Shigella Infection

Updated: Apr 03, 2018
Author: Jaya Sureshbabu, MBBS, MRCPCH(UK), MRCPI(Paeds), MRCPS(Glasg), DCH(Glasg); Chief Editor: Russell W Steele, MD 


Practice Essentials

Shigella organisms are a group of gram-negative, facultative intracellular pathogens. They were recognized as the etiologic agents of bacillary dysentery or shigellosis in the 1890s. Shigella were discovered over 100 years ago by a Japanese microbiologist named Shiga, for whom the genus is named. Shigella was adopted as a genus in the 1950s. These organisms are members of the family Enterobacteriaceae and tribe Escherichieae; they are grouped into 4 species: Shigelladysenteriae, Shigellaflexneri, Shigellaboydii, and Shigellasonnei, also known as groups A, B, C, and D, respectively.[1]  They are nonmotile, non – spore forming, rod shaped, and nonencapsulated. Subgroups and serotypes are differentiated from each other by their biochemical characteristics (e.g., ability to ferment D-mannitol) and antigenic properties. Group A has 15 serotypes, group B has 8 serotypes, group C has 19 serotypes, and group D has 1 serotype.

This illustration depicts a three-dimensional (3D) This illustration depicts a three-dimensional (3D), computer-generated image of a number of rod-shaped, drug-resistant, Shigella sp. bacteria. The artistic recreation was based upon scanning electron microscopic (SEM) imagery. Note that the exterior of the Shigella bacteria is fimbriated, covered by numerous thin, hair-like projections, imparting a furry appearance. Courtesy of the Centers for Disease Control (CDC)/James Archer.

Geographic distribution and antimicrobial susceptibility varies with different species. S dysenteriae serotype 1 causes deadly epidemics, S boydii is restricted to the Indian subcontinent, and S flexneri and S sonnei are prevalent in developing and developed countries, respectively. S flexneri, enteroinvasive gram-negative bacteria, is responsible for the worldwide endemic form of bacillary dysentery.


Shigella infection is a major public health problem in developing countries where sanitation is poor. Humans are the natural reservoir, although other primates may be infected. No natural food products harbor endogenous Shigella species, but a wide variety of foods may be contaminated.

Shigellosis is spread by means of fecal-oral transmission. Other modes of transmission include ingestion of contaminated food or water (untreated wading pools, interactive water fountain), contact with a contaminated inanimate object, and certain mode of sexual contact. Vectors like the housefly can spread the disease by physically transporting infected feces.

The infectivity dose (ID) is extremely low. As few as 10 S dysenteriae bacilli can cause clinical disease, whereas 100-200 bacilli are needed for S sonnei or S flexneri infection. The reasons for this low-dose response are not completely clear. One possible explanation is that virulent Shigellae can withstand the low pH of gastric juice. Most isolates of Shigella survive acidic treatment at pH 2.5 for at least 2 h.[2]

The incubation period varies from 12 hours to 7 days but is typically 2-4 days; the incubation period is inversely proportional to the load of ingested bacteria. The disease is communicable as long as an infected person excretes the organism in the stool, which can extend as long as 4 weeks from the onset of illness. Bacterial shedding usually ceases within 4 weeks of the onset of illness; rarely, it can persist for months. Appropriate antimicrobial treatment can reduce the duration of carriage to a few days.

DNA-DNA hybridization studies demonstrate that E.Coli  share more than 75% nucleotide similarity with Shigella species and Shigella species appears to be metabolically inactive biogroups of E.coli.[3]


Virulence in Shigella species involves both chromosomal-coded and plasmid-coded genes. Virulent Shigella strains produce disease after invading the intestinal mucosa; the organism only rarely penetrates beyond the mucosa.[4]

The characteristic virulence trait is encoded on a large (220 kb) plasmid responsible for synthesis of polypeptides that cause cytotoxicity. Shigellae that lose the virulence plasmid are no longer pathogenic. Escherichia coli (E coli O157:H7) that harbor this plasmid clinically behave as Shigella bacteria.[5]

Siderophores, a group of plasmid-coded genes, control the acquisition of iron from host cells from its protein-bound state. In the extra intestinal phase of infection by gram-negative bacteria, iron becomes one of the major factors that limit further growth. This limitation occurs because most of the iron in human body is sequestered in hemoproteins (i.e., hemoglobin, myoglobin) or iron-chelating proteins involved in iron transport (transferrin and lactoferrin). Many bacteria can secrete iron chelating compounds, or siderophores, which chelate iron from the intestinal fluids and which bacteria then take up to obtain iron for its metabolic needs. These siderophores are under the control of plasmids and are tightly regulated by genes such that, under low iron conditions, expression of the siderophore system is high.

