Infectious Disease and Microbiology – Shigellosis

Shigellosis is an acute bacterial intestinal infection caused by Shigella species. Clinical disease ranges from mild watery diarrhea to severe inflammatory dysentery characterized by bloody, mucoid stools, abdominal cramps, fever, and tenesmus.

Shigella organisms are small, gram-negative, nonmotile, non-spore-forming facultative anaerobic bacilli belonging to the Enterobacterales. They are highly adapted to humans, who constitute the major reservoir.

The four major species are Shigella sonnei, S. flexneri, S. dysenteriae, and S. boydii.

S. sonnei predominates in many higher-income countries, whereas S. flexneri remains an important cause in lower-resource settings. S. dysenteriae type 1 is particularly important because it produces Shiga toxin and has historically caused severe epidemic dysentery.

Transmission occurs predominantly by the fecal–oral route, either directly from person to person or indirectly through contaminated food, water, hands, or fomites.

An important microbiologic characteristic of Shigella is its extremely low infectious dose. Ingestion of only a small number of organisms can produce disease. Consequently, person-to-person transmission can occur readily.

Important risk groups include young children, childcare attendees and workers, household contacts, travelers to areas with inadequate sanitation, people experiencing homelessness, residents of crowded institutions, and men who have sex with men (MSM).

Outbreaks are particularly associated with crowding, inadequate sanitation, poor access to clean water, childcare settings, institutions, and settings involving close person-to-person contact.

After ingestion, Shigella survives passage through the stomach and reaches the intestine. The organisms primarily infect the colon, invading the intestinal epithelium and producing an intense inflammatory response.

Shigella penetrates the colonic mucosa, multiplies intracellularly, and spreads from cell to cell. The resulting epithelial destruction, ulceration, and intense neutrophilic inflammation account for the characteristic blood, mucus, and leukocytes in the stool.

S. dysenteriae type 1 produces Shiga toxin, which inhibits protein synthesis by targeting the 60S ribosomal subunit. Systemic effects of the toxin can contribute to hemolytic uremic syndrome (HUS).

The incubation period is usually approximately 1–3 days, although it can vary depending on the infecting strain and inoculum.

Illness frequently begins with fever, malaise, anorexia, abdominal cramps, and watery diarrhea. In more severe disease, the diarrhea subsequently becomes inflammatory and bloody.

The classic manifestation is bacillary dysentery: frequent passage of small-volume stools containing blood and mucus, accompanied by severe abdominal cramping and tenesmus.

Tenesmus is the painful and persistent sensation of needing to defecate despite an empty or nearly empty rectum. It reflects intense inflammation of the distal colon and rectum.

Physical examination may demonstrate fever, abdominal tenderness, hyperactive bowel sounds, and signs of dehydration. Severe disease may produce systemic toxicity.

Young children are particularly vulnerable to dehydration, electrolyte abnormalities, hypoglycemia, and neurologic complications.

Most uncomplicated cases are self-limited, but severe shigellosis can produce substantial fluid and electrolyte losses. Assessment of hydration status is therefore one of the most important components of initial evaluation.

When diagnostic testing is indicated, modern stool molecular testing or stool culture can identify Shigella. Culture remains particularly useful because an isolate can undergo antimicrobial susceptibility testing, which has become increasingly important because antimicrobial resistance is common.

Patients with bloody diarrhea, severe illness, fever with inflammatory diarrhea, immunocompromise, outbreak-associated disease, or significant epidemiologic/public-health implications are particularly likely to benefit from stool testing.

Fecal leukocytes or inflammatory markers can support the presence of inflammatory diarrhea but are not specific for shigellosis and generally do not establish the diagnosis.

Blood cultures are not routinely positive in uncomplicated disease. They may be appropriate in patients with severe systemic illness, suspected bacteremia, or significant immunocompromise.

Laboratory evaluation in severe cases may demonstrate metabolic acidosis, electrolyte abnormalities, renal dysfunction, or hypoglycemia. When HUS is suspected, the CBC, platelet count, peripheral blood smear, creatinine, and markers of hemolysis become particularly important.

Imaging is not routinely required for uncomplicated shigellosis. Abdominal imaging is reserved primarily for suspected complications such as toxic megacolon, intestinal obstruction, perforation, or another acute abdominal process.

