UK planted CHOLERA in Zimbabwe

UK wants Rhodesia back.
UK wants to establish LEGAL PRECEDENT of "humanitarian intervention"
which, of course, can be used by those who are
a) willing to sow the destruction and able to hide their involvement,
a time-tested and well-rehearsed SPECIAL OP by UK and US and Israel
b) in charge of the doctrinal system, who control the media,
remember how the BBC was pro-Iraq-War???

therefore:

The UK could have easily planted the Cholera bacteria.

Just a little well-poisoning and then a big MORAL IDIGNATION

Cholera is an infectious disease. It is caused by a bacteria Vibrio cholerae. This bacteria usually lives in water. Vibrio cholera is more common where fresh water mixes with salt water, like where rivers enter the ocean. It is more common in water with lots of algae.

Cholera is an acute intestinal illness, causing abdominal pain, watery diarrhoea, and vomiting. The diarrhoea and vomiting, in turn, can cause very bad dehydration of the body, leading to death if untreated. Dehydration is losing too much water and salts.

Most of the treatment for cholera is giving people fluids (water) and electrolytes (salts). For most people with cholera, fluids and electrolytes are given by mouth. This can be done with 80-90% of people. The best way to give this by mouth is WHO-ORS: World Health Organization Oral Rehydration Solution. (Oral means by mouth. Rehydration means to give back fluids and electrolytes to someone who is dehydrated. Solution is a mixture of salts and water.)

Some people cannot take enough fluids and electrolytes by mouth. Usually this is because vomiting is so bad. These people must be given treatment intravenously. (Intravenous means into a vein. Intravenous fluids and electrolytes are given through a needle into a person's vein.) This is necessary because if people cannot drink enough fluids and electrolytes, they can die quickly.

Transmission to humans occurs through ingesting food or water that is contaminated with cholera vibrios. The major reservoir for cholera was long assumed to be humans themselves, but considerable evidence exists that aquatic environments can serve as reservoirs of the bacteria. Vibrio cholerae is a Gram-negative bacterium that produces cholera toxin, an enterotoxin, whose action on the mucosal epithelium lining of the small intestine is responsible for the disease's infamous characteristic, exhaustive diarrhea.[1] In its most severe forms, cholera is one of the most rapidly fatal illnesses known, and a healthy person may become hypotensive within an hour of the onset of symptoms; infected patients may die within three hours if medical treatment is not provided.[1] In a common scenario, the disease progresses from the first liquid stool to shock in 4 to 12 hours, with death following in 18 hours to several days, unless oral rehydration therapy is provided

The diarrhea associated with cholera is acute and so severe that, unless oral rehydration therapy is started promptly, the diarrhea may within hours result in severe dehydration (a medical emergency), or even death.

Author Susan Sontag wrote that cholera was more feared than some other deadly diseases because it dehumanized the victim. Diarrhea and dehydration were so severe that the victim could literally shrink into a wizened caricature of his or her former self before death.[5] Other symptoms include rapid dehydration, nosebleed, rapid pulse, dry skin, tiredness, abdominal cramps, nausea, leg cramps, and vomiting.

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,[17][18] 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.[19]

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 malnourished.

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.[20] 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.

[edit] Transmission
Drawing of Death bringing the cholera, in Le Petit Journal

Persons infected with cholera suffer acute diarrhea. This highly liquid diarrhea, referred to as rice-water stool, is loaded with bacteria that can infect water used by other people. Cholera is transmitted from person to person through ingestion of water contaminated with the cholera bacterium, usually from faeces or other effluent. 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 supplies. Any infected water and any foods washed in the water, as well as shellfish living in the affected waterway, can cause an infection. Cholera is rarely spread directly from person to person. V. cholerae harbors naturally in the zooplankton of fresh, brackish, and salt water, attached primarily to their chitinous exoskeleton.[21] Both toxic and non-toxic strains exist. Non-toxic strains can acquire toxicity through a lysogenic bacteriophage.[22] Coastal cholera outbreaks typically follow zooplankton blooms, thus making cholera a zoonotic disease.

