Shigellosis

The Pathogen

• Medical Microbiology 9e, p. 1961-2004

Epidemiology

• Transmission: predominantly fecal-oral, via person-to-person contact, fomites, contaminated food/water, and increasingly as an STI (especially in MSM)
• Extremely low infective dose: as few as 10 organisms for S. dysenteriae; 50-180 for other species - the lowest of any enteric pathogen
• ~80-165 million cases/year worldwide; ~150,000 deaths globally (GBD 2019), ~95,000 in children under 5
• Second most common cause of diarrheal death worldwide, after rotavirus; most common bacterial cause
• Accounts for 64% of dysentery cases attributable fraction
• In the US: ~500,000 cases/year; S. sonnei causes ~75-80% of US cases
• High-risk groups: children <5, elderly, residents of care homes/institutions, daycare attendees, MSM, travelers, immunocompromised patients
• Goldman-Cecil Medicine, p. 2069-2075

Pathogenesis

1. Shigella is acid-resistant, allowing survival through the stomach at a very low inoculum
2. Organisms are taken up by M (microfold) cells in the colonic epithelium (and ileal Peyer patches)
3. After proliferating within M cells, bacteria escape into the lamina propria, where they are phagocytosed by macrophages and induce apoptosis
4. The resultant inflammatory response damages surface epithelium, allowing Shigella in the lumen and lamina propria to access the basolateral surface of colonic epithelial cells - entry is far more efficient from the basolateral than the apical side
5. All Shigella spp. carry virulence plasmids encoding a Type III secretion system that injects bacterial proteins directly into the host cytoplasm
6. S. dysenteriae serotype 1 additionally produces Shiga toxin (Stx), which inhibits eukaryotic protein synthesis, causing host cell death and endothelial damage (mechanism for HUS)

• Robbins Pathologic Basis of Disease, p. 2916-2918

Morphology / Histopathology

• Most prominent in the left colon; ileum may also be involved (due to M-cell tropism over Peyer patches)
• Macroscopically: hemorrhagic, ulcerated mucosa; pseudomembranes may be present
• Histologically: early cases resemble acute self-limited colitis (e.g., Campylobacter colitis)
• Later: aphthous ulcers form over lymphoid follicles due to M-cell tropism
• Intraepithelial neutrophils are prominent (cryptitis/crypt abscesses)

Fig. 17.31 - Bacterial enterocolitis (Robbins Pathologic Basis of Disease). These panels illustrate patterns of acute colitis seen with enteric bacterial infections, including neutrophil infiltration, crypt abscesses, and mucosal erosion.

Clinical Features

• Crampy abdominal pain, fever, nausea/vomiting
• High-volume, non-bloody diarrhea

• Low-volume, grossly bloody diarrhea with mucus
• Tenesmus (painful urge to defecate)
• Fever, headache, myalgias
• Severe dehydration and circulatory collapse if untreated

• S. sonnei: high-volume watery diarrhea, fewer systemic signs - typically milder
• S. flexneri, S. dysenteriae, S. boydii: more likely to cause frank dysentery with severe systemic symptoms

• Rosen's Emergency Medicine, p. 1162-1165

Complications

Diagnosis

• Stool culture on selective media (e.g., MacConkey, XLD, Hektoen agar): >90% sensitivity in first 3 days; 75% after 1 week
• Multiplex PCR / NAATs (enteric panels): now considered the gold standard; detect Shigella directly and rapidly
• Stool microscopy: fecal leukocytes (WBCs in stool) are characteristic - useful screen
• Blood cultures: if bacteremia/sepsis is suspected
• Sigmoidoscopy: not routinely needed but shows friable, hyperemic, ulcerated mucosa

Treatment

• Oral rehydration salts (ORS) for mild-moderate dehydration
• IV fluids for severe dehydration or inability to tolerate oral intake

• All moderate-to-severe or dysenteric disease
• Immunocompromised patients
• Malnourished children
• Elderly patients
• Public health indications (food handlers, healthcare workers)
• Asymptomatic/recovering patients generally do not require antibiotics unless public health concerns apply

Antimicrobial resistance is a major and growing problem. Treatment should always be guided by local resistance patterns and in vitro susceptibility testing. Multidrug-resistant (MDR) and extensively drug-resistant (XDR) Shigella - particularly S. sonnei and S. flexneri - are increasingly reported globally.

• Rosen's Emergency Medicine, p. 1175-1178; Goldman-Cecil Medicine, p. 2100-2115

Prevention and Control

• Handwashing with soap is the single most effective preventive measure
• Safe water supply and sanitation
• Proper food handling; isolating infected food-handlers
• Infection control in institutional settings
• No licensed vaccine is currently available - though several are in clinical development (this remains a major global health gap)

Key Summary Points

• Shigellosis is the most common cause of bacillary dysentery worldwide
• Very low infective dose (as few as 10 organisms) makes it highly contagious
• Pathogenesis is through colonic epithelial invasion via M cells and Type III secretion
• Classic presentation: fever + watery diarrhea progressing to bloody diarrhea + tenesmus
• S. dysenteriae type 1 produces Shiga toxin and can cause HUS
• Diagnosis: stool culture or NAAT (multiplex PCR)
• Treatment: rehydration + antibiotics (fluoroquinolones or azithromycin; guided by susceptibility)
• Growing antimicrobial resistance is a major global threat

Shigellosis - Quick Overview

What causes it?

• Gram-negative bacteria: Shigella sonnei (mildest, common in developed countries), S. flexneri (developing countries), S. dysenteriae (most severe), S. boydii
• Spread by fecal-oral route - person to person, contaminated food/water, or sexually (MSM)
• Extremely contagious - as few as 10 organisms can cause infection

What are the symptoms?

• Fever + crampy abdominal pain
• Starts as watery diarrhea, progresses to bloody diarrhea with mucus
• Tenesmus (painful urge to pass stool)
• Nausea, vomiting, headache

Who gets it?

• Children under 5 are most vulnerable
• People in crowded/poor-sanitation settings, daycare centers, nursing homes

How is it treated?

• Rehydration (ORS or IV fluids) - most important
• Antibiotics (ciprofloxacin or azithromycin) for moderate-severe cases
• Avoid anti-diarrheal drugs like loperamide

Key danger

• S. dysenteriae type 1 produces Shiga toxin, which can cause Hemolytic Uremic Syndrome (HUS) - kidney failure, anemia, low platelets