Intestinal infection with Vibrio cholerae results in the loss of large volumes of watery stool, leading to severe and rapidly progressing dehydration and shock. Without adequate and appropriate rehydration therapy, severe cholera kills about half of affected individuals. Cholera toxin, a potent stimulator of adenylate cyclase, causes the intestine to secrete watery fluid rich in sodium, bicarbonate, and potassium, in volumes far exceeding the intestinal absorptive capacity. Cholera has spread from the Indian subcontinent where it is endemic to involve nearly the whole world seven times during the past 185 years. V cholerae serogroup O1, biotype El Tor, has moved from Asia to cause pandemic disease in Africa and South America during the past 35 years. A new serogroup, O139, appeared in south Asia in 1992, has become endemic there, and threatens to start the next pandemic. Research on case management of cholera led to the development of rehydration therapy for dehydrating diarrhoea in general, including the proper use of intravenous and oral rehydration solutions. Appropriate case management has reduced deaths from diarrhoeal disease by an estimated 3 million per year compared with 20 years ago. Vaccination was thought to have no role for cholera, but new oral vaccines are showing great promise.

BackgroundThe global burden of cholera is largely unknown because the majority of cases are not reported. The low reporting can be attributed to limited capacity of epidemiological surveillance and laboratories, as well as social, political, and economic disincentives for reporting. We previously estimated 2.8 million cases and 91,000 deaths annually due to cholera in 51 endemic countries. A major limitation in our previous estimate was that the endemic and non-endemic countries were defined based on the countries’ reported cholera cases. We overcame the limitation with the use of a spatial modelling technique in defining endemic countries, and accordingly updated the estimates of the global burden of cholera.Methods/Principal FindingsCountries were classified as cholera endemic, cholera non-endemic, or cholera-free based on whether a spatial regression model predicted an incidence rate over a certain threshold in at least three of five years (2008-2012). The at-risk populations were calculated for each country based on the percent of the country without sustainable access to improved sanitation facilities. Incidence rates from population-based published studies were used to calculate the estimated annual number of cases in endemic countries. The number of annual cholera deaths was calculated using inverse variance-weighted average case-fatality rate (CFRs) from literature-based CFR estimates. We found that approximately 1.3 billion people are at risk for cholera in endemic countries. An estimated 2.86 million cholera cases (uncertainty range: 1.3m-4.0m) occur annually in endemic countries. Among these cases, there are an estimated 95,000 deaths (uncertainty range: 21,000-143,000).Conclusion/SignificanceThe global burden of cholera remains high. Sub-Saharan Africa accounts for the majority of this burden. Our findings can inform programmatic decision-making for cholera control.

SUMMARY Vibrio parahaemolyticus is recognized as a cause of food-borne gastroenteritis, particularly in the Far East, where raw seafood consumption is high. An unusual increase in admissions of V. parahaemolyticus cases was observed at the Infectious Diseases Hospital in Calcutta, a city in the northeastern part of India, beginning February 1996. Analysis of the strains revealed that a unique serotype, O3:K6, not previously isolated during the surveillance in Calcutta accounted for 50 to 80% of the infections in the following months. After this report, O3:K6 isolates identical to those isolated in Calcutta were reported from food-borne outbreaks and from sporadic cases in Bangladesh, Chile, France, Japan, Korea, Laos, Mozambique, Peru, Russia, Spain, Taiwan, Thailand, and the United States. Other serotypes, such as O4:K68, O1:K25, and O1:KUT (untypeable), that had molecular characteristics identical to that of the O3:K6 serotype were subsequently documented. These serotypes appeared to have diverged from the O3:K6 serotype by alteration of the O:K antigens and were defined as “serovariants” of the O3:K6 isolate. O3:K6 and its serovariants have now spread into Asia, America, Africa, and Europe. This review traces the genesis, virulence features, molecular characteristics, serotype variants, environmental occurrence, and global spread of this unique clone of V. parahaemolyticus.

