Cholera disease , history of cholera disease , transmission of cholera , colonization of intestine , vaccination in cholera and treatment of cholera.

 Cholera

When Vibrio cholerae bacteria are present in food or water, it can result in cholera, an acute intestinal infection. It has a brief one to five day incubation period and releases a toxin that causes painless, watery diarrhea and vomiting that can swiftly result in severe dehydration and death.

Gram-negative, straight or curved rod-shaped bacteria with a single polar flagellum make up the genus Vibrio. Both respiratory and fermentative metabolism are possible in bacteria. Most species have positive oxidase activity. Human pathogens include V. parahaemolyticus and V. cholerae. While V.parahaemolyticus is an invasive pathogen that mostly affects the colon, V. Another new human pathogen that causes cholera, Vibrio vulnificus, is noninvasive and affects the small intestine by releasing an enterotoxin. wound infections, gastroenteritis, or the "primary septicaemia" syndrome.

History

Cholera regularly expanded over the 19th century from India's Ganges delta to the rest of the world before retreating to South Asia. Millions of people died as a result of six epidemics that were documented in Europe, Africa, and the Americas. Cholera is mostly spread via tainted food and water and is closely associated with unclean environmental conditions.

The key factors causing the disease to spread are a lack of accessible, clean drinking water, inadequate sanitation, and an unsanitary atmosphere. One of the fundamental measures of social progress and a hazard to public health on a worldwide scale continues to be cholera. While the disease is no longer a problem in nations with basic hygienic standards, it nevertheless poses a concern in practically all developing nations with significant populations.

In 2006, there were significantly more cholera cases reported to WHO than there had been in the late 1990s. A total of 236 896 cases, including 6311 deaths, were recorded from 52 different countries, which is a 79% increase over the cases reported in 2005.

   Cholera Toxin

The cholera toxin causes the intestinal mucosa cells to release H20, Na+, K+, Cl-, and HCO3- into the small intestine lumen as well as activate the adenylate cyclase enzyme, increasing intracellular cAMP levels. The monosialosyl ganglioside (GM1 ganglioside) receptor, which is found on the surface of intestinal mucosal cells, is what causes the action.

During the colonisation phase, the bacterium develops the invasin neuraminidase, which has the intriguing feature of degrading gangliosides to the monosialosyl form, which is the particular receptor for the toxin. Once within the cell, the A1 subunit enzymatically transfers NAD's ADP ribose to a protein known as Gs or Ns, which controls the adenylate cyclase system on the interior of mammalian cells' plasma membranes. Fragment A1 functions as an enzyme that catalyses the transfer of the NAD's ADP-ribosyl moiety to a part of the adenylate cyclase system. A regulatory protein (GS) and GTP ordinarily activate adenylate cyclase (AC).

Transmission

The extremely liquid diarrhoea caused by cholera infection is full of bacteria that can spread in filthy environments to contaminate other people's water supplies. People can contract cholera from one another by drinking water that has been tainted with feces.

Other cholera patients who allow their diarrheal output to enter streams, groundwater, or drinking water supplies are often the sources of contamination. Any contaminated water, food that has been washed in it, and fish and shellfish that are present in the impacted streams can all spread infection. Rarely does cholera spread from person to person. In fresh, brackish, and salt water planktons, V. cholerae naturally exists, mostly associated to copepods. There are both poisonous and non-toxic strains. Zooplankton blooms are frequently followed by coastal cholera epidemics.

Colonization of Intestine

Adhesins, neuraminidase, intestinal motility, chemotaxis, and toxin synthesis are some of the traits of pathogenic V. cholerae that facilitate colonisation. The production of neuraminidase and proteases may help V. cholerae penetrate the mucus layer of the small intestine since it is resistant to bile salts (mucinases). Additionally, they are able to survive the propulsion of the gut motility due to their own swimming prowess and chemotaxis towards the gut mucosa.

Hemagglutinin, a surface protein that agglutinates red blood cells, and a collection of outer membrane proteins made by the acf (accessory colonisation factor) genes are two other potential adhesins in V. cholerae. It has been demonstrated that acf mutants are less able to colonise the gastrointestinal system. V. cholerae may use these nonfimbrial adhesins to mediate a tighter attachment to host cells than is possible with fimbriae alone, according to certain theories.

Vaccine

The live, attenuated strain of V. cholerae used to create the oral vaccinations. The ideal characteristics of such a bacterium would be to lack the ability to create toxin molecules while yet having all the pathogenicity components necessary for colonisation of the small intestine. In a perfect world, it would only create the B component of the toxin, which would encourage the production of antibodies that could block the native toxin's ability to bind to epithelial cells.

To address the Bengal strain of Vibrio cholerae, which has started to spread epidemically throughout Southeast Asia and the Indian subcontinent, a new vaccine has been created. The Bengal strain varies from previously isolated epidemic strains in that it expresses a unique polysaccharide capsule and belongs to the serogroup 0139 rather than the 01 subgroup. Since immunity against 0139 Vibrio cholerae is not conferred by prior exposure to 01 Vibrio cholerae, populations are affected by the Bengal type of cholera.

The noncellular vaccine has a low to zero LPS and other contaminants content and is comparatively harmless. For active vaccination against Vibriocholerae O139 and other bacterial species expressing related surface polysaccharides, the vaccine will be employed. Additionally, human or other antibodies produced by this vaccination may be used to recognise Vibrio cholerae Bengal in order to diagnose infections and monitor the bacterium's presence in the environment.

Treatment

The simplest and most effective way to treat cholera is to restore any salts and bodily fluids that have been lost due to vomiting and diarrhea as away. Patients who get extremely dehydrated need to be given intravenous fluids, though they can be treated with Oral Rehydration Solution, a mixture of sugar and salts that needs to be combined with water and consumed in large doses. Less than 1% of cholera patients die when they receive early rehydration.

In extreme situations, an efficient antibiotic can shorten both the length of Vibrio discharge and the amount and duration of diarrhoea. The typical antibiotic of choice is tetracycline, however resistance to it is rising. Cotrimoxazole, erythromycin, doxycycline, chloramphenicol, and furazolidone are further useful antibiotics.

antibiotics prescribed for cholera

a single tablet of 300 mg of doxycycline

500 mg or 12.5 mg/kg of tetracycline, four times daily

three days.

TMP 5 mg/kg, sulfamethoxazole and trimethoprim (TMP/SMX),

TMP 160 mg and SMX 800 mg twice daily for three days at SMX 25 mg/kgc.

Furazolidone, 100 mg pill, 4 times daily for 3 days, 1.25 mg/kg.

If the aforementioned antibiotics are unavailable or Vibrio cholerae O1 is resistant to them, erythromycin or chloramphenicol may be employed.

For adults, doxycycline is the antibiotic of choice, but not for expectant mothers.

The recommended antibiotic for kids is TMP-SMX.

In all age groups, tetracycline is equally effective.

For pregnant women, furazolidone is the antibiotic of choice.

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