Shopping on line can be easy, simple and save you lots of money. It can also take a lot of your time, frustrate you, and result in unwanted purchases. Now the same can be said for regular high street shopping, but with the vast opportunity presented by the Internet it will pay you to spend a few minutes reading this and understanding how to better optimize your Cholera shopping experience:

1. Compare - without doubt the biggest advantage that the Cholera offers shoppers today is the ability to compare thousands of Cholera at a time. This is a great thing, but not necessarily all the time! Too much can be daunting at times so take advantage of the great comparison sites and where possible let them do the hard work for you.

2. Research - if it has been said it will be on the internet. Ignorance is no longer a justifiable reason for buying the wrong thing. Take the time to research in detail everything that you could possible want to know about

3. Testimonials - don't know anybody that has bought a Cholera? Wrong! If the Cholera is good the internet will let you know. Use the Internet as a friend and get testimonials before you buy.

4. Questions - Got a question about Cholera then search the Forums, FAQ's, Blogs etc. Don't be afraid to ask .....

5. Reputation - Never heard of the company selling Cholera? Don't worry, no reason why you should know every company in the world, but you know someone that does! Use the internet to find out what people are saying about Cholera and build up a picture of their reputation for sales, returns, customer service, delivery etc.

6. Returns - still worried that even after all of the above your Cholera wont be what you want? Check out the returns policy. There is so much competition now that someone, somewhere is bound to offer the terms that you are comfortable with.

7. Feedback - happy with your Cholera then let people know, after all you are depending on others people input in your buying decision, so why not give a little back.

8. Security - check for the yellow padlock on the Cholera site before you buy, and the s after http:/ /i.e. https:// = a secure site

9. Contact - got a question about Cholera, or want to leave a comment then check out the sites contact page. Reputable companies have them and respond.

10. Payment - ready to pay for your Cholera, then use your credit card or PayPal! Be aware of companies that don't accept them, there may be genuine reasons but given the huge amount of choice you have when buying online there is no reason at all not to buy via credit card or PayPal.

{{DiseaseDisorder infobox | Name = Cholera | ICD10 = {{ICD10|A|00| |a|00--> | ICD9 = {{ICD9|001--> | Image = cholera bacteria SEM.jpg | Caption = ''[Vibrio cholerae'': The bacterium that causes cholera ([Scanning electron microscope image) | DiseasesDB = 2546 | ICDO = | OMIM = | MedlinePlus = 000303 | eMedicineSubj = med | eMedicineTopic = 351 | eMedicine_mult = {{eMedicine2|ped|382--> | MeshName = Cholera | MeshNumber = C01.252.400.959.347 | -->

Cholera (or Asiatic cholera or epidemic cholera) is a severe diarrheal disease caused by the bacterium Vibrio cholerae. Transmission to humans is by ingesting contaminated water or food. The major reservoir for cholera was long assumed to be humans, but some evidence suggests that it is the aquatic environment.

V. cholerae is a Gram-negative bacteria which produces cholera toxin, an enterotoxin, whose action on the mucosal epithelium lining of the small intestine is responsible for the characteristic massive diarrhea of the disease. In its most severe forms, cholera is one of the most rapidly fatal illnesses known: A healthy person may become hypotension 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. WHO Cholera

Symptoms Symptoms include those of general GA tract (stomach) upset and Diarrhea#Acute diarrhea. Symptoms may also include terrible muscle and stomach cramps, vomiting and fever in early stages. In a later stage the diarrhea becomes "rice water stool" (almost clear with flecks of white). Symptoms are caused by massive body fluid loss induced by 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. The toxin actually catalyzes the covalent modification of Gαs protein by transferring an ADP-ribose to an arginine residue at the GTPase active site. This ADP-ribosylation prevents Gαs from hydrolyzing GTP, thus causing the protein to become permanently activated. As ions flow into the intestinal lumen (lining), body fluids (mostly water) flow out of the body due to osmosis leading to massive diarrhea as the fluid is expelled from the body. The body is "tricked" into releasing massive amounts of fluid into the small intestine which shows up in up to 36 liters of liquid diarrhea in a six day period in adults with accompanying massive dehydration. Radical dehydration can bring death within a day through collapse of the circulatory system.