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Cholera has historically occurred in periodic epidemics, with the most severe epidemics limited to a few countries, namely Bangladesh, India, and countries in Africa and South America. During the past three decades, however, this disease has occurred in geographical areas from which it had seemingly disappeared almost a century ago (35). Including these new appearances, epidemics have been reported in over 75 countries in South America, Africa, and Asia during the past decade (38). In addition, each year sporadic cases are reported in other countries around the world (38).Interestingly, cholera is one of the few bacterial diseases known for its pandemicity, and until 1992, all epidemics of cholera were caused by Vibrio cholerae serogroup O1. In the latter part of 1992, a newly recognized O139 serogroup was isolated in areas surrounding the Bay of Bengal and was linked to major epidemics, first in Madras on the eastern coast of India and then in the southern part of Bangladesh. Later it was detected in neighboring countries and has continued to persist in that geographic region (6, 28).In 1992 in Bangladesh during a 12-week period, there were approximately 220,000 cases of cholera caused by serotype O139, with over 8,000 deaths, more deaths than in all of Latin America that same year (31,35). Cholera is known to be a disease with a high mortality (Ϸ60% if untreated); with adequate treatment (intravenous and oral rehydration therapy, supplemented with appropriate antibiotics) the mortality drops to Ͻ1.0% (5, 26). The large numbers of deaths indicate that adequate therapy was not available to the many persons who died (6,35).In the recent history of cholera, most major epidemics originated in coastal regions, including both the South American epidemic that began in the coastal regions of Peru, spreading to 21 countries, including Mexico, and the new O139 outbreak in India and Bangladesh. In Dhaka City and a rural area of Bangladesh, Matlab, cholera occurs year-round, with a distinct pattern of two peaks of disease, one in the spring and the other in the fall (16,30).The presence of V. cholerae O1 year-round via its commensal association with plankton was established by Colwell and coworkers using direct detection methods (17). It is still not certain what triggers the continuing seasonal epidemics of cholera in Bangladesh and what determines the persistence and multiplication of V. cholerae O1 and O139 in the choleraendemic regions of the world. However, coexistence of V. cholerae O1 and O139 serogroups in association with plankton has

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The relationship among (i ) the local incidence of cholera, (ii) the prevalence in the aquatic environment of Vibrio cholerae, and (iii) bacterial viruses that attack potentially virulent O1 and O139 serogroup strains of this organism (cholera phages) was studied in Dhaka, Bangladesh. Over nearly a 3-year period, we found that significantly more environmental water samples contained either a phage or a phage-susceptible V. cholerae strain than both (P < 0.00001). The number of cholera patients varied seasonally during this period and frequently coincided with the presence of pathogenic V. cholerae strains in water samples that otherwise lacked detectable cholera phages. Interepidemic periods were characterized by water samples containing cholera phages but no viable bacteria. Our data support the conclusion that cholera phages can influence cholera seasonality and may also play a role in emergence of new V. cholerae pandemic serogroups or clones.bacteriophage ͉ seasonality ͉ epidemiology ͉ emergence ͉ lysogeny E pidemics of cholera caused by toxigenic Vibrio cholerae belonging to the O1 or O139 serogroups are a major public health problem in many developing countries of Asia, Africa, and Latin America (1). Cholera epidemics occur with seasonal regularity in the Ganges delta region of Bangladesh and India. Epidemics usually occur twice during a year, with the highest number of cases just after the monsoon during September to December. A somewhat smaller peak of cholera cases also is observed during the spring, between March and May. Although V. cholerae is a human pathogen, these bacteria constitute part of the normal aquatic flora in estuarine environments, and water is clearly a vehicle for transmission of V. cholerae. Although the seasonality of cholera in Bangladesh and elsewhere has been temporally associated with numerous physical and biological parameters (2), these associations do not directly cause epidemics, nor do they end them. More than a century of public health experience has shown that toxigenic O1 and O139 V. cholerae cells cause cholera epidemics and that the elimination of these cells from drinking water ends cholera epidemics. The parameters that directly modulate the level of viable cells belonging to the pathogenic clones of V. cholerae O1 and O139 in the Ganges delta aquatic environment remain unknown. Furthermore, the fact that pathogenic strains of V. cholerae are clonally distinct from environmental, nonpathogenic V. cholerae strains (1) undermines proposed mechanisms of seasonality and pandemic spread that are based on data from studies measuring the abundance of all Vibrio species in the aquatic environment (2).Bacterial viruses (phages) are known to play a critical role in the evolution of pathogenic bacterial species, and V. cholerae in particular. For example, cholera toxin genes are transferred to nontoxigenic strains by means of a lysogenic filamentous phage, CTX⌽ (3). Here we show that the presence of bacterial viruses acting on V. cholerae O1 or O139 (cholera phages or vibriopha...

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