Monday, May 23, 2011

Human-associated factors in cholera outbreak


Until 1970s, it had been believed that the humans were the major reservoirs of V. cholerae and that the organism was incapable of persisting outside the host. However, with the finding that the bacteria can remain as VBNCs in water for long time, the aquatic environment had been widely considered to be the major reservoir of the organism. This shifted the importance from human-to-human transmission to environment–to-human transmission. However, the environmental hypothesis could not explain many aspects of cholera outbreak. Moreover, there are many reports indicating the importance of human factors in cholera outbreak.

1.  Using a model incorporating high asymptomatic ratio and rapidly waning immunity, King et al. (2008) found that the asymptomatic ratio in cholera is very high and that the environmental reservoir is directly responsible for relatively few infections only. Thus, the disease outbreak pattern may depend on the prevalence of human inapparent infections.
2. During the seventh pandemic cholera in Peru, V. cholerae O1 could be isolated from 3% of the total randomly selected, symptom-free individuals with no signs of cholera or diarrhea indicating inapparent infections (Pugliell et al. 1992)
3. As already given in the previous blogs, there are number of reports on the import of the organism from one region to another with the help of human carriers.
4. Cholera outbreak in non-estuarine regions of Zimbabwe, a landlocked country in the middle of Africa, suggest that human-to-human transmission contribute more to the outbreak of cholera than the environment-to-human transmission (Mukandavire et al. 2011)
5. In countries of Africa, the funeral activities (Gunnlaugsson et al. 1998) and the practice of eating together with fingers from the same bowl during funeral feasts (Mukandavire et al. 2011) have been a major cause of cholera spread during an outbreak, indicating the importance of human-associated factors.
6. Epidemiological investigations on cholera outbreak in a psychiatric hospital in Singapore showed that the organism was transmitted through person-to-person contact (Goh et al. 1990).
7. As indicated in the previous blog, cholera outbreak during heavy rainfall and drought may be indicative of human factors rather than environmental factor.
8. Low socioeconomic status, unhygienic practices, lack of latrine facilities, poverty, war and migration, overcrowding etc. (i.e.human factors) are linked to the outbreak of cholera
9. The passage of V. cholerae through human gut would make it ‘hyperinfectious’ that may contribute to the explosive spread of cholera (Merrell et al. 2002; Hartley et al. 2006). Thus, the human host not only allows the growth of the organism but also help in the human-to-human spread. This also underlines the role of hygienic practices in preventing the spread of cholera (Codeco and Coelho 2006).

Thus, the importance of human-to-human transmission can not be overlooked even though the climate theory continues to underestimate or ignore the human factors in cholera outbreak.

Next- Prejudice or hijacking the science?

King et al. 2008. Inapparent infections and cholera dynamics. Nature 454(7206): 877-U29
Puglielli et al. 1992. Symptomless carriage of Vibrio cholerae in Peru. Lancet 339(800): 1056-1057
Mukandavire et al. 2011. Estimating the reproductive numbers for the 2008-2009 cholera outbreaks in Zimbabwe. Proc Natl Acad Sci U S A
Gunnlaugsson et al. 1998. Funerals during the 1994 cholera epidemic in Guinea-Bissau, West Africa: the need for disinfection of bodies of persons dying of cholera. Epidemiol Infect. 120(1):7-15.
Goh et al. 1990. Person-to-person transmission of cholera in a psychiatric hospital. J Infect. 20(3):193-200
Merrell et al. 2002. Host induced epidemic spread of the cholera bacterium. Nature 417(6889):642-5
Hartley et al. 2006. Hyperinfectivity: a critical element in the ability of V. cholerae to cause epidemics? PLoS Med. 3(1):e7
Codeco, C. T. and Coelho, F. C. 2006. Trends in cholera epidemiology. PLoS Med. 3(1):e42.


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