Shigellosis is an acute infection of the intestine caused by the gram-negative Shigella
The genus Shigella is distributed worldwide. It is the typical cause of inflammatory dysentery, which causes 5 to 20% of diarrheal illness in many areas (1).
Each year in the United States, there are approximately 450,000 cases (5.7/100,000 people) of shigellosis, leading to 5,400 hospitalizations and 38 deaths. Children < 5 years of age have the highest rate of infection (2). Worldwide,Shigellacauses an estimated 80 to 165 million cases and 600,000 deaths yearly, with most cases and deaths in children (1).
Shigella is divided into 4 major subgroups:
A (S. dysenteriae)
B (S. flexneri)
C (S. boydii)
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 United States (3).
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. Sexual transmission is also known to occur between men who have sex with men (4).
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 young 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 United States, except in travelers returning from endemic areas) produces Shiga toxin, which causes marked watery diarrhea and sometimes hemolytic-uremic syndrome.
References
1. Centers for Disease Control and Prevention: Shigellosis: CDC Yellow Book 2024. Accessed January 25, 2024.
2. Centers for Disease Control and Prevention: AboutShigellaInfection. Accessed January 25, 2024.
3. Shad AA, Shad WA. Shigella sonnei: virulence and antibiotic resistance.Arch Microbiol. 2021;203(1):45-58. doi:10.1007/s00203-020-02034-3
4. McNeil CJ, Kirkcaldy RD, Workowski K. Enteric Infections in Men Who Have Sex With Men.Clin Infect Dis. 2022;74(Suppl_2):S169-S178. doi:10.1093/cid/ciac061
Symptoms and Signs of Shigellosis
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
Episodes of gripping abdominal pain
Urgency to defecate (tenesmus)
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 weeks. Significant dehydration and electrolyte loss with circulatory collapse and death occur mainly in adults with immunocompromise 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 second week.
Complications of shigellosis
Hemolytic-uremic syndrome (HUS) may complicate shigellosis due to S. dysenteriae type 1 in children. HUS, if it occurs, develops about 7 days (but up to 3 weeks) after the first symptoms of shigellosis, when the diarrhea is resolving. HUS is signaled by the development of lethargy and decreasing urine output.
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 (mostly S. flexneri 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
Stool culture
Polymerase chain reaction (PCR) testing
1).
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 Clostridioides 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.
Diagnosis reference
1. Beal SG, Tremblay EE, Toffel S, Velez L, Rand KH. A Gastrointestinal PCR Panel Improves Clinical Management and Lowers Health Care Costs.J Clin Microbiol. 2017;56(1):e01457-17. Published 2017 Dec 26. doi:10.1128/JCM.01457-17
Treatment of Shigellosis
Supportive care
Fluid loss due to shigellosis is treated symptomatically with oral or IV fluids.
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:
Children
Older adults
Patients with immunocompromise
Patients with moderate to severe disease
For adults, the following antibiotics may be used:
For children, the following antibiotics may be used:
Many ShigellaS. sonnei and S. flexneri (1). Treatment of XDR shigellosis often requires a carbapenem but generally should be directed by infectious disease consultation.
Treatment reference
1. Centers for Disease Control and Prevention (CDC): Increase in Extensively Drug-Resistant Shigellosis in the United States, February 24, 2023.
Prevention of Shigellosis
Hands should be washed thoroughly before handling food. Soiled garments, sheets, and blankets 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.
Vaccines are being developed, and field trials in endemic areas hold promise (1). However, immunity is generally type specific, so presumably the vaccine would need to be polyvalent or contain an antigen common to multiple serotypes.
Prevention reference
1. MacLennan CA, Grow S, Ma LF, Steele AD. TheShigellaVaccines Pipeline.Vaccines (Basel). 2022;10(9):1376. Published 2022 Aug 24. doi:10.3390/vaccines10091376
Key Points
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 United States, 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 adults with immunocompromise and children < 2 years.
