Shigella species are gram-negative bacteria of the family Enterobacteriaceae. They cause watery or bloody diarrhea, or the dysentery syndrome and occasionally lead to systemic complications, such as the hemolytic-uremic syndrome, leukemoid reactions, and autoimmune phenomena such as reactive arthritis. Shigella are pathogens only for humans and primates with a low ID.«, of a few hundred to a few thousand organisms. Ubiquitous in distribution, they principally cause illness in children, especially where the infection is endemic, suggesting immunity is acquired. Less commonly, shigellosis occurs in nonimmune adults. Severe persistent bacteremic disease has been documented in immunocompromised patients with the acquired immune deficiency syndrome (AIDS).
Shigella invade the colonic mucosa, a step essential for virulence, and divide and spread from cell to cell within the intestinal epithelial cell layer. This process requires both chromosomal and plasmid genes, many of which have now been determined. Cytokines are produced, neutrophils recruited and there is an intense inflammatory response. The most characteristic lesions involve inflammation and ulceration of the colonic mucosa, resulting in the clinical presentation of dysentery, characterized by both blood and pus in the stools of infected patients.
There are four species of Shigella: S. dysenteriae (group A, 10 types), S. flexneri (group B, 6 serotypes and 14 subtypes). S. boydii (group C, 18 serotypes), and S. sonnei (group D, 1 serotype and 20 colicin types). Shigella are nonmotile and generally nonen-capsulated. Like other Enterobacteriaceae, they display O (somatic) and K (capsular) antigens. Accurate serotyping of Shigella isolates using specific anti-0 antigen antibody is best done after heating test organisms to denature K antigens which can obscure the seroreactivity of O antigens. Many immunologically defined Shigella O antigens are shared with serotypes of Escherichia coli or other gram-negative bacilli. Specific antibody responses occur to S. dysenteriae 1 (the only member of the genus to produce Shiga toxins), S. flexneri 6, and S. sonnei; group responses to S. flexneri 1-5 also develop.
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