Regulatory genes control expression of virulence genes. Shiga toxin (Stx) is not essential for virulence of S dysenteriae type 1 but contributes to the severity of dysentery. Both plasmid-encoded virulence traits and chromosome-encoded factors are essential for full virulence of shigellae.

Regarding chromosomally encoded enterotoxin, many pathogenic features of Shigella infection are due to the production of potent cytotoxins known as Stx, a potent protein synthesis–inhibiting exotoxin. Shigella strains produce distinct enterotoxins. These are a family of cytotoxins that contain 2 major immunologically non–cross-reactive groups called Stx1 and Stx2. The homology sequences between Stx1 and Stx2 are 55% and 57% in subunits A and B, respectively.

These toxins are lethal to animals; enterotoxic to ligated rabbit intestinal segments; and cytotoxic for vero, HeLa, and some selected endothelial cells (human renal vascular endothelial cells) manifesting as diarrhea, dysentery, and hemolytic-uremic syndrome (HUS).[6] Stx1 is synthesized in significant amount by S dysenteriae serotype 1 and S flexneri 2a and E coli (Shigella toxin–producing E coli [ShET]).[7]

Stx1 and Stx2 are both encoded by a bacteriophage inserted into the chromosome. Stx1 increases inflammatory cytokine production by human macrophages, which, in turn, leads to a burst of interleukin (IL)-8. This could be relevant in recruiting neutrophils to the lamina propria of the intestine in hemorrhagic colitis and accounts for elevated levels of IL-8 in serum of patients with diarrhea-associated HUS.

Stxs have 2 subunits. Stx is transported into nucleoli. Stx nucleolar movement is carrier-dependent and energy-dependent. Subunit A is a 32-kD polypeptide that, when digested by trypsin, generates A1 with a 28-kD fragment and another small fragment, A2, which is 4 kD. A1 fraction acts like N -glycosidase; it removes single adenine residue from 28S rRNA of ribosome and inhibits protein synthesis. The A2 fraction is a pentamer polypeptide of 7.7-kD protein and is required to bind the A1 fraction to the B subunit. The main function of the B subunit is the binding of toxins to the cell surface receptor, typically globotriaosylceramide (Gb3), on the brush border of intestinal epithelial cells.[8]

In summary, events that occur on exposure to Shigella toxin are as follows:

  • The B subunit of holotoxin binds to the Gb3 receptor on the cell surface of brush-border cells of the intestines.

  • The receptor-holotoxin complex is endocytosed.

  • The complex moves to Golgi apparatus and then to the endoplasmic reticulum.

The A1 subunit is released and it targets 28S RNA of the ribosome, inhibiting protein synthesis. Stxs may play a role in the progression of mucosal lesions after colonic cells are invaded, or they may induce vascular damage in the colonic mucosa. Stx adheres to small-intestine receptors and blocks the absorption of electrolytes, glucose, and amino acids from intestinal lumen. The B subunit of Stx binds the host's cell glycolipid in the large intestine and in other cells, such as renal glomerular and tubular epithelia. The A1 domain internalized by means of receptor-mediated endocytosis and causes irreversible inactivation of the 60S ribosomal subunit, inhibiting protein synthesis and causing cell death, microvascular damage to the intestine, apoptosis in renal tubular epithelial cells, and hemorrhage (as blood and mucus in the stool).

Chromosomal genes control lipopolysaccharide (LPS) antigens in cell walls. LPS plays an important role in resistance to nonspecific host defense encountered during tissue invasion. These genes help in invasion, multiplication, and resistance to phagocytosis by tissue macrophages. LPS enhances the cytotoxicity of Stx on human vascular endothelial cells. Shigella chromosomes share most of their genes with E coli K12 strain MG1655, and the diversity of putative virulence genes acquired by means of bacteriophage-mediated lateral gene transfer is extensive. As a result of convergent evolution involving the gain and loss of functions, Shigella species have become highly specific human pathogens with variable epidemiologic and pathologic features.