Treatment In general, patients must receive as much fluid as they lose, which can be up to 36 L, due to diarrhea.

Treatment usually consists of aggressive rehydration (restoring the lost body fluids) and oral rehydration salt with commercial or hand-mixed sugar-salt solutions (1 tsp salt + 8 tsp sugar in 1 litre of clean/boiled water) or massive injections of liquid given intravenously via an IV in advanced cases. See: Oral rehydration therapy for easily made rehydration solutions. Without treatment the death rate is as high as 50%; with treatment the death rate can be well below 1%.

Tetracycline antibiotics may have a role in reducing the duration and severity of cholera, although drug-resistance is occurring. Oral tetracycline was recommended for reducing the period of vibrio excretion and need for parenteral fluid. Initially cholera vibrios were universally susceptible to all antibiotics active against gram negative bacilli, but since 1979 multiple drug resistant strain have become increasingly common and their effects on overall mortality are questioned. Other antibiotics that have been used include ciprofloxacin and azithromycin, although again, drug-resistance has now been described.

Epidemiology Prevention Although cholera can be life-threatening, it is nearly always easily prevented, in principle, if proper sanitation practices are followed. In the United States and Western Europe, because of advanced water treatment and sanitation systems, cholera is no longer 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. Good sanitation practices, if instituted in time, are usually sufficient to stop an epidemic. There are several points along the transmission path at which the spread may be halted:

Susceptibility Recent epidemiology 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, 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.

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 malnutrition.

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. 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.

Transmission of Death (personification) bringing the cholera, in Le Petit Journal.

Persons infected with cholera have massive diarrhea. This highly liquid diarrhea, which is often compared to "rice water," is loaded with bacteria that can spread under unsanitary conditions to infect water used by other people. Cholera is transmitted from person to person through ingestion of feces contaminated water loaded with the cholera bacterium. The source of the contamination is typically other cholera patients when their untreated diarrhea discharge is allowed to get into waterways or into groundwater or drinking water supply. Any infected water and any foods washed in the water, and shellfish living in the affected waterway can cause an infection. Cholera is rarely spread directly from person to person. V. cholerae occurs naturally in the plankton of fresh water, brackish water, and Seawater, attached primarily to copepods in the zooplankton. Both toxic and non-toxic strains exist. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage. Coastal cholera outbreaks typically follow algal bloom. This makes cholera a zoonosis.

Laboratory diagnosis Stool and Swab collected in the acute stage of the disease are useful specimens for laboratory diagnosis. A number of special media have been employed for the cultivation for cholera vibrios. They are classified as follows:

Holding or transport media
  • Venkataraman-ramakrishnan (VR) medium
  • Cary-Blair medium: This the most popularly carrying media. This is a buffered solution of sodium chloride, sodium thioglycollate, disodium phosphate and calcium chloride at pH 8.4.


  • Plating media
  • Alkaline bile salt agar: The colonies are very similar to those on Nutrient Agar.
  • Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium: Cholera vibrios produce small translucent colonies with a greyish black centre.
  • TCBS medium: This the mostly widely used medium. This medium contains thiosulphate, citrate, bile salts and sucrose. Also in osters and lobster in some cases. Cholera vibrios produce flat 2-3 mm in diameter, yellow nucleated colonies.


