Shigella is a bacterium that belongs to a small group of pathogens (including E. coli O157:H7 and Cryptosporidium) that can infect the gut after the ingestion of relatively few organisms, and can cause sudden and severe diarrhea (gastroenteritis) in humans. When ingested, Shigella bacteria penetrate the lining of the intestine, causing swelling and possibly causing sores to develop (Mayo Clinic, 2007, April 14).
Volunteer experiments have demonstrated that shigellosis – the illness caused by the ingestion of Shigella bacteria, which is also known as “bacillary dysentery” – can occur after ingestion of fewer than 200 bacteria (DuPont, et. al. 1989), making Shigella one of the most communicable and severe forms of the bacterial-induced diarrheas (Gomez, et.al. 2002).
Shigella is named after Kiyoshi Shiga, a Japanese scientist who discovered Shigella dysenteriae type 1 in 1896 during a large epidemic of dysentery in Japan (Keusch & Acheson, 1996). Since that time, several types of Shigella bacteria have been discovered – S. dysenteriae, S. flexneri, S. boydii, and S. sonnei – all named after the lead workers who discovered them (CDC, 2005, October 13).
Shigella thrives in the human intestine and is commonly spread both through food and by person-to-person contact. About 25,000 laboratory-confirmed cases of shigellosis are reported each year in the U.S. (Mead, et al., 1999); however, many cases go undiagnosed and/or unreported and the Centers for Disease Control and Prevention (CDC) estimates that 450,000 total cases of shigellosis occur in the United States every year (Baer, et al., 1999; CDC, 2005, October 13).
No group of individuals is immune to shigellosis, but certain individuals are at increased risk. Small children acquire Shigella at the highest rate. Persons infected with HIV experience shigellosis much more commonly than other individuals, but this may largely be due to an increased risk among men having sex with men (Baer, et al., 1999).
In developing countries, S. flexneri is the most predominant cause of shigellosis, but S. dysinteriae type 1 is the most frequent cause of epidemic and endemic disease. In developed countries such as the United States, S. sonnei is the predominant cause of Shigellosis; S. sonnei is involved in over 75% of cases reported annually in the US (Keusch & Acheson, 1996).
How is Shigella transmitted?
The ultimate source of Shigella bacteria is the infected excrement of a previously infected individual. A new case of bacillary dysentery occurs after the organism is ingested and approximately 20 percent of cases of shigellosis are transmitted via contaminated food or water (Mead, et.al. 1999). Food can become contaminated due to unsanitary practices followed by food workers, but may also become contaminated during harvest or processing. Contamination of drinking water by Shigella is a problem that generally only occurs in the developing world (Barzilay, Weinberg & Eley, 1999).
Symptoms of Shigella Infection
Most people who are infected with Shigella develop diarrhea, fever, and abdominal cramps. Severity of the disease ranges from mild to very severe diarrhea. Diarrhea is bloody 25-50 percent of the time and most often contains mucus. Rectal spasms, medically termed “tenesmus,” are common. The illness starts 12 hours to 6 days, usually 1-2 days, after exposure (MMWR Surveillance Summaryes, 1996).
Dehydration is also a common symptom of Shigella infection.
Shigellosis usually resolves in 5 to 7 days, although it may be several months before a victim’s bowel habits are entirely normal. In some persons, especially young children, the elderly, and immune compromised persons, the diarrhea can be so severe that the patient needs to be hospitalized. The hospitalization rate for shigellosis is estimated to be in excess of 50,000 per year in the United States (Mead, et al., 1999).
In addition to common symptoms of Shigellosis, some children who run high fevers have seizures, although it is not known whether the seizures are a result of the fever or the Shigella infection itself (Mayo Clinic, 2007, April 14).
What are the serious and long-term risks of Shigella infection?
Shigellosis is more severe than other forms of gastroenteritis. This is because when Shigella bacteria multiply in the human gut they invade cells and result in much tissue destruction (Philpott, Edgeworth & Sansonetti, 2000). Also, many strains produce a toxin called “shiga toxin” which is very potent and destructive. Shiga toxin is very similar to the verotoxin of E. coli O157:H7.
