Dysentery causes and management and approach
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Dysentery — Causes, Approach & Management
Definition
Dysentery is a diarrheal illness in which the stool contains an inflammatory exudate of polymorphonuclear leukocytes (PMNs), mucus, and blood. It results from invasion of the colonic mucosa by infectious pathogens. — Sleisenger and Fordtran's Gastrointestinal and Liver Disease
Causes
1. Bacillary Dysentery (Bacterial)
| Organism | Notes |
|---|---|
| Shigella spp. | Most classic cause; four species — S. dysenteriae (most severe), S. flexneri, S. sonnei (mildest, most common in developed countries), S. boydii |
| Enteroinvasive E. coli (EIEC) | Genetically closely related to Shigella; identical mechanism |
| Campylobacter jejuni | Common cause of dysentery syndrome |
| Salmonella spp. | Non-typhoidal, can cause bloody diarrhea |
| Yersinia enterocolitica | Particularly in children |
| Vibrio parahaemolyticus | Seafood-associated |
| STEC (EHEC) | Enterohemorrhagic E. coli (e.g., O157:H7); produces Shiga toxin; associated with HUS |
2. Protozoal Dysentery (Amebic)
| Organism | Notes |
|---|---|
| Entamoeba histolytica | Causes amebic colitis/dysentery; 15–33% of infected individuals develop dysentery; gradual onset over 3–4 weeks |
3. Other
- Trichuris trichiura (whipworm) at high worm loads can cause dysentery and rectal prolapse
Pathogenesis
Shigella (prototype bacillary dysentery):
- Triggers uptake via M cells in the colon
- Escapes macrophages by inducing apoptosis → intense inflammatory response
- Invades enterocytes basolaterally via macropinocytosis using a Type III Secretion System (T3SS)
- Spreads cell-to-cell via actin polymerization (IcsA protein)
- Releases ShET1/ShET2 toxins → watery first-phase diarrhea; S. dysenteriae 1 also produces Shiga toxin (Stx) → cytotoxicity, risk of HUS
- Result: focal ulcers, microabscesses, crypt abscesses, loss of goblet cells, mucosal destruction
Entamoeba histolytica: trophozoites invade colonic mucosa → flask-shaped ulcers; microscopically show erythrophagocytic trophozoites with few PMNs (unlike bacterial dysentery which shows abundant PMNs) — Harrison's Principles of Internal Medicine 22E
Clinical Features
Bacillary Dysentery (Shigella)
- Incubation: 1–3 days
- Phase 1: Watery, non-bloody diarrhea (enterotoxin-mediated)
- Phase 2 (classic dysentery): Frequent small-volume stools with blood, mucus, and pus; tenesmus; painful defecation
- Fever, abdominal cramps
- Usually 1–2 days until dysenteric phase (faster than amebic)
- Complications: Bacteremia (rare, <5%), HUS (S. dysenteriae type 1), toxic megacolon, reactive arthritis (Reiter syndrome), seizures in children (Ekiri syndrome)
Amebic Dysentery (E. histolytica)
- Incubation: 11–21 days (can be weeks)
- Gradual onset over 3–4 weeks
- Diarrhea with mucus ± visible/microscopic blood
- Fever present in a minority (unlike bacterial)
- Abdominal tenderness
- Complications: Toxic megacolon (0.5%), ameboma (mimics colon cancer), intussusception/perforation (especially children), amebic liver abscess
Diagnostic Approach
History & Examination
- Travel history (amebic if returning traveler, endemic area)
- Duration: rapid onset → bacterial; gradual 3–4 weeks → amebic
- Fever prominent → bacterial (especially Shigella); fever absent/mild → amebic
- Risk: MSM → Shigella; raw seafood → Vibrio/Salmonella
Investigations
| Test | Purpose |
|---|---|
| Stool microscopy | RBCs, WBCs (PMNs = bacterial); trophozoites with ingested RBCs = amebic |
| Stool culture | Gold standard for Shigella; use rectal swab for highest yield; media: MacConkey, Hektoen, XLD agar |
| Stool antigen assay (ELISA) | Preferred for E. histolytica |
| Multiplex PCR (FilmArray) | Rapid molecular diagnosis; increasingly standard |
