Various Diseases

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Saturday, January 9, 2010

Cholera

From Wikipedia, the free encyclopedia

 

Cholera, sometimes known as Asiatic or epidemic cholera, is an infectious gastroenteritis caused by enterotoxin-producing strains of the bacterium Vibrio cholerae.[1][2] Transmission to humans occurs through eating food or drinking water contaminated with Vibrio cholerae from other cholera patients. 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 most salient characteristic, exhaustive diarrhea.[1] In its most severe forms, cholera is one of the most rapidly fatal illnesses known, and a healthy person's blood pressure may drop to hypotensive levels 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 (or, in more serious cases, intravenous) rehydration therapy is provided.[3][4]
It is estimated that most cases of cholera are unreported due to poor surveillance systems, particularly in Africa. Fatality rates are 5% of total cases in Africa, and less than 1% elsewhere.[5] For a map of recent international outbreaks, see:[3]


Treatment

In most cases cholera can be successfully treated with oral rehydration therapy. Prompt replacement of water and electrolytes is the principal treatment for cholera, as dehydration and electrolyte depletion occur rapidly. Oral rehydration therapy or ORT is highly effective, safe, and simple to administer. In situations where commercially produced ORT sachets are too expensive or difficult to obtain, alternative homemade solutions using various formulas of water, sugar, table salt, baking soda, and fruit offer less expensive methods of electrolyte repletion. In severe cholera cases with significant dehydration and the administration of intravenous rehydration solutions may be necessary.
Antibiotics shorten the course of the disease, and reduce the severity of the symptoms. However oral rehydration therapy remains the principal treatment. Tetracycline is typically used as the primary antibiotic, although some strains of V. cholerae exist that have shown resistance. Other antibiotics that have been proven effective against V. cholerae include cotrimoxazole, erythromycin, doxycycline, chloramphenicol, and furazolidone.[6] Fluoroquinolones such as norfloxacin also may be used, but resistance has been reported.[7]
Rapid diagnostic assay methods are available for the identification of multidrug resistant V. cholerae.[8] New generation antimicrobials have been discovered which are effective against V. cholerae in in vitro studies.[9]
The success of treatment is significantly affected by the speed and method of treatment. If cholera patients are treated quickly and properly, the mortality rate is less than 1%; however, with untreated cholera the mortality rate rises to 50–60%.

Diagnosis

In epidemic situations a clinical diagnosis is made by taking a history of symptoms from the patient and by a brief examination only. Treatment is usually started without or before confirmation by laboratory analysis of specimens.
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.[15]
A number of special media have been employed for the cultivation for cholera vibrios. They are classified as follows:

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 is the most widely-used carrying medium. This is a buffered solution of sodium chloride, sodium thioglycollate, disodium phosphate and calcium chloride at pH 8.4.
  3. Autoclaved sea water

Enrichment media

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

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.

Biochemistry

Most of the V. cholerae bacteria in the contaminated water consumed by the host do not survive the highly acidic conditions of the human stomach.[24] 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.


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.[25] 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. 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.[25] 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."


 



 

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