dysentery(redirected from Amoebic dysentry)
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dysentery(dĭs`əntĕr'ē), inflammation of the intestine characterized by the frequent passage of feces, usually with blood and mucus. The two most common causes of dysentery are infection with a bacillus (see bacteriabacteria
[pl. of bacterium], microscopic unicellular prokaryotic organisms characterized by the lack of a membrane-bound nucleus and membrane-bound organelles. Once considered a part of the plant kingdom, bacteria were eventually placed in a separate kingdom, Monera.
..... Click the link for more information. ) of the Shigella group, and infestation by an amebaameba
, common name for certain one-celled organisms belonging to the phylum Sarcodina of the kingdom Protista. Amebas were previously classified as members of the animal kingdom.
..... Click the link for more information. , Entamoeba histolytica. Both bacillary and amebic dysentery are spread by fecal contamination of food and water and are most common where sanitation is poor. They are primarily diseases of the tropics, but may occur in any climate.
It is estimated that in some parts of the tropics 80% of the children acquire bacillary dysentery before the age of five; the mortality rate is high among infants and the aged if the infection is not treated, preferably with a broad-spectrum antibiotic. In adults bacillary dysentery usually subsides spontaneously, but treatment is desirable to prevent recurrence.
Amebic dysentery is prevalent in regions where human excrement is used as fertilizer; in some such regions over half the population probably harbors the amebic cyst. The cyst is the inactive, resistant stage in which the ameba is transmitted from one host to another; the active form is that which causes damage. Both cysts and active amebas are excreted in the feces of an infected person, but only the cysts are hardy enough to survive outside the body. A person recovering from the infection, or one with an inactive case, passes mostly cysts; such a person is a more likely source of contamination than one with an active case. When cysts are ingested with contaminated food or water they are transformed in the intestine into active amebas. If these remain within the lumen of the intestine they are relatively innocuous, but if they invade the intestinal wall they cause ulceration, dysentery, and usually pain. In severe cases the resulting dehydration may lead to prostration.
Amebic dysentery may occur in acute or chronic form. In prolonged infections the amebas may invade the blood vessels of the intestine and be carried to other parts of the body, where they cause amebic abcesses. Abcesses of the liver and brain are especially dangerous; destruction of liver tissue is the most frequent complication of amebic dysentery. Infection by amebas, whether of the intestine alone or of other parts of the body, is called amebiasis. Infections are diagnosed by finding cysts or active amebas in the feces. However, the disease is easily misdiagnosed for several reasons. Entamoeba histolytica may be harbored without causing symptoms (although it may be passed on and cause the disease in others); it is easily confused with harmless amebas of the human intestine, especially Entamoeba coli; it commonly coexists with bacteria that may in some cases be the cause of the symptoms.
A combination of drugs is generally used to treat amebic dysentery: an amebicide (metronidazole or tinidazole) to eliminate the organism from the intestinal tract, an antibiotic to eradicate associated bacterial infection, and a drug to combat infection of the liver and other tissues. Preventive measures include the protection of water supplies from contamination and the washing of hands by food handlers.
an acute or chronically recurring infectious disease of man which most seriously affects the large intestine.
Baciilary dysentery. Bacillary dysentery is caused by various representatives of the group of dysentery bacteria, the most significant of which are the Flexner and Sonne species—rods that inhabit the folds (and sometimes become embedded in the cells) of the mucous membrane of the lower portion of the large intestine, the sigmoid colon, and the rectum. The causative agent of the dysentery is discharged with the patient’s stool. Dysentery bacteria may retain their viability outside the body for a long time, especially in water, milk, and various food products (contaminated by the hands of the patient or of those caring for the patient). Flies play an active role in spreading the condition. The spread of dysentery is fostered by poor sanitary practices and violation of the rules of hygiene. Most often affected are children during the first two years of life. Outbreaks of dysentery are not uncommon in children’s institutions.
The causative agent of dysentery enters the body orally through raw water, food, and dirty hands. Because of the acid content of the stomach, some of the dysentery bacteria are destroyed, but those that survive move to the intestine, causing various inflammatory and necrotic processes (most often catarrhal changes in the mucous membrane and sometimes surface erosions, deeper ulcers, or filmy fibrin deposits). As the dysentery bacteria die off and as a result of their vital processes, poisonous substances (toxins) are formed. These are absorbed through the mucous membrane of the large intestine and enter the blood stream, causing systemic poisoning (intoxication). Diarrhea occurs as a result of intestinal lesions. Blood and mucus are found mixed with the stools. The sigmoid colon goes into spasm (convulsive contraction), which accounts for the pain accompanying the urge to defecate.
The incubation period averages two or three days, but may be anywhere from one to five. The disease begins with slight chills, pain in the lower abdomen, and frequent bowel movements. The feces become loose. In some persons repeated vomiting begins within a day (mainly in Sonne dysenteries). After the first 24 hours mucus is found in the stools, often with streaks or small clots of blood. By the second day stool frequency reaches 10-15 times a day or more. Often there is the false urge to defecate (tenesmus), that is, the urge is not accompanied by a discharge of fecal matter. Sometimes a small clump of mucus streaked with blood is discharged from the rectum. The diagnosis is established on the basis of examination of the mucous membrane of the lower portion of the large intestine (rectoscopy) and bacteriological examination of the stools. All symptoms of the dysentery peak on the second and third days. The temperature reaches 38°-39.5°C and appetite and sleep are disturbed. With timely initiation of the proper treatment, the stools become less frequent by the fourth day, and gradually, during the next three to five days, the mucus and blood disappear from the discharge. However, in 1-2 percent of the cases there may be a transition to a chronic form of the disease in which relapses lasting two or three weeks may appear at three- or four-month intervals.
