- Facultative anaerobes (def).
- There are 4 species of Shigella:
S. dysenteriae, S. flexneri, S. boydii, and S. sonnei.
- The intestinal tract of infected
- Humans are the only reservoir
for Shigella. Transmitted by the fecal-oral route.
- 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.
- 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.
- In the outer membrane of the gram-negative
cell wall, the lipopolysaccharide functions as an endotoxin .
- A variety of cell wall adhesins
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
- 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
causing hemolytic uremic syndrome (HUS).
- 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.
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Updated: Feb. 2, 2005
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