More than one million deaths occur in the developing world yearly due to infections with Shigella. The victims are mostly children (Philpott, Edgeworth & Sansonetti, 2000). In the United States, it is estimated that about 700 persons die yearly from shigellosis (Mead, 1999). Small children and the elderly are at greatest risk to experience mortality from a Shigella infection.
Complications of shigellosis include severe dehydration, seizures in small children, rectal bleeding, and invasion of the blood stream by the bacterium. Other complications include:
Reiter’s Syndrome (Reactive Arthritis). Up to 3 percent of persons who are infected with Shigella may later develop a syndrome that includes joint pain and swelling, irritation of the eyes, and sometimes painful urination. This is a reaction to the previous gastroenteritis and is called “reactive arthritis.” It occurs because of protein mimicry; basically, the immune system, intending to fight Shigella, attacks the self (Ringrose, 2001).
Reiter’s Syndrome is most common in persons with the HLA-B27 genetic makeup. (Testing for this is readily available.) Reiter’s Syndrome can last for months or years, can lead to chronic arthritis, and may be difficult to treat.
Toxic megacolon. Toxic megacolon is characterized by abdominal pain and swelling, fever, and weakness. This complication occurs when a person’s colon becomes paralyzed, preventing them from having bowel movements or from passing gas. Without treatment, a person’s colon may rupture, causing a life-threatening condition that requires emergency surgery (Mayo Clinic, 2007, April 14).
Hemolytic uremic syndrome (HUS). HUS is a rare complication of shigellosis, more commonly caused by E. coli O157:H7 (Mayo Clinic, 2007, April 14). Development of HUS usually results in a low red blood cell count (hemolytic anemia), low platelet count (thrombocytopenia) and acute kidney failure. The kidney, pancreas, and brain are the organs most likely to be damaged during the acute phase of HUS.
How is Shigellosis Diagnosed?
Determining that Shigella is the cause of an illness depends on laboratory tests that identify the bacteria in the stool of an infected person. The laboratory can also do special tests to tell which species of Shigella the person has and which antibiotics would be best to treat it. Shigella is not a normal inhabitant in the colon, but the culture tests are sometimes falsely negative. This is because Shigella is somewhat difficult to isolate from a stool specimen because it has characteristics that are similar to normal colon bacteria.
Newer methods are being developed to identify foodborne pathogens, like Shigella, in food samples. These tests often work by locating segments of RNA unique to the organism.
Treatment for Shigella Infection
Although shigellosis is usually a self-limited illness, antibiotics can shorten the course, and in the most serious cases, might be life saving. When oral therapy is adequate, a fluoroquinolone antibiotic is the recommended first-line treatment for non-pregnant adults (Gilbert, Moellering & Sande, 2001). Ciprofloxacin 500 mg twice daily for three days is often prescribed. Alternative antimicrobial agents include trimethoprim-sulfamethoxazole, azithromycin, and ceftriaxone.
If you believe you have become ill with Shigellosis, contact your healthcare provider, who will be able to prescribe the best course of treatment.
The bacteria remain active during the illness and for a week or two after an infected individual recovers. It’s possible for a person to carry Shigella without developing symptoms, but then pass the illness to others (Mayo Clinic, 2007, April 14).
How to Prevent Shigella Infection
The spread of Shigella from an infected person can be stopped by frequent and careful hand washing with soap and water (Doyle, Ruoff & Weinberg, 2000). Ill individuals and all of their contacts should practice this, and all children’s handwashing should be supervised both in day care centers and at home (Krilov, et al., 1996). Young children with a Shigella infection, or with diarrhea of any cause, should not be in contact with uninfected children.
If a child in diapers has shigellosis, everyone who changes the child’s diapers should be sure the diapers are disposed of properly in a closed-lid garbage can, and should wash his or her hands carefully with soap and warm water immediately after changing the diapers. After use, the diaper changing area should be wiped down with disinfectant, such as household bleach or bactericidal wipes.
At swimming pools, maintaining a chlorine level of at least 0.5-PPM will kill Shigella. At swimming beaches, children not yet toilet trained should be excluded from public swimming areas; stay clear if this rule is broken. Children with diarrhea should never be taken to public swimming areas.