[edit] Potential human contribution to transmissibility

Cholera bacteria grown in vitro encounter difficulty subsequently growing in humans without additional stomach acid buffering. In a 2002 study at Tufts University School of Medicine, it was found that stomach acidity is a principal factor that contributes to epidemic spread.[23] In their findings, the researchers found that human colonization creates a hyperinfectious bacterial state that is maintained after dissemination and that may contribute to epidemic spread of the disease. When these hyperinfectious bacteria underwent transcription profiles, they were found to possess a unique physiological and behavioral state, characterized by high expression levels of genes required for nutrient acquisition and motility, and low expression levels of genes required for bacterial chemotaxis. Thus, the spread of cholera can be expedited by host physiology.

[edit] Laboratory diagnosis

Stool and swab samples collected in the acute stage of the disease, before antibiotics have been administered, are the most useful specimens for laboratory diagnosis. If an epidemic of cholera is suspected, the most common causative agent is Vibrio cholerae O1. If V. cholerae serogroup O1 is not isolated, the laboratory should test for V. cholerae O139. However, if neither of these organisms is isolated, it is necessary to send stool specimens to a reference laboratory. Infection with V. cholerae O139 should be reported and handled in the same manner as that caused by V. cholerae O1. The associated diarrheal illness should be referred to as cholera and must be reported as a case of cholera to the appropriate public health authorities [24].

A number of special media have been employed for the cultivation for cholera vibrios. They are classified as follows:

[edit] Holding or transport media

1. Venkataraman-ramakrishnan (VR) medium: This medium has 20g Sea Salt Powder and 5g Peptone dissolved in 1L of distilled water.
2. Cary-Blair medium: This the most widely-used carrying media. This is a buffered solution of sodium chloride, sodium thioglycollate, disodium phosphate and calcium chloride at pH 8.4.
3. Autoclaved sea water

[edit] Enrichment media

1. Alkaline peptone water at pH 8.6
2. Monsur's taurocholate tellurite peptone water at pH 9.2

[edit] Plating media

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

Direct microscopy of stool is not recommended as it is unreliable. Microscopy is preferred only after enrichment, as this process reveals the characteristic motility of Vibrios and its inhibition by appropriate antiserum. Diagnosis can be confirmed as well as serotyping done by agglutination with specific sera.

[edit] Biochemistry of the V. cholerae bacterium
TEM image of Vibrio cholerae

Most of the V. cholerae bacteria in the contaminated water that a host drinks do not survive the very acidic conditions of the human stomach.[25] The few bacteria that do survive conserve their energy and stored nutrients during the passage through the stomach by shutting down much protein production. When the surviving bacteria exit the stomach and reach the small intestine, they need to propel themselves through the thick mucus that lines the small intestine to get to the intestinal wall where they can thrive. V. cholerae bacteria 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 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 longer. The bacteria stop producing the protein flagellin, thus again conserving energy and nutrients by changing the mix of proteins that they manufacture in response to the changed chemical surroundings. On reaching the intestinal wall, V. cholerae start producing the toxic proteins that give the infected person a watery diarrhea. This carries the multiplying new generations of V. cholerae bacteria out into the drinking water of the next host.if proper sanitation measures are not in place.
Cholera Toxin. The delivery region (blue) binds membrane carbohydrates to get into cells. The toxic part (red) is activated inside the cell (PDB code: 1xtc)

Microbiologists have studied the genetic mechanisms 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.[26] Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that interact 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 chloride 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.[27]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 separate, 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.[26] 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."[26]

[edit] History

[edit] Origin and spread

Cholera was originally endemic to the Indian subcontinent, with the Ganges River likely serving as a contamination reservoir. The disease spread by trade routes (land and sea) to Russia, then to Western Europe, and from Europe to North America during the Irish immigration period. Cholera is now no longer considered a pressing health threat in Europe and North America due to filtering and chlorination of water supplies, but still heavily affects populations in developing countries.

* 1816-1826 - First cholera pandemic: Previously restricted, the pandemic began in Bengal, and then spread across India by 1820. The cholera outbreak extended as far as China and the Caspian Sea before receding.
* 1829-1851 - Second cholera pandemic reached Europe, London and Paris in 1832. In London, the disease claimed 6,536 victims; in Paris, 20,000 succumbed (out of a population of 650,000) with about 100,000 deaths in all of France.[28] The epidemic reached Russia (see Cholera Riots), Quebec, Ontario and New York in the same year and the Pacific coast of North America by 1834. [29]