A 3-kb plasmid that harbors information for the production of bacteriocin by S flexneri strains has been described. The production of this bacteriocin may be related to dysenteric diarrhea these bacterial strains produce.

Intestinal adherence factor

Intestinal adherence factor favors colonization in vivo and in animal models. This is 97-kD outer-membrane protein (OMP) encoded by each gene on chromosomes. This codes for intimin protein, and an anti-intimin response is observed in children with HUS.[9]


The host response to primary infection is characterized by the induction of an acute inflammation, which is accompanied by polymorphonuclear cell (PMN) infiltration, resulting in massive destruction of the colonic mucosa. Apoptotic destruction of macrophages in subepithelial tissue allows survival of the invading shigellae, and inflammation facilitates further bacterial entry.

Gross pathology consists of mucosal edema, erythema, friability, superficial ulceration, and focal mucosal hemorrhage involving the rectosigmoid junction primarily.

Microscopic pathology consists of epithelial cell necrosis, goblet cell depletion, PMN infiltrates and mononuclear infiltrates in lamina propria, and crypt abscess formation.

Shigella bacteria invade the intestinal epithelium through M cells and proceed to spread from cell to cell, causing death and sloughing of contiguously invaded epithelial cells and inducing a potent inflammatory response resulting in the characteristic dysentery syndrome. In addition to this series of pathogenic events, only S dysenteriae type 1 has the ability to elaborate the potent Shiga toxin that inhibits protein synthesis in eukaryotic cells and that may lead to extraintestinal complications, including hemolytic-uremic syndrome and death. Invasion of M cells, the specialized cells that cover the lymphoid follicles of the mucosa, overlying Peyer patches, may be the earliest event.[2]



United States

In 2013, the average annual incidence of shigellosis in the United States was 4.82 cases per 100,000 individuals.[10]  State public health laboratories reported 7,746 laboratory confirmed Shigella infections to the CDC in 2012. Of the 7,746 laboratory confirmed isolates, 6,867 were identified to species level. Distribution by species was similar to previous years, with S sonnei accounting for the largest percentage of infections (75%), followed by S flexneri (12%), S boydii (0.8%), and S dysenteriae (0.3%).The reporting jurisdictions with the highest incidence rates were Nebraska (13.2 %), New Jersey (7.6%), and Minnesota (7.1%).[11] The highest incidence per 100,000 population for shigellosis (27.77 cases) was among children younger than 5 years.

The largest outbreak of Shigellosis since 1988 took place in Michigan in 2016.[12]


The overall incidence of Shigella infection in 2012 was 2.5 cases per 100,000 population, and the rate of HUS in pediatric patients younger than 15 years is 0.49 cases per 100,000 population. Compared with the previous 10 years (2002–2011), a larger portion of Shigella infections in 2012 were reported from January through March. More than 95% of Shigella infections may be asymptomatic. Hence, the actual incidence may be 20 times higher than reported. The CDC estimates that 450,000 total cases of shigellosis occur in the United States every year. The latest major outbreak is reported from Illinois in February 2010 due to S sonnei.


Worldwide, the incidence of shigellosis is estimated to be 164.7 million cases per year, of which 163.2 million were in developing countries, where 1.1 million deaths occurred. About 60% of all episodes and 61% of all deaths attributable to shigellosis involved children younger than 5 years. The incidence in developing countries may be 20 times greater than that in developed countries. Although the relative importance of various serotypes is not known, an estimated 30% of these infections are caused by S dysenteriae.

Case-fatality rates for S dysenteriae infections may approach 30%. Patients with malnutrition are at increased risk of having complicated course. Shigella infection in malnourished children often causes a vicious cycle of further impaired nutrition, recurrent infection, and further growth retardation.


Although shigellosis-related mortality is rare in developed countries, S dysenteriae infection is associated with substantial morbidity and mortality rates in the developing world.

Case fatality is as high as 15% among patients with S dysenteriae type 1 who require hospitalization; this rate is increased by delayed arrival and treatment with ineffective antibiotics. Infants, non-breastfed children, children recovering from measles, malnourished children, and adults older than 50 years have a more severe illness and a greater risk of death

The overall mortality rate in developed countries is less than 1%.

In the Far East and Middle East, the mortality rates for S dysenteriae infections may be as high as 20-25%.


