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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

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

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

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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