Shigella

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A Microbial Biorealm page on the genus Shigella


Contents

Classification

Higher order taxa:

Bacteria, Proteobacteria, Gammaproteobacteria, Enterobacteriales, Enterobacteriaceae

Species:

Shigella dysenteriae, S. flexneri, S. boydii, and S. sonnei

Description

Shigella is a non-spore forming, non-motile, rod-shaped Gram-negative bacterium which aids in the facilitation of intracellular pathogens. It is able to survive the proteases and acids of the intestinal tract, which allows the bacteria to infect in very small amounts. As few as 10 cells have been reported to cause infection. Shigellosis primarily affects humans.

Shigella was initially recognized as the causal agent of shigellosis (also known as bacillary dysentery) in the 1890s and became an official genus in the 1950s. Each species has its own niche, representing its primary environmental and competitive habitat. S. dysenteriae serogroup A causes deadly epidemics mainly in developing countries, S. boydii serogroup C is restricted to the Indian subcontinent, and S. flexneri serogroup B and S. sonnei serogroup D are prevalent in developing and developed countries, respectively. S. flexneri is also responsible for the worldwide endemic form of shigellosis.

Genome structure

The four different species of Shigella vary greatly in the genomic structure. The largest species, S. sonnei, contains 4,825,265 base pairs. S. flexneri contains 4,607,203 base pairs, S. boydii contains 4,519,823 base pairs and the smallest species, S. dysenteriae, contains 4,369,232 base pairs.

Shigella shares many genes with Escherichia coli, especially those of E. coli K12 strain MG1655.

Life Cycle

The Shigella life cycle begins with penetration of colonic mucosa. This results in degradation of the epithelium and acute inflammatory colitis in the lamina propria. This causes leakage of blood, inflammation in the colon, and mucus into the intestinal lumen.


Metabolism

Shigella pathogens use a mixed acid fermentation pathway to metabolize substrates. Products of this anaerobic pathway include ethanol, acetic acid, lactic acid, succinic acid, formic acid, and carbon dioxide.


Pathology

Transmission

Fecal-oral transmission is the main route of Shigella infection. Other modes of transmission include ingestion of contaminated food or water, contact with infected objects, or sexual contact. Outbreaks of Shigella infection are common in places with poor sanitation standards.

Infection

Shigella induces macrophage death to disseminate into the surrounding epithelial cells, activating the host immune response which includes inflammation at high concentrations. Shigella dysenteriae is the most common source for shiga toxins, which inhibit protein synthesis in the endothelium lining to produce bloody diarrhea.

Frequency

Worldwide, there are approximately 165 million cases of Shigella infection and 1 million Shigella-related deaths annually, with 98% of those cases occurring in third world or developing nations. Of the various strains of Shigella, S. sonnei is the cause of 78% of infections. S. flexneri and S. boydii are responsible for most of the remaining 22% of cases. The occurrence of S. dysenteriae is rare in developed countries, where sanitation conditions are satisfactory, but account for 30% of cases in under-developed areas. The majority of infections are reported during the summer season and occur mostly in teenagers and adolescents under the age of 15, hypothetically due to poor hygiene techniques. It is difficult to accurately gauge of the actual number of cases that occur, as it is estimated that 90-95% of Shigella infections are asymptomatic and thus unreported.

Current Research

High Prevalence of Antimicrobial Resistance among Shigella Isolates in the United States Tested by the National Antimicrobial Resistance Monitoring System from 1999 to 2002, Sivapalasingam, S., Nelson, J. M., Joyce, K., Hoekstra, M., Angulo, F. J., and Mintz, E. D. This information on shigella's resistance to various antibiotics will help in treating shigellosis. Click this hyperlink for the full text of this article.


References

Hale, Thomas L. Genetic Basis of Virulence in Shigella Species. Dept. of Enteric Infections, Walter Reed Amry Institute of Research. Washington, D. C.: American Society for Microbiology, 1991. 206-224. 10 Nov. 2006 <http://mmbr.asm.org/cgi/reprint/55/2/206.pdf>.

Hale, Thomas L., and Gerald T. Keusch. "Shigella." GSBS At UTMB. The Graduate School of Biomedical Sciences at UTMB. 10 Nov. 2006 <http://www.gsbs.utmb.edu/microbook/ch022.htm>.

Sivapalasingam, S. "High Prevalence of Antimicrobial Resistance among Shigella Isolates in the United States Tested by the National Antimicrobial Resistance Monitoring System from 1999 to 2002." PubMed Central. New York, NY: NYU School of Medicine, 2006. 17 Nov. 2006 <http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16377666#N0x84ceb98.0x92357c0#N0x84ceb98.0x92357c0>.

Sureshbabu, Jaya, and Poothirikovil Venugopalan. "Shigella Infection." EMedicine From WebMD. 12 Sept. 2006. WebMD. 10 Nov. 2006 <http://www.emedicine.com/ped/topic2085.htm>.

Toebe, Carol. "Microbial Metabolism." CCSF. City College of San Francisco. 17 Nov. 2006 <http://cloud.ccsf.edu/Departments/Biology/ctoebe/metab.htm>.

Edited by Deidre DeSilva, Kayleigh Erazmus, and Megan Harney under Dr. Kirk Bartholomew of Sacred Heart University, Fairfield, CT and Adam Meade of Bowling Green State University, Bowling Green, OH.

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