  • Biochemistry of the V. cholerae bacterium Most of the V. cholerae bacteria in the contaminated water that a potential host drinks do not survive the very acidic conditions of the stomachHartwell LH, Hood L, Goldberg ML, Reynolds AE, Silver LM, and Veres RC (2004). Genetics: From Genes to Genomes. Mc-Graw Hill, Boston: p. 551-552, 572-574 (using the turning off and turning on of gene expression to make toxin proteins in cholera bacteria as a "comprehensive example" of what is known about the mechanisms by which bacteria change the mix of proteins they manufacture to respond to the changing opportunities for surviving and thriving in different chemical environments). But the few bacteria that manage to survive the stomach's acidity conserve their nutrient during the perilous passage through the stomach by shutting down much protein production. When the surviving bacteria manage to exit the stomach and reach the favorable conditions of the small intestine, they need to propel themselves through the thick mucous membrane that lines the small intestine to get to the intestinal wall where they can thrive. So they start up production of the hollow cylindrical protein flagellin to make flagella, the curly whip-like tails that they rotate to propel themselves through the pasty mucus that lines the small intestine.

    Once the cholera bacteria reach the intestinal wall, they do not need the flagella propellers to move themselves any more, so they stop producing the protein flagellin, thus again conserving energy and nutrients by changing the mix of proteins that they manufacture, responding to the changed chemical surroundings. And on reaching the intestinal wall, they start producing the toxic proteins that give the infected person a watery diarrhea which carries the multiplying and thriving new generations of V. cholerae bacteria out into the drinking water of the next host—if proper sanitation measures are not in place.



    Microbiologists have studied the gene expression by which the V. cholerae bacteria turn off the production of some proteins and turn on the production of other proteins as they respond to the series of chemical environments they encounter, passing through the stomach, through the mucous layer of the small intestine, and on to the intestinal wall. Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that ineract with host cell mechanisms to pump chloride ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The choride and sodium ions create a salt water environment in the small intestines which through osmosis can pull up to six liters of water per day through the intestinal cells creating the massive amounts of diarrhea. The host can become rapidly dehydrated if an appropriate mixture of dilute salt water and sugar is not taken to replace the blood's water and salts lost in the diarrhea.

    By inserting separately, successive sections of V. cholerae DNA into the DNA of other bacteria such as E. coli that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which V. cholerae responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered that there is a complex cascade of regulatory proteins that control expression of V. cholerae virulence determinants. In responding to the chemical environment at the intestinal wall, the V. cholerae bacteria produce the TcpP/TcpH proteins which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein. ToxT then directly activates expression of virulence genes that produce the toxins that cause diarrhea in the infected person and that permit the bacteria to colonize the intestine. Current research aims at discovering "the signal that makes the cholera bacteria stop swimming and start to colonize (that is, adhere to the cells of) the small intestine."p. 574

    History Origin and spread Cholera was originally endemic (epidemiology) to the Indian subcontinent, with the Ganges River likely serving as a contamination reservoir. It spread by trade routes (land and sea) to Russia, then to Western Europe, and from Europe to North America. It is now no longer considered an issue in Europe and North America, due to water filtration and chlorination of the water supply.



    Famous cholera victims The crying and pathos in the last movement of Pyotr Ilyich Tchaikovsky's (c. 1840-1893) last symphony made people think that Tchaikovsky had a premonition of death. "A week after the premiere of his Symphony No. 6 (Tchaikovsky), Tchaikovsky was dead--6 November 1893. The cause of this indisposition and stomach ache was suspected to be his intentionally infecting himself with cholera by drinking contaminated water. The day before, while having lunch with Modest Tchaikovsky (his brother and biographer), he is said to have poured faucet water from a pitcher into his glass and drunk a few swallows. Since the water was not boiled and cholera was once again rampaging Saint Petersburg, Russia, such a connection was quite plausible ...."Meumayr A (1997). Music and Medicine: Chopin, Smetana, Tchaikovsky, Mahler: Notes on Their Lives, Works, and Medical Histories. Med-Ed Press: pp. 282-283 (summarizing various theories on what killed the composer Pyotr Ilyich Tchaikovsky, including his brother Modest Tchaikovsky's idea that Tchaikovksy drank cholera infested water the day before he became ill)..