The differential diagnosis of bloody inflammatory diarrhea includes Campylobacter, Salmonella, Shiga toxin-producing Escherichia coli (STEC), Yersinia enterocolitica, Clostridioides difficile, and Entamoeba histolytica, among other infectious and noninfectious causes.

Distinguishing Shigella from STEC can be especially important because antibiotic treatment is generally avoided in suspected STEC infection due to concern for an increased risk of HUS.

The foundation of treatment is fluid and electrolyte replacement. Oral rehydration is preferred whenever the patient can drink adequately, whereas severe dehydration or inability to tolerate oral fluids may require intravenous isotonic fluids.

Antibiotics are not automatically required for every mild case of shigellosis. They are particularly considered for severe disease, dysentery, immunocompromised patients, patients at increased risk of complications, and circumstances in which shortening fecal shedding may have important public-health benefits.

When antimicrobial therapy is indicated, treatment should increasingly be guided by local resistance patterns and, whenever possible, antimicrobial susceptibility testing.

Depending on susceptibility and clinical circumstances, treatment options can include azithromycin, ciprofloxacin, or ceftriaxone. However, resistance to several traditional agents has become increasingly important, and empiric choices should therefore reflect current local and public-health recommendations.

Multidrug-resistant and extensively drug-resistant (XDR) Shigella have emerged in multiple regions. Resistance can involve ampicillin, trimethoprim-sulfamethoxazole, fluoroquinolones, azithromycin, and third-generation cephalosporins, making microbiologic diagnosis and susceptibility testing particularly valuable in severe or persistent disease.

Antimotility medications such as loperamide and diphenoxylate should generally be avoided in bloody or severe inflammatory diarrhea, because slowing intestinal transit can potentially worsen invasive disease or delay pathogen clearance.

Children with diarrhea should continue appropriate feeding and nutritional support rather than undergoing unnecessary dietary restriction. In settings where recommended for childhood acute diarrhea, zinc supplementation can reduce the duration and severity of diarrheal illness.

Hospitalization may be necessary for patients with severe dehydration, inability to maintain oral intake, significant electrolyte or metabolic abnormalities, severe systemic toxicity, HUS, seizures or encephalopathy, toxic megacolon, or other major complications.

One of the most important complications is hemolytic uremic syndrome, particularly associated with Shiga-toxin-producing S. dysenteriae type 1.

HUS is characterized by the classic triad of:

Microangiopathic hemolytic anemia + thrombocytopenia + acute kidney injury.

Neurologic manifestations, particularly seizures, can occur in young children with severe shigellosis. Fever, electrolyte abnormalities, hypoglycemia, and encephalopathy may contribute.

Severe colonic inflammation and tenesmus can occasionally cause rectal prolapse, particularly in young children.

Other gastrointestinal complications include toxic megacolon, intestinal obstruction, colonic perforation, and severe colitis, although these are uncommon.

A delayed complication is reactive arthritis, classically involving asymmetric arthritis of the lower extremities following gastrointestinal infection. Susceptibility has historically been associated with HLA-B27, although reactive arthritis can occur without it.

Prevention centers on meticulous hand hygiene, safe food preparation, adequate sanitation, safe drinking water, and preventing fecal contamination of food and environmental surfaces.

Because shigellosis is highly transmissible, infected individuals should avoid preparing food for others while infectious. Special occupational or return-to-childcare requirements may apply to food handlers, healthcare workers, childcare workers, and young children attending childcare, according to local public-health regulations.

Shigellosis is a notifiable disease in many jurisdictions, and suspected outbreaks require public-health involvement.

Most otherwise healthy patients recover completely. Prognosis becomes less favorable with severe dehydration, malnutrition, very young age, immunocompromise, HUS, encephalopathy, or severe colonic complications.

A useful clinical pattern to remember is:

Fecal–oral transmission + extremely low infectious dose → fever and watery diarrhea → bloody/mucoid small-volume stools + cramps + tenesmus = Shigellosis.

S. dysenteriae type 1 → Shiga toxin → HUS

Diagnosis → stool testing/culture + susceptibility testing when indicated

Treatment → rehydration first + selective susceptibility-guided antibiotics + avoid antimotility drugs in dysentery.