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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 is supportive, mostly with rehydration; antibiotics (eg, ampicillin, trimethoprim/sulfamethoxazole) are optional.
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, B, C, and D, which are 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. Direct spread is by the fecal-oral route. Indirect spread is by contaminated food and fomites. Flies serve as vectors. 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.
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.
Complications:
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
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's stain. Stool cultures are diagnostic and should be obtained. In patients with symptoms of dysentery (bloody and mucoid stools), the differential diagnosis should include invasive Escherichia coli, Salmonella, Yersinia, and Campylobacter infections; amebiasis; 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, it averages 13,000/μL. Hemoconcentration is common, as is diarrhea-induced metabolic acidosis.
Treatment
Fluid loss is treated symptomatically with oral or IV fluids (see discussed in Shock and Fluid Resuscitation: Intravenous Fluid Resuscitation). 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, or TMP/SMX one double-strength tablet q 12 h is the treatment of choice. For children, treatment is TMP/SMX 4 mg/kg (of the TMP component) po q 12 h. Many Shigella isolates are likely to be resistant to ampicillin and tetracycline.
Prevention
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 August 2009 by Burke A. Cunha, MD
Content last modified February 2012
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