    Other famous people who succumbed to the disease include:



    Research The major contributions to fighting cholera were made by physician and self-trained scientist John Snow (physician) (1813-1858), who found the link between cholera and contaminated drinking water in 1854 and Henry Whitehead, an Anglican minister, who helped John Snow track down and verify the source of the disease, an infected well in London. Their conclusions and writings were widely distributed and firmly established for the first time a definite link between germs and disease. Clean water and good sewage treatment, despite their major engineering and financial cost, slowly became a priority throughout the major developed cities in the world from this time onward. Robert Koch, 30 years later, identified V. cholerae with a microscope as the bacillus causing the disease in 1885. The bacterium had been originally isolated thirty years earlier (1855) by Italian anatomist Filippo Pacini, but its exact nature and his results were not widely known around the world.

    Cholera has been a laboratory for the study of evolution of virulence. The province of Bengal in British Raj was partitioned into West Bengal (a state in India) and East Pakistan in 1947. Prior to partition, both regions had cholera pathogens with similar characteristics. After 1947, India made more progress on public health than East Pakistan (now Bangladesh). As a consequence, the strains of the pathogen which succeeded in India had a greater incentive in the longevity of the host and are less virulent than the strains prevailing in Bangladesh, which uninhibitedly draw upon the resources of the host population, thus rapidly killing many in it.

    Other historical information In the past, people travelling in ships would hang a yellow flag if one or more of the crew members suffered from cholera. Boats with a yellow flag hung would not be allowed to disembark at any harbor for an extended period of time, typically 30 to 40 days.

    The French writer Jean Giono's novel "Le Hussard sur la toit" ("The Horseman on the Roof") is set in the south of France during the cholera epidemic of 1832.

    False report of cholera A persistent myth states that Chicago 1885 cholera epidemic myth of cholera and typhoid fever in 1885. This story has no factual basis. In 1885 there was a torrential rainstorm that flushed the Chicago river and its attendant pollutants into Lake Michigan far enough that the city's water supply was contaminated. Fortunately, cholera was not present in the city and this is not known to have caused any deaths. It did, however, cause the city to become more serious about their sewage treatment.

    Cholera morbus The term cholera morbus was used in the 19th and early 20th century to describe both non-epidemic cholera and gastrointestinal diseases that mimicked cholera. The term is not in current use, but is found in many older references. Archaic Medical Terms.

    References

    External links

    {{DiseaseDisorder infobox | Name = Cholera | ICD10 = {{ICD10|A|00| |a|00--> | ICD9 = {{ICD9|001--> | Image = cholera bacteria SEM.jpg | Caption = ''[Vibrio cholerae'': The bacterium that causes cholera ([Scanning electron microscope image) | DiseasesDB = 2546 | ICDO = | OMIM = | MedlinePlus = 000303 | eMedicineSubj = med | eMedicineTopic = 351 | eMedicine_mult = {{eMedicine2|ped|382--> | MeshName = Cholera | MeshNumber = C01.252.400.959.347 | -->

    Cholera (or Asiatic cholera or epidemic cholera) is a severe diarrheal disease caused by the bacterium Vibrio cholerae. Transmission to humans is by ingesting contaminated water or food. The major reservoir for cholera was long assumed to be humans, but some evidence suggests that it is the aquatic environment.

    V. cholerae is a Gram-negative bacteria which produces cholera toxin, an enterotoxin, whose action on the mucosal epithelium lining of the small intestine is responsible for the characteristic massive diarrhea of the disease. In its most severe forms, cholera is one of the most rapidly fatal illnesses known: A healthy person may become hypotension 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. WHO Cholera

    Symptoms Symptoms include those of general GA tract (stomach) upset and Diarrhea#Acute diarrhea. Symptoms may also include terrible muscle and stomach cramps, vomiting and fever in early stages. In a later stage the diarrhea becomes "rice water stool" (almost clear with flecks of white). Symptoms are caused by massive body fluid loss induced by 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. The toxin actually catalyzes the covalent modification of Gαs protein by transferring an ADP-ribose to an arginine residue at the GTPase active site. This ADP-ribosylation prevents Gαs from hydrolyzing GTP, thus causing the protein to become permanently activated. As ions flow into the intestinal lumen (lining), body fluids (mostly water) flow out of the body due to osmosis leading to massive diarrhea as the fluid is expelled from the body. The body is "tricked" into releasing massive amounts of fluid into the small intestine which shows up in up to 36 liters of liquid diarrhea in a six day period in adults with accompanying massive dehydration. Radical dehydration can bring death within a day through collapse of the circulatory system.