No racial predilection is known.


No sexual predilection is known.


According to recent CDC reports, Shigella infection accounted for 28% of all the enteric bacterial infections.[13] Children younger than 5 years had 7% of total reported cases, a rate indicating a disproportionate disease burden in this population.




See the list below:

  • Populations that are at high-risk for shigellosis include the following:

    • Children in daycare centers (< 5 y) and their caregivers

    • Persons in custodial institutions

    • International travelers

    • Homosexual men

    • People living in crowded conditions with poor sanitary facilities and inadequate clean water supply (eg, refugee camps, shelters for displaced people)

    • People with human immunodeficiency virus (HIV) infection[14]

  • Symptoms include the following:

    • Sudden onset of severe abdominal cramping, high-grade fever, emesis, anorexia, and large-volume watery diarrhea. Seizures may be an early manifestation.

    • Abdominal pain, tenesmus, urgency, fecal incontinence, and small-volume mucoid diarrhea with frank blood (fractional stools) may subsequently occur.

  • Signs include the following:

    • Elevated temperatures (as high as 106 º F) are documented in approximately one third of cases, and a generally toxic appearance is noticed.

    • Tachycardia and tachypnea may occur secondary to fever and dehydration. Depending on the degree of dehydration, dry mucous membranes, hypotension, prolonged capillary refill time, and poor skin turgor may be present.

    • Abdominal tenderness is usually central and lower, although it may be generalized.

  • Extra intestinal manifestations are as follows:

    • CNS symptoms include severe headache, lethargy, meningismus, delirium, and convulsions lasting less than 15 minutes, especially with S dysenteriae.[15] Severe toxic encephalopathy is rare, but lethal complications occur when initial symptoms are followed by sensory obtundation, seizures, coma, and death in 6-48 hours. The pathogenesis of neurologic manifestations during shigellosis is unclear. However, data now clearly demonstrate that Stx is not responsible.

    • Regarding HUS, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure have been reported with S dysenteriae because of vasculopathy mediated by Stx. The principal organ affected in Stx1-mediated HUS is the kidney. This is presumed to be the consequence of the high renal blood flow and abundant baseline expression and high inducibility of the Stx glycolipid receptor Gbe in the glomerular microcirculation. Manifestations of the disease arise due to 2 primary pathogenetic mechanisms: (1) direct Stx-mediated injury to vascular endothelial cells that leads to tissue ischemia and dysfunction and (2) a systemic inflammatory response triggered by Stx-mediated release of a wide range of cytokines and chemokines, including IL-6, IL-8, and tumor necrosis factor-alpha.

    • Septicemia is rare, except in malnourished children with S dysenteriae infection. Septicemia is sometimes caused by other gram-negative organisms and is related to loss of mucosal integrity by Shigella infection.

    • Profound dehydration and hypoglycemia is more common with S dysenteriae infection.

    • Shigellasepsis may be complicated with disseminated intravascular coagulation (DIC), bronchopneumonia, and multiple organ failure in lethal cases.

    • Arthritis, urethritis, conjunctivitis syndrome is commonly observed in adults carrying human leukocyte antigen (HLA)-B27 histocompatibility antigen.

    • Cholestatic hepatitis, if present, is usually mild.

    • Myocarditis is identified with cardiogenic shock, arrhythmias, and heart block.

    • Rectal prolapse, toxic megacolon, and intestinal obstruction may be present.

    • Shigellosis in the first 6 months of life is rare probably due to presence of antibodies to both virulence plasmid-coded antigens and lipopolysaccharides in the breast milk. Shigellosis in the neonatal period results from mother-to-infant fecal-oral transmission during labor and delivery, usually from asymptomatic mothers.

    • Symptoms usually begin on the third day of life.

    • Septicemia and chronic diarrhea are common.

    • Fever may be absent.

    • Diarrhea is not usually bloody.

    • Intestinal perforation and mortality are more common in this group than in older children.

  • Shigellosis in patients with HIV infection is often a protracted, chronic, relapsing disease (even when treated with antibiotics). Bacteremia is rare, although it can occur in immunocompromised or malnourished patients.[14]


See the list below:

  • Physical examination during acute illness reveals a febrile ill-appearing child. Fever with a temperature as high as 39-40 º C may be noted.

