Shigellosis – an acute infectious disease characterized by symptoms of intoxication and defeat of the predominantly the distal colon. Some patients can turn into chronic form.
Causes of Shigellosis
The source of infection – patients and bacillicarriers. Shigellosis is recorded throughout the year with higher incidence during the warm season. The mechanism of transmission – fecal-oral and contact-household, water, food. A role in the spread of infection is played by insect vectors – flies, cockroaches. The infectious dose is 200 to 300 living cells, which is usually sufficient for the development of the disease.
- In symptomatic cases, the disease begins acutely after a 3-7-day incubation period with fever, intoxication, single or repeated vomiting. At the same time or somewhat later symptoms of colitis. Acute course with complete recovery in 2-3 weeks – the most common outcome of dysentery.
- Intoxication of varying severity (malaise, chills, headache, fever, cramps, vomiting).
- Colitis syndrome
- Dull pain all over the abdomen constant nature, which then become acute cramping, localized in the lower abdomen, usually on the left or above the pubis.
- Tenesmus (drawing pain in the rectum, extending to the sacrum, during defecation and within 5-15 minutes after it), false urge to defecate,
- Initially the stools of patients abundant (10-25 per day), soon to be significantly reduced in number and acquires the appearance and smell of grated potatoes. It consists of mucus and blood, and at a later period the pus and impurities. Characterized by the separation of the last portion, consisting of mucus (rectal spittle).
- Often see an increase in the liver, lesions of the pancreas and disturbance of vascular permeability.
Diagnostics and treatment of Shigellosis
Most significantly the diagnosis is confirmed by bacteriological methods – isolation of Shigella from feces and vomit.
If satisfactory sanitary conditions of patients in most cases can be treated at home. Subject to hospitalization of persons with severe dysentery, as well as elderly people, children under 1 year, patients with severe concomitant diseases; also hospitalization and is carried out on epidemic indications.
Shigelloses in the pathogenesis of infection there are two phases: enteral and colonic. The severity of the manifested clinical features of variants of the disease. When Shigella infection overcomes nonspecific protection factors oral cavity and the acidic barrier of the stomach, then attached to the enterocytes in the small intestine by secreting an enterotoxins and cytotoxins. With the death of Shigella results in the release of endotoxin (lipopolysaccharide complex), the absorption of which causes the development of intoxication syndrome.
In the colon the interaction of Shigella with the mucous membrane passes through several stages. Specific proteins of the outer membrane of Shigella interact with receptors of the plasma membrane of colonocytes, which causes adhesion, and then the invasion of pathogens in epithelial cells and submucosal layer. There is an active multiplication of Shigella in the intestinal cells; they are released hemolysin provides for the development of the inflammatory process. Inflammation supports the cytotoxic enterotoxin secreted by Shigella. With the death of pathogens excreted lipopolysaccharide complex that catalyzes the overall toxic response. The most severe form of dysentery called Shigella Grigorieva-Shigi able to distinguish in vivo heat-labile protein exotoxin a (toxin Sigi). Homogeneous preparations of the toxin Sigi simultaneously exhibit cytotoxic activity, enterotoxicity and neurotoxicity, and this defines the low infectious (contagious) dose of pathogen and the severity of the clinical course of the disease. Currently there are reports that sheptone toxins can be other types of Shigella. As a result of the action of Shigella and the response of the microorganism to develop functional disorders of the intestine and microcirculatory processes, serous edema and destruction of mucous membrane of the colon. Under the action of toxins of Shigella in the colon develops acute catarrhal or fibrinous-necrotic inflammation, with possible formation of erosions and ulcers. Dysentery constantly proceeds with the phenomena of dysbiosis (dysbacteriosis) preceding or accompanying the development of the disease. In the end it all determines the development of exudative diarrhea when hypermotor dyskinesia of the colon.