    Treatment In general, patients must receive as much fluid as they lose, which can be up to 36 L, due to diarrhea.

    Treatment usually consists of aggressive rehydration (restoring the lost body fluids) and oral rehydration salt with commercial or hand-mixed sugar-salt solutions (1 tsp salt + 8 tsp sugar in 1 litre of clean/boiled water) or massive injections of liquid given intravenously via an IV in advanced cases. See: Oral rehydration therapy for easily made rehydration solutions. Without treatment the death rate is as high as 50%; with treatment the death rate can be well below 1%.

    Tetracycline antibiotics may have a role in reducing the duration and severity of cholera, although drug-resistance is occurring. Oral tetracycline was recommended for reducing the period of vibrio excretion and need for parenteral fluid. Initially cholera vibrios were universally susceptible to all antibiotics active against gram negative bacilli, but since 1979 multiple drug resistant strain have become increasingly common and their effects on overall mortality are questioned. Other antibiotics that have been used include ciprofloxacin and azithromycin, although again, drug-resistance has now been described.

    Epidemiology Prevention Although cholera can be life-threatening, it is nearly always easily prevented, in principle, if proper sanitation practices are followed. In the United States and Western Europe, because of advanced water treatment and sanitation systems, cholera is no longer 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. Good sanitation practices, if instituted in time, are usually sufficient to stop an epidemic. There are several points along the transmission path at which the spread may be halted:

    Susceptibility Recent epidemiology 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, 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.

    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 malnutrition.

    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. 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.

    Transmission of Death (personification) bringing the cholera, in Le Petit Journal.

    Persons infected with cholera have massive diarrhea. This highly liquid diarrhea, which is often compared to "rice water," is loaded with bacteria that can spread under unsanitary conditions to infect water used by other people. Cholera is transmitted from person to person through ingestion of feces contaminated water loaded with the cholera bacterium. The source of the contamination is typically other cholera patients when their untreated diarrhea discharge is allowed to get into waterways or into groundwater or drinking water supply. Any infected water and any foods washed in the water, and shellfish living in the affected waterway can cause an infection. Cholera is rarely spread directly from person to person. V. cholerae occurs naturally in the plankton of fresh water, brackish water, and Seawater, attached primarily to copepods in the zooplankton. Both toxic and non-toxic strains exist. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage. Coastal cholera outbreaks typically follow algal bloom. This makes cholera a zoonosis.

    Laboratory diagnosis Stool and Swab collected in the acute stage of the disease are useful specimens for laboratory diagnosis. A number of special media have been employed for the cultivation for cholera vibrios. They are classified as follows:

    Holding or transport media
  • Venkataraman-ramakrishnan (VR) medium
  • Cary-Blair medium: This the most popularly carrying media. This is a buffered solution of sodium chloride, sodium thioglycollate, disodium phosphate and calcium chloride at pH 8.4.


  • Plating media
  • Alkaline bile salt agar: The colonies are very similar to those on Nutrient Agar.
  • Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium: Cholera vibrios produce small translucent colonies with a greyish black centre.
  • TCBS medium: This the mostly widely used medium. This medium contains thiosulphate, citrate, bile salts and sucrose. Also in osters and lobster in some cases. Cholera vibrios produce flat 2-3 mm in diameter, yellow nucleated colonies.