  • The patient's hydration status should be carefully assessed. Especially note dryness of the oral mucosa, lack of tears, decreased urine output, and loss of skin turgor.

  • Abdominal examination may reveal generalized mild-to-moderate tenderness with no guarding or rigidity.

  • In a child who presents with febrile seizures, careful neurologic examination is mandatory to exclude meningitis.


See the list below:

  • The primary mode of transmission of Shigella infection is fecal-oral contamination by the gram-negative aerobic bacilli.

  • Contaminated food usually looks and smells normal. Food may become contaminated by infected food handlers who forget to wash their hands with soap after using the bathroom. Vegetables can become contaminated if they are harvested from a field with sewage in it.

  • Outbreaks of shigellosis have also occurred among men who have sex with men.

  • Travellers from developed to developing regions and soldiers serving under field conditions are also at an increased risk to develop shigellosis.

  • Shigellosis can be caused by exposure to contaminated treated water and, more likely, from untreated recreational water.



Differential Diagnoses



Laboratory Studies

See the list below:

  • Hematology

    • The total WBC count reveals no consistent findings. A shift to the left (increased number of band cells) in the differential WBC count in a patient with diarrhea suggests bacillary dysentery. Leukopenia or leukemoid reactions are occasionally detected.

    • In HUS, anemia and thrombocytopenia occur.

    • Bacteremia is rare, even in severe disease, possibly due to the superficial nature of Shigella infection; the organism rarely penetrates beyond the mucosa.

    • Blood culture should be obtained in children who appear toxic, very young, severely ill, malnourished, or immunocompromised because of their increased risk of bacteremia.

  • Stool examination

    • Isolation of Shigella from feces or rectal swab specimen is diagnostic but lacks specificity. Routine microscopy may reveal sheets of leukocytes on methylene-blue stained stool smear, which is a sensitive test for colitis but not specific for Shigella species.

    • In approximately 70% of patients with shigellosis, fecal blood or leukocytes (confirming colitis) are detectable in the stool.

  • Stool culture

    • A sample for stool culture should be obtained in all suspected cases of shigellosis.

    • The yield from stool cultures is greatest early in the course of disease. Guidelines for obtaining specimens to improve the yield are as follows:

      • Process specimens immediately after collection.

      • If processing is delayed, use a transport medium (eg, buffered glycerol saline).

      • Collect more than one stool or rectal (not anal) swab and inoculate them promptly on at least 2 different culture media.

      • Specimens should be plated lightly onto MacConkey, xylose-lysine-deoxycholate, Hektoen enteric, or Salmonella-Shigella, or eosin-methylene blue agars.

    • If processing is delayed, a rectal-swab sample can be placed in Cary-Blair transport medium or buffered glycerol saline.

    • After overnight incubation, colorless, nonlactose-fermenting colonies may be tested by means of latex agglutination to establish a preliminary identification of Shigella infection.

    • Antimicrobial susceptibility tests of all confirmed isolates should be performed by using the agar diffusion technique. The agar and broth-dilution methods are also widely used. The new Epsilometer strip method (E test) is used to accurately determine the minimum inhibitory concentration (MIC).

    • Despite meticulous care in obtaining and processing specimens from patients infected with Shigella species, approximately 20% may fail to yield Shigella organisms.

  • Enzyme immunoassay: An enzyme immunoassay for Stx is used to detect S dysenteriae type 1 in the stool.

  • Rapid techniques: With rapid techniques, gene probes or polymerase chain reaction (PCR) primers are directed toward virulence genes (invasion plasmid locus).

  • Other testing modalities, such as fluorescent antibody test and enzyme-linked DNA probes, are available in research laboratories.

  • A systematic review and meta-analysis by Tickell et al reported that the sensitivity of dysentery for laboratory-confirmed Shigella infection ranged from 1·9% to 85·9% in the time period between 1977 and 2016, with sensitivity decreasing over time (p=0·04).[16]

Other Tests

Additional diagnostic tools, such as gene probes and PCR analysis of stool for specific genes such as ipaH, virF, or virA can detect cases not diagnosed by culture but are usually available in research laboratories.[17]



Medical Care

The clinician should rapidly assess the patient's fluid and electrolyte status and institute parenteral or oral hydration along with antipyretics as needed. Prompt recognition and treatment of seizures and raised intracranial pressure are essential. Nutritional supplementation of vitamin A (200,000 IU) can hasten clinical resolution in malnourished children.[18, 19]

