Shigellosis (Bacillary Dysentery)
Summary
Shigellosis is an acute invasive intestinal infection caused by bacteria of the genus Shigella. Unlike Cholera (which is secretory), Shigellosis causes inflammatory colitis, leading to the classic triad of fever, abdominal cramps, and bloody diarrhoea (dysentery). It is notoriously highly infectious, with an infectious dose of as few as 10-100 organisms. The clinical spectrum ranges from mild watery diarrhoea (common in high-income countries with S. sonnei) to fulminant dysentery and HUS (common in low-income settings with S. dysenteriae).
Key Facts
- Definition: Acute bacterial colitis caused by Shigella species.
- Prevalence: 80-165 million cases annually worldwide; ~600,000 deaths.
- Mortality/Morbidity: Mortality is concentrated in children <5 years in developing nations.
- Key Management: Rehydration is paramount. Antibiotics shorten duration and reduce shedding but must be weighed against resistance.
- Critical Threshold: Development of HUS (Haemolytic Uraemic Syndrome) requires urgent nephrology input.
- Key investigation: Stool Culture is identifying; PCR is faster.
Clinical Pearls
The Infectious Dose: Shigella is the "special forces" of bacteria. While you need 100,000 Salmonella or 100,000,000 Cholera bacteria to get sick, you only need 10 Shigella organisms. This makes it spread like wildfire in daycares and households.
Neurotoxin Effect: S. dysenteriae type 1 produces Shiga Toxin (Stx), but all Shigella species can provoke seizures in children (known as "Ekiri" syndrome in Japan), often before the diarrhoea even starts.
Reiter's Triad: Remember "Can't see, can't pee, can't climb a tree." Shigellosis is a classic trigger for Reactive Arthritis (Urethritis/Cervicitis + Uveitis + Arthritis), particularly in HLA-B27 positive individuals.
Why This Matters Clinically
In the developed world, Shigella is a top cause of outbreaks in childcare centers and among men who have sex with men (MSM). In the developing world, it is a leading killer of children. Recognizing dysentery early allows for public health containment and appropriate antibiotic stewardship (as multidrug resistance is exploding).
Incidence & Prevalence
- Global: A major cause of childhood mortality in sub-Saharan Africa and South Asia.
- Developed World: Frequent focal outbreaks.
- Seasonality: Peaks in summer months (fly vectors) and rainy seasons (water contamination).
The Four Species (By Severity)
| Species | Group | Severity | Distribution |
|---|---|---|---|
| S. dysenteriae | Group A | Severe | Developing world. The epidemic killer. Produces Shiga Toxin. |
| S. flexneri | Group B | Moderate | Developing world. Commonest cause of endemic dysentery. |
| S. boydii | Group C | Mild-Mod | Rare. Mostly Indian subcontinent. |
| S. sonnei | Group D | Mild | Developed world (UK/USA). Watery diarrhoea, often no blood. |
Mneumonic: "Dirty Fingers Bring Shigella" (Group A, B, C, D)
Demographics
- Age: Peak incidence in children 1-4 years (fecal-oral hygiene difficulty).
- Sex: Equal in children. In adults, MSM (Men who have Sex with Men) have disproportionately high rates due to oro-anal contact.
Risk Factors
Modifiable:
- Sanitation: Poor water supply, lack of latrines.
- Hygiene: Poor handwashing (fecal-oral).
- Crowding: Refugee camps, daycare centres, barracks.
- Sexual behaviour: Oro-anal contact.
| Risk Factor | Mechanism |
|---|---|
| Travel | Exposure to endemic Group A/B strains. |
| MSM | Direct transmission of multidrug resistant strains. |
| Achlorhydria | Reduced stomach acid lowers infectious dose even further (PPI use). |
Mechanism: The "Rocket" Invasion
Shigella is non-motile (no flagella) outside cells, but highly motile inside cells.
Step 1: Acid Resistance
- Shigella survives pH 2.5 in the stomach, explaining the incredibly low infectious dose.
Step 2: M-Cell Entry (The Trojan Horse)
- In the colon, Shigella targets M-cells (Microfold cells) overlying Peyer's patches.
- It crosses the epithelium via M-cells to reach the sub-epithelial macrophage.
Step 3: Macrophage Apoptosis
- Once eaten by a macrophage, Shigella escapes the vacuole and triggers macrophage apoptosis (cell death).
- This releases IL-1beta, triggering massive inflammation (recruiting neutrophils).
Step 4: Basolateral Invasion
- Released from the dead macrophage, Shigella attacks the intestinal epithelial cells from underneath (basolateral side), which is less protected than the luminal side.
