Dysentery

Definition And Classification

Core Definition

• Presence of grossly visible blood in stools.
• Consequence of colonic mucosal infection by bacterial or amebic pathogens.
• Differentiated from acute watery diarrhea; denotes inflammatory enterocolitis.
• Frequent, small-volume mucoid stools.
• Accompanied by fever, abdominal pain, tenesmus (ineffectual defecation, straining, suprapubic discomfort).
• Clinically distinct from non-inflammatory bloody diarrhea (larger volume, minimal systemic toxicity).

Primary Categories

• Bacillary Dysentery: Bacterial etiology; significantly more common in pediatric populations.
• Amebic Dysentery: Parasitic etiology; insidious onset; less frequent in children.

Etiology And Pathogens

Pathogen Category	Specific Organisms	Clinical Signatures
Bacterial (Bacillary)	Shigella species (S. dysenteriae, S. flexneri, S. boydii, S. sonnei)	Most common cause globally. S. flexneri dominates developing nations; S. dysenteriae causes severe epidemics.
	Enteroinvasive Escherichia coli (EIEC)	Genetically/clinically resembles Shigella; watery diarrhea progressing to dysentery.
	Enterohemorrhagic E. coli (EHEC)	Causes hemorrhagic colitis; massive bloody stools; high risk of hemolytic uremic syndrome (HUS).
	Salmonella (Nontyphoidal)	Fever, cramps, vomiting; prolonged shedding; risk of bacteremia in infants/immunocompromised.
	Campylobacter jejuni	High fever, severe abdominal pain mimicking appendicitis; aphthoid ulcers on endoscopy.
	Yersinia enterocolitica	Prolonged symptoms; pseudoappendicitis (right lower quadrant pain); exudative pharyngitis.
	Clostridioides difficile	Post-antibiotic onset; pseudomembranous colitis.
Parasitic (Amebic)	Entamoeba histolytica	Insidious onset; causes deep flask-shaped mucosal ulcers; potential extraintestinal dissemination (liver abscess).
Viral	Adenovirus (types 11 & 21)	Rare cause of dysentery; typically seen in immunocompromised hosts.

Pathophysiology

Mechanisms Of Mucosal Invasion

• Pathogens traverse intestinal epithelial barrier.
• Shigella pathogenesis: Invades M cells, utilizes cell-cell and basolateral invasion.
• Induces macrophage apoptosis, releasing interleukin-1β (IL-1β) and IL-8.
• Triggers massive polymorphonuclear leukocyte (neutrophil) transmigration.
• Disrupts tight junction proteins (claudin-1, ZO-1); dephosphorylates occludin.
• Epithelial barrier destruction creates microabscesses and frank mucosal ulcerations.

Toxin-Mediated Damage

• Enterotoxins induce secretory fluid loss early in disease course (watery diarrhea phase).
• Shiga toxin (S. dysenteriae type 1, EHEC): Inhibits cellular protein synthesis.
• Triggers endothelial damage, precipitating microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury (HUS).

Clinical Features

Acute Disease Progression

• Incubation period: Typically 1-5 days.
• Prodrome: High fever, malaise, anorexia, occasional vomiting.
• Initial phase: Watery, large-volume diarrhea.
• Dysenteric phase: Transition to frequent, small-volume stools mixed with overt blood and mucus.
• Abdominal examination: Diffuse tenderness, hyperactive or hypoactive bowel sounds.

Pathogen-Specific Manifestations

• Shigellosis: High fever >40°C, severe tenesmus, potential neurological manifestations (seizures).
• Amebiasis: Gradual, insidious onset; less prominent fever; right upper quadrant pain if liver abscess present.

Differential Diagnosis

Disease Category	Key Differentiating Features
Intussusception	Episodic severe colicky pain; red currant-jelly stools (blood and mucoid exudate); palpable right upper quadrant mass; target sign on ultrasound.
Cow Milk Protein Allergy	Occurs in infants; bloody loose stools; eczema; anemia; resolves with maternal dietary restriction or hypoallergenic formula.
Inflammatory Bowel Disease (IBD)	Chronic course (>2-4 weeks); weight loss; extraintestinal manifestations (aphthous ulcers, joint pains, erythema nodosum, iritis); family history.
Necrotizing Enterocolitis	Premature neonates; abdominal distension; feed intolerance; systemic hemodynamic instability; pneumatosis intestinalis on radiography.
Pseudomembranous Colitis	Recent broad-spectrum antibiotic exposure; C. difficile toxins A/B positive.
Vasculitides	Henoch-Schönlein purpura (palpable purpura, arthritis, hematuria); Hemolytic Uremic Syndrome (pallor, oliguria, petechiae).
Anal Fissure	Painful defecation; hard stools; blood streaking on stool exterior; visible mucosal tear.