Basic food safety precautions will also help to prevent shigellosis. Shigella organisms are killed by heat used in cooking. People who have shigellosis or any diarrhea should not prepare food for others until they have been shown to no longer be carrying the bacterium.
Drink water only if it has been chlorinated (most tap water) or treated with ozone (most bottled water) and then you know it will not contain pathogenic bacteria.
Consume only pasteurized dairy products.
In the developing world, shigellosis is far more common and is present in most communities most of the time. Simple precautions taken while traveling to the developing world can also prevent shigellosis (Weinberg, 1996). Drink beverages only if they are imported (e.g. Evian), carbonated (e.g. cola – without ice), boiled (e.g. coffee) or have been in contact with alcohol for a prolonged period (e.g. wine or beer, not mixed drinks). Eat a cooked diet with the exception of fruits you peel yourself.
- Filiberto’s Shigella Outbreak
- Gate Gourmet Shigella Outbreak
- Royal Fork Shigella Outbreak
- Senor Felix Shigella Outbreak
- Shipley Sales Cantaloupe Salmonella Outbreak
- Viva Mexico Shigella Outbreak
- Baer JT, Vugia DJ, Reingold AL, Aragon T, Angulo FJ, and Bradford WZ. (1999). HIV Infection as a Risk Factor for Shigellosis. Emerg Inftect Dis. 5(6): 820-23.
- Barzilay JI, Weinberg WG, and Eley JW. (1999). The water we drink. New Brunswick, NJ: Rutgers University Press.
- CDC. (2005, October 13). Shigella: Technical Fact Sheet. Retrieved August 17, 2007 from Centers for Disease Control Web site: http://www.cdc.gov/ncidod/dbmd/diseaseinfo/shigellosis_t.htm.
- Doyle MP, Ruoff KL, and Weinberg WG. (2000). Reducing transmission of infectious agents in the home. Dairy, Food and Environmental Sanitation. 20:330-337.
- DuPont HL, Levine MM, Hornick RB, Formal SB. (1989). Inoculum size in shigellosis and implications for expected mode of transmission. J Infect Dis. Jun;159(6):1126.
- Gilbert DN, Moellering RC, and Sande MA. (2001). The Sanford guide to antimicrobial therapy 2001. Hyde Park VT: Antimicrobial Therapy, Inc.
- Gomez HF, Ochoa TJ, Herrera-Sinsua I, Carlin LG and Cleary TG. (2002). Lactoferrin Protects Rabbits from Shigella flexneri-Induced Inflammatory Interitis. Infect. Immun. 70(12): 7050-7053.
- Keusch, GT and Acheson, DWD. (1996). Shigella Infection. In Paradise LJ, Bendellini M, and Friedman, H. (Ed.), Enteric Infections and Immunity. New York: Plenum.
- Krilov LR, Barone SR, Mandel FS, Cusack TM, Gaber DJ, Rubino JR. (1996). Impact of an infection control program in a specialized preschool. Am J Infect Control. 24:167-73.
- Mayo Clinic. (2007, April 14). Shigella. Retrieved August 22, 2007 from Mayo Clinic Web site, http://www.mayoclinic.com/health/shigella/DS00719.
- Mead PM, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, Griffin PM, and Tauxe RV. (1999). Food-related Illness and Death in the United States. Emerg. Infect. Dis. 5:607-625.
- MMWR Surveillance Summaries. 1996. Guidelines for confirmation of foodborne-disease outbreaks. October 25, 1996 / 45:59-66. Atlanta, GA: Centers for Disease Control and Prevention.
- Philpott DJ, Edgeworth JD, and Sansonetti PJ. (2000). The pathogenesis of Shigella flexneri infection: lessons from in vitro and in vivo studies. Philos Trans R Soc Lond B Biol Sci. 355:575-86.
- Ringrose JH, Muijsers AO, Pannekoek Y, Yard BA, Boog CJP, Van Alphen L, Dankert J, and Feltkamp TEW. (2001). Influence of infection of cells with bacteria associated with reactive arthritis on the peptide repertoire presented by HLA-B27. J Med Microbiol. 50:385-9.
- Weinberg WG. (1996). No Germs Allowed! How to avoid infectious diseases at home and on the road. New Brunswick, NJ: Rutgers University Pre