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Members of the
genus Shigella cause a readily communicable infectious colitis,
bacillary dysentery.
Bacillary
dysentery has historically affected troops in the field, prisoners of
war, victims of natural disaster (
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)
and those living in unsanitary overcrowded conditions.
The disease
was distinguished from amebic dysentery in 1896 by Shiga who
recognized the first representative of the genus now known as Shigella
dysenteriae.
The four
species of Shigella ( S. dysenteriae, S. flexneri, S. boydii and S.
sonnei ) are gram negative bacilli. These are among the most virulent
enteropathogens. Disease is produced by ingestion of as few as
10 to 100 organisms, and there are few asymptomatic carriers.
The shigellae
are worldwide and are most conspicuous in tropical and developing
countries, where they are a major cause of morbidity and mortality. In
the developed countries, S. flexneri and S. sonnei are more common,
and infection is sporadic.
The lesions,
limited to the colon, are destructive as evidenced by the bloody
mucoid stools characteristic of shigellosis. Unlike the salmonella
infection which also invade and colonize the intestinal mucosa,
shigellae have no significant animal reservoir.
Shiga toxin
contributes to the profuse diarrhea and precedes dysentery in some
patients. This enterotoxin activates membrane-associated adenyl
cyclase. Thus shiga toxin like cholera toxina and and E. coli
enterotoxin induces hypersecretion of fluid and electrolytes from
mucosa of the terminal ileum.
Water and
electrolyte balance must be maintained to prevent dehydration,
prostration and impaired mental status.
Mode of
transmission:
Transmission occurs by the fecal-oral route.
Clinical
presentation:
Symptoms appear 2 to 5 days after the ingestion of bacteria. The dose
of organisms and the status of host defenses influence the incubation
period and severity.
Shigella
infection ranges from mild diarrhea to incapacitating and
life-threatening dysentery, the latter caused primarily by S.
dysenteriae.
Diffuse
involvement of the colon is associated with high fever, shaking
chills, toxemia and shock.
Appropriate
antibiotic therapy is critical in shortening the illness, preventing
relapse and reducing transmission.
Pathological
Features:
The key to the
pathogenecity of Shigella is its ability to invade and multiply in the
epithelium and lamina propria of the terminal ileum and colon.
The mucosa
becomes edematous and hyperemic and is covered by pus and mucus.
The mucosa
becomes soft and friable and irregular superficial ulcerations
appears.
The ulcerated
mucosa becomes covered with a granular, dirty-yellow pseudomembrane.
Sloughed
pseudomembrane, together with blood tinged mucus comprise the
characteristic dysenteric stool of shigellosis.
Microscopic
features:
There is a
predominantly mononuclear leukocytic infiltrate within the lamina
propria. The surfaces of the ulcers are covered with an acute,
suppurative, neutrophilic reaction accompanied by congestion, marked
edema, fibrin deposition, and thromboses of small vessels.
The epithelium
persists only in the depths of the crypts and goblet cells contain no
mucus in the acute stage.
As the disease
progresses, the ulcer margins are transformed into active granulation
tissue.
When the
disease remits, the granulation tissue fills the defect and the ulcers
heal by regeneration of the mucosal epithelium.
Epithelial
regeneration is rapid and healing is complete in 2
weeks.
Investigations:
Detection methods
for Shigella include conventional culture methods, immunological
methods, and molecular microbiological methods.
Conventional
culture of Shigella in foods is often problematic due to the lack of
appropriate selective media.
Immunological
methods for Shigella have been researched, yet there is only one
commercially available test kit.
Molecular
microbiological methods such as PCR, oligonucleotide microarrays, and
rep-PCR have also been developed for the detection and identification
of Shigella.
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