Zinc supplementation (20 mg elemental zinc for 14 d) has been shown to reduce the duration of diarrhea, improve weight gain during recovery, and result in better immune response to the Shigella along with decreased incidence of diarrheal illness in the subsequent 6 months in malnourished children.[17, 20, 21]

Methods to use bacteriophages to control bacterial infections are being developed and these include the combination of broad host range phages. Within the cocktails, the phages can alter their host range in situ and can be used to treat certain bacterial disease as well as decontaminate food handling premises. Interest in phage therapy has increased and well controlled, well designed blinded studies are on way which will eventually answer many of the questions derived from earlier studies.[22, 12, 23]

Surgical Care

Surgical care may be required for complications (eg, intestinal perforation).


See the list below:

  • Consult a neurologist if seizures and altered sensorium predominate.

  • Consult a nephrologist if HUS is suspected (eg, for patients with anemia, thrombocytopenia, oliguria, and renal failure).


The diet may need to be restricted according to the severity of the disease.


No restrictions are necessary.



Medication Summary

Various antimicrobial agents are effective in the treatment of shigellosis, although options are becoming limited because of globally emerging drug resistance. Resistance of Shigella species to sulfonamides, tetracyclines, ampicillin, and trimethoprim-sulfamethoxazole (TMP-SMX) has been reported worldwide, and these agents are not recommended as empirical therapy.

The World Health Organization (WHO) recommends that all suspected cases of shigellosis based on clinical features be treated with effective antimicrobials (antibiotics).[24] The choice of antimicrobial drug has changed over the years as resistance to antibiotics has occurred, with different patterns of resistance being reported around the world. Evidence is insufficient to consider any class of antibiotic superior in efficacy in treating Shigella dysentery. The following antibiotics are used to treat Shigella dysentery:

  • Beta-lactams: Ampicillin, amoxicillin, third-generation cephalosporins (cefixime, ceftriaxone), and pivmecillinam (not available in the United States)

  • Quinolones: Nalidixic acid, ciprofloxacin, norfloxacin, and ofloxacin

  • Macrolides: Azithromycin

  • Others: sulfonamides, tetracycline, cotrimoxazole, and furazolidone.

Most clinical infections with S sonnei are self-limited (48-72 h) and may not require antimicrobial therapy.

If an ampicillin and TMP-SMX resistant strain is isolated or if susceptibility is unknown, parenteral ceftriaxone sodium, fluoroquinolone (eg, ciprofloxacin, ofloxacin), azithromycin dihydrate (off-label indication), or oral cefixime are the drugs of choice.[9, 25, 26] Amoxicillin is less effective than ampicillin for treatment of ampicillin-sensitive strains. Oral first- and second-generation cephalosporins are inadequate despite in vitro susceptibility. Recently, Shigella isolates with decreased susceptibility to azithromycin (DSA-Shigella), with minimum inhibitory concentration (MIC) greater than 16 µ g/mL has been described by the CDC.[27]

In June 2015, the Centers for Disease Control and Prevention (CDC) warned that they received reports of infections with Shigella strains that are not susceptible to ciprofloxacin and/or azithromycin.  CDC is seeing resistance to ciprofloxacin in 1.6% of the Shigella cases tested and resistance to azithromycin in approximately 3%. The CDC added that most cases have been reported among gay, bisexual, and other men who have sex with men in Illinois, Minnesota, and Montana and among international travelers, but cases are also occurring among other populations.[28, 29, 30]

Because shigellosis is self-limiting, some authorities recommend withholding antibiotic therapy. When an effective antibiotic is given, clinical improvement is anticipated within 48 hours. This lessens the risk of serious complications and death, shortens the duration of symptoms, and hastens the elimination of Shigella and the subsequent spread of infection. The risk of continued shedding of organisms in stool increases the risk of transmission of further disease among contacts argues against withholding antimicrobial treatment.[31]

Antimicrobial therapy is typically administered for 5 days. Antibiotic treatment decreases the duration of illness, person-to-person spread, and cases in household contacts. Treatment in malnourished children (eg, in developing countries) is likely to reduce the risk of worsening malnutrition morbidity after shigellosis. In persons infected with S dysenteriae type 1, early administration of effective antibiotics decreases Shiga toxin (Stx) concentrations in the stool and lowers HUS risk. However, the risk of HUS caused by E coli O157-H7 may be increased with the early administration of antibiotics. Prophylactic antibiotics are not recommended for contacts.

