Shigellosis¶
Chapter 172 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Shigella is a non-spore-forming, gram-negative bacillus causing bacillary dysentery, with four serogroups (A-D) and 150+ serotypes.
- Global burden: ~165 million cases annually (1966–1997), 69% in children <5 years; 500,000–1.1 million deaths/year, with declining mortality due to improved nutrition.
- Transmission via fecal-oral route, contaminated food/water, or person-to-person contact; multidrug resistance is a growing concern.
- Clinical features include watery diarrhea progressing to dysentery (bloody/mucopurulent stools), with complications like HUS, toxic megacolon, and postinfectious arthritis.
- Antibiotic treatment (ciprofloxacin, ceftriaxone, azithromycin) is recommended for all cases, with duration varying by Shigella type and patient status.
1. DEFINITION & OVERVIEW¶
Shigellosis is an acute bacterial infection caused by Shigella species, characterized by dysentery (inflammation of the colon with bloody stools). Discovered by Kiyoshi Shiga in 1897, Shigella differs from E. coli by being nonmotile, non-lactose fermenting, and lacking lysine decarboxylase. Four serogroups (A-D) are clinically significant, with S. dysenteriae type 1 causing the most severe disease.
Recommended Antimicrobial Therapy for Shigellosis¶
| ANTIMICROBIAL AGENT | CHILDREN | ADULTS | LIMITATIONS |
|---|---|---|---|
| Ciprofloxacin | 15 mg/kg 2 times/day for 3 days PO | 500 mg 2 times/day for 3 days PO | First-line; resistance emerging |
| Pivmecillinam | 20 mg/kg 4 times/day for 5 days PO | 100 mg 4 times/day for 5 days PO | Costly; emerging resistance |
| Ceftriaxone | 50–100 mg/kg once/day IM for 2–5 days | — | Efficacy not validated in adults |
| Azithromycin | 6–20 mg/kg once/day for 1–5 days PO | 1–1.5 g once/day for 1–5 days PO | Efficacy not validated |
1.1 Pathogenesis¶
Shigella invades colonic epithelial cells via a type III secretion system, inducing cytoskeletal rearrangements for intracellular survival. The 215-kb virulence plasmid encodes genes for invasion, toxin production (Shiga toxin in S. dysenteriae), and immune evasion. Shiga toxin inhibits protein synthesis in endothelial cells, contributing to hemolytic-uremic syndrome (HUS).
1.2 Clinical Phases¶
Four phases: incubation (1–4 days), watery diarrhea, dysentery (bloody stools), and postinfectious recovery. Severe cases may present with fever, dehydration, and systemic complications.
2. EPIDEMIOLOGY¶
Global burden: 165 million cases annually (1966–1997), 69% in children <5 years. Mortality: 500,000–1.1 million/year, declining due to improved nutrition. Endemic in developing countries (99% of cases), with outbreaks in daycare centers and refugee camps. S. dysenteriae type 1 causes severe epidemics, while S. sonnei is more common in industrialized nations.
2.1 Transmission¶
Fecal-oral route (hand-to-mouth), contaminated food/water, or flies in impoverished areas. Sexual transmission possible. High infectivity with minimal inoculum (100 CFU).
2.2 Risk Factors¶
Poor hygiene, malnutrition, immunocompromise, and overcrowding. Children <5 years and elderly are most vulnerable to severe complications.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Shigella species (A-D) are non-spore-forming, gram-negative rods. Key virulence factors: type III secretion system, Shiga toxin (S. dysenteriae), and plasmid-encoded genes for invasion. Pathogenesis involves epithelial cell invasion, cytokine release (IL-1 β , IL-8), and apoptosis of macrophages, leading to colonic inflammation and systemic complications.
3.1 Virulence Mechanisms¶
Type III secretion system injects effectors into host cells, enabling intracellular survival. Shiga toxin (A1-B5) binds to Gb3 receptors, inhibiting protein synthesis and causing endothelial damage. S. dysenteriae type 1 is most virulent.
3.2 Immune Response¶
NF- κ B activation drives pro-inflammatory cytokines (IL-1 β , IL-8), leading to neutrophil infiltration and epithelial barrier disruption. Caspase-1 activation contributes to pyroptosis and systemic inflammation.