Step 5: Actin Polymerization (The Rocket)
- Inside the cell, Shigella uses a protein (IcsA) to hijack the host cell's actin cytoskeleton.
- It builds an "actin tail" that propels it like a rocket through the cytoplasm and punches through the cell wall into the adjacent cell.
- This cell-to-cell spread allows it to evade the immune system and destroy the mucosa, creating ulcers (bloody stool).
Shiga Toxin (Stx) Mechanism
- Produced primarily by S. dysenteriae type 1.
- Action: Cleaves ribosomal RNA, halting protein synthesis.
- Target: Endothelial cells of the glomerulus (kidney) and brain.
- Result: HUS (kidney failure, low platelets, hemolytic anaemia).
Symptoms
Typical Presentation (The "Dysentery Phase"):
Atypical/Complicated:
Signs
Red Flags
[!CAUTION] Red Flags — Seek immediate help if:
- Oliguria/Anuria: Failure to pass urine (Signs of Acute Kidney Injury/HUS).
- Pallor + Bruising: Signs of HUS (Haemolysis + Thrombocytopenia).
- Rigid Abdomen: Toxic Megacolon or Perforation.
- Altered Mental Status: Seizure or metabolic derangement.
Structured Approach
General:
- Dehydration Assessment: This is the priority.
- Mild: Thirsty, alert.
- Moderate: Irritable, sunken eyes, skin pinch goes back slowly.
- Severe: Lethargic, weak pulse, skin pinch goes back very slowly (>2s).
Abdominal:
- Distension: Check for Toxic Megacolon (rare but fatal).
- Bowel Sounds: Usually hyperactive (tinkling) in gastroenteritis, absent in ileus/megacolon.
Neurological:
- Check for neck stiffness (Ekiri syndrome can mimic meningitis).
Special Tests
- Stool Inspection: Is it "currant jelly"? Is it frank blood? Melaena? (Shigella is usually fresh blood mixed with mucus).
Laboratory Tests
| Test | Expected Finding | Purpose |
|---|---|---|
| FBC | Leukocytosis with "left shift". | Marked neutrophil response to bacterial invasion. |
| U&E / Creatinine | Hypokalaemia, Elevated Urea/Cr. | Monitor dehydration and screen for HUS. |
| CRP | High (>00). | Differentiates invasive colitis from viral GE. |
| Blood Culture | Often Negative. | Shigella bacteraemia is rare (unlike Salmonella) but fatal. |
Stool Studies (The Gold Standard)
- Culture: Gold standard. Requires selective media (MacConkey or XLD agar).
- PCR (Multiplex): Now common. Detects ipaH gene. Highly sensitive, results in hours.
- Microscopy: Faecal leukocytes (Poly-morphs) are abundant. If you see RBCs but NO leukocytes, think Amoeba (Entamoeba histolytica), not Shigella.
Imaging
Not routinely indicated.
- Abdominal X-ray: If toxic megacolon suspected (dilated transverse colon >6cm).
- CT Abdomen: If considering appendicitis or perforation (wall thickening prominent).
Diagnostic Criteria
Haemolytic Uraemic Syndrome (HUS) Triad:
- Microangiopathic Haemolytic Anaemia (Low Hb, Schistocytes on film).
- Thrombocytopenia (Low Platelets).
- Acute Kidney Injury (High Creatinine).
Management Algorithm
(See Section 2 for ASCII)
Conservative Management (Mild/S. sonnei)
Rehydration is the cornerstone.
- Oral Rehydration Solution (ORS): WHO formula (low osmolarity).
- Zinc supplementation: In children <5 years, reduces duration and severity.
- Antimotility Agents (Loperamide): CONTRAINDICATED. Slowing the gut retains the toxin and bacteria, increasing risk of toxic megacolon and HUS.
Medical Management (Antibiotics)
Indicated for Dysentery, Immunocompromise, or Public Health control.
| Drug Class | Drug | Dose (Adult) | Considerations |
|---|---|---|---|
| Fluoroquinolone | Ciprofloxacin | 500mg BD x 3 days | First line. Resistance is rising. |
| Macrolide | Azithromycin | 500mg OD x 3 days | First line for children (Cipro safety debate). |
| Cephalosporin | Ceftriaxone | 1-2g IV OD | For severe inpatient illness/sepsis. |
| Trimethoprim | TMP-SMX | Resistance widespread | Rarely used now unless sensitivity proven. |
Note on Resistance: Multi-drug resistant (MDR) and Extensively Drug Resistant (XDR) S. sonnei is spreading in MSM communities globally. Always check sensitivity.
