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Shigella



Shigella

Photomicrograph of Shigella sp. in a stool specimen
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Shigella
Castellani & Chalmers 1919
Species

S. boydii
S. dysenteriae
S. flexneri
S. sonnei

This article is about the bacteria. For the disease, see shigellosis

Shigella is a genus of Gram-negative, non-motile, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis, Shigella also cause disease in other primates, but not in other mammals.[1]

Additional recommended knowledge

Contents

Classification

Shigella species are classified by four serogroups:

  • Serogroup A: S. dysenteriae (12 serotypes)
  • Serogroup B: S. flexneri (6 serotypes)
  • Serogroup C: S. boydii (23 serotypes)
  • Serogroup D: S. sonnei (1 serotype)

Group AC are physiologically similar; S. sonnei (group D) can be differentiated on the basis of biochemical metabolism assays.[2]

Pathogenesis

Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as ten bacterial cells can be enough to cause an infection. Shigella cause dysentery that results in the destruction of the epithelial cells of the intestinal mucosa in the cecum and rectum. Some strains produce enterotoxin and Shiga toxin, similar to the verotoxin of E. coli O157:H7.[3] Both Shiga toxin and verotoxin are associated with causing hemolytic uremic syndrome.

Shigella invade the host through epithelial cells of the large intestine. Using a Type III secretion system acting as a biological syringe, the bacterium injects IpaD protein into cell, triggering bacterial invasion and the subsequent lysis of vacuolar membranes using IpaB and IpaC proteins. It utilizes a mechanism for its motility by which its IcsA protein triggers actin polymerization in the host cell (via N-WASP recruitment of Arp2/3 complexes) in a "rocket" propulsion fashion for cell-to-cell spread.

The most common symptoms are diarrhea, fever, nausea, vomiting, stomach cramps, and straining to have a bowel movement. The stool may contain blood, mucus, or pus (e.g. dysentery). In rare cases, young children may have seizures. Symptoms can take as long as a week to show up, but most often begin two to four days after ingestion. Symptoms usually last for several days, but can last for weeks. Shigella is implicated as one of the pathogenic causes of reactive arthritis worldwide.[4]

Severe dysentery can be treated with ampicillin, TMP-SMX, or fluoroquinolones such as ciprofloxacin.

References

  1. ^ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0-8385-8529-9. 
  2. ^ Hale TL, Keusch GT (1996). Shigella: Structure, Classification, and Antigenic Types. in: Baron's Medical Microbiology (Baron S et al, eds.), 4th ed., Univ of Texas Medical Branch. ISBN 0-9631172-1-1. 
  3. ^ Hale TL, Keusch GT (1996). Shigella. in: Baron's Medical Microbiology (Baron S et al, eds.), 4th ed., Univ of Texas Medical Branch. ISBN 0-9631172-1-1. 
  4. ^ Hill Gaston JS, Lillicrap MS (2003). "Arthritis associated with enteric infection". Best practice & research. Clinical rheumatology 17 (2): 219-39. PMID 12787523.

See also

TSI slant, a selective test for enteric bacteria such as Shigella and Salmonella

 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Shigella". A list of authors is available in Wikipedia.
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