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Shigellosis

  • Author: Joyann A Kroser, MD, FACP, FACG, AGAF; Chief Editor: BS Anand, MD  more...
 
Updated: Jun 22, 2016
 

Practice Essentials

Shigellosis is a type of food poisoning caused by infection with the Shigella species. It is a major public health problem in developing countries where sanitation is poor. Shigellosis is spread by means of fecal-oral transmission.

Signs and symptoms

Certain populations are at an increased risk for shigellosis including children in daycare, incarcerated persons, international travelers, homosexual men, people with HIV, and those who live in crowded, unsanitary conditions.

Shigellosis follows a self-limited course ranging from 3 days to 1 week. It rarely lasts as long as a month.

Symptoms of shigellosis include the following:

  • Acute bloody diarrhea
  • Abdominal cramping
  • Tenesmus
  • Urgency
  • Fever
  • Occasional vomiting
  • Dehydration

See Clinical Presentation for more detail.

Diagnosis

A sample of stool for culture should be obtained in all suspected cases of shigellosis. Specimens should be processed immediately after collection. Other lab tests, such as a WBC count, may be performed in persons with severe symptoms or to rule out other causes.

See Workup for more detail.

Management

Antibiotic treatment is indicated in most patients. Avoid antimotility agents because they have the potential to worsen symptoms and may predispose to toxic dilation of the colon.

Clear liquids followed by a low residue, lactose-free diet are recommended until symptoms of shigellosis resolve.

See Treatment and Medication for more detail.

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Pathophysiology

Shigella organisms cause bacillary dysentery,[1, 2, 3] a disease that has been described since early recorded history.

Shigella species (eg, S dysenteriae, S flexneri, S sonnei, S boydii) are aerobic, nonmotile, glucose-fermenting, gram-negative rods that are highly contagious,[2, 4] causing diarrhea after ingestion of as few as 180 organisms.[5]

Shigella species cause damage by 2 mechanisms, as follows: (1) invasion of the colonic epithelium, which is dependent on a plasmid-mediated virulence factor,[1, 2, 3] and (2) production of an enterotoxin, which is not essential for colitis but enhances the virulence.

The organism is spread by fecal-oral contact; via infected food or water; during travel; or in long-term care facilities, day care centers, or nursing homes.[6]

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Epidemiology

United States data

Approximately 450,000 cases of shigellosis are estimated to occur annually in the United States.

International data

Shigellosis occurs worldwide, and it tends to occur whenever war, natural calamities (eg, earthquakes, floods), or unhygienic living conditions result in overcrowding and poor sanitation. S boydii and S dysenteriae occur more commonly internationally. Disease from Shigella species causes an estimated 1 million deaths and 165 million cases of diarrhea annually worldwide.

Race-, sex-, and age-related demographics

No racial or sexual differences exist in Shigella infections. However, reactive arthritis, which is a triad of arthritis, urethritis, and conjunctivitis, occurs most commonly in men aged 20-40 years, and it occurs 2-4 weeks after infection with the Shigella species. Reactive arthritis is associated with the human leukocyte antigen (HLA)–B27 phenotype. The arthritis is asymmetrical and can be chronic and relapsing.

Shigellosis is most common in children aged 6 months to 5 years.

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Prognosis

Postinfection carriage is generally less than 3-4 weeks. Mild cramps and diarrhea may continue for many days to weeks after treatment of shigellosis.

Morbidity/mortality

Infection with Shigella species may be associated with extragastrointestinal complications.

  • Bacteremia occurs primarily in malnourished children and carries a mortality rate of 20% as a result of renal failure, hemolysis, thrombocytopenia, gastrointestinal hemorrhage, and shock. [7, 8]
  • Hemolytic uremic syndrome may complicate infections with  Shigella species and  Escherichia coli, and it carries a mortality rate of greater than 50%. [5] Hemolytic uremic syndrome is characterized by acute hemolysis, renal failure, uremia, and disseminated intravascular coagulation.
  • Metabolic disturbances: Hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone (ADH) secretion may occur.
  • Leukemoid reaction: An elevated WBC count of 50,000/mm 3 occurs in approximately 4% of patients, mainly in pediatric patients aged 2-10 years.
  • Neurologic disease: Seizures, the most common neurologic complication, are always associated with fever and are generalized. They are typically nonrecurring and uncomplicated. Seizures are least common with  S dysenteriae. The prevalence of seizures is approximately 10% across all ages.
  • Encephalopathy with lethargy, confusion, and headache has been noted in up to 40% of children hospitalized with  Shigella infections.
  • Reactive arthritis (also known as Reiter syndrome) may occur.

Complications

Complications from shigellosis may be intestinal or systemic.

Intestinal complications

Proctitis or rectal prolapse is common in infants and young children. This is induced by invasion of the organism into the colonic mucosa, causing severe inflammation of the rectum and distal colon.[9, 10]

Toxic megacolon occurs primarily in the setting of S dysenteriae infection. The pathogenesis is unclear, but it occurs in patients with pancolitis and seems to be related to the intensity of inflammation rather than being mediated by the Shiga toxin.[9, 10]

Intestinal obstruction can develop from severe colonic disease. The incidence of this complication in one series of 1211 patients with shigellosis was 2.5%.[11]  The patients with obstruction were more likely to be infected with type 1 S dysenteriae.

Colonic perforation is an extremely rare complication of shigellosis. It occurs primarily in infants or severely malnourished patients and is associated with infection due to type 1 S dysenteriae or S flexneri.[12]

Systemic complications

Shigella bacteremia has a reported incidence of 0-7%. Signs that correlate with bacteremia are leukocytosis, hypothermia, temperature above 39.5ºC, severe dehydration, and lethargy. Bacteremia is more common among children than in adults, occurring primarily in younger than 5 years.[13, 14]  In one study, among the 22 cases of bacteremia described in adults, one third of patients were older than 65 years, and more than half had an underlying disease (most commonly diabetes).[15]  However, infection with human immunodeficiency virus (HIV) does not appear to confer a significant predisposition to Shigella bacteremia.

Bacteremia is associated with an increased risk of death.[14]  Young malnourished children are at greatest risk. Additionally, the mortality rate associated with Shigella bacteremia may be higher in the setting of human immunodeficiency virus (HIV) infection.[16]  Antibiotic therapy is recommended in all patients who become bacteremic with Shigella.

Metabolic disturbances may occur. Substantial volume depletion is uncommon in shigellosis, because the stool volume is usually very low. In one study, hyponatremia, defined as serum sodium levels below 120 meq/L, was noted in 29% of patients hospitalized with diarrhea due to type 1 S dysenteriae. [17]  However, the hyponatremia is generally caused by the syndrome of inappropriate antidiuretic hormone secretion, not volume depletion. Protein-losing enteropathy may also be observed. Increased catabolism secondary to fever, stool protein loss, decreased intake owing to anorexia, and malabsorption can exacerbate preexisting malnutrition.

Leukemoid reaction, defined as a white blood cell (WBC) count of 50,000/mm3 or more, has been observed in Bangladesh among approximately 4% of patients, most commonly in children between the ages of 2 and 10 years. In contrast, a study conducted in the United States found no association between disease severity and an elevated WBC count.[18]

Neurologic complications associated with Shigella infection may arise, of which seizures are the most common. These tend to be generalized seizures. Although they are not associated with specific neurologic deficits, they have been associated with a higher risk of death. Seizures occur almost exclusively among children younger than 15 years. The occurrence of seizures has been observed during infection with all serotypes of Shigella, and they are associated with fever (often >39ºC), an increased proportion of immature leukocytes, low serum sodium levels, and high serum potassium levels. Analysis of cerebrospinal fluid (CSF) obtained by lumbar puncture is typically normal, although up to 15% may demonstrate mild lymphocytic pleocytosis with up to 12 cells.[19]

In addition to seizures, other neurologic findings have been described in up to 40% of children hospitalized with Shigella infection, including encephalopathy with lethargy, confusion, and headache.[20]  Obtundation, coma, and posturing are rare. In cases of fatal encephalopathy, cerebral edema has been observed at autopsy.

A particularly lethal form of shigellosis, known as Ekiri syndrome, was responsible for 15,000 deaths per year in Japan during the pre-World War II era. Ekiri syndrome was associated with S sonnei infection, and it was characterized by the rapid development of seizures and coma in patients with high fever and few dysenteric symptoms. The mechanism of the fulminant course of this disease remains unclear.[9]

Reactive arthritis is an uncommon complication that may follow S flexneri infection. It can occur alone or in association with conjunctivitis and urethritis. The arthritis is a sterile inflammatory arthritis. Symptoms develop 1-2 weeks following symptoms of dysentery, regardless of whether or not the dysentery was treated with antibiotics. Approximately 70% of patients with post-shigellosis reactive arthritis are HLA-B27 positive.[21]

Hemolytic-uremic syndrome (HUS) is a relatively uncommon disease; however, it is the most frequent cause of acute renal failure among infants and young children worldwide. About 90% of cases of pediatric HUS follow a diarrheal prodrome that is most commonly due to infection with enterohemorrhagic Escherichia coli (particularly type O157:H7) but that may also be induced by infection with type 1 S dysenteriae.[9, 22]

At the end of the first week and during the recovery phase of diarrheal or dysenteric symptoms, patients with HUS present with a combination of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure (initially oliguric and then anuric). These patients may be considered to have thrombotic thrombocytopenic purpura (TTP) if fever and transient neurologic symptoms are also present. Seizures occur in approximately 10% of affected patients, and stroke or cerebral edema occur in 5%.

The pathogenesis of HUS or TTP involves cytotoxic damage to the vascular endothelium. In most studies, Shiga toxin production by type 1 S dysenteriae is thought to be directly involved.

Other manifestations can also occur. In young girls, Shigella can cause vaginitis or vulvovaginitis, with or without diarrhea.[23]  Rarely, keratitis or conjunctivitis and acute myocarditis may develop.[24, 25]

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Contributor Information and Disclosures
Author

Joyann A Kroser, MD, FACP, FACG, AGAF Adjunct Clinical Associate Professor of Medicine, Gastroenterology, and Hepatology, Drexel University College of Medicine; Adjunct Professor of Medicine, Temple University School of Medicine

Joyann A Kroser, MD, FACP, FACG, AGAF is a member of the following medical societies: American College of Physicians, Alpha Omega Alpha, Crohn's and Colitis Foundation of America, American College of Gastroenterology, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Pennsylvania Medical Society, Phi Beta Kappa, Philadelphia County Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Amandeep Singh, MBBS Resident Physician, Department of Internal Medicine, Crozer Chester Medical Center

Amandeep Singh, MBBS is a member of the following medical societies: American Academy of Family Physicians, American College of Gastroenterology, American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Aaron Glatt, MD Chief Administrative Officer, Executive Vice President, Mercy Medical Center, Catholic Health Services of Long Island

Aaron Glatt, MD is a member of the following medical societies: American College of Chest Physicians, American Association for Physician Leadership, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Infectious Diseases Society of America, International AIDS Society, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Ronnie Fass, MD, FACP, FACG Chief of Gastroenterology, Head of Neuroenteric Clinical Research Group, Southern Arizona Veterans Affairs Health Care System; Professor of Medicine, Division of Gastroenterology, University of Arizona School of Medicine

Ronnie Fass, MD, FACP, FACG is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Neurogastroenterology and Motility Society, American Society for Gastrointestinal Endoscopy, Israeli Medical Association

Disclosure: Received grant/research funds from Takeda Pharmaceuticals for conducting research; Received consulting fee from Takeda Pharmaceuticals for consulting; Received honoraria from Takeda Pharmaceuticals for speaking and teaching; Received consulting fee from Vecta for consulting; Received consulting fee from XenoPort for consulting; Received honoraria from Eisai for speaking and teaching; Received grant/research funds from Wyeth Pharmaceuticals for conducting research; Received grant/research funds f.

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