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Shigella

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Shigella stool
Photomicrograph of Shigella sp. in a stool specimen
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Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Shigella
Castellani & Chalmers 1919
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S. boydii
S. dysenteriae
S. flexneri
S. sonnei

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

Shigella is a genus of Gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis, Shigella causes disease in primates, but not in other mammals.[1] It is only naturally found in humans and apes.[2] During infection, it typically causes dysentery.[3] The genus is named after Kiyoshi Shiga, who first discovered it in 1898.

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 A–C are physiologically similar; S. sonnei (group D) can be differentiated on the basis of biochemical metabolism assays.[4] Three Shigella groups are the major disease-causing species: S. flexneri is the most frequently isolated species worldwide and accounts for 60% of cases in the developing world; S. sonnei causes 77% of cases in the developed world, compared to only 15% of cases in the developing world; and S. dysenteriae is usually the cause of epidemics of dysentery, particularly in confined populations such as refugee camps.[5]

Pathogenesis[]

Shigella infection is typically via ingestion (fecal–oral contamination); depending on age and condition of the host as few as 100 bacterial cells can be enough to cause an infection.[6] Shigella causes 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.[7] 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, flatulence, and constipation. The stool may contain blood, mucus, or pus. 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.[8]

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

Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with that of E. coli K12 strain MG1655[9]

Identification[]

Shigella species are negative for motility and are non-lactose fermenters. (However, S. sonnei can ferment lactose).[10] They typically do not produce gas from carbohydrates (with the exception of certain strains of S. flexneri) and tend to be overall biochemically inert. Shigella should also be Urea Hydrolysis negative . When inoculated to a Triple Sugar Iron slant they react as follows: K/A, gas -, H2S -. Indole reactions are mixed, positive and negative, with the exception of S. sonnei which is always indole negative.

See also[]

  • TSI slant, a selective test for enteric bacteria such as Shigella and Salmonella
  • Infectious diarrhea
  • Diarrheal diseases
  • Traveler's diarrhea
  • Enterotoxigenic Escherichia coli

References[]

  1. ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. ISBN 0-8385-8529-9. 
  2. ↑ doi:10.1007/s10669-006-8666-3
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  3. ↑ Mims, Playfair, Roitt, Wakelin, Williams (1993). Medical Microbiology (1st ed.). Mosby. p. A.24. ISBN 0-3974-4631-4. 
  4. ↑ 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. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1269. 
  5. ↑ World Health Organization. Shigellosis.
  6. ↑ Levinson W, "Chapter 18. Gram-Negative Rods Related to the Enteric Tract" (Chapter). Levinson W: Review of Medical Microbiology and Immunology, 10e
  7. ↑ 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. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.chapter.1257. 
  8. ↑ Hill Gaston JS, Lillicrap MS (2003). "Arthritis associated with enteric infection". pp. 219–39. Digital object identifier:10.1016/S1521-6942(02)00104-3. PMID 12787523. 
  9. ↑ Yang F et al. (2005). "Genome dynamics and diversity of Shigella species, the etiologic agents of bacillary dysentery". pp. 6445–58. Digital object identifier:10.1093/nar/gki954. PMC 1278947. PMID 16275786. 
  10. ↑ Ito H, Kido N, Arakawa Y, Ohta M, Sugiyama T, Kato N (October 1991). "Possible mechanisms underlying the slow lactose fermentation phenotype in Shigella spp". pp. 2912–7. PMC 183896. PMID 1746953. http://aem.asm.org/cgi/pmidlookup?view=long&pmid=1746953. 

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