Shigella

Shigella species

Organism

Shigella are a moderately-sized, non-motile, gram-negative bacilli.
Facultative anaerobes (def).
There are 4 species of Shigella: S. dysenteriae, S. flexneri, S. boydii, and S. sonnei.

Habitat

The intestinal tract of infected humans.

Source

Humans are the only reservoir for Shigella. Transmitted by the fecal-oral route.

Epidemiology

Over 23,600 cases of shigellosis were reported in the U.S. in 1998 but most cases are not reported. An estimated 450,000 are thought to occur each year in the U.S.
The most common cause of shigellosis in developed countries is S. flexneri.
70% of all Shigella infections occur in children under the age of 15.

Clinical Disease

Symptoms of shigellosis include diarrhea, bloody stool, abdominal cramps, and fever. The incubation period is 1-3 days.
Initial profuse watery diarrhea typically appears first as a result of enterotoxin. Within 1-2 days this progresses to Abdominal cramps and tenesmus (def), with or without bloody stool. Classic shigellosis presents itself as lower abdominal cramps and stool abundant with blood and pus develops as the Shigella invade the mucosa of the colon.

Pathogenicity

In the outer membrane of the gram-negative cell wall, the lipopolysaccharide functions as an endotoxin .
A variety of cell wall adhesins (def) enable the bacterium to make a more intimate contact with mucosal cells.
It is thought that Shigella first transit the mucous membrane of the colon by passing through M cells (see Fig. 1). (M cells are phagocytic cells in the mucous membrane whose function is to sample microbes from the intestinal lumen and pass them on to the lymphoid tissue of the Peyer's patch in order to activate the immune defenses against intestinal microbes). Once across the mucosa, the Shigella use invasins (def) to enter the epithelial cells from the underside (see Fig. 1). Once inside they escape from the vacuole into the cytoplasm and multiply. Now they move through the host cell and spread to adjacent host cells by a unique process called actin-based motility whereby actin filaments polymerize at one end of the bacterium producing comet-like tails that propel the Shigella through the cytoplasm of the host cell. When they reach the boundary of that cell, the actin filaments push the Shigella across that membrane and into the adjacent cell (see Fig. 1). As the Shigella grow and spread within the epithelial cells, those epithelial cells die and provoke a strong inflammatory response leading to the symptoms of dysentery.
Shigella survive phagocytosis by inducing a programmed cell death called apoptosis in macrophages.
S. dysenteriae produce Shiga toxin that disrupts host cell protein synthesis resulting in damage to the intestinal epithelium. In some people it also damages glomerular endothelial cells (def) causing hemolytic uremic syndrome (HUS).

Treatment

Treatment is guided by antibiotic susceptibility testing. Empiric therapy often uses fluoroquimolone or trimethoprim-sulfamethoxazole (TMP-SMX)* (see antibiotic table).

*Drugs may change with time.

For a more detailed article on Shigella infections, see Shigella Infection, by Walid Abuhammour, MD, FAAP, Associate Professor of Pediatrics, Michigan State University; Director of Pediatric Infectious Disease, Department of Pediatrics, Hurley Medical Center and Ilyas Burny, MD, Staff Physician, Department of Pediatrics, Hurley Medical Center.