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. This strain is responsible for the epidemic on Hispaniola and may cause more severe episodes of cholera and higher death rates.
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.
Cholera is endemic in approximately 50 countries and has the potential to emerge in dramatic epidemics; unfortunately, most cases go unreported. V. cholerae O1 is 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 large cholera epidemic began in Haiti, just 10 months after a devastating earthquake destroyed the Haitian capital of Port-au-Prince and surrounding areas. Cholera is likely to persist in Haiti at endemic levels with the potential for localized outbreaks and elevated case counts, especially during the rainy season, for the foreseeable future. After it emerged in Haiti, cholera spread to a number of other countries, including the Dominican Republic and Cuba. Sporadic cases associated with travel to or from the Caribbean may continue to occur.
From 2001 through 2013, 123 confirmed cases of cholera in the United States were acquired abroad; of these, 63 were associated with the epidemic in Hispaniola. Risk of infection is highest for travelers who are traveling to countries where cholera is endemic or there is an active epidemic. Haiti continues to be the primary source of travel-associated cholera cases, even though cases among US travelers in 2013 declined to 2010 levels. 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 of acquiring cholera. 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, several cases of cholera have been reported among US health care workers caring for cholera patients in Haiti and in the United States.
Cholera most commonly manifests as watery diarrhea in an afebrile person. Severe cholera is characterized by acute, profuse watery diarrhea, described as “rice-water stools,” and often nausea and vomiting and can rapidly lead to severe 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, case-fatality rates (CFRs) are <1%.
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 agar may be used for isolation and identification. Reagents for serogrouping V. cholerae isolates are available in 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 <1%. Antibiotics reduce fluid requirements and duration of illness and are indicated for moderate and severe cases. Whenever possible, antimicrobial susceptibility testing should inform treatment choices, which may include doxycycline, tetracycline, erythromycin, azithromycin, or ciprofloxacin. Multidrug-resistant isolates are emerging, particularly in South Asia, with resistance to quinolones, trimethoprim-sulfamethoxazole, and tetracycline. The strain from Hispaniola is also multidrug resistant; however, it is still sensitive to doxycycline and tetracycline. Zinc supplementation reduces the severity and duration of cholera and other diarrheal diseases in children in resource-limited areas.
Safe food and water precautions and frequent handwashing are critical in preventing cholera (see Chapter 2, Food & Water Precautions). Chemoprophylaxis is not indicated.
No cholera vaccine is currently licensed in the United States. Two oral vaccines are prequalified by WHO and are available in many countries outside the United States: Dukoral (Crucell, the Netherlands) and Shanchol (ShanthaBiotechnics, India). No country or territory requires vaccination against cholera as a condition for entry.
Gaffga NH, Tauxe RV, Mintz ED. Cholera: a new homeland in Africa? Am J Trop Med Hyg. 2007 Oct;77(4):705–13.
Haitian Ministry of Public Health and Population (MSPP). Ministere de la SantePubliqueet de la Population. Port-au-Prince, Haiti: Haitian Ministry of Public Health and Population; 2013 [cited 2014 Jun 19]. Available from: http://mspp.gouv.ht.
Harris JB, Larocque RC, Charles RC, Mazumder RN, Khan AI, Bardhan PK. Cholera’s western front. Lancet. 2010 Dec 11;376(9757):1961–5.
Harris JB, LaRocque RC, Qadri F, Ryan ET, Calderwood SB. Cholera. Lancet. 2012 Jun 30;379(9835):2466–76.
Loharikar A, Newton AE, Stroika S, Freeman M, Greene KD, Parsons MB, et al. Cholera in the United States, 2001–2011: a reflection of patterns of global epidemiology and travel. Epidemiol Infect. 2014 May 27:1–9.
Lucas ME, Deen JL, von Seidlein L, Wang XY, Ampuero J, Puri M, et al. Effectiveness of mass oral cholera vaccination in Beira, Mozambique. N Engl J Med. 2005 Feb 24;352(8):757–67.
Schilling KA, Cartwright EJ, Stamper J, Locke M, Esposito DH, Balaban V, et al. Diarrheal illness among US residents providing medical services in Haiti during the cholera epidemic, 2010–2011. J Travel Med. 2014 Jan-Feb;21(1):55–7.
Sur D, Lopez AL, Kanungo S, Paisley A, Manna B, Ali M, et al. Efficacy and safety of a modified killed-whole-cell oral cholera vaccine in India: an interim analysis of a cluster-randomised, double-blind, placebo-controlled trial. Lancet. 2009 Nov 14;374(9702):1694–702.
World Health Organization. Cholera, 2012. Wkly Epidemiol Rec. 2013 Aug 2;88(31):321–34.