Shigella

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Shigella
Photomicrograph of Shigella sp. in a stool specimen
Scientific classification Edit this classification
Domain: Bacteria
Phylum: Pseudomonadota
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Shigella
Castellani & Chalmers 1919
Species

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

Shigella is a

facultatively anaerobic, non–spore-forming, nonmotile, rod-shaped, and is genetically closely related to Escherichia. The genus is named after Kiyoshi Shiga, who discovered it in 1897.[1]

Shigella causes disease in primates, but not in other mammals; it is the causative agent of human shigellosis.[2] It is only naturally found in humans and gorillas.[3][4] During infection, it typically causes dysentery.[5]

Shigella is a leading cause of bacterial diarrhea worldwide, with 80–165 million annual cases (estimated)[6] and 74,000 to 600,000 deaths.[6][7] It is one of the top four pathogens that cause moderate-to-severe diarrhea in African and South Asian children.[8]

Classification

Shigella species are classified by three serogroups and one serotype:

Groups AC are physiologically similar; S. sonnei (group D) can be differentiated on the basis of biochemical metabolism assays.[12] 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.[13]

Each of the Shigella genomes includes a virulence plasmid that encodes conserved primary virulence determinants. The Shigella chromosomes share most of their genes with those of E. coli K12 strain MG1655.[14]

Phylogenetic studies indicate Shigella is more appropriately treated as a subgroup of Escherichia[15] (see Escherichia coli#Diversity for details).

Pathogenesis

Shigella infection is typically by

hemolytic-uremic syndrome.[12]

Because they do not interact with the apical surface of epithelial cells — preferring the basolateral side — Shigella species invade the host through the

M-cells interspersed in the epithelia of the small intestine.[17] Shigella uses a type-III secretion system that acts as a biological syringe to translocate toxic effector proteins to the target human cell. The effector proteins can alter the metabolism of the target cell — leading, for example, to the lysis of vacuolar membranes or reorganization of actin polymerization to facilitate intracellular motility of Shigella bacteria inside the host cell. For instance, the IcsA effector protein (an autotransporter, not a type-III secretion-system effector) triggers actin reorganization by N-WASP recruitment of Arp2/3 complexes, promoting cell-to-cell spread.[18]

After infection, Shigella cells multiply

seizures. Symptoms can take as long as a week to appear, 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.[21]

Discovery

The Shigella genus is named after Japanese physician Kiyoshi Shiga, who researched the cause of dysentery. Shiga entered the Tokyo Imperial University School of Medicine in 1892, during which he attended a lecture by Shibasaburo Kitasato. Shiga was impressed by Kitasato's intellect and confidence, so after graduating, he went to work for him as a research assistant at the Institute for Infectious Diseases. In 1897, Shiga focused his efforts on what the Japanese referred to as a sekiri (dysentery) outbreak. Such epidemics were detrimental to the Japanese people and occurred often in the late 19th century. The 1897 sekiri epidemic affected >91,000, with a mortality rate of >20%.[22] Shiga studied 32 dysentery patients and used Koch's postulates to successfully isolate and identify the bacterium causing the disease. He continued to study and characterize the bacterium, identified its methods of (Shiga-) toxin production, and worked to create a vaccine for the disease.[citation needed]

See also

References

  1. PMID 12054222
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  2. ]
  3. on June 30, 2013.
  4. ^ "Shigellosis" (PDF). European Association of Zoo and Wildlife Veterinarians. Archived from the original (PDF) on 2015-09-27.
  5. .
  6. ^ . Retrieved 22 June 2016.
  7. .
  8. .
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  11. .
  12. ^ .
  13. ^ "Shigellosis" (PDF). State of the art of new vaccine research and development. Immunization, Vaccines and Biologicals. World Health Organization. 2006. pp. 10–2. Archived (PDF) from the original on 2015-09-27.
  14. PMID 16275786
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  15. .
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  18. .
  19. ^ Todar, Kenneth. "Shigella and Shigellosis". Todar's Online Textbook of Bacteriology.[self-published source]
  20. PMID 11553531
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  21. .
  22. .

External links