation by the health care system is vital to avoid excess deaths.
We thank John Savill, Deidre Davis, Darrel Cecil, Temas Ikanofi, Leomeldo Latorre, and Louisa Wanma for laboratory support; and Anthony Gomes, Irwin Law, and Eigil Sorensen for technical advice.
- Seas C, Miranda J, Gil AI, Leon-Barua R, Patz J, Huq A, New insights on the emergence of cholera in Latin America during 1991: the Peruvian experience. Am J Trop Med Hyg. 2000;62:513–7.
- Lobitz B, Beck L, Huq A, Wood B, Fuchs G, Faruque S, Climate and infectious disease: use of remote sensing for detection of Vibrio cholerae by indirect measurement. Proc Natl Acad Sci U S A. 2000;97:1438–43.
- Lipp EK, Rivera ING, Gil AI, Espeland EM, Choopun N, Louis VR, Direct detection of Vibrio cholerae and ctxA in Peruvian coastal water and plankton by PCR. Appl Environ Microbiol. 2003;69:3676–80.
- Colwell RR, Seidler RJ, Kaper J, Joseph SW, Garges S, Lockman H, Occurrence of Vibrio cholerae serotype O1 in Maryland and Louisiana estuaries. Appl Environ Microbiol. 1981;41:555–8.
- Simanjuntak CH, Larasati W, Arjoso S, Putri M, Lesmana M, Oyofo BA, Cholera in Indonesia in 1993–1999. Am J Trop Med Hyg. 2001;65:788–97.
- Agtini MD, Soeharno R, Lesmana M, Punjabi NH, Simanjuntak C, Wangsasaputra F, The burden of diarrhoea, shigellosis, and cholera in North Jakarta, Indonesia: findings from 24 months surveillance. BMC Infect Dis. 2005;5:89.
- Keasler SP, Hall RH. Detecting and biotyping Vibrio cholerae O1 with multiplex polymerase chain reaction. Lancet. 1993;341:1661.
- Colwell RR. Global climate and infectious disease: the cholera paradigm. Science. 1996;274:2025–31.
- McMichael A. Planetary overload—global environmental change and the health of the human species. Cambridge (UK): Cambridge University Press; 1993.
- National Institute of Water and Atmospheric Research. Climate developments in June 2009 [cited 2010 Nov 23]. http://www.niwa.co.nz/our-science/climate/publications/all/icu/2009-07/month