* 1849 - Second major outbreak in Paris. In London, it was the worst outbreak in the city's history, claiming 14,137 lives, over twice as many as the 1832 outbreak. In 1849 cholera claimed 5,308 lives in the port city of Liverpool, England, and 1,834 in Hull, England.[28] An outbreak in North America took the life of former U.S. President James K. Polk. Cholera spread throughout the Mississippi river system killing over 4,500 in St. Louis[28] and over 3,000 in New Orleans[28] as well as thousands in New York.[28] In 1849 cholera was spread along the California and Oregon trail as hundreds died on their way to the California Gold Rush, Utah and Oregon.[28]
* 1852-1860 - Third cholera pandemic mainly affected Russia, with over a million deaths. In 1853-4, London's epidemic claimed 10,738 lives.
* 1854 - Outbreak of cholera in Chicago took the lives of 5.5% of the population (about 3,500 people).[28] The Soho outbreak in London ended after removal of the handle of the Broad Street pump by a committee instigated to action by John Snow.[30]

* 1863-1875 - Fourth cholera pandemic spread mostly in Europe and Africa.

1892 Cholera outbreak in Hamburg, Germany, hospital ward
1892 Cholera outbreak in Hamburg, Germany, disinfection team

* 1866 - Outbreak in North America. In London, a localized epidemic in the East End claimed 5,596 lives just as London was completing its major sewage and water treatment systems--the East End was not quite complete. William Farr, using the work of John Snow et al. as to contaminated drinking water being the likely source of the disease, was able to relatively quickly identify the East London Water Company as the source of the contaminated water. Quick action prevented further deaths.[28] Also a minor outbreak at Ystalyfera in South Wales. Caused by the local water works using contaminated canal water, it was mainly its workers and their families who suffered, 119 died. In the same year more than 21,000 people died in Amsterdam, The Netherlands.
* 1881-1896 - Fifth cholera pandemic ; The 1892 outbreak in Hamburg, Germany killed 8,600 people. Although generally held responsible for the virulence of the epidemic, the city government went largely unchanged. This was the last serious European cholera outbreak.
* 1899-1923 - Sixth cholera pandemic had little effect in Europe because of advances in public health, but major Russian cities and the Ottoman Empire were particularly hard hit by cholera deaths.
* 1961-1970s - Seventh cholera pandemic began in Indonesia, called El Tor after the strain, and reached Bangladesh in 1963, India in 1964, and the USSR in 1966. From North Africa it spread into Italy by 1973. In the late 1970s, there were small outbreaks in Japan and in the South Pacific. There were also many reports of a cholera outbreak near Baku in 1972, but information about it was suppressed in the USSR.
* January 1991 to September 1994 - Outbreak in South America, apparently initiated when a ship discharged ballast water. Beginning in Peru there were 1.04 million identified cases and almost 10,000 deaths. The causative agent was an O1, El Tor strain, with small differences from the seventh pandemic strain. In 1992 a new strain appeared in Asia, a non-O1, nonagglutinable vibrio (NAG) named O139 Bengal. It was first identified in Tamil Nadu, India and for a while displaced El Tor in southern Asia before decreasing in prevalence from 1995 to around 10% of all cases. It is considered to be an intermediate between El Tor and the classic strain and occurs in a new serogroup. There is evidence of the emergence of wide-spectrum resistance to drugs such as trimethoprim, sulfamethoxazole and streptomycin.
* November 2008 - Doctors Without Borders reported an outbreak in a refugee camp in Congo's eastern provincial capital of Goma. Some 45 cases were reportedly treated between November 7th through 9th.

Wikinews
Wikinews has related news:

* Wikinews Shorts: November 25, 2008#53 die in Zimbabwe after cholera outbreak
* Number of Zimbabwe cholera deaths nears 500

* November 2008 - More than an estimated 11,000 people in Zimbabwe are believed to be infected with more than 550 recorded deaths observed during a current and ongoing outbreak. The number of people infected is believed to be significantly higher and the government is accused of underestimating the spread of the epidemic. The outbreak is a result of mismanagement of water purification infrastructure. Subsequent outbreaks are being observed in neighbouring countries as the medical infrastructure in Zimbabwe is severely crippled by hyperinflation leading to several Zimbabwean citizens seeking medical care elsewhere. The continuing closure of several local hospitals and the scarcity of basic medical commodities such as medicines and personnel is believed to be a major contributor to the spread. According to the World Health Organisation, Zimbabwe's government has asked for urgent international help to tackle its cholera outbreak.[31]