Complications

Intestinal Complications

• Toxic Megacolon: Colonic dilation >6 cm; risk of imminent rupture; associated with Shigella, C. difficile, EHEC, E. histolytica.
• Intestinal Perforation: High mortality; free air under diaphragm on upright radiograph.
• Rectal Prolapse: Secondary to severe tenesmus and perineal muscle fatigue.
• Amebic Specific: Amebic appendicitis, colonic strictures, amebomas (granulomatous masses).

Extraintestinal Complications

• Renal: Hemolytic uremic syndrome (S. dysenteriae type 1, STEC).
• Neurological: Seizures, encephalopathy (Shigella, STEC).
• Rheumatologic: Reactive arthritis, erythema nodosum (Shigella, NTS, Campylobacter, Yersinia).
• Neuromuscular: Guillain-Barré syndrome (Campylobacter jejuni).
• Hepatic: Amebic liver abscess (E. histolytica).

Diagnostic Evaluation

Laboratory Investigations

• Complete Blood Count (CBC): Assess for leukocytosis, bandemia (leukemoid reaction in Shigella); evaluate smear for schistocytes (HUS screen).
• Metabolic Panel: Assess baseline renal function (BUN, Creatinine) and profound dyselectrolytemia (hypokalemia, metabolic acidosis).
• Fecal Biomarkers: Elevated fecal calprotectin or lactoferrin denotes mucosal inflammation.
• Stool Microscopy: Numerous polymorphonuclear leukocytes indicate invasive bacterial colitis. Pyknotic or absent leukocytes suggest amebic dysentery (amebae destroy neutrophils).

Microbiological Assays

• Stool Culture: Isolate Salmonella, Shigella, Campylobacter (requires microaerobic conditions, 42°C), Yersinia.
• Toxin Assays: C. difficile toxin A/B EIA, Glutamate Dehydrogenase (GDH) antigen test, NAAT.
• Molecular Panels: Multiplex PCR / Nucleic Acid Amplification Tests (NAAT) highly sensitive for rapid pathogen identification.
• Parasitology: Enzyme immunoassay (EIA) or PCR for E. histolytica; direct microscopy for trophozoites/cysts (requires minimum 3 separate samples).

Endoscopy And Histology (If Refractory or IBD Suspected)

• Campylobacter: Friable mucosa, aphthoid ulcers, crypt abscesses, neutrophilic infiltrate.
• Shigella: Patchy mucosal edema, loss of vascular pattern, pseudomembranes, crypt depletion.
• E. histolytica: Deep, flask-shaped ulcer craters covered with purulent necrotic material.

Management Protocol

Resuscitation And Supportive Care

• Hydration: Primary intervention. Utilize low-osmolarity Oral Rehydration Solution (ORS) for mild-moderate dehydration.
• Intravenous Therapy: Isotonic crystalloid fluid resuscitation (20 mL/kg bolus) mandated for shock, severe dehydration, or intractable vomiting.
• Nutritional Rehabilitation: Continue breastfeeding; institute early refeeding with age-appropriate unrestricted diet to repair mucosa.
• Zinc Supplementation: Administer 10-20 mg/day elemental zinc for 10-14 days. Reduces severity, duration, and prevents recurrence.
• Contraindications: Strictly avoid antimotility agents (loperamide, diphenoxylate). Prolong pathogen clearance, exacerbate tissue invasion, precipitate toxic megacolon/ileus.

Antimicrobial Pharmacotherapy

Bacillary Dysentery (Empiric and Directed)

• Do not delay therapy for culture results in toxic patients.
• Severe/Hospitalized Cases: Intravenous Ceftriaxone (50-100 mg/kg/day for 3-5 days) represents first-line empiric therapy.
• Stable/Outpatient Cases: Oral Azithromycin (10-12 mg/kg/day on day 1, followed by 5-6 mg/kg/day for 4 days) or Oral Cefixime.
• Fluoroquinolones: Ciprofloxacin (15 mg/kg/dose BID for 3 days) highly effective but restricted use in pediatrics unless alternative unavailable or pathogen sensitivity confirmed.
• Refractory Shigellosis: Adjust therapy based strictly on local resistance patterns and culture sensitivities.

Amebic Dysentery

• First-Line Tissue Agent: Metronidazole (15 mg/kg/day divided TID for 5-7 days) or Tinidazole (50 mg/kg single dose, max 2 g, for 3 days).
• Follow-up Luminal Agent: Mandatory eradication of colonized cysts post-metronidazole therapy to prevent relapse. Utilize Paromomycin (25-35 mg/kg/day divided TID for 7 days) or Iodoquinol.

Clostridioides difficile Colitis

• Immediate cessation of offending antibiotic.
• First-Line Therapy: Oral Metronidazole (30 mg/kg/day divided QID) or Oral Vancomycin (40 mg/kg/day divided QID for 10-14 days). Oral Vancomycin preferred for severe/fulminant disease.
• Recurrent/Refractory: Pulsed-tapered Oral Vancomycin, Fidaxomicin, or Fecal Microbiota Transplantation (FMT).