Shigellosis is an acute infection of the intestine caused by Shigella sp. Symptoms include fever, nausea, vomiting, and diarrhea that is usually bloody. Diagnosis is clinical and confirmed by stool culture. Treatment of mild infection is supportive, mostly with rehydration; antibiotics (eg, ciprofloxacin, azithromycin, ceftriaxone) are given to severely ill and high-risk patients with bloody diarrhea or immunocompromise and may shorten the duration of illness and decrease contagiousness.
The genus Shigella is distributed worldwide and is the typical cause of inflammatory dysentery, responsible for 5 to 10% of diarrheal illness in many areas. Shigella is divided into 4 major subgroups: A (S. dysenteriae), B (S. flexneri), C (S. boydii), and D (S. sonnei). Each subgroup is further subdivided into serologically determined types. S. flexneri and S. sonnei are more widespread than S. boydii and the particularly virulent S. dysenteriae. S. sonnei is the most common isolate in the US.
The source of infection is the feces of infected people or convalescent carriers; humans are the only natural reservoir for Shigella. Direct spread is by the fecal-oral route. Indirect spread is by contaminated food and fomites. Flies serve as vectors. Because Shigella are relatively resistant to gastric acid, ingestion of as few as 10 to 100 organisms can cause disease. Epidemics occur most frequently in overcrowded populations with inadequate sanitation. Shigellosis is particularly common among younger children living in endemic areas. Adults usually have less severe disease.
Convalescents and subclinical carriers may be significant sources of infection, but true long-term carriers are rare. Infection imparts little or no immunity.
Shigella organisms penetrate the mucosa of the colon, causing mucus secretion, hyperemia, leukocytic infiltration, edema, and often superficial mucosal ulcerations. Shigella dysenteriae type 1 (not commonly present in the US, except in travelers returning from endemic areas) produces Shiga toxin, which causes marked watery diarrhea and sometimes hemolytic-uremic syndrome (see also Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic-Uremic Syndrome (HUS)).
Symptoms and Signs
The incubation period is 1 to 4 days. The most common presentation, watery diarrhea, is indistinguishable from other bacterial, viral, and protozoan infections that induce secretory activity of intestinal epithelial cells.
In adults, initial symptoms may be episodes of gripping abdominal pain, urgency to defecate, and passage of formed feces that temporarily relieves the pain. These episodes recur with increasing severity and frequency. Diarrhea becomes marked, with soft or liquid stools containing mucus, pus, and often blood. Rectal prolapse and consequent fecal incontinence may result from severe tenesmus. However, adults may present without fever, with nonbloody and nonmucoid diarrhea, and with little or no tenesmus. The disease usually resolves spontaneously in adults—mild cases in 4 to 8 days, severe cases in 3 to 6 wk. Significant dehydration and electrolyte loss with circulatory collapse and death occur mainly in debilitated adults and children < 2 yr.
Rarely, shigellosis starts suddenly with rice-water or serous (occasionally bloody) stools. The patient may vomit and rapidly become dehydrated. Infection may manifest as delirium, seizures, and coma but with little or no diarrhea. Death may occur in 12 to 24 h.
In young children, onset is sudden, with fever, irritability or drowsiness, anorexia, nausea or vomiting, diarrhea, abdominal pain and distention, and tenesmus. Within 3 days, blood, pus, and mucus appear in the stools. The number of stools may increase to ≥ 20/day, and weight loss and dehydration become severe. If untreated, children may die in the first 12 days. If children survive, acute symptoms subside by the 2nd wk.
The hemolytic-uremic syndrome may complicate shigellosis due to S. dysenteriae type 1 in children. Secondary bacterial infections may occur, especially in debilitated and dehydrated patients. Severe mucosal ulcerations may cause significant acute blood loss. Patients (particularly those with the HLA-B27 genotype) may develop reactive arthritis (arthritis, conjunctivitis, urethritis) after shigellosis (and other enteritides).
Other complications are uncommon but include seizures in children, myocarditis, and, rarely, intestinal perforation. Infection does not become chronic and is not an etiologic factor in ulcerative colitis.
Diagnosis is facilitated by a high index of suspicion during outbreaks and in endemic areas and by the presence of fecal leukocytes on smears stained with methylene blue or Wright stain. Stool cultures are diagnostic and should be obtained; for severely ill or at-risk patients, antimicrobial sensitivity testing is done. In patients with symptoms of dysentery (bloody and mucoid stools), the differential diagnosis should include invasive Escherichia coli, Salmonella, Yersinia, and Campylobacter infections; amebiasis; Clostridium difficile infection, and viral diarrheas.
The mucosal surface, as seen through a proctoscope, is diffusely erythematous with numerous small ulcers. Although leukopenia or marked leukocytosis may be present, WBC count averages 13,000/μL. Hemoconcentration is common, as is diarrhea-induced metabolic acidosis.
Fluid loss is treated symptomatically with oral or IV fluids (see Intravenous Fluid Resuscitation). Antidiarrheal drugs (eg, loperamide) may prolong illness and should not be used. Antibiotics can reduce the symptoms and shedding of Shigella but are not necessary for healthy adults with mild illness. However, certain patients, including the following, should usually be treated:
For adults, a fluoroquinolone (such as ciprofloxacin 500 mg po q 12 h for 3 to 5 days), azithromycin 500 mg po on day 1 and 250 mg once/day for 4 days, or ceftriaxone 2 g/day IV for 5 days. Many Shigella isolates are likely to be resistant to ampicillin, trimethoprim/sulfamethoxazole (TMP/SMX), and tetracyclines.
Hands should be washed thoroughly before handling food, and soiled garments and bedclothes should be immersed in covered buckets of soap and water until they can be boiled. Appropriate isolation techniques (especially stool isolation) should be used with patients and carriers.
A live oral vaccine is being developed, and field trials in endemic areas hold promise. However, immunity is generally type specific.
Last full review/revision February 2014 by Larry M. Bush, MD; Maria T. Perez, MD
Content last modified March 2014