Antidiarrheal medications (diphenoxylate hydrochloride with atropine [Lomotil] or loperamide [Imodium]) should not be used because of the risk of prolonging the illness. WHO has introduced the use of zinc for 10-14 days as part of a diarrheal disease control program in addition to oral rehydration therapy. Initiating zinc at the time of diarrhea leads to shorter duration and fewer loose stools.[21, 32]

A child with typical dysentery that responds to initial empirical antibiotic treatment should continue taking the same drug for a full 5-day course, even if the stool culture is negative.

Immunity and vaccination

Once someone has had Shigella infection, they are not likely to become infected with that specific type again for at least several years. However, they can still become infected with other types of Shigella. Presumably, this immunity could be due to secretory IgA. Circulating antibodies can be detected in immune individuals.

Presently, no US Food and Drug Administration (FDA)–approved vaccines are available. However, research is underway to develop live oral vaccines to prevent shigellosis.[33, 34] Three approaches to Shigella vaccine development that are under active investigation are (1) parenteral O–specific polysaccharide conjugate vaccine, (2) nasal proteasomes delivering Shigella lipopolysaccharide, and (3) live attenuated invasive Shigella deletion mutants that are administered orally.

Researchers have launched an early-stage human clinical trial of two related candidate vaccines to prevent infection with Shigella. The trial is being conducted at the Cincinnati Children’s Hospital Medical Center, one of the eight NIAID-funded Vaccine and Treatment Evaluation Units in the United States funded by the National Institute of Allergy and Infectious Diseases (NIAID).[35]


Class Summary

Ampicillin and TMP-SMZ are effective for susceptible strains; amoxicillin is less effective than this because of its rapid absorption high in the GI tract. The oral route is preferred except for seriously ill patients. In the United States, sentinel surveillance data from 2003-2006 indicated that 94% of S sonnei and 67% of S flexneri organisms were resistant to ampicillin and TMP-SMZ. The WHO now recommends that clinically diagnosed cases of Shigella dysentery be treated with ciprofloxacin as first line treatment, and pivmecillinam (not available in the United States), ceftriaxone, or azithromycin as second line treatment and lists the others as ineffective (WHO 2005a).[36] . However, resistance to quinolones has also been observed since the late 1990s, and some authors have questioned the effectiveness of this class for Shigella. The choice of antibiotic to use as first line against Shigella dysentery should be governed by periodically updated local antibiotic sensitivity patterns of Shigella isolates.

Ciprofloxacin (Cipro)

First-line treatment for shigellosis. Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes. Continue treatment for total of 5 days, even empirical treatment in patient with typical bloody diarrhea who responds clinically with negative stool culture. (7-14 d typical)

Ceftriaxone (Rocephin)

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 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 presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder 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 < 25 mcg/mL to 85% bound at 300 mcg/mL.

Azithromycin (Zithromax)

Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It has enhanced activity against gram-negative organisms. Concentrates in phagocytes and fibroblasts, as demonstrated with in vitro incubation techniques; hence, plasma concentrations are very low but tissue concentrations are very high. It has a long tissue half-life and once daily dosage is recommended. In vivo data suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues.

Ampicillin (Principen)

Broad-spectrum penicillin. Interferes with bacterial cell-wall synthesis during active replication, causing bactericidal activity against susceptible organisms.

Nalidixic acid (NegGram)

First-generation quinolone. Blocks bacterial DNA gyrase. Useful in patients with sulfas and cephalosporin allergy. WHO guidelines state most Shigella strains are now resistant to nalidixic acid.

Cefixime (Suprax)

Third-generation oral cephalosporin with broad activity against gram-negative bacteria. By binding to one or more of the penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth. For outpatient use in drug-resistant Shigella infections.

Trimethoprim and sulfamethoxazole (Bactrim, Cotrim)

Combination effective for shigellosis in the past, but WHO states most Shigella strains are now resistant. Produces sequential blockade in folic acid synthesis. Effect frequently synergistic and bactericidal.