Public Health Management
- Notification: Shigellosis is a Notifiable Disease in most jurisdictions (UK/USA/AUS).
- Exclusion:
- General: Stay home until 24-48h symptom free.
- High Risk (Food handlers, Healthcare, Childcare): "Clearance" samples (2 negative stool samples 24h apart) often required before return to work.
Disposition
- Admit if: Severe dehydration, inability to tolerate oral fluids (vomiting), confusion/seizure, bloody stools in infant.
- Discharge if: Tolerating ORS, vitals stable.
Immediate
- Dehydration/Shock: Hypovolaemic or Septic.
- Seizures: Febrile or Toxin-mediated.
- Rectal Prolapse: Common in children due to severe tenesmus.
Early (Days)
- Haemolytic Uraemic Syndrome (HUS): Occurs in ~10-15% of S. dysenteriae type 1 cases. Leading cause of acute renal failure in children globally.
- Toxic Megacolon: Colonic dilation + sepsis. High perforation risk.
- Intestinal Perforation: Rare.
Late (Weeks)
- Reactive Arthritis (Reiter's Syndrome):
- Triad: Arthritis, Uveitis, Urethritis.
- Occurs 2-4 weeks post infection.
- Strong HLA-B27 association.
- Post-Infectious IBS: Chronic functional bowel disturbance.
Natural History
- Without antibiotics, illness lasts 7-10 days.
- With antibiotics, fever resolves in 1 day, diarrhoea in 2-3 days.
- Shedding stops quickly (days) with treatment vs weeks without.
Outcomes
- Mortality: <1% in treated cases. Up to 15-20% in untreated S. dysenteriae type 1 pandemics.
- Kidney Function: Most recover from HUS, but 3-5% develop End Stage Renal Disease (ESRD).
Key Guidelines
- IDSA (Infectious Diseases Society of America) — Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea.
- WHO (World Health Organization) — Guidelines for the control of shigellosis. Focuses on developing world outbreaks.
Landmark Papers
The Vietnam/Thailand Studies (Fluoroquinolones)
- Established Ciprofloxacin as superior to Ampicillin/TMP-SMX in the 1990s.
- Clinical Impact: Shifted global first-line therapy.
Holt et al. (2012) - Genomic Epidemiology
- Tracking the spread of MDR Shigella sonnei.
- Key finding: Global spread of MDR strains is separate from local endemic strains.
Evidence Strength
| Intervention | Level | Key Evidence |
|---|---|---|
| Oral Rehydration | 1a | Universal consensus (WHO) |
| Antibiotics for Dysentery | 1a | Cochrane reviews (shortens illness by ~2.5 days) |
| Loperamide Avoidance | 2b | Observational studies linking to adverse outcomes |
What is Shigellosis?
Shigellosis is a gut infection caused by Shigella bacteria. It is sometimes called "dysentery." It causes severe inflammation in the bowel, leading to diarrhoea that often contains blood or slime (mucus), along with fever and bad stomach cramps.
How did I get it?
It is incredibly contagious. You only need to swallow a microscopic amount of invisible germs to get sick. You usually get it from:
- Touching surfaces (door handles, toys) touched by an infected person.
- Eating food prepared by someone who didn't wash their hands well.
- Drinking contaminated water.
- Changing nappies.
How is it treated?
- Fluids: The most important thing is to drink plenty of fluids (water, rehydration salts) to replace what you are losing.
- Antibiotics: Unlike mild food poisoning, we often give antibiotics for Shigella to help you recover faster and stop you spreading it to others.
- Hygiene: You must be fastidious about hand washing. Do not prepare food for others.
What to expect
- You will feel wretched for a few days with cramps and needing to rush to the toilet.
- With antibiotics, you should feel better within 48 hours.
- You must stay off work/school until 48 hours after the last episode of diarrhoea.
When to seek help
- If there is a lot of blood in the poo.
- If you cannot keep fluids down.
- If a child becomes very pale and stops peeing (signs of kidney problems).
Primary Guidelines
- Shane AL et al. 2017 Infectious Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea. Clin Infect Dis. 2017;65(12):e45-e80. PMID: 29194529
- World Health Organization. Guidelines for the control of shigellosis, including epidemics due to Shigella dysenteriae type 1. WHO; 2005.
Key Trials
- Christopher PR et al. Antibiotic therapy for Shigella dysentery. Cochrane Database Syst Rev. 2010;(8):CD006784. PMID: 20687081
Further Resources
- CDC: Shigella - Shigellosis
- UK Health Security Agency: Shigella: guidance, data and analysis
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.