|Classification and external resources|
|ICD-10||A09.0, A03.9, A06.0, A07.9|
|ICD-9-CM||004, 007.9, 009.0|
It is caused by a number of types of infection such as bacteria, viruses, parasitic worms, or protozoa. It is a type of gastroenteritis. The mechanism is an inflammatory disorder of the intestine, especially of the colon.
Signs and symptoms
In developed countries, the most common form of dysentery is bacillary dysentery which is typically a mild illness, causing symptoms normally consisting of mild stomach pains and frequent passage of stool or diarrhea. Symptoms normally present themselves after one to three days and are usually no longer present after a week. The frequency of urges to defecate, the large volume of liquid feces passed, and the presence of mucus, pus and blood depends on the pathogen that is causing the disease. Temporary lactose intolerance can occur. In some caustic occasions severe abdominal pain, fever, shock, and delirium can all be symptoms.
In extreme cases, dysentery patients may pass over one litre of fluid per hour. More often, individuals will complain of nausea, abdominal pain, and frequent watery and usually foul-smelling diarrhea, accompanied by mucus and blood, rectal pain, and fever. Vomiting, rapid weight-loss, and generalized muscle aches sometimes also accompany dysentery. On rare occasions, the amoebic parasite will invade the body through the bloodstream and spread beyond the intestines. In such cases, it may more seriously infect other organs such as the brain, lungs, and the liver.
Dysentery results from viral infections, bacterial infections, or parasitic infestations. These pathogens typically reach the large intestine after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on.
Each specific pathogen has its own mechanism or pathogenesis, but in general the result is damage to the intestinal lining, leading to the inflammatory immune response. This can cause elevated temperature, painful spasms of the intestinal muscles (cramping), swelling due to water leaking from capillaries of the intestine (edema), and further tissue damage by the body's immune cells and the chemicals, called cytokines, they release to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases the entry of pathogenic organisms into the bloodstream.
Some microorganisms – for example, bacteria of the genus Shigella – secrete substances known as cytotoxins, which kill and damage intestinal tissue on contact. Viruses directly attack the intestinal cells, taking over their metabolic machinery to make copies of themselves, which leads to cell death.
Definitions of dysentery can vary by region and by medical specialty. The U. S. Centers for Disease Control and Prevention (CDC) limits its definition to "diarrhea with visible blood." Others define the term more broadly. These differences in definition must be taken into account when defining mechanisms. For example, using the CDC definition requires that intestinal tissue be so severely damaged that blood vessels have ruptured, allowing visible quantities of blood to be lost with defecation. Other definitions require less specific damage.
Dysentery caused by amoebiasis, an infection by the amoeba Entamoeba histolytica, which is found mainly in tropical areas, is known as amoebic dysentery. Proper treatment of the underlying infection of amoebic dysentery is important; insufficiently treated amoebiasis can lie dormant for years and subsequently lead to severe, potentially fatal, complications.
When amoebas inside the bowel of an infected person are ready to leave the body, they group together and form a shell that surrounds and protects them. This group of amoebas is known as a cyst, which is then passed out of the person's body in the feces and can survive outside the body. If hygiene standards are poor; for example, if the person does not dispose of the feces hygienically, it can contaminate the surroundings, such as nearby food and water. If another person then eats or drinks food or water that has been contaminated with feces containing the cyst, that person will also become infected with the amoeba. Amoebic dysentery is particularly common in parts of the world where human feces are used as fertilizer. After entering the person's body through the mouth, the cyst will travel down into the stomach. The amoebas inside the cyst are protected from the stomach's digestive acid. From the stomach, the cyst will travel to the intestines where it will break open and release the amoebas, causing the infection. The amoebas can burrow into the walls of the intestines and cause small abscesses and ulcers to form. The cycle then begins again.
A clinical diagnosis may be made by taking a history and doing a brief examination. Treatment is usually started without or before confirmation by laboratory analysis.
The mouth, skin, and lips may appear dry due to dehydration. Lower abdominal tenderness may also be present.