[edit] Genetic Diversity in the Pandemic Cholera Spread

Amplified fragment length polymorphism (AFLP) fingerprinting of the pandemic isolates of Vibrio Choleraehas revealed variation in the genetic structure. Two clusters have been identified: Cluster I and Cluster II. Cluster I consists mainly of strains from the 1960s and 1970s, while cluster II contains mainly strains from the 1980s and 1990s, based on a the change in the clone structure. This grouping of strains is best seen in the strains from the African Continent.[32]

[edit] Famous cholera victims

The pathos in the last movement of Tchaikovsky's (c. 1840-1893) last symphony made people think that Tchaikovsky had a premonition of death. "A week after the premiere of his Sixth Symphony, 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 (his brother and biographer), he is said to have poured tap water from a pitcher into his glass and drunk a few swallows. Since the water was not boiled and cholera was once again rampaging St. Petersburg, such a connection was quite plausible ...."[33]

Other famous people who succumbed to the disease include:

* Major General Edward Hand, Adjutant General of the Continental Army and congressman
* James K. Polk, eleventh president of the United States
* Mary Abigail Fillmore, daughter of U.S. president Millard Fillmore
* Elizabeth Jackson, mother of U.S. president Andrew Jackson
* Elliott Frost, son of American poet Robert Frost[citation needed]
* Nicolas Léonard Sadi Carnot
* Georg Wilhelm Friedrich Hegel
* Samuel Charles Stowe, son of Harriet Beecher Stowe
* Carl von Clausewitz
* George Bradshaw
* Adam Mickiewicz
* August von Gneisenau
* William Jenkins Worth
* John Blake Dillon
* Daniel Morgan Boone, founder of Kansas City, Missouri, son of Daniel Boone
* James Clarence Mangan
* Mohammad Ali Mirza Dowlatshahi of Persia
* Ando Hiroshige, Japanese ukiyo-e woodblock print artist.
* Juan de Veramendi, Mexican Governor of Texas, father-in-law of Jim Bowie
* Grand Duke Constantine Pavlovich of Russia
* William Godwin, father of Mary Shelley
* Judge Daniel Stanton Bacon, father-in-law of George Armstrong Custer
* Inessa Armand, mistress of Lenin and the mother of Andre, his son.
* Honinbo Shusaku, famous go player.
* Henry Louis Vivian Derozio, Eurasian Portuguese Poet and Teacher. Resided in India.
* Alexandre Dumas, père, French author of The Three Musketeers and The Count of Monte Cristo, also contracted cholera in the 1832 Paris epidemic and almost died, before he wrote these two novels.
* Jane Gibs
* Charles X of France

One of the major contributions to fighting cholera was made by physician and self-trained scientist John Snow (1813-1858), who found the link between cholera and contaminated drinking water in 1854.[28] In addition, Henry Whitehead, an Anglican minister, helped Snow track down and verify the source of the disease, which turned out to be an infected well in London. Their conclusions 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. The Russian-born bacteriologist Waldemar Haffkine developed the first cholera vaccine around 1900, along with that of the plague.

Cholera has been a laboratory for the study of evolution of virulence. The province of Bengal in British India was partitioned into West Bengal 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 that 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 victims.

More recently, in 2002, Alam et al studied stool samples from patients at the International Centre for Diarrhoel Disease (ICDDR) in Dhaka, Bangladesh. From the various experiments they conducted, the researchers found a correlation between the passage of V. cholerae through the human digestive system and an increased infectivity state. Furthermore, the researchers found that the bacterium creates a hyper-infected state where genes that control biosynthesis of amino acids, iron uptake systems, and formation of periplasmic nitrate reductase complexes were induced just before defecation. These induced characteristics allow the cholera vibrios to survive in the rice water stools, an environment of limited oxygen and iron, of patients with a cholera infection.[23]

[edit] False historical report of cholera

A persistent myth states that 90,000 people died in Chicago of cholera and typhoid fever in 1885, but this story has no factual basis.[34] 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. However, because cholera was not present in the city, there were no cholera-related deaths, though the incident caused the city to become more serious about its sewage treatment.

[edit] Cholera morbus

The term cholera morbus was used in the 19th and early 20th centuries to describe both non-epidemic cholera and other gastrointestinal diseases (sometimes epidemic) that resembled cholera. The term is not in current use, but is found in many older references.[35] The other diseases are now known collectively as gastroenteritis.

[edit] Other historical information

In the past, people traveling 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, typically 30 to 40 days.[36]

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