Trace Elements/Metals

Class Summary

WHO has introduced the use of zinc for 10-14 days as part of a diarrheal disease control program in addition to oral rehydration therapy. Initiating zinc at the time of diarrhea leads to shorter duration and fewer loose stools.[21, 32]

Zinc (Galzin, Zinimin, ZnCl2)

Zinc supplementation has been found to decrease duration and severity of diarrheal episodes.




See the list below:

  • Meticulous hand hygiene is the single most important measure to decrease transmission. In situations where access to clean water or soap is limited, waterless hand sanitizers may be an effective option.

  • For individuals who travel to highly endemic areas, recommend that all fruits and vegetables be washed, peeled, and cooked (see the CDC Web site).

  • In developed countries, person-to-person transmission is the most common source of infection. In developing countries, water contaminated with human waste is the most common source for infection.

  • Encourage prolonged breastfeeding in infants because the incidence of disease is markedly decreased in breastfed babies.

  • The following measures help prevent person-to-person transmission of Shigella species:

    • Education of families and child-care center personnel in handwashing techniques, especially after toilet use

    • Avoidance of food preparation by personnel who change diapers in daycare centers

    • Exclusion of febrile children with diarrhea from daycare centers

    • Proper handling and refrigeration of food, even after cooking

    • Use of universal precautions and isolation of persons with diarrhea in institutions and hospitals

    • Exclusion from daycare centers of symptomatic children, attendees, and staff members with documented Shigella gastroenteritis until diarrhea has ceased and 2 stool culture tests are negative for Shigella

    • 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 and the child’s hands carefully with soap and warm water immediately after changing the diapers. After use, the diaper changing area should be wiped down with a disinfectant.

    • Exclusion of infected people as food handlers and measures to decrease contamination of food by house flies

    • People with diarrhea due to this waterborne pathogen should not use recreational water venues for 2 weeks after symptoms resolve.

    • Improvements in worker hygiene during vegetable and fruit picking and packing may prevent shigellosis caused by contaminated produce.

    • Appropriate case reporting to health authorities is essential to take effective measures to prevent further transmission.


See the list below:

  • Dehydration is the most common complication of shigellosis.

  • Other reported complications include the following:

    • CNS complications

      • Seizures were previously thought to be caused by the elaboration of Stx. The etiology is presently uncertain.[37]

      • Syndrome of inappropriate secretion of antidiuretic hormone with profound hyponatremia may occur.

      • Lethargy, meningismus, delirium, seizures, and hypoglycemia may be observed.

      • Encephalopathy and meningitis are rare and may be lethal.

    • HUS associated with strains that produce Stx (eg, S dysenteriae serotype 1 and S flexneri 2a)[38, 39]

    • Septicemia and DIC, particularly in malnourished children

    • Arthritis

      • Postinfectious arthritis is a late complication of S flexneri infection, especially in persons with HLA-B27 marker.

      • Arthritis, conjunctivitis, urethritis syndrome is most common in adults with HLA-B27 marker (occurs 2-5 wk after enteritis).

    • GI complications

      • Cholestatic hepatitis

      • Rectal prolapse

      • Toxic megacolon

      • Pseudomembranous colitis

      • Protein-losing enteropathy

    • Other manifestations

      • Conjunctivitis, iritis, corneal ulcers, cystitis, myocarditis, and vaginitis are uncommon.

      • Ekiri syndrome is a rare syndrome that consists of extreme toxicity, seizures, hyperpyrexia, and headache; it can be rapidly fatal due to brain edema.[37]


See the list below:

  • Most patients recover even without treatment, although illness is more prolonged and more severe if not treated.

    • The fever usually lessens within 24 hours.

    • Frequency of stool decreases within 2-3 days.

    • Carrier state usually ceases within 4 weeks of onset of illness even without antimicrobial treatment and chronic carrier state (>1 y) is rare.

  • The overall mortality rate in developed countries is less than 1%. In the Far East and Middle East, the mortality rates for infections of S dysenteriae may be as high as 20-25%.

  • Severely malnourished children with shigellosis and hypoglycemia, hypothermia, altered consciousness, and/or bronchopneumonia are at high risk of dying.


Questions & Answers


What is the Shigella infection?

What is the pathophysiology of Shigella infection?

What is the pathophysiology of virulence in Shigella infection?

What events occur following exposure to Shigella toxin?

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What is the pathology of Shigella infection?

What is the prevalence of Shigella infection in the US?

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Which populations are at high-risk for Shigella infection?

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