Stool and blood tests
Dysentery is managed by maintaining fluids by using oral rehydration therapy. If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for intravenous fluid replacement. In ideal situations, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an amoebicidal drug to kill the parasite, and an antibiotic to treat any associated bacterial infection.
If shigella is suspected and it is not too severe, letting it run its course may be reasonable — usually less than a week. If the shigella is severe, antibiotics, such as ciprofloxacin or TMP-SMX may be useful. However, many strains of shigella are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. If necessary, a doctor may have to reserve antibiotics for those at highest risk for death, including young children, people over 50, and anyone suffering from dehydration or malnutrition.
With correct treatment, most cases of amoebic and bacterial dysentery subside within ten days, and most individuals will achieve a full recovery within two to four weeks after beginning proper treatment. If the disease is left untreated, the prognosis varies with the immune status of the individual patient and the severity of disease. Extreme dehydration can prolong recovery and significantly raises the risk for serious complications.
Society and culture
The seed, leaves, and bark of the kapok tree have been used in traditional medicine by indigenous peoples of the rain-forest regions in the Americas, West-Central Africa, and South East Asia to treat this disease. Bacillus subtilis was marketed throughout America and Europe from 1946 as an immunostimulatory aid in the treatment of gut and urinary tract diseases such as Rotavirus and Shigella, but declined in popularity after the introduction of cheap consumer antibiotics, despite causing less chance of allergic reaction and significantly lower toxicity to normal gut flora.
- 1216 – King John of England died of dysentery at Newark Castle on 18 October 1216.
- 1422 – King Henry V of England died suddenly from dysentery in 1422. He was 35 years old.
- 1596 – Sir Francis Drake, Vice Admiral, died of dysentery on 27 January 1596 while attacking San Juan, Puerto Rico. He was buried at sea in a lead coffin, near Portobelo.
- 1605 – Akbar the Great, ruler of the Mughal Empire of South Asia, died of dysentery. On 3 October 1605, he fell ill with an attack of dysentery, from which he never recovered. He is believed to have died on or about 27 October 1605, after which his body was buried at a mausoleum in Agra, present-day India.
- 1675 – Jacques Marquette died of dysentery on his way north from what is today Chicago, traveling to the mission where he intended to spend the rest of his life.
- 1676 – Nathaniel Bacon died of dysentery after taking control of Virginia following Bacon's Rebellion. He is believed to have died in October, 1676, allowing Virginia's ruling elite to regain control. 
- 19th century – As late as the nineteenth century, the 'bloody flux,' it is estimated, killed more soldiers and sailors than did combat. Typhus and dysentery decimated Napoleon's Grande Armée in Russia. More than 80,000 Union soldiers died of dysentery during the American Civil War.
- 1896 – Phan Đình Phùng, a Vietnamese revolutionary who led rebel armies against French colonial forces in Vietnam, died of dysentery as the French surrounded his forces on January 21, 1896.
- 1930 – The French explorer and writer, Michel Vieuchange, died of dysentery in Agadir on 30 November 1930, on his return from the "forbidden city" of Smara. He was nursed by his brother, Doctor Jean Vieuchange, who was unable to save him. The notebooks and photographs, edited by Jean Vieuchange, went on to become bestsellers.
- 1942 – The Selarang Barracks Incident in the summer of 1942 during World War II involved the forced crowding of 17,000 Anglo-Australian prisoners-of-war (POWs) by their Japanese captors in the areas around the barracks square for nearly five days with little water and no sanitation after the Selarang Barracks POWs refused to sign a pledge not to escape. The incident ended with the capitulation of the Australian commanders due to the spreading of dysentery among their men.
Vaccines currently in development may eventually become a critical part of the strategy to reduce the incidence and severity of diarrhea, particularly among children in low-resource settings. For example, Shigella is a longstanding World Health Organization (WHO) target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent this disease should be feasible. Currently, no licensed vaccine targeting Shigella exists. The development of vaccines against these types of infection has been hampered by technical constraints, insufficient support for coordination, and a lack of market forces for research and development. Most vaccine development efforts are taking place in the public sector or as research programs within biotechnology companies. Several vaccine candidates are currently in various phases of research and development, including a number of ongoing clinical trials.
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