4. CLINICAL FEATURES¶
Symptoms: fever, watery diarrhea progressing to dysentery (bloody/mucopurulent stools), abdominal cramps, tenesmus. Severe cases in malnourished children and elderly may present with dehydration, bacteremia, or toxic megacolon. Postinfectious complications include HUS, reactive arthritis (HLA-B27+), and neurological manifestations (toxic encephalopathy).
4.1 Complications¶
HUS (55–70% incidence): microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure. Toxic megacolon: colonic dilation, risk of perforation. Reactive arthritis: HLA-B27+ patients develop arthritis, ocular inflammation, and urethritis.
4.2 Mortality¶
42% mortality in children 1–4 years during S. dysenteriae type 1 epidemics. Mortality declines with improved nutrition and antibiotic use.
5. DIFFERENTIAL DIAGNOSIS¶
Distinguish from Salmonella, Campylobacter, E. coli, and parasites (E. histolytica). Consider inflammatory bowel disease (IBD) in industrialized countries. Key differentiators: Shigella presents with dysentery, while Salmonella often causes systemic symptoms. E. histolytica is diagnosed via stool microscopy (trophozoites).
5.1 Laboratory Differentiation¶
Stool microscopy: E. histolytica shows trophozoites with few PMNs; Shigella shows high PMN counts. Culture on selective media (Hektoen, Salmonella-Shigella agar) identifies non-lactose-fermenting colonies.
6. INVESTIGATIONS & DIAGNOSIS¶
Stool culture on selective media (Hektoen, xylose-lysine-deoxycholate) is the gold standard. Molecular methods (PCR, mass spectrometry) are emerging. Serotyping and genome sequencing aid in outbreak tracking. Shiga toxin detection via ELISA confirms S. dysenteriae type 1.
6.1 Diagnostic Criteria¶
Clinical suspicion (dysentery, recent travel to endemic areas) + stool culture confirmation. PCR for virulence genes (ipA, ipB, ipC) or Shiga toxin detection in severe cases.
7. MANAGEMENT & TREATMENT¶
Antibiotics (ciprofloxacin, ceftriaxone, azithromycin) reduce duration and complications. Public health measures: isolation, hygiene education, and outbreak control. Resistance to first-line agents is widespread; second-line agents are used in resistant cases. Treatment duration: 3–10 days depending on Shigella type and patient status.
7.1 Antibiotic Resistance¶
Multidrug resistance due to plasmid-mediated gene transfer. Fluoroquinolone resistance (87% in US, 5% in India) necessitates alternative regimens. Resistance to ampicillin, trimethoprim-sulfamethoxazole, and tetracycline is common.
7.2 Supportive Care¶
Oral rehydration therapy for dehydration. Avoid loperamide in severe cases. Monitor for HUS and toxic megacolon requiring hospitalization.
8. PROGNOSIS & COMPLICATIONS¶
Most cases resolve within 1 week with treatment. Mortality: 5–10% in severe cases, higher in malnourished children. Long-term complications: stunted growth, chronic arthritis, and renal damage in HUS survivors. Postinfectious complications may persist for months.
8.1 Long-Term Outcomes¶
Malnourished children face stunted growth and chronic malnutrition. HUS survivors may develop chronic kidney disease. Reactive arthritis can persist for years, requiring immunosuppressive therapy.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: No specific risks; treat with safe antibiotics. Pediatrics: Focus on hydration and nutrition. Elderly: Higher risk of complications; monitor for sepsis. Immunocompromised: Prolonged treatment (7–10 days) and resistance monitoring.
9.1 Public Health¶
Hygiene education, outbreak containment, and antibiotic stewardship are critical. Vaccines are under development but not yet available.
10. KEY POINTS & CLINICAL PEARLS¶
- Shigella is a leading cause of dysentery in developing countries. 2. Antibiotics reduce morbidity and mortality but resistance is widespread. 3. HUS and toxic megacolon are life-threatening complications requiring immediate intervention. 4. Hygiene and sanitation are key to prevention. 5. Treatment duration varies by Shigella type and patient risk factors.