shigellosis– an acute infectious disease characterized by symptoms of general intoxication and damage mainly to the distal colon. Some patients may become chronic. Etiology. The causative agents are gram-negative non-motile (generic trait) bacteria of the genus Shigella of the Enterobacteriaceae family. Varieties: Shigella dysenteriae, Shigellaflexneri, Shigella sonnei. In India, lesions caused by Shigella boydii predominate. Epidemiology. The only natural reservoir of Shigella is man. The likelihood of developing the disease is higher in individuals with weakened resistance and pathology of the gastrointestinal tract. The source of infection is sick persons and bacteria carriers: the carrier period is 1-4 weeks, but may be lengthened. The main ways of transmission are fecal-oral and household contact, through water, food products. A certain role is played by insect vectors – flies, cockroaches, which transfer the pathogen with their limbs to food products. The infectious dose is 200-300 living cells, which is traditionally sufficient for the development of the disease. Dysentery is registered throughout the year with an increase in the incidence in the warm season. Pathogenesis. The lesions are due to the ability of Shigella to penetrate into the cells of the colon mucosa, multiply in them and infect neighboring cells, as well as leave phagosomes and enter the cytoplasm of neutrophils and macrophages. The reproduction of shigella in epithelial cells causes their death and leads to the penetration of bacteria into the underlying tissues with the development of mucosal defects (catarrhal, catarrhal-hemorrhagic, less often catarrhal and ulcerative lesions) and an inflammatory reaction in the submucosa with the release of blood cells into the intestinal lumen. The genes encoding the entire complex of these virulence properties are located in the chromosome and plasmids. All virulent strains contain plasmids encoding the synthesis of certain surface proteins. The pathogenicity factor is a cytotoxin (Shiga toxin), which causes cell death and fluid influx into the lesion. The toxin causes cell death, disrupts protein synthesis, absorption of Na

    • and water, which leads to the accumulation of fluid in the submucosa. Also, Shiga toxin has hemolytic activity in vitro, which is sometimes used for its identification. A certain role belongs to endotoxin, which exhibits the entire spectrum of activity characteristic of endotoxins of gram-negative bacteria.

clinical picture.

    • In clinically manifest cases, the disease begins acutely after a 3-7-day incubation period with fever, intoxication, single or repeated vomiting. Simultaneously or somewhat later, symptoms of colitis are detected. An acute course with complete recovery after 2-3 weeks is the most common outcome of dysentery.
    • Intoxication of varying severity (malaise, chills, headache, fever, convulsions, vomiting).
    • colitis syndrome
    • Dull pains throughout the abdomen of a permanent nature, which then become acute cramping, localized in the lower abdomen, often on the left or above the pubis.
    • Tenesmus (drawing pains in the rectal area, radiating to the sacrum, during defecation and for 5-15 minutes after it), false urge to defecate,
    • Initially, the stool of the sick is plentiful (10-25 per day), soon it is significantly reduced in number and takes on the appearance and smell of grated potatoes. It consists of mucus and blood, and in a later period, impurities of pus. Characteristic separation in the last portion, consisting of mucus (rectal spit).
    • An increase in the liver, pancreatic lesions and impaired vascular permeability are often observed.
    • Newborns and children of the first year of life do not get sick often: the disease proceeds atypically, with symptoms of enteritis.
    • Severity indicators
    • The severity of the local inflammatory process: hemocolitis, severe pain syndrome, prolapse of the rectal mucosa
    • Severity of intoxication: severe fever, repeated vomiting
    • Syndromes that threaten the life of the patient (neurotoxicosis, toxicosis with exicosis, infectious toxic shock).

Research methods

    • Detection of pathogens in the feces of a sick person
    • Bacteriological examination of feces
    • Immunofluorescence study of faeces and the reaction of coal agglomeration of coprofiltrates
    • Sigmoidoscopy: signs of inflammation of the distal colon of varying severity, can be catarrhal (in mild forms), catarrhal-hemorrhagic, erosive, ulcerative, fibrinous (in severe forms). At the site of erosions and large hemorrhages, changes in the mucous membrane in the form of red spots persist for a long time, which is important for retrospective diagnosis.
    • Detection of serum antibodies to pathogen Ag and increase in their titer in agglutination reactions, indirect and passive hemagglutination
    • Coprological examination: they detect mucus, a large number of leukocytes, erythrocytes, and the absence of detritus.

The differential diagnosis is acute colitis and enterocolitis of other etiologies.


    • Diet. First – No. 4, then – No. 2, before discharge – No. 15.
    • Etiotropic therapy: antibacterial agents are indicated for children, the elderly, as well as for severe and complicated forms of dysentery. The duration of treatment is determined by the severity of the disease and the presence of complications, as a rule, it is 7-10 days.
    • Trimethoprim-sulfamethoxazole (co-trimoxazole, biseptol) 7.5-20 mg / kg / day (trimethoprim) in 2 doses 12 hours later (traditionally 2 tablets containing 80 mg trimethoprim and 400 mg sulfamethoxazole); children of the first year of life 10 mg / kg / day (trimethoprim) in 2 divided doses.
    • Norfloxacin 400 mg orally twice daily (adults).
    • Ciprofloxacin 500 mg orally twice a day (adults).
    • Furazolidone 5 mg/kg/day orally in 4 doses for 5 days (adults and children).
    • Ampicillin or tetracycline (many strains are resistant to these products).
    • With dehydration – oral (in severe forms – intravenous) rehydration.
    • The appointment of anticholinergics is not recommended.

Flow. Chronic shigellosis can be recurrent or continuous. The disease may be asymptomatic. Complications

    • intestinal bleeding
    • Intestinal perforation
    • Peri- and paraproctitis
    • Peritonitis
    • Infectious-toxic shock
    • hypovolemic shock
    • Toxic megacolon
    • pneumonia
    • rectal prolapse
    • Intestinal intussusception
    • urinary tract infection
    • Intestinal dysbacteriosis
    • Cerebral edema in neurotoxicosis in children.

Prevention. Isolation of the sick person for the entire period of treatment. Convalescents in children’s preschool groups are admitted after negative results of bacteriological examination. Persons who have had dysentery are actively observed by infectious disease specialists (dispensary registration) for 1 month. In the event of an outbreak of dysentery in children’s groups, contacts are monitored for 7 days with a daily examination of all babies and control of the nature of the stool. The facility is being disinfected. Compliance with sanitary and hygienic rules for the preparation, storage and sale of food and water, maintaining the anti-epidemic regime of children’s groups. Synonym. Bacterial dysentery ICD. AOZ Shigellosis Literature. 129:75-77

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