Cholera

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Cholera
ICD-10 code:
ICD-9 code: 001

Cholera (also called Asiatic cholera) is an infectious disease, caused by bacteria that are typically ingested by drinking water that is contaminated by improper sanitation, or by eating improperly cooked fish, especially shellfish. Symptoms include diarrhea, abdominal cramps, nausea, vomiting, and dehydration. Death is generally due to the dehydration caused by the illness. When cholera is left untreated, it generally has a high death rate. Treatment typically consists of aggressive rehydration. With treatment, death rates plummet. Cholera was first described in a scientific manner by the physician Garcia de Orta in the 16th century.

Contents

Pathology

Susceptibility

Cholera produces potentially lethal secretory diarrhea through a pathway that involves the cystic fibrosis transmembrane conductance regulator, CFTR (Gabriel 1994). This discovery led to the hypothesis that carriers for cystic fibrosis, who have lower levels of functional CFTR, are protected from the severe effects of cholera because they don't lose water as quickly as other people. This might explain the high incidence of cystic fibrosis among populations which were formerly exposed to cholera. However, no evidence of resistance in vivo has been observed in humans, and studies in mice have produced conflicting results (Gabriel 1994, Cuthbert 1995, Hogenauer 2000).

Recent genetic research has determined that a person's susceptibility to cholera (and other diarrheas) is affected by their blood type. Those with type O blood are the most susceptible. Those with type AB are the most resistant, virtually immune. Between these two extremes are the A and B blood types, with type A being more resistant than type B.

Vibrio cholerae: The bacteria that causes cholera (SEM image)
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Vibrio cholerae: The bacteria that causes cholera (SEM image)

About one million Vibrio cholerae bacteria must 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.

Transmission

Cholera is transmitted through ingestion of substances contaminated with the bacterium. The contamination usually occurs when untreated sewage is released into waterways, affecting the water supply, any foods washed in the water, and shellfish living in the affected waterway — it is rarely spread directly from person to person. The resulting diarrhea allows the bacterium to spread to other people under unsanitary conditions.

Symptoms

Symptoms include those of general GI tract upset: profuse diarrhea (eg 1L/hour), abdominal cramps, fever, nausea and vomiting. Also those of the resulting dehydration: thirst, muscle cramps, weakness, loss of tissue turgor, sunken eyes and wrinkled skin, severe metabolic acidosis with potassium depletion, anuria, circulatory collapse and cyanosis. Death is through circulatory volume shock, and can occur within hours.

Causes of symptoms

More information at Vibrio cholerae

The root causes of these symptoms are the enterotoxins that V. cholerae produces. The main enterotoxin, known as cholera toxin, interacts with G proteins and cyclic AMP in the intestinal lining to open ion channels. As ions flow into the intestinal lumen, water follows from osmotic pressure.

History

Origin

Cholera originated in India or elsewhere in Asia, with the Ganges River likely serving as a contamination reservoir.

Discovery

The scientists with major contributions to fighting cholera were John Snow, who found the link between cholera and drinking water in 1854, and Robert Koch, who identified Vibrio cholerae as the bacillus causing the disease. The bacterium was originally isolated thirty years earlier by Italian anatomist Filippo Pacini, but his results were not widely known at all.

Spread

Cholera was originally endemic in India, but spread by trade routes (land and sea) to Russia, then to Western Europe, and from Europe to North America. Major cholera epidemics struck the United States in 1832 (An interesting side-note, when the epidemic reached Canada in 1832, the victims blamed the British and accused them of creating the disease), 1849, and 1866. (The 1849 outbreak took the life of former U.S. President James K. Polk.) Cholera is now no longer considered an issue in Europe and North America, due to filtering and chlorination of the water supply.

In the past, people travelling in ships would hang a yellow flag if one of the crews suffered from cholera. Boats with a yellow flag hung would not be allowed to disembark at any habour. (See Love in the Time of Cholera)

Treatment

Prevention

Although cholera can be life-threatening, it is easily prevented and treated. In the United States and Western Europe, because of advanced water and sanitation systems, cholera is not a major threat. The last major outbreak of cholera in the United States was in 1911. However, everyone, especially travelers, should be aware of how the disease is transmitted and what can be done to prevent it.

Simple sanitation is usually sufficient to stop an epidemic. There are several points along the transmission path at which the spread may be halted:

  • Sickbed: Proper disposal and treatment of waste produced by cholera victims.
  • Sewage: Treatment of general sewage before it enters the waterways.
  • Sources: Warnings about cholera contamination posted around contaminated water sources.
  • Sterilization: Boiling, filtering, and chlorination of water before use.

Filtration and boiling is by far the most effective means of halting transmission. In general, education and sanitation are the limiting factors in prevention of cholera epidemics.

Sources

References:

  • Cholera facts from the United States FDA website: http://vm.cfsan.fda.gov/~MOW/chap7.html
  • Gabriel, S.E. et al; Cystic fibrosis heterozygote resistance to cholera toxin in the cystic fibrosis mouse model; Science: 1994, v 266, 5182; pp 107-109
  • Cuthbert, A.W. et al; The genetic advantage hypothesis in cystic fibrosis heterozygotes: a murine study; J Physiol: 1995, v 482; pp 449-454
  • Hogenauer, C. et al; Active intestinal chloride secretion in human carriers of cystic fibrosis mutations: an evaluation of the hypothesis that heterozygotes have subnormal active intestinal chloride secretion; Am J Hum Genet: 2000, v 67, i 6, pp 1422-1427

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