| Sigmoidoscopy/colonoscopy | Flask-shaped ulcers (amebic) vs diffuse mucosal inflammation with ulcers (Shigella) |
| Blood culture | If toxic/septic; positive in <5% of Shigella, but important to obtain |
| CBC | Leukocytosis |
| Serology | Amebic serology useful for invasive amebiasis |
Fecal specimens are required for diagnosis, as other organisms can cause a dysentery syndrome (Campylobacter, V. parahaemolyticus, Salmonella). — Sleisenger and Fordtran's
Management
General Principles
- Rehydration (oral or IV depending on severity) is the cornerstone
- Avoid antidiarrheal agents (loperamide, opioids) in dysentery — they can worsen illness and increase complications — Jawetz, Melnick & Adelberg's Medical Microbiology
- Fever management (antipyretics)
Bacillary Dysentery (Shigellosis)
Antibiotic treatment is recommended for severe infections and to prevent secondary spread. Antimotility agents are contraindicated. — Jawetz
| Setting | Drug of Choice | Alternative |
|---|---|---|
| Adults (uncomplicated) | Ciprofloxacin 500 mg BID × 3 days | Azithromycin 500 mg × 3 days |
| Severe/hospitalized | IV ciprofloxacin; ceftriaxone | — |
| Multidrug-resistant (MDR) | Azithromycin; cefixime | Pivmecillinam |
| Children | Azithromycin (where fluoroquinolone resistance is high) | Ceftriaxone |
| Pregnancy | Ceftriaxone | Azithromycin |
Resistance note: Increasing resistance to ampicillin, TMP-SMX, nalidixic acid is widespread. Fluoroquinolone resistance emerging in Asia and spreading globally. Susceptibility testing is essential when available. — Harrison's Principles of Internal Medicine 22E
Empirical antibiotics should be guided by local resistance patterns.
Amebic Dysentery (E. histolytica)
Metronidazole plus a luminal amebicide is the treatment of choice. — Katzung's Basic and Clinical Pharmacology 16th ed.
| Step | Drug | Dose |
|---|---|---|
| Tissue amebicide (kills invasive trophozoites) | Metronidazole | 500–750 mg TID × 7–10 days |
| Luminal amebicide (eliminates gut cyst carriage — mandatory to prevent relapse) | Iodoquinol OR Paromomycin | Iodoquinol 650 mg TID × 20 days; Paromomycin 500 mg TID × 7 days |
| Alternative tissue amebicide | Tinidazole | 2 g/day × 3–5 days |
- Metronidazole alone is insufficient — luminal agent must always be added
- Tetracyclines and erythromycin are alternatives for moderate colitis but are NOT effective against extraintestinal disease
- Amebic liver abscess: metronidazole ± drainage (usually not required)
Empirical Approach to Dysentery in Clinical Practice
Bloody diarrhea + fever + PMNs in stool
↓
Send stool cultures, PCR panel, stool microscopy
↓
Is patient TOXIC / IMMUNOCOMPROMISED / SEVERE?
YES → Empirical antibiotics (ciprofloxacin ± ceftriaxone IV)
NO → Await cultures; hydrate
↓
Travel history / insidious onset / trophozoites in stool?
YES → Consider amebic dysentery → metronidazole + luminal amebicide
NO → Bacterial dysentery (Shigella most likely)
Empirical antibiotic therapy is considered in patients with fever, toxic appearance, or dysentery. — Rosen's Emergency Medicine
Key Differentiating Points: Bacillary vs Amebic Dysentery
| Feature | Bacillary (Shigella) | Amebic (E. histolytica) |
|---|---|---|
| Onset | Rapid (1–2 days) | Gradual (3–4 weeks) |
| Fever | Prominent | Mild/absent in most |
| Stool microscopy | Many PMNs | Erythrophagocytic trophozoites, few PMNs |
| Complications | HUS, bacteremia | Liver abscess, toxic megacolon |
| Treatment | Antibiotics (fluoroquinolone/azithromycin) | Metronidazole + luminal amebicide |
Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease; Harrison's Principles of Internal Medicine 22E; Goldman-Cecil Medicine; Katzung's Basic and Clinical Pharmacology 16th ed.; Jawetz, Melnick & Adelberg's Medical Microbiology; Rosen's Emergency Medicine
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