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Shigella dysenteriae*


Diseases | Sites and Sources | Diagnostic Factors | Virulence Factors | Treatment and Prevention | Commentary

Synonyms
Shiga's bacillus
Classification
facultative anaerobic, gram- bacteria, rods


Diseases


Dysentery
fever diarrhea, inflammatory diarrhea, bloody
fecal leukocytes pus abdominal pain
tenesmus dehydration  


Hemolytic-Uremic Syndrome
anemia thrombocytopenia renal failure
hematuria blood in stool  


Sites and Sources

contaminated food, source contaminated water, source fecal-oral route, source
day care centers, source GI tract, pathogen  

Diagnostic Factors

growth on selective media culture on MacConkey's agar or EMB growth on MacConkey's and EMB agars
hydrogen sulfide- indole+ lactose-
no gas produced in TSI non motile urease-


Virulence Factors

toxin cytotoxin Shiga toxin
endotoxin enterotoxin siderophore (iron binding protein)
invasin induced phagocytosis lysis of the phagosome
intracellular growth induction of endocytosis by epithelial cells  

Treatment and Prevention

sanitation hand washing ciprofloxacin
trimethoprim-sulfamethoxazole ampicillin  

Commentary

Shigella dysenteriae, as are all Shigellae, is strictly a human pathogen. It is spread by the fecal-oral route and is highly communicable. It is estimated that less than 100 Shigella can start an infection, whereas it can take tens of millions of, for instance, cholera vibrios to cause disease. Transmission is by contaminated fingers, food, or water. Children in group care are considered to be at high risk, because of poor hygiene and close contact. The organisms multiply in the small intestine, then invade the large intestine. Disease is caused by the invasion of the colonic epithelial cells and multiplication of the organisms within these cells and the lamina propria with attendant cell death and tissue destruction. This produces acute inflammation and ulceration of the mucosa. Shigella dysenteriae, in contrast to S. flexneri, S. sonnei, and S. boydii, can also cause cell death by the production of Shiga toxin, an A-B type toxin with 1 A subunit and 5 B subunits. As with other A-B type toxins, the B subunits bind to the cell, injecting the A subunit into the cell. The A subunit cleaves a specific adenine residue from the 28S ribosomal RNA in the 60S ribosome, inhibiting protein synthesis and causing cell death. Hemolytic-uremic syndrome can occur if the Shiga toxin attacks the renal endothelial cells, to which it has some affinity. Rarely, in contrast to invasive Salmonella, is there invasion beyond the intestinal mucosa or local lymph nodes. Invasion of the bloodstream is rare. Genes coded for by a large "virulence" plasmid are apparently responsible for the ability of S. dysenteriae to penetrate and multiply within cells. It is known that the organism induces its endocytosis by epithelial cells, lyses the endocytic vesicle (the phagosome), multiplies in the cytoplasm, and causes cell death. Shigellae are members of the family Enterobacteriaceae. The identification of the Enterobacteriaceae is complicated and involves a large number of tests. Of primary importance is the fermentation of lactose, which Escherichia and Klebsiellae can accomplish, but which Shigella, Salmonella, and Proteus cannot. Other characteristics which can distinguish between the members of the family Enterobacteriaceae include indole, urease, hydrogen sulfide, and gas production. A variety of commercial products to test for these attributes quickly and simultaneously are available. One of these uses a plastic strip with 20 or so wells containing different kinds of dehydrated media. A single colony to be identified is suspended in 5 ml of saline, and this is used to both rehydrate and innoculate the media.


  Updated: September 3, 1999
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