Shigella

  • TRANSMISSION ROUTE: Direct contact, ingestion

Definition

Shigella are gram-negative, nonmotile, non-spore-forming, nonencapsulated, facultative-anaerobic rods that cause bacillary dysentery (shigellosis) in humans and other primates. The infection affects the intestines.

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Natural Habitat and Features

Shigella was named for Kiyoshi Shiga, a Japanese physician and bacteriologist, who first isolated S. dysenteriae in 1896. There are four recognized species. Other Shigella spp. that were named in the first half of the twentieth century have either been moved to other genera (for example, Shigella galinarum is now Salmonella galinarum) or subsumed into one of the four recognized species (for example, S. ambigua is now S. dysenteriae type II). These bacteria are closely related to Escherichia coli and share most genes with E. coli strain K12.

Shigella spp. infections occur only naturally in primates. Other animals are not normally infected, but infections have been induced in a few animals used as models for the disease and its treatment. Infection is usually fecal to oral and can occur anytime food or water becomes contaminated with infected feces. Infection also can occur during certain sex practices. Good hygiene, including thorough handwashing with soap and water after fecal elimination, is the best way to prevent shigellosis.

Symptoms

The most common site for bacterial growth is in the large intestine. A dose of as few as ten organisms is enough to cause infection in some persons. Symptoms usually occur twenty-four to forty-eight hours after ingestion of Shigella-contaminated food or water. Shigella spp. thrive in the large intestine and, because of their virulence plasmid, have the ability to invade intestinal epithelial cells. This invasion leads to the most common symptoms of shigellosis: diarrhea, abdominal cramps, nausea, and vomiting. In addition, blood, pus, and mucus are often present in the stool because invasion often leads to ulceration of the colonic epithelium.

The disease is usually self-limiting and lasts about one week in healthy adults, by which time the immune system disposes of the invading bacteria. In infants, small children, and those debilitated from other illnesses, the disease may last longer; dehydration caused by diarrhea and vomiting can lead to severe problems. Damaging enterotoxins and Shiga toxins are coded by the virulence plasmid and are produced by most strains. Shiga toxins can cause hemolytic uremic syndrome, which leads to anemia and kidney failure. Some non- Shigella spp. also contain Shiga toxins because plasmid transfer can occur across species lines. A small percentage of persons with S. flexneri may develop Reiter’s syndrome, which causes joint pain, eye irritation, and painful urination. Reiter’s syndrome can last months or even years and can lead to difficult-to-treat chronic arthritis.

Treatment

Persons often remain infective for up to two weeks after the dysentery symptoms abate because bacteria remain in the intestine for one to two weeks after recovery. For several years after infection, persons may retain immunity against the particular Shigella strain that infected them, but they are susceptible to other strains. Rehydration is the main treatment for shigellosis; however, antibiotic therapy can be used in severe cases. The antibiotics of choice are ampicillin, trimethoprim/sulfamethoxazole, nalidixic acid, ciprofloxacin, and azithromycin. Because resistance plasmids are easily transferred between members of the Enterobacteriaceae, antibiotic resistant Shigella strains are becoming more widespread. Further, the CDC has warned about the worrisome increase in drug-resistant varieties of shigellosis. Various Shigella vaccines have been investigated and live attenuated vaccines have been tested; however, no broad-spectrum Shigella vaccine is available.

Serotypes

S. dysenteriae has fifteen serotypes and is the major cause of epidemic dysentery. This disease usually occurs in less-developed countries with poor sanitation and is often seen in Africa, Southeast Asia, and the Indian sub-continent. Fecal to oral transmission usually occurs because of sewage-contaminated water. S dysenteriae type I causes the most severe form of shigellosis. It is especially severe in malnourished and otherwise debilitated persons; life-threatening complications often occur. More than 30 percent of dysentery cases worldwide are caused by S. dysenteriae.

S. flexneri, with six serotypes, is the most common cause of endemic dysentery worldwide and accounts for more than 60 percent of shigellosis in less-developed countries. The main sources are contaminated water and food caused by poor sanitation and the use of human waste to fertilize crop plants. Neither S. dysenteriae nor S. flexneri are major pathogens in areas where good sanitation leads to the availability of clean water and proper disposal of fecal wastes. In the developed world, less than 15 percent of shigellosis cases can be traced to S. flexneri and even less to S. dysenteriae. S. sonnei has a single serotype and is biochemically different than the other Shigella spp. The only known reservoir of S. sonnei is the human intestinal tract, and this bacterium does not survive for extended periods in other locations. It is most commonly transmitted by infected food handlers who have poor hygiene and is the most common cause of endemic shigellosis in developed countries. Approximately 77 percent of shigellosis in developed countries and 70 percent in the United States is caused by S sonnei, which is less virulent than other Shigella spp. and causes a milder form of shigellosis. Occasional outbreaks have occurred in the United States and have been traced to S. sonnei-infected food handlers. The CDC reported an increase in drug-resistant strains of Shingella, which included S. sonnei and S. flexneri. The increase in drug-resistant strains led to an increase in cases and a perceived shift in the demographics of who was being infected.

S. boydii, with nineteen known serotypes, is the most genetically diverse of the Shigella spp. As in other Shigella spp., most S. boydii serotypes are similar to E. coli; however, there are some that seem to share genes with Vibrio cholerae. Although S. boydii has worldwide distribution, it is most common on the Indian subcontinent. It affects all primates, including humans, and can survive for extended periods in the soil. It is responsible for only a small percentage of human shigellosis in the rest of the world.

Bibliography

Dall, Chris. “CDC Warns of Increase in Extensively Drug-Resistant Shigellosis.” University of Minnesota, 28 Feb. 2023, www.cidrap.umn.edu/antimicrobial-stewardship/cdc-warns-increase-extensively-drug-resistant-shigellosis. Accessed 21 Oct. 2024.

Garrity, George M., editor. The Proteobacteria. Bergey’s Manual of Systematic Bacteriology, vol. 2, 2nd ed., Springer, 2005.

Madigan, Michael T., and John M. Martinko. Brock Biology of Microorganisms. 12th ed., Pearson/Prentice Hall, 2010.

Niyogi, S. K. “Shigellosis.” Journal of Microbiology, vol. 43, 2005, pp. 133-43.

Procop, Gary W., and Bobbi S. Pritt, editors. Pathology of Infectious Diseases. Elsevier Saunders, 2015.

Romich, Janet A. Understanding Zoonotic Diseases. Thomson Delmar Learning, 2008.

"Shigella Infection." Mayo Clinic, Mayo Foundation for Medical Education and Research, 17 Sep. 2024, www.mayoclinic.org/diseases-conditions/shigella/basics/definition/con-20028418. Accessed 21 Oct. 2024.

"Shigella—Shigellosis." Centers for Disease Control and Prevention, US Department of Health and Human Services, 3 Aug. 2016, www.cdc.gov/shigella/general-information.html. Accessed 21 Oct. 2024.