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Epidemiology and Pathology

Shigellosis occurs almost exclusively in primates, particularly in man. Human carriers are common where the disease is prevalent and are the only important reservoir of shigellosis. Fecal pollution of water supply, contamination of food by infected food handlers, or transfer of the bacilli by flies are the principal means of transmission. Epidemics are common after mild infections are overlooked. In epidemics, cultures may be positive in up to 25% of apparently healthy contacts. About 3% of patients who recover from an attack of bacillary dysentery become symptom-free carriers for varying periods of time.

There appears to be a seasonal incidence to the occurrence of bacillary dysentery in the tropics and subtropics. Epidemics are more common during the rainy season and shortly thereafter. During hot dry summers, epidemics are rare. In the rainy season in the tropics, people crowd together indoors and are more susceptible to chills. The rains inhibit people from defecating at a safe distance from their village and the damp soil allows the bacilli to flourish. Under these conditions, dysentery generally spreads rapidly. The house fly is a common carrier of the bacilli. The seasonal incidence of shigellosis corresponds directly to the maximum prevalence of swarming flies. Contaminated water is another important mode of spread. The shigellae can survive in water for 3 weeks but for a much shorter time when exposed to sunlight. Several outbreaks of Flexner and Sonne dysentery have been traced to contaminated milk or food, especially in England and Europe. Susceptibility to infection is likewise important; persons new to the tropics, especially young children, are more likely to acquire dysentery than local inhabitants. Patients whose resistance has been lowered by other diseases, such as malaria, tuberculosis or AIDS, are also particularly susceptible.

The genus Shigella is complex and contains numerous serotypes which can be classified into four species.

Shigella dysenteriae with ten antigenically distinct serotypes, including Shiga's bacillus (type 1), Schmitz's bacillus (type 2), and the Large-Sachs organisms, which do not ferment mannitol.

Shigella flexneri types 1-5, and type 6 (Newcastle bacillus). These serotypes are all antigenically interrelated and ferment mannitol.

Shigella boydii, containing 13 antigenically distinct serotypes which also ferment mannitol.

Shigella sonnei, which ferments mannitol and is a late lactose fermenter.

Shigellae are gram-negative, non-motile, rod shaped bacilli 1-3 micra long. They are present in great numbers in the feces and intestinal mucosa early in the infection. The organisms are killed by chemical agents and sunlight, but can survive for long periods in water, ice, and the mucinous discharges of active patients. Thus, those caring for dysenteric patients are at high risk for infection because soiled sheets and gowns harbor many bacilli.

Pathologically, shigellosis is characterized by an acute diffuse inflammation of the colon with initial hyperemia of the mucosa, followed by edema, hemorrhage, and infiltration with leukocytes and macrophages. This process often extends into the submucosa, causing marked thickening of the intestinal wall. Epithelial necrosis and desquamation with formation of a membrane are followed by sinuous ulceration, originating on the tops of the intestinal folds and often extending deep into the submucosa and occasionally into the muscularis; perforation is rare. Inflammation is not usually uniformly distributed throughout the colon but is most severe in the distal portion from sigmoid colon to anus. The terminal ileum is occasionally involved. Secondary bacterial infection occurs once ulcerative lesions have developed, and may be important in the subsequent development of a chronic state of the disease. In patients in whom dysentery has been of long duration, adjacent ulcers may be joined by ulcerating channels beneath bridges of hyperplastic mucosa.

In chronic bacillary dysentery, there is usually extensive scarring and fibrosis of the colon, indolent ulceration, and a continued subacute or chronic inflammation which periodically becomes acute. There are successive periods of exacerbation and remission, and the disease differs little, both clinically and pathologically, from chronic idiopathic ulcerative colitis. During periods of active disease there may be fever and diarrhea with varying amounts of blood, mucus, and cellular debris in the stools. There is often disturbance of normal motor function with retention in the right colon. Considerable fibrosis of the mucosa and submucosa may complicate such chronically recurrent infections. Mucosal retention cysts may form as the result of incomplete healing, and these cysts may harbor Shigella bacilli which are intermittently discharged by chronic carriers.

In severe dysentery caused by the Shiga bacillus, toxic nephritis is a common cause of death and emboli are often seen in the liver and spleen.

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