  • Biochemistry of the V. cholerae bacterium Most of the V. cholerae bacteria in the contaminated water that a potential host drinks do not survive the very acidic conditions of the stomachHartwell LH, Hood L, Goldberg ML, Reynolds AE, Silver LM, and Veres RC (2004). Genetics: From Genes to Genomes. Mc-Graw Hill, Boston: p. 551-552, 572-574 (using the turning off and turning on of gene expression to make toxin proteins in cholera bacteria as a "comprehensive example" of what is known about the mechanisms by which bacteria change the mix of proteins they manufacture to respond to the changing opportunities for surviving and thriving in different chemical environments). But the few bacteria that manage to survive the stomach's acidity conserve their nutrient during the perilous passage through the stomach by shutting down much protein production. When the surviving bacteria manage to exit the stomach and reach the favorable conditions of the small intestine, they need to propel themselves through the thick mucous membrane that lines the small intestine to get to the intestinal wall where they can thrive. So they start up production of the hollow cylindrical protein flagellin to make flagella, the curly whip-like tails that they rotate to propel themselves through the pasty mucus that lines the small intestine.

    Once the cholera bacteria reach the intestinal wall, they do not need the flagella propellers to move themselves any more, so they stop producing the protein flagellin, thus again conserving energy and nutrients by changing the mix of proteins that they manufacture, responding to the changed chemical surroundings. And on reaching the intestinal wall, they start producing the toxic proteins that give the infected person a watery diarrhea which carries the multiplying and thriving new generations of V. cholerae bacteria out into the drinking water of the next host—if proper sanitation measures are not in place.



    Microbiologists have studied the gene expression by which the V. cholerae bacteria turn off the production of some proteins and turn on the production of other proteins as they respond to the series of chemical environments they encounter, passing through the stomach, through the mucous layer of the small intestine, and on to the intestinal wall. Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that ineract with host cell mechanisms to pump chloride ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The choride and sodium ions create a salt water environment in the small intestines which through osmosis can pull up to six liters of water per day through the intestinal cells creating the massive amounts of diarrhea. The host can become rapidly dehydrated if an appropriate mixture of dilute salt water and sugar is not taken to replace the blood's water and salts lost in the diarrhea.

    By inserting separately, successive sections of V. cholerae DNA into the DNA of other bacteria such as E. coli that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which V. cholerae responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered that there is a complex cascade of regulatory proteins that control expression of V. cholerae virulence determinants. In responding to the chemical environment at the intestinal wall, the V. cholerae bacteria produce the TcpP/TcpH proteins which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein. ToxT then directly activates expression of virulence genes that produce the toxins that cause diarrhea in the infected person and that permit the bacteria to colonize the intestine. Current research aims at discovering "the signal that makes the cholera bacteria stop swimming and start to colonize (that is, adhere to the cells of) the small intestine."p. 574

    History Origin and spread Cholera was originally endemic (epidemiology) to the Indian subcontinent, with the Ganges River likely serving as a contamination reservoir. It spread by trade routes (land and sea) to Russia, then to Western Europe, and from Europe to North America. It is now no longer considered an issue in Europe and North America, due to water filtration and chlorination of the water supply.



    Famous cholera victims The crying and pathos in the last movement of Pyotr Ilyich Tchaikovsky's (c. 1840-1893) last symphony made people think that Tchaikovsky had a premonition of death. "A week after the premiere of his Symphony No. 6 (Tchaikovsky), Tchaikovsky was dead--6 November 1893. The cause of this indisposition and stomach ache was suspected to be his intentionally infecting himself with cholera by drinking contaminated water. The day before, while having lunch with Modest Tchaikovsky (his brother and biographer), he is said to have poured faucet water from a pitcher into his glass and drunk a few swallows. Since the water was not boiled and cholera was once again rampaging Saint Petersburg, Russia, such a connection was quite plausible ...."Meumayr A (1997). Music and Medicine: Chopin, Smetana, Tchaikovsky, Mahler: Notes on Their Lives, Works, and Medical Histories. Med-Ed Press: pp. 282-283 (summarizing various theories on what killed the composer Pyotr Ilyich Tchaikovsky, including his brother Modest Tchaikovsky's idea that Tchaikovksy drank cholera infested water the day before he became ill)..

    Other famous people who succumbed to the disease include:



    Research The major contributions to fighting cholera were made by physician and self-trained scientist John Snow (physician) (1813-1858), who found the link between cholera and contaminated drinking water in 1854 and Henry Whitehead, an Anglican minister, who helped John Snow track down and verify the source of the disease, an infected well in London. Their conclusions and writings were widely distributed and firmly established for the first time a definite link between germs and disease. Clean water and good sewage treatment, despite their major engineering and financial cost, slowly became a priority throughout the major developed cities in the world from this time onward. Robert Koch, 30 years later, identified V. cholerae with a microscope as the bacillus causing the disease in 1885. The bacterium had been originally isolated thirty years earlier (1855) by Italian anatomist Filippo Pacini, but its exact nature and his results were not widely known around the world.

    Cholera has been a laboratory for the study of evolution of virulence. The province of Bengal in British Raj was partitioned into West Bengal (a state in India) and East Pakistan in 1947. Prior to partition, both regions had cholera pathogens with similar characteristics. After 1947, India made more progress on public health than East Pakistan (now Bangladesh). As a consequence, the strains of the pathogen which succeeded in India had a greater incentive in the longevity of the host and are less virulent than the strains prevailing in Bangladesh, which uninhibitedly draw upon the resources of the host population, thus rapidly killing many in it.

    Other historical information In the past, people travelling in ships would hang a yellow flag if one or more of the crew members suffered from cholera. Boats with a yellow flag hung would not be allowed to disembark at any harbor for an extended period of time, typically 30 to 40 days.

    The French writer Jean Giono's novel "Le Hussard sur la toit" ("The Horseman on the Roof") is set in the south of France during the cholera epidemic of 1832.

    False report of cholera A persistent myth states that Chicago 1885 cholera epidemic myth of cholera and typhoid fever in 1885. This story has no factual basis. In 1885 there was a torrential rainstorm that flushed the Chicago river and its attendant pollutants into Lake Michigan far enough that the city's water supply was contaminated. Fortunately, cholera was not present in the city and this is not known to have caused any deaths. It did, however, cause the city to become more serious about their sewage treatment.

    Cholera morbus The term cholera morbus was used in the 19th and early 20th century to describe both non-epidemic cholera and gastrointestinal diseases that mimicked cholera. The term is not in current use, but is found in many older references. Archaic Medical Terms.

    References

    External links



    Cholera
    Cholera is an infectious disease caused by a bacterium that affects the absorption of water in the small intestine.

    WHO | Cholera
    Cholera is an acute intestinal infection caused by ingestion of food or water contaminated with the bacterium Vibrio cholerae. It has a short incubation period, from less than one ...

    Cholera in the 19th Century
    The following images are examples of documents relating to cholera outbreaks in 19th Century Dundee, Scotland.

    Cholera - Wikipedia, the free encyclopedia
    Cholera, sometimes known as Asiatic cholera or epidemic cholera, is an infectious gastroenteritis caused by the bacterium Vibrio cholerae. [1] [2] Transmission to humans occurs ...

    HPA - Cholera
    Cholera ... Cholera. Cholera is an acute intestinal infection caused by the bacterium Vibrio cholerae.Cholera is spread by contaminated water and food.

    Disease Listing: Cholera General Information | CDC DFBMD
    FAQ on cholera from the Centers for Disease Control.

    Gresham College | Home
    Exists to provide free public lectures which have been given for over 400 years. Includes a guide to subjects and digital archive of past lectures.

    Definition: cholera from Online Medical Dictionary
    The Online Medical Dictionary is a searchable dictionary of definitions from medicine, science and technology.

    BBC NEWS | World | South Asia | Cholera-hit Indians 'face hunger'
    Tribal people are facing starvation in eastern India where cholera has killed scores in recent weeks.

    Cholera News
    World Health Today provides Plagues & Epidemics News from the most comprehensive global news network on the internet. International News and analysis on epidemics, diseases ...

     

    Cholera



     
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