cholera(redirected from Asiatic cholera)
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Related to Asiatic cholera: Colera, Cólera
Asiatic cholera,acute infectious disease caused by strains of the bacterium Vibrio cholerae that have been infected by bacteriophagesbacteriophage
, virus that infects bacteria and sometimes destroys them by lysis, or dissolution of the cell. Bacteriophages, or phages, have a head composed of protein, an inner core of nucleic acid—either deoxyribonucleic acid (DNA) or ribonucleic acid (RNA)—and a
..... Click the link for more information. . The bacteria, which are found in fecal-contaminated food and water and in raw or undercooked seafood, produce a toxintoxin,
poison produced by living organisms. Toxins are classified as either exotoxins or endotoxins. Exotoxins are a diverse group of soluble proteins released into the surrounding tissue by living bacterial cells. Exotoxins have specific reaction sites in the host; e.g.
..... Click the link for more information. that affects the intestines causing diarrhea, vomiting, and severe fluid and electrolyte loss. This overwhelming dehydration is the outstanding characteristic of the disease and is the main cause of death. Cholera has a short incubation period (two or three days) and runs a quick course. In untreated cases the death rate is high, averaging 50%, and as high as 90% in epidemics, but with effective treatment the death rate is less than 1%. The intravenous and oral replacement of body fluids and essential electrolytes and the restoration of kidney function are more important in therapy than the administration of antibacterial drugs. In regions of Asia, Africa, and South America where public sanitation is poor the disease is still endemic or epidemic; vaccination is recommended for people living in those areas. Although a cholera vaccine was developed in the late 1800s, an inexpensive oral vaccine that could be easily given in countries where cholera is most common did not become widely available until the 2010s. A theory of evolutionary biologists holds that the cystic fibrosiscystic fibrosis
, inherited disorder of the exocrine glands (see gland), affecting children and young people; median survival is 25 years in females and 30 years in males.
..... Click the link for more information. gene, a common but lethal recessive gene carried by approximately one in twenty Caucasians, affords those carriers partial protection against cholera.
See C. E. Rosenberg, The Cholera Years (1962).
A severe diarrheal disease caused by infection of the small bowel of humans with Vibrio cholerae, a facultatively anaerobic, gram-negative, rod-shaped bacterium. Cholera is transmitted by the fecal-oral route. Cholera has swept the world in seven pandemic waves. These involved the Western Hemisphere several times in the 1800s, and again in Peru in 1991. Whereas previous cholera outbreaks were associated with high mortality rates, through understanding of its pathophysiology it can now be said that no one should die of cholera who receives appropriate treatment soon enough.
Cholera produces a secretory diarrhea caused by the protein cholera enterotoxin (CTX). The toxin causes hypersecretion of chloride and bicarbonate and inhibition of sodium absorption in host membranes leading to the secretion of the large volumes of isotonic fluid which constitute the diarrhea of severe cholera. Treatment consists of replacing the fluids and electrolytes lost in the voluminous cholera stool. This can be done intravenously or orally. Appropriate antibiotics can also be used. The incubation period may be less than one day or up to several days; properly treated, the patient should recover in 4 or 5 days. The disease produces immunization, and convalescents rarely get cholera again.
Despite the fact that the cholera bacteria were first discovered by Robert Koch in 1883 and a cholera vaccine was introduced 3 years later, there is still no effective, economical, and nonreactogenic vaccine. Use of a killed whole-cell vaccine administered parenterally (via injection) was eliminated because of expense, reactogenicity, and lack of efficacy. Experimental vaccines currently being evaluated include genetically engineered living attentuated preparations administered orally (or intranasally), killed whole-cell vaccines administered orally, and conjugated vaccines (polysaccharide and toxin antigens) administered parenterally. Efforts are also being made to include cholera antigens transgenically in edible plants.
A complicating feature is the fact that of approximately 150 recognized serogroups of V. cholerae, until 1992 only two, classical (first described by Koch) and El Tor (recognized later), of serogroup O1 have been responsible for all epidemic cholera. In 1992 a recently recognized serogroup, O139, caused epidemic cholera in India and Bangladesh and, for a time, replaced the resident El Tor vibrios. O139 and El Tor are antigenically distinct, so a new vaccine will be required for O139. The emergence of O139 raises the specter that other serogroups of V. cholerae may acquire virulence and epidemicity.
