Cholera is an acute bacterial, intestinal infection caused by toxigenic Vibrio cholerae O-group 1 or O-group 139. Many other serogroups of V. cholerae, with or without the cholera toxin gene (including the nontoxigenic strains of the O1 and O139 serogroups), can cause a choleralike illness. Only toxigenic strains of serogroups O1 and O139 have caused widespread epidemics and are reportable to the World Health Organization (WHO) as “cholera.”
V. cholerae O1 has 2 biotypes, classical and El Tor, and each biotype has 2 distinct serotypes, Inaba and Ogawa. The symptoms of infection are indistinguishable, although more people infected with the El Tor biotype remain asymptomatic or have only a mild illness. Globally, most cases of cholera are caused by O1 El Tor organisms. In recent years, an El Tor variant that has characteristics of both classical and El Tor biotypes and may be more virulent than older El Tor strains has emerged in Asia and spread to Africa and the Caribbean.
Toxigenic V. cholerae O1 and O139 are free-living bacterial organisms found in fresh and brackish water, often in association with copepods or other zooplankton, shellfish, and aquatic plants. Cholera infections are most commonly acquired from drinking water in which V. cholerae is found naturally or into which it has been introduced from the feces of an infected person. Other common vehicles include contaminated fish and shellfish. Other foods, including produce, are less commonly implicated. Direct transmission from person to person, even to health care workers during epidemics, has been reported but is not frequent.
Since 1961, the seventh pandemic of cholera, caused by V. cholerae serogroup O1, biotype El Tor, has spread from Indonesia through most of Asia into Eastern Europe and Africa, and from North Africa to the Iberian Peninsula. In 1991, an extensive epidemic began in Peru and spread to neighboring countries in the Western Hemisphere. Although few cases of cholera occur in South or Central America, V. cholerae O1 remains endemic in much of Africa and South and Southeast Asia. V. cholerae O139 spread rapidly through Asia in the early 1990s but has since remained localized to a few areas in Asia. In October 2010, a cholera epidemic began in Haiti, just 10 months after a devastating earthquake destroyed the Haitian capital of Port-au-Prince and surrounding areas. During the first year of the outbreak, 480,577 cases and 6,673 deaths were reported. In the early weeks of the outbreak, the case-fatality ratio (CFR) was 3%–4%, but declined after improvements in access to care; the CFR for Haiti was 0.84% in 2011 compared with 2.22% in 2010. In November 2010, cholera was first reported in the neighboring Dominican Republic, with 21,432 cases and 363 deaths reported by December 2011. Cholera is likely to persist in Haiti at endemic levels because of the lack of safe water and sanitation infrastructure, with the potential for localized outbreaks and seasonal spikes in cases associated with heavy rainfall. Sporadic cases associated with travel to or from Hispaniola may continue to occur.
Most cholera cases go unreported. In 2011, 58 countries reported 589,854 cholera cases and 7,816 cholera deaths (CFR, 1.3%) to WHO. The 2011 global cholera case numbers represent an 85% increase from 2010. Since 2010, there has been a geographic shift in cholera incidence from Africa to the Americas as a result of the Haiti outbreak, which accounted for 55% and >57% of all cholera cases reported in 2010 and 2011, respectively. From 2001 through 2009, >90% of cholera cases were reported from Africa, including 98% of cases and 99% of deaths during 2009. Cholera has the potential to emerge in dramatic epidemics, as was seen with the massive outbreaks that affected Zimbabwe in 2008 and 2009, with close to 100,000 cases and >4,000 deaths reported, and with the current epidemic in Haiti, with >500,000 cases and 7,000 deaths reported during 2010 and 2011.
From 1999 through 2011, 86 confirmed cases of cholera in the United States were acquired abroad; of these, 40 were associated with the epidemic in Hispaniola in 2010 and 2011. Travelers who follow the usual tourist itineraries and who observe safe food and water recommendations and hygiene precautions while in countries reporting cholera have virtually no risk. The risk is increased for those who drink untreated water, do not follow proper hygiene recommendations, or eat raw or poorly cooked food, especially seafood, in endemic or outbreak settings. Although rare, 2 cases of cholera have been reported among volunteer US health care workers caring for cholera patients during the peak period of the epidemic in Haiti; recent evidence shows that lack of handwashing supplies at treatment centers may lead to diarrheal illness and other health care–associated infections.
Two reports of cholera have been associated with food served on international flights, most recently in 1992, during the Latin American epidemic, on a flight from Argentina to Los Angeles. CDC consequently advised the International Air Transport Association that prepackaged oral rehydration salts should be carried on international flights and that certain food items (such as shrimp) prepared in cities with cholera epidemics should not be served. Airline flights have not been implicated in any subsequent cases of cholera.
Cholera infection is most often asymptomatic or results in a mild gastroenteritis. Severe cholera is characterized by acute, profuse watery diarrhea, described as “rice-water stools,” and often nausea and vomiting, leading to volume depletion. Signs and symptoms include tachycardia, loss of skin turgor, dry mucous membranes, hypotension, and thirst. Additional symptoms, including muscle cramps, are secondary to the resulting electrolyte imbalances. If untreated, rapid loss of body fluids can lead to severe dehydration, hypovolemic shock, and death within hours. With adequate and timely rehydration, CFRs are <1%. Most people infected with toxigenic V. cholerae will be asymptomatic or have mild diarrhea.
Cholera is confirmed through culture of a stool specimen or rectal swab. Cary-Blair medium can be used for transport, and selective media such as taurocholate-tellurite-gelatin agar and thiosulfate-citrate-bile salts (TCBS) agar may be used for isolation and identification. Reagents for serogrouping V. cholerae isolates are available in all state health department laboratories. Commercially available rapid test kits do not yield an isolate for antimicrobial susceptibility testing and subtyping and should not be used for routine diagnosis. All isolates obtained in the United States should be sent to CDC via state health department laboratories for cholera toxin testing and subtyping. Cholera is a nationally reportable disease.
Rehydration is the cornerstone of cholera treatment. Oral rehydration solution and, when necessary, intravenous fluids and electrolytes, if administered in a timely manner and in adequate volumes, will reduce CFRs to well under 1%. Antibiotics reduce fluid requirements and duration of illness. Antimicrobial therapy is indicated for moderate and severe cases, which can be treated with doxycycline, tetracycline, erythromycin, azithromycin, or ciprofloxacin. Whenever possible, antimicrobial susceptibility testing should inform treatment choices. Zinc supplementation reduces the severity and duration of cholera and other diarrheal diseases in children in resource-limited areas.
No cholera vaccine is currently licensed in the United States. Two oral vaccines are prequalified by WHO and are available outside the United States: Dukoral (Crucell, the Netherlands) and Shanchol (Shantha Biotechnics, India). CDC does not recommend cholera vaccines for US travelers because of the low risk of cholera and the unavailability of vaccines in the United States. No country or territory requires vaccination against cholera as a condition for entry.
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