Cholera risk factors: Difference between revisions
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{{Cholera}} | {{Cholera}} | ||
{{CMG}}; '''Associate Editors-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto: | {{CMG}}; '''Associate Editors-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, MBBS]] [mailto:psingh13579@gmail.com], {{SaraM}} | ||
==Overview== | ==Overview== | ||
Certain factors have been found to be associated with an increased | 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 [[ABO blood group system|blood group O]] are most prone, while patients with [[ABO blood group system|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.<ref name="pmid4014172">{{cite journal| author=Glass RI, Holmgren J, Haley CE, Khan MR, Svennerholm AM, Stoll BJ et al.| title=Predisposition for cholera of individuals with O blood group. Possible evolutionary significance. | journal=Am J Epidemiol | year= 1985 | volume= 121 | issue= 6 | pages= 791-6 | pmid=4014172 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4014172 }} </ref><ref name="pmid10892490">{{cite journal| author=Rabbani GH, Greenough WB| title=Food as a vehicle of transmission of cholera. | journal=J Diarrhoeal Dis Res | year= 1999 | volume= 17 | issue= 1 | pages= 1-9 | pmid=10892490 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10892490 }} </ref><ref name="pmid19212328">{{cite journal| author=Larocque RC, Sabeti P, Duggal P, Chowdhury F, Khan AI, Lebrun LM et al.| title=A variant in long palate, lung and nasal epithelium clone 1 is associated with cholera in a Bangladeshi population. | journal=Genes Immun | year= 2009 | volume= 10 | issue= 3 | pages= 267-72 | pmid=19212328 | doi=10.1038/gene.2009.2 | pmc=2672110 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19212328 }} </ref><ref name=Cholera-outbreak> 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</ref> | ||
==Risk factors== | |||
===Blood | ==Risk Factors== | ||
===Contaminated Sources=== | |||
=== | Risk factors for foodborne cholera may include:<ref name="pmid22099118">{{cite journal| author=O'Connor KA, Cartwright E, Loharikar A, Routh J, Gaines J, Fouché MD et al.| title=Risk factors early in the 2010 cholera epidemic, Haiti. | journal=Emerg Infect Dis | year= 2011 | volume= 17 | issue= 11 | pages= 2136-8 | pmid=22099118 | doi=10.3201/eid1711.110810 | pmc=3310583 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22099118 }} </ref><ref name="pmid10892490">{{cite journal| author=Rabbani GH, Greenough WB| title=Food as a vehicle of transmission of cholera. | journal=J Diarrhoeal Dis Res | year= 1999 | volume= 17 | issue= 1 | pages= 1-9 | pmid=10892490 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10892490 }} </ref> | ||
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. | *Consumption of contaminated water | ||
===Decreased | *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:<ref name=Cholera-outbreak> 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</ref> | |||
*Poor sanitation | |||
*Unsafe drinking water | |||
*Increased person-to-person transmission | |||
===Other Risk Factors=== | |||
====Blood Group==== | |||
Recent [[epidemiology|epidemiologic research]] suggests that an individual's susceptibility to cholera (and other [[diarrhea]]l 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.<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> | |||
====Genetics==== | |||
*Variants in the innate immunity protein BPIFB1 (LPLUNC1) are associated with susceptibility to cholera.<ref name="pmid19212328">{{cite journal| author=Larocque RC, Sabeti P, Duggal P, Chowdhury F, Khan AI, Lebrun LM et al.| title=A variant in long palate, lung and nasal epithelium clone 1 is associated with cholera in a Bangladeshi population. | journal=Genes Immun | year= 2009 | volume= 10 | issue= 3 | pages= 267-72 | pmid=19212328 | doi=10.1038/gene.2009.2 | pmc=2672110 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19212328 }} </ref> | |||
*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==== | |||
* Use of [[antacid]]s | * Use of [[antacid]]s | ||
===Decreased Immunity=== | ====Decreased Immunity==== | ||
* [[Malnutrition|Malnourished]] patients | * [[Malnutrition|Malnourished]] patients | ||
==References== | ====Hypochlorhydria==== | ||
*[[Retinol]] deficiency | |||
== References == | |||
{{Reflist|2}} | {{Reflist|2}} | ||
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{{WS}} | |||
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[[Category:Infectious disease]] | |||
[[Category:Pediatrics]] |
Latest revision as of 20:55, 29 July 2020
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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
- 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
- Use of antacids
Decreased Immunity
- Malnourished patients
Hypochlorhydria
- Retinol deficiency
References
- ↑ 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.
- ↑ 2.0 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.
- ↑ 3.0 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.
- ↑ 4.0 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
- ↑ 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.
- ↑ 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.