diease

Cholera


OVERVIEW OF Cholera :

Cholera results in ingestion of the contaminated foods and water by the bacterium called Vibrio cholera. It might result in the acute diarrhoeal symptoms. It is also known as the Vibrio cholera.


STRUCTURE of Cholera :

Structure:

It is an gram negative bacteria. It is an aerobic but also can survive without oxygenic environment. It is a comma shaped bacteria. Its antigen includes Flagella H antigen and Somatic O antigen. It uses flagella for the locomotion. But it cannot survive in acidic pH.


EPIDEMIOLOGY :

In India, kolkata city in west bengal state in the ganges delta has been described as the "homeland of cholera", with regular outbreaks and pronounced seasonality.  The seasonal variation in India is during the March to April


CAUSES :

Contaminated foods and water

Poor sanitization

Sewage

Sea food

Raw fruits and vegetables

Grains

The stomach acid acts as a greater defense mechanism. When this bacteria comes into contact with the acid, it might result in degradation of the bacteria. The patients taking the H2 receptor blockers and other antacids might easily get the infection.

Raw or undecooked shellfish


PATHOPHYSIOLOGY :

Mostly bacteria do not survive in the acidic environment of the human being.  These surveying bacteria exit the stomach and reach the small intestine they must propel themselves through the thick mucus that lines the small intestine to reach the intestinal walls where they can attach and thrive. Once the cholera bacteria enters the intestinal wall they are not dependendant on flagella for locomotion. The bacteria stop producing the protein flagellin to conserve energy and nutrients by changing the mix of proteins that they express in response to the changed chemical surroundings. The toxic proteins produces by the vibrio cholera produces the watery diarrhoea. This carries the multiplying new generations of V. cholera bacteria out into the drinking water of the next host if proper sanitation measures are not in place.

The cholera toxin is an oligomeic compound made up of six protein subunits a single copy of the subunit A and five copies of the subunit B connected by the disulfide bond. The A1 portion of the A subunit is an enzyme that ADP-ribosylates G proteins, while the A2 chain fits into the central pore of the B subunit ring. Upon binding, the complex is taken into the cell via receptor-mediated endocytosis. Once inside the cell, the disulfide bond is reduced, and the A1 subunit is freed to bind with a human partner protein called ADP-ribosylation factor 6 (Arf6).[30] Binding exposes its active site, allowing it to permanently ribosylate the Gs alpha subunit of the heterotrimeric G protein. This results in constitutive cAMP production, which in turn leads to the secretion of water, sodium, potassium, and bicarbonate into the lumen of the small intestine and rapid dehydration. The gene encoding the cholera toxin was introduced into V. cholerae by horizontal gene transfer. Virulent strains of V. cholerae carry a variant of a temperate bacteriophage.

The cholera toxins interacts with the host cell and enhances the pumping of chloride ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The combination of sodium and chloride ions results in salt water environment in the small intestine which increases the osmosis reaction pull up to six litres of water per dat through the intestinal cells, creating the massive amounts of diarrhoes. The host can become rapidly dehydrated unless treated properly.

 

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 a complex cascade of regulatory proteins controls 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, causing diarrhea in the infected person and allowing the bacteria to colonize the intestine. Currentresearch 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."

 


ROUTES OF TRANSMISSION :

The main routes of transmission occurs by faeco-oral route by contamination with food and water.

Poor sanitization might result in infection. Uncooked food might also results in transmission of the disease.


COMMON CLINICAL SIGNS AND SYMPTOMS :

Diarrhoea: Water loss greater than 1 litre per day. Rice watery stools are common.

Nausea and vomiting: Vomiting occurs especially in the early stage of cholera and can lasts for hours.

Dehydration: Dehydration can result in fluid loss which might result in the mild to severe.

Signs and symptoms of cholera dehydration include irritability, fatigue, sunken eyes, a dry mouth, extreme thirst, dry and shriveled skin that's slow to bounce back when pinched into a fold, little or no urinating, low blood pressure, and an irregular heartbeat.

Muscle cramps: This might occurs due to potassium, sodium and chloride.

 Shock:This is one of the most serious complications of dehydration. It occurs when low blood volume causes a drop in blood pressure and a drop in the amount of oxygen in your body. If untreated, severe hypovolemic shock can cause death in minutes.

 

 


DIAGNOSTIC :

Stool culture:

Isolation of the organisms and susceptibility profile. V. cholerae can be isolated from stool using selective media such as thiosulfate citrate bile sucrose (TCBS) agar or taurocholate tellurite gelatin

Agar. Serogroup and serotype can be assigned by testing with specific antibodies. The transport media includes Cary-Blair media.

Molecular and Rapid tests:

This includes immunochromatographic lateral flow devices such as dipsticks which can detect the presence of the O1 or O139 antigen in rice water stool samples.

Accurate molecular testing for V. cholerae (eg, PCR), including tests that use dried fecal spots, is also feasible, but the practical use of molecular tests has been primarily limited to epidemiologic research and surveillance.

Darkfield microscopy of fresh rice-water stools (at 400x magnification) can also be used to rapidly evaluate for the presence of highly motile Vibrios, whose shooting star-like motion can be inhibited by the subsequent addition of specific antibodies.Darkfield microscopy is quite specific for V. cholerae but lacks sufficient sensitivity for it to be used reliably for diagnosis.

 


TREATMENT AND PROGNOSIS :

Fluid therapy:

This can be better achieved by Oral Rehydration therapy. Rice fluids are  preferable than glucose fluids. Ringer’s lactate is often a efficient solution when added with potassium.

Electrolytes:

Potassium can be given as a supplement. Coconut water can be given to equalize the potassium loss.

Antibiotics:

Doxycycline

Cotrimaxazole

Erythromycin

Tetracycline

Chloramphenicol

Ciprofloxacin

Azithromycin

Zinc Supplementation:

Antibiotics combined with Zinc gives the better results.

Vaccination :

Vaccines such as Vaxchora or inactivated strains of bacterial toxins are available.

 


PROGNOSIS :

The prognosis increases when treated at an early stage. The mortality rate (50-60%) might increases if treatment is denied


PREVENTION :

Avoid consuming contaminated food and water

Follow proper sanitary protocol

Clean the surrounding

Stay hydrated and take lots of fluids and electrolytes

Heat the food before eating.


Medicines used in the Treatment :

Doxycycline

Cotrimaxazole

Erythromycin

Tetracycline

Chloramphenicol

Ciprofloxacin

Azithromycin

Zinc Supplementation: