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.[1] 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 infected with human immunodeficiency virus (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:

See Presentation for more detail.


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.


Antibiotic treatment is indicated in most patients. Avoid antimotility agents because they have the potential to worsen the 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.


Shigellosis occurs when Shigella species invade the epithelial lining of the terminal ileum, colon, and rectum, causing diarrhea and bacillary dysentery that ranges from mild to severe disease. It is a major public health problem in developing countries where sanitation is poor but also exists in industrialized nations among the homeless and those with low and middle income.[1]  

Shigellosis is highly infectious and spreads by fecal-oral transmission. Shigella sonnei and Shigella flexneri cause 90% of the cases of shigellosis; Shigella dysenteriae has produced epidemic shigellosis. Left untreated, fulminant dysentery may occur and is potentially fatal. No vaccine against Shigella species exists yet, however, several are under development.[2, 3, 4, 5]


Shigella organisms cause bacillary dysentery,[6, 7, 8] 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,[7, 9] causing diarrhea after ingestion of as few as 180 organisms.[10]

These pathogens cause damage by two mechanisms, (1) invasion of the colonic epithelium, which is dependent on a plasmid-mediated virulence factor,[6, 7, 8] and (2) production of an enterotoxin, which is not essential for colitis but enhances the virulence.

Lapaquette et al indicate that S flexneri uses a calcium/calpain-dependent mechanism to cause sumoylation inhibition, thereby allowing pathogenic bacterial entry.[11]  

The organism is spread by fecal-oral contact via infected food or water, during travel or in long-term care facilities, daycare centers, or nursing homes.[12]


United States data

Shigellosis is the third most common cause of bacterial gastroenteritis in the United States.[13] Approximately 500,000 cases of shigellosis are estimated to occur annually in the United States.[14]

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 700,000 deaths and 165 million cases of diarrhea annually worldwide.[15]

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 asymmetric and can be chronic and relapsing.

Shigellosis is most common in children aged 6 months to 5 years.[2, 15]


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


Infection with Shigella species may be associated with extragastrointestinal 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.[18, 19]

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.[18, 19]

Intestinal obstruction can develop from severe colonic disease. The incidence of this complication in one series of 1211 patients with shigellosis was 2.5%.[20]  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.[21]

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 those younger than 5 years.[22, 23]  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).[24]  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.[23]  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.[25]  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. [26]  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 in 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.[27]

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.[28]

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.[29]  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 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.[18]

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.[30]

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.[18, 31]

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.[32]  Rarely, keratitis or conjunctivitis and acute myocarditis may develop.[33, 34]

History and Physical Examination


Manifestations of shigellosis generally begin within 1-2 days of infection and can include a range of the following signs and symptoms[1, 14] :

Physical examination

Clinical findings may include the following:

Laboratory Studies

Laboratory studies generally reveal the following findings:


Sigmoidoscopy is not necessary in most cases of shigellosis.

If distinguishing between dysentery and the acute presentation of idiopathic ulcerative colitis is urgently necessary, a colonic biopsy may be useful if it is performed within 4 days of the onset of symptoms. Histologic findings of shigellosis include the following:

Medical Care

General supportive care of patients with shigellosis includes the following:[36]

Antimotility agents should be avoided. They have the potential to worsen symptoms and may predispose to toxic dilation of the colon.

For fluid and electrolyte supplementation, oral rehydration solutions are preferable.


Consult a gastroenterologist or an infectious diseases expert if the Shigella infection is prolonged or if the patient experiences a severe course of shigellosis that is unresponsive to antibiotics.

Patient education

Educate patients about proper hygiene. Careful handwashing and stool precautions should prevent the dissemination of shigellosis. Thus, primary preventive measures should include universal availability of potable water, provision of sanitation methods, and improved personal and food hygiene.[2]


A vaccine for shigellosis is not currently available. Until a vaccine is available, the following measures can help prevent the dissemination of shigellosis:

Medication Summary

Shigella infection produces a self-limited diarrheal illness that lasts 5-7 days and may not require antibiotics in individuals who are otherwise healthy.[14] However, for public health reasons, most experts recommend treating any person whose stool culture is positive for Shigella species. Moreover, antibiotics have been shown to decrease the duration of fever and diarrhea by about 2 days. The shorter duration of shedding with antibiotic therapy can reduce the risk of person-to-person spread. Antibiotic treatment is definitely recommended for infirm or older patients, malnourished children, patients infected with human immunodeficiency virus (HIV) infection, food handlers, health care workers, and children in day care centers.[37]  However, antibiotic-resistant strains of Shigella have emerged, posing therapeutic challenges.[15, 38]

Ampicillin was widely used in the past but is no longer an effective empiric treatment in the United States because of antibiotic resistance.[39] In fact, antibiotic resistance to Shigella species is widespread and increasing worldwide. Thus, antibiotic susceptibility testing is essential for the management of patients with suspected Shigella infection.

At present, ciprofloxacin, azithromycin, and ceftriaxone are the mainstays of treatment for shigellosis. However, in some regions increasing evidence exists of decreased susceptibility or full resistance to these agents.[3, 40, 41]

In a study comprising 90 patients with shigellosis from 2008 to 2013 who had acquired Shigella as traveler's diarrhea or domestically acquired diarrhea, Toro et al detected the highest resistance for trimethoprim/sulfamethoxazole (81.8%), followed by ampicillin (37.8%) and ciprofloxacin (23.3%).[42]

Given the widespread resistance to ciprofloxacin as well as trimethoprim-sulfamethoxazole and azithromycin, a third-generation cephalosporin is appropriate empiric therapy in the setting of acute illness.[37, 43] The treatment of choice for HIV-infected patients is a quinolone for 5 days.

Ceftriaxone (Rocephin)

Clinical Context:  Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin binding proteins. Exerts antimicrobial effect by interfering with the synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Highly stable in the presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of the dose is excreted unchanged in urine, and the remainder is secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding have been reported to decrease from 95% bound at plasma concentrations

Ciprofloxacin (Cipro)

Clinical Context:  Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, bacterial growth.

Trimethoprim-sulfamethoxazole (Bactrim, Septra, Bactrim DS, Cotrim)

Clinical Context:  Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Reasonable drug of choice (DOC) in the United States due to few resistant strains.

Dosing may be based on TMP component.

Azithromycin (Zithromax)

Clinical Context:  Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks the dissociation of peptidyl tRNA from ribosomes, causing the arrest of RNA-dependent protein synthesis. Nucleic acid synthesis is not affected.

Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that the concentration in phagocytes may contribute to drug distribution in inflamed tissues.

Treats mild-to-moderate microbial infections.

Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half-life.

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.[44, 45]

What is shigellosis?Which patients are at highest risk for shigellosis?What are the signs and symptoms of shigellosis?How is shigellosis diagnosed?How is shigellosis treated?How is shigellosis transmitted?What is the pathophysiology of shigellosis?What is the US prevalence of shigellosis?What is the global prevalence of shigellosis?Which patient groups have the highest prevalence of shigellosis?What is the mortality and morbidity associated with shigellosis?What are the possible intestinal complications of shigellosis?What are the possible systemic complications of shigellosis?What is the prognosis of shigellosis?Which clinical history findings are characteristic of shigellosis?Which physical findings are characteristic of shigellosis?What are the differential diagnoses for Shigellosis?What is the role of lab tests in the workup of shigellosis?What is the role of sigmoidoscopy in the workup of shigellosis?Which histologic findings are characteristic of shigellosis?What is included in supportive care for shigellosis?Which specialist consultations are beneficial to patients with shigellosis?What is included in patient education about shigellosis?How is shigellosis prevented?What is the role of medication in the treatment of shigellosis?Which medications in the drug class Antibiotics are used in the treatment of Shigellosis?


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

Disclosure: Nothing to disclose.


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

Disclosure: Nothing to disclose.

Specialty Editors

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, Chairman, Department of Medicine, Chief, Division of Infectious Diseases, Hospital Epidemiologist, South Nassau Communities Hospital

Disclosure: Nothing to disclose.

Chief Editor

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

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

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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