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:
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.
An episode of shigellosis imparts serotype-specific immunity for at least several years. But patients may have additional episodes of shigellosis caused by other serotypes.
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.
The incubation period for Shigella 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. Fever may be present.
In adults, initial symptoms of shigellosis may be
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 weeks. Significant dehydration and electrolyte loss with circulatory collapse and death occur mainly in debilitated adults and children < 2 years.
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 hours.
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 week.
The hemolytic-uremic syndrome may complicate shigellosis due to S. dysenteriae type 1 in children.
Bacteremia may occur, especially in children under 5 years of age and in adults over 65 with underlying disease.
Severe mucosal ulcerations may cause significant acute blood loss.
Patients (particularly those with the human leukocyte antigen [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 of shigellosis 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 enterohemorrhagic E. coli, Salmonella, Yersinia, and Campylobacter infections; amebiasis; and Clostridium difficile infection.
The mucosal surface, as seen through a proctoscope, is diffusely erythematous with numerous small ulcers. Although leukopenia or marked leukocytosis may be present, white blood cell count averages 13,000/mcL (13 × 109/L). Hemoconcentration is common, as is diarrhea-induced metabolic acidosis.
Fluid loss due to shigellosis is treated symptomatically with oral or IV fluids.
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, the following antibiotic regimens may be used:
For children, the following antibiotic regimens may be used:
Many Shigella isolates are likely to be resistant to ampicillin, trimethoprim/sulfamethoxazole (TMP/SMX), and tetracyclines, but patterns of resistance vary by geographic region.
Hands should be washed thoroughly before handling food. Soiled garments and bedclothes should be immersed in covered buckets of soap, water, and disinfectant until they can be washed in hot water. 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 so presumably the vaccine would need to be polyvalent or contain an antigen common to multiple serotypes.
Shigella species are a highly contagious cause of dysentery; humans are the only reservoir.
Watery diarrhea may be accompanied by abdominal pain and marked urgency to defecate; stools may contain mucus, pus, and often blood.
S. dysenteriae type 1 (not common in the US, except in returning travelers) produces Shiga toxin, which may cause hemolytic-uremic syndrome.
Significant dehydration and electrolyte loss with circulatory collapse and death occur mainly in debilitated adults and children < 2 years.
Supportive care is usually adequate, but give antibiotics (a fluoroquinolone, azithromycin, ceftriaxone) to young children and to older, debilitated, or severely ill patients; resistance to ampicillin, trimethoprim/sulfamethoxazole (TMP/SMX), and tetracyclines is common.
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