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Epidemiology. Pathogenesis



Epidemiology

The source of infection are patients with acute dysentery and bacillicarriers (which present less danger). The patients with mild and subclinic forms of dysentery present epidemiological significance because they are not treated and are not isolated. Bacillicarriers are of less significance because the pathologic process has a transitory character. The mechanism of infection transference is fecal-oral. The factors of transference are dirty hands, contaminated food and water, flies. Contact, food and water routes of infection are distinguished depending on the predominanting factors of transference. Dysentery bacilli may be introduced into cooked foods, thus milk and other dairy products should be under control because they are a good medium for preservation and rapid growth of Sh. Sonnei. Water route of infection spreading is most typical for Sh. Flexneri, that is why group cases of illness and even epidemics appear. Sporadic cases of the disease take place frequently if infection is carried over by contact route. This route of transference usually takes place in younger children.

Among the patients with dysentery, children occupy up to 70 % of cases. Morbidity in 1-year-old children is the lowest, and it is the highest among the children from 2 to 7 years of age. Immunity in dysentery is typospecific that is why recurrent cases may occur.

Pathogenesis

Infection in dysentery is peroral only. The portal of entry is gastro-intestinal tract. The infectious dose has great importance due to its influence on the duration of the incubative period and severity of the disease course. Condition of the body, local function of gastro-intestinal tract, common immunity have significance in development of the infectious process.

On getting into the stomach, the pathogens perish partially due to the influence of proteolytic enzymes and hydrochloric acid in the gastric juice. Remaining pathogens get into the small intestine and can stay there for several days, then they get into the large intestine where they reproduce and disintegrate in great quantity, increasing the inflammatory process. The Shigellae have a selective ability to adhesion (sticking) to colonocytes of the large bowel. Virulent Shigellae strains have an ability to intracellular invasion. Endotoxin is the leading factor, determining the character of morphologic lesion, specific of course and severity of the disease. It attacks the whole structure of intestinal wall: enterocytes cells of mucous membrane, vascular and nervous structures. Entering the blood, endotoxin causes common toxic influence on the vascular and nervous systems of the body and its vegetative centers. The effect of an exotoxin an enterocytes and the mechanism of diarrhea were described earlier in the book.

The most significant morphologic lesions appear in the distal part of the large bowel. Several morphologic forms of dysenteric colitis are distinguished: catarrhal, fibrinous, diphtheritic and ulcerous.



  

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