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Shigella

Shigella

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Shigella
So closely related to Escherichia coli, particularly Enteroinvasive E. coli, that some authors call Shigella an E. coli biogroup.
Shigella is an intercellular pathogen that only infects humans.
Asymptomatic carriers are a key reservoir.
Virulence factors
Encoded on a plasmid, but regulated by chromosomal genes; this means that the plasmid, alone, is not enough to promote virulence.
Type three secretion systems inject effectors
Ipa's A-D, facilitate invasion of epithelial cells and macrophages.
Within host cells, Shigella lyses phagosomes and replicates within the cytoplasm; notice that this is unlike Salmonella, which replicates within special vacuoles.
Actin tails facilitate Shigella migration to adjacent cells, which allows the bacteria to spread without exposure to agents of innate immunity.
Shigellosis
Primarily affects small children; outbreaks are associated with daycares and preschools, and other places where fecal-oral transmission via contaminated hands is likely.
Shigella has a low infectious dose.
Upon infection, Shigella enterotoxin initially causes watery diarrhea.
Then, as bacteria invade the colon mucosa, bloody diarrhea with pus, cramping, and fever occur. The presence of neutrophils, red blood cells, and mucus in the stool is a helpful diagnostic criterion.
Most patients with Shigellosis recover on their own; supportive care to prevent dehydration is all that is needed. In severe cases, antibiotics can be administered.
There are multiple pathogenic strains of Shigella:
Shigella sonnei is responsible for most cases of Shigellosis in the U.S.
Shigella flexneri is responsible for most cases of Shigellosis in developing countries.
Shigella dysenteriae causes dysentery, the most severe form of Shigellosis.
    • These strains produce Shiga exotoxin, which impairs protein synthesis. As a result, damaged intestinal epithelium produces bloody diarrhea.
Damaged renal endothelial cells can lead to Hemolytic uremia syndrome (HUS); this occurs most often in infected children.

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