The best ways to avoid cholera are by chlorination of water, sanitary disposal of sewage, and avoidance of raw or improperly cooked seafood, which may have become infected by ingesting infected plankton in epidemic areas.
an acute infectious disease of man that tends to occur in epidemics; it is a quarantine disease. The causative agent is the cholera vibrio, which was isolated in pure culture by R. Koch in 1883. It grows in an alkaline medium, surviving in food for several hours to several days and in bodies of water for several months. The vibrio is sensitive to common disinfectants, acids, and sunlight; it dies within 5 min at 80°C and instantaneously at 100°C.
Cholera has been known since antiquity. The historical focuses of epidemics are the basins of the Ganges and Brahmaputra rivers in India, owing to the areas’ humidity, the high population density, and the use of contaminated water for drinking. Cholera was brought to other countries from India, causing devastating epidemics. There were six pandemics from 1817 through 1926, each lasting from six to 23 years. They engulfed Afghanistan, Iran, Southeast Asia, and the Far East; the third and fourth pandemics spread to Africa, Europe, and America. All the pandemics affected Russia, which they reached by way of Afghanistan, Iran, and Turkey, generally beginning in Astrakhan, Transcaucasia, and Middle Asia and spreading to most of Russia’s provinces. In 1848 alone, more than 1.7 million persons were victims of cholera in Russia; of them, about 700,000 died.
Cholera was eradicated in the USSR by 1926 as a result of social changes, improvements in sanitation and hygiene, and measures undertaken to control epidemics. The seventh pandemic, which occurred in the second half of the 20th century, was caused not by the vibrio of the typical (Asian) cholera but by the El Tor biotype. Spreading from a focus in Indonesia in 1961, it extended to Southeast Asia, the Far East, and the Near East, reaching Africa in 1970. There were also outbreaks in Italy, Yugoslavia, Czechoslovakia, and other countries of Europe. In the USSR, outbreaks were recorded in the Kara-Kalpak ASSR and Khorezm Oblast (1965) and in Astrakhan, Odessa, and Kerch’ (1970), but they were quickly suppressed.
The source of infection by cholera is either a person affected by the disease or a carrier of the vibrio. Infection follows entry of the vibrio into the gastrointestinal tract, generally with contaminated water or food. The disease may also be transmitted by flies. Incorrect water supply sanitation is the major factor in the transmission of cholera. The disease spreads when untreated waste water is discharged into bodies of open water and when people subsequently drink nondisinfected water or swim in polluted bodies of water.
The incubation period of cholera varies from a few hours to five days, the average being two or three days. Typically, the disease sets in with diarrhea, which is marked by 30 to 40 or more watery stools daily, containing flakes that resemble cooked rice. The gastroenteritis phase soon follows, marked by vomiting, and symptoms of intoxication increase. Dehydration and the loss of body salts produce an algid condition, manifested by lowered blood pressure, convulsions, dyspnea, and decreased body temperature (to 35°–34°C or lower). The facial features become gaunt and pinched and the eyes sunken. The tongue and the mucous membranes of the mouth become dry, and the voice becomes hoarse. In mild cases there may be a single attack of diarrhea and vomiting, while the patient’s general condition remains satisfactory. Diagnosis is based on clinical findings, epidemiological data, and the results of laboratory tests. Of primary importance is bacteriological examination, achieved by culturing excreta and vomitus on alkaline media.
In the treatment of cholera, the water-salt balance is restored by injecting saline solutions into the tissues; the total volume of fluid injected into an adult may amount to 30–100 liters over a period of several days. Tetracycline and other antibiotics are also used. Prevention consists in observing general rules of sanitation, treating waste water, protecting bodies of water from contamination, providing properly treated drinking water, and strictly inspecting the production and sale of food products. Of particular importance are the observance of border health regulations, examination and periodic checkups of persons arriving from cholera locales, bacteriological analysis of water, and medical examination of individuals with symptoms suggestive of cholera.
Cholera patients must be hospitalized, and persons who have come in contact with them are also hospitalized and examined. Persons in an epidemic focus are kept under quarantine and are examined in order to detect those who have the disease or are bacteria carriers. Disinfection measures and occasionally chemo-prophylaxis are carried out. After a focus of cholera is freed of the disease, convalescents and bacteria carriers are periodically inspected, and the population of the area is vaccinated.
REFERENCESKorobkova, E. I. Mikrobiologiia i epidemiologiia kholery, 2nd ed. Moscow, 1959.
Zhukov-Verezhnikov, N. N., I. K. Musabaev, and N. K. Zav’ialova. Klinika, lechenie i profilaktika kholery. Tashkent, 1966.
Burgasov, P. N. Kholera El’-Tor, 2nd ed. Moscow, 1976.
L. M. MARCHUK and V. L. VASILEVSKII