Cholera risk factors: Difference between revisions

Jump to navigation Jump to search
No edit summary
Line 7: Line 7:
===Blood group===
===Blood group===
* Recent [[epidemiology|epidemiologic research]] suggests that an individual's susceptibility to cholera (and other [[diarrhea]]l infections) is affected by their [[blood type]]: Those with [[type O blood]] are the most susceptible,<ref name=Swerdlow_1994>{{cite journal |author=Swerdlow D, Mintz E, Rodriguez M, Tejada E, Ocampo C, Espejo L, Barrett T, Petzelt J, Bean N, Seminario L |title=Severe life-threatening cholera associated with blood group O in Peru: implications for the Latin American epidemic |journal=J Infect Dis |volume=170 |issue=2 |pages=468-72 |year=1994 |id=PMID 8035040}}</ref><ref name=Harris_2005>{{cite journal |author=Harris J, Khan A, LaRocque R, Dorer D, Chowdhury F, Faruque A, Sack D, Ryan E, Qadri F, Calderwood S |title=Blood group, immunity, and risk of infection with ''Vibrio cholerae'' in an area of endemicity |journal=Infect Immun |volume=73 |issue=11 |pages=7422-7 |year=2005 |pmid=16239542}}</ref> 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.
* Recent [[epidemiology|epidemiologic research]] suggests that an individual's susceptibility to cholera (and other [[diarrhea]]l infections) is affected by their [[blood type]]: Those with [[type O blood]] are the most susceptible,<ref name=Swerdlow_1994>{{cite journal |author=Swerdlow D, Mintz E, Rodriguez M, Tejada E, Ocampo C, Espejo L, Barrett T, Petzelt J, Bean N, Seminario L |title=Severe life-threatening cholera associated with blood group O in Peru: implications for the Latin American epidemic |journal=J Infect Dis |volume=170 |issue=2 |pages=468-72 |year=1994 |id=PMID 8035040}}</ref><ref name=Harris_2005>{{cite journal |author=Harris J, Khan A, LaRocque R, Dorer D, Chowdhury F, Faruque A, Sack D, Ryan E, Qadri F, Calderwood S |title=Blood group, immunity, and risk of infection with ''Vibrio cholerae'' in an area of endemicity |journal=Infect Immun |volume=73 |issue=11 |pages=7422-7 |year=2005 |pmid=16239542}}</ref> 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.
===Genetics===
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.
===Decreased gastric acidity===
===Decreased gastric acidity===
* As from the use of [[antacid]]s)
* As from the use of [[antacid]]s
===Decreased Immunity===
===Decreased Immunity===
* A weakened [[immune system]]
* [[Malnutrition|Malnourished]].
* [[Malnutrition|Malnourished]].
===Genetics===
==References==
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 ==
{{Reflist|2}}
{{Reflist|2}}
== External links ==
[[Category:Neurotoxins]]
[[Category:Neurotoxins]]
[[Category:Foodborne illnesses]]
[[Category:Foodborne illnesses]]

Revision as of 16:29, 5 April 2012

Cholera Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Cholera from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications, and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Other diagnostic studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Case Studies

Case #1

Cholera risk factors On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Cholera risk factors

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Cholera risk factors

CDC on Cholera risk factors

Cholera risk factors in the news

Blogs on Cholera risk factors

Directions to Hospitals Treating Cholera

Risk calculators and risk factors for Cholera risk factors

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

Blood group

  • 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.

Genetics

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.

Decreased gastric acidity

Decreased Immunity

References

  1. McLeod K (2000). "Our sense of Snow: John Snow in medical geography". Soc Sci Med. 50 (7–8): 923–35. PMID 10714917.
  2. WHO Cholera [1]
  3. 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.
  4. 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.
  5. 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.


Template:WikiDoc Sources