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Cholera risk factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Priyamvada Singh, MBBS [2], Sara Mehrsefat, M.D. [3]

Overview

Certain factors have been found to be associated with an increased risk of contracting cholera. Among these decreased immunity, decreased gastric pH, certain blood groups (patients with blood group O are most prone, while patients with blood group AB are least prone), and genetics are the most commonly associated factors. The greatest risk occurs in over-populated communities and refugee settings characterized by poor sanitation, unsafe drinking water, and increased person-to-person transmission.[1][2][3][4]

Risk Factors

Contaminated Sources

Risk factors for foodborne cholera may include:[5][2]

  • Consumption of contaminated water
  • Consumption of rice products
  • Consumption of specific vegetables or fruits

Risk factors for sporadic cholera include:

  • Consumption of under-cooked shellfish

Overcrowding and Displacement

The greatest risk of developing cholera is present in over-populated communities affected by massive displacement and overcrowding, commonly due to natural disasters or political/economical instability (e.g., earthquakes, hurricanes, refugee camps) by means of:[4]

  • Poor sanitation
  • Unsafe drinking water
  • Increased person-to-person transmission

Other Risk Factors

Blood Group

Recent epidemiologic research suggests that an individual’s susceptibility to cholera (and other diarrheal infections) is affected by his/her blood type. Those with type O blood are the most susceptible, while those with type AB are the most resistant. Between these two extremes are the A and B blood types, with type A being more resistant than type B.[6][7]

Genetics

Decreased Gastric Acidity

Decreased Immunity

Hypochlorhydria

References

  1. Glass RI, Holmgren J, Haley CE, Khan MR, Svennerholm AM, Stoll BJ; et al. (1985). “Predisposition for cholera of individuals with O blood group. Possible evolutionary significance”. Am J Epidemiol. 121 (6): 791–6. PMID 4014172.
  2. 2.0 2.1 Rabbani GH, Greenough WB (1999). “Food as a vehicle of transmission of cholera”. J Diarrhoeal Dis Res. 17 (1): 1–9. PMID 10892490.
  3. 3.0 3.1 Larocque RC, Sabeti P, Duggal P, Chowdhury F, Khan AI, Lebrun LM; et al. (2009). “A variant in long palate, lung and nasal epithelium clone 1 is associated with cholera in a Bangladeshi population”. Genes Immun. 10 (3): 267–72. doi:10.1038/gene.2009.2. PMC 2672110. PMID 19212328.
  4. 4.0 4.1 World Health Organization. Assessing the Outbreak response and improving preparedness (2004) http://apps.who.int/iris/bitstream/10665/43017/1/WHO_CDS_CPE_ZFk_2004.4_eng.pdf
  5. O’Connor KA, Cartwright E, Loharikar A, Routh J, Gaines J, Fouché MD; et al. (2011). “Risk factors early in the 2010 cholera epidemic, Haiti”. Emerg Infect Dis. 17 (11): 2136–8. doi:10.3201/eid1711.110810. PMC 3310583. PMID 22099118.
  6. Swerdlow D, Mintz E, Rodriguez M, Tejada E, Ocampo C, Espejo L, Barrett T, Petzelt J, Bean N, Seminario L (1994). “Severe life-threatening cholera associated with blood group O in Peru: implications for the Latin American epidemic”. J Infect Dis. 170 (2): 468–72. PMID 8035040.
  7. Harris J, Khan A, LaRocque R, Dorer D, Chowdhury F, Faruque A, Sack D, Ryan E, Qadri F, Calderwood S (2005). “Blood group, immunity, and risk of infection with Vibrio cholerae in an area of endemicity”. Infect Immun. 73 (11): 7422–7. PMID 16239542.
  8. Bertranpetit J, Calafell F (1996). “Genetic and geographical variability in cystic fibrosis: evolutionary considerations”. Ciba Found Symp. 197: 97–114, discussion 114-8. PMID 8827370.


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