Amoebic dysentery. Amoebic dysentery is the principal form of amoebiasis. It arises as the result of the penetration and proliferation in the tissues of the large intestine of the dysentery amoeba. Incidence of the disease is usually sporadic (that is, it appears in isolated cases). In the majority of those infected, the dysentery amoeba multiplies only in the contents of the upper sections of the large intestine, causing neither lesions of the intestinal wall nor disturbances of intestinal activity. These persons are healthy carriers and help to spread the disease. Infection may occur from a patient in the chronic stage of the disease who is discharging cysts of the amoeba in his stool (these cysts may survive outside the body for several weeks). The paths of transmission of the causative agent are the same as in bacillary dysentery and other intestinal infections and invasions.
Having penetrated the wall of the large intestine, the dysentery amoeba multiplies there, forming a primary abscess that opens into the lumen of the intestine. Ulcers develop with undermined margins. Hollow ulcers may lead to perforation of the intestine, which creates the possibility of peritonitis, cicatricial stenosis of the intestine, intestinal hemorrhage, ameboma (a specific granuloma of the large intestine), and metastatic amoebic abscesses of the liver and other internal organs and tissues.
The incubation period may last from one week to three months or more. In the acute manifestation of the disease diagnosis must be confirmed (as in bacillary dysentery) by discovery of the causative agent. In uncomplicated cases, elevated temperature and the symptoms of systemic intoxication are absent. With incorrect treatment or without treatment, the disease takes a chronic course (alternate periods of exacerbation and remission). In exacerbations of chronic dysentery the symptoms are analogous to those in the acute form of the disease. Remissions may last a year or longer. Forms of the disease without clearly expressed manifestations are often encountered.
Treatment of dysentery must be conducted in special hospitals for infectious diseases. Antibiotics, such as Levomycetin and tetracycline, are used according to specially developed rules, as well as chemotherapeutic preparations, such as nitrofurans, sulfanilamide preparations, and Entero-Septol. Emetine, Yatren, metronidazole, and vaccines are used for amoebic dysentery. Special diets are prescribed during the acute period of the disease and for three or four weeks after the disappearance of the principal symptoms of the disease.
Dysenteries can be prevented by improving the sanitary conditions of an area, by better treatment of the water supply, and by improving the sewage disposal system of population points, as well as by the observance of the rules of personal hygiene and proper culinary treatment and storage of food products. Bacillary carriers are not permitted to work for food stores, food enterprises, the water supply system, or in child care. Bacteriophage is used in children’s collectives. Healthy carriers of the dysentery amoeba are disinfected with Yatren (without having to leave work).
K. V. BUNIN and V. B. SCHENSNOVICH
Dysentery in animals. Dysentery is a collective term for the diseases of swine and sheep whose principal symptom is a wasting diarrhea. Swine dysentery, first described by the American scientist L. Doyle in 1921, is caused by the microbe Vibrio suis. It affects predominantly the young stock (from one to six months). The source of infection is diseased swine and the bacterial carriers. The disease is widespread and causes great economic loss. The latent period of the disease lasts 10-15 days. The principal clinical symptoms are diarrhea and weight loss. The basis of prevention is observance of the veterinary and sanitary requirements of keeping swine, a nutritionally balanced diet, and obligatory disinfection of the premises where the animals are kept. Antibiotics are used in treatment. Anaerobic dysentery of lambs is caused by the spore-forming bacillus Clostridium perfringens (Type B); this was first established in the USSR in 1936 by M. D. Polykovskii. The disease most often affects lambs, especially of the fine-wooled varieties, at the age of one to five days (during the period of mass lambing). Since the causative agent can survive for long periods in the soil, the disease may occur repeatedly in the same places. Sick animals, which discharge the causative agent in their feces, are the source of infection. The occurrence of dysentery in lambs is fostered by poor conditions in keeping and feeding the animals. The latent period of the disease is several hours. Lamb dysentery most often appears during the first two or three days of life. The sick lambs die very quickly after the onset of diarrhea. Economic loss through lamb dysentery is quite considerable. The principal preventive measure is observance of the rules of hygiene of animal husbandry. A specific serum and antibiotics are used for treatment.
REFERENCESSeppi, I. V. Dizenteriia. Moscow, 1963.
Schensnovich, V. B., and N. N. Plotnikov. “Amebnaia dizenteriia.” In Mnogotomnoe rukovodstvo po mikrobiologii, klinike i epidemiologii infektsionnykh boleznei, vol. 9. Moscow, 1968.
“Dizenteriia svinei.” “Dizenteriia iagniat.” In Veterinarnaia entsiklopediia, vol. 2. Moscow, 1969. Pages 806, 810.