Cholera risk factors: Difference between revisions
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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.<ref name=Bertranpetit_1996>{{cite journal |author=Bertranpetit J, Calafell F |title=Genetic and geographical variability in cystic fibrosis: evolutionary considerations |journal=Ciba Found Symp |volume=197 |issue= |pages=97-114; discussion 114-8 |year=1996 |pmid=8827370}}</ref> 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. | 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.<ref name=Bertranpetit_1996>{{cite journal |author=Bertranpetit J, Calafell F |title=Genetic and geographical variability in cystic fibrosis: evolutionary considerations |journal=Ciba Found Symp |volume=197 |issue= |pages=97-114; discussion 114-8 |year=1996 |pmid=8827370}}</ref> 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. | ||
== References == | == References == | ||
Revision as of 16:20, 5 April 2012
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]
Overview
Choleria is a severe bacterial gastrointestinal, diarrheal disease. In its most severe forms, cholera is one of the most rapidly fatal illnesses known. A healthy person may become hypotensive within an hour of the onset of symptoms and may die within 2-3 hours if no treatment is provided. More commonly, the disease progresses from the first liquid stool to shock in 4-12 hours, with death following in 18 hours to several days without rehydration treatment.[1][2]
Risk factors
Recent epidemiologic research suggests that an individual's susceptibility to cholera (and other diarrheal infections) is affected by their blood type: Those with type O blood are the most susceptible,[3][4] 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.[citation needed]
About one million V. cholerae bacteria must typically be ingested to cause cholera in normally healthy adults, although increased susceptibility may be observed in those with a weakened immune system, individuals with decreased gastric acidity (as from the use of antacids), or those who are malnourished.
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.[5] 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.
References
- ↑ McLeod K (2000). "Our sense of Snow: John Snow in medical geography". Soc Sci Med. 50 (7–8): 923–35. PMID 10714917.
- ↑ WHO Cholera [1]
- ↑ 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.
- ↑ 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.
- ↑ 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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