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[edit | edit source]

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[edit | edit source]

Contaminated Sources[edit | edit source]

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[edit | edit source]

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[edit | edit source]

Blood Group[edit | edit source]

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[edit | edit source]

• Variants in the innate immunity protein BPIFB1 (LPLUNC1) are associated with susceptibility to cholera.^[3]
• It has also been hypothesized that the cystic fibrosis genetic mutation has been maintained in humans due to a selective advantage: heterozygous carriers of the mutation (who are thus not affected by cystic fibrosis) are more resistant to V. cholerae infections.^[8] In this model, the genetic deficiency in the cystic fibrosis transmembrane conductance regulator channel proteins interferes with bacteria binding to the gastrointestinal epithelium, thus reducing the effects of an infection.

Decreased Gastric Acidity[edit | edit source]

• Use of antacids

Decreased Immunity[edit | edit source]

• Malnourished patients

Hypochlorhydria[edit | edit source]

• Retinol deficiency

References[edit | edit source]

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