Bacillary and Amoebic Dysentery

Dysentery = Syndrome

Bloody, mucoid, painful diarrhea + tenesmus. 2 dominant causes differ in mechanism/stool/treatment.

Bacillary Dysentery (Shigellosis)

Organism: Shigella, non-motile Gram-negative rod, Enterobacteriaceae, genetically VERY close to E. coli. 4 species/serogroups: S. dysenteriae (A, MOST virulent/severe/epidemic), S. flexneri (B, commonest developing countries), S. boydii (C), S. sonnei (D, commonest industrialized countries, milder).

Pathogenesis: VERY LOW infective dose (10-100 organisms) — acid-resistant, survives gastric transit well. → efficient person-to-person/fomite spread, not just food/water. INVASIVE mechanism: M cells → colonic epithelium invasion → cell-to-cell spread (actin motility), NO bloodstream crossing needed. Contrast cholera’s non-invasive toxin-only mechanism. Invasion → intense inflammation, ulceration, micro-abscess → blood+mucus in stool (tissue destruction, not secretory).

S. dysenteriae type 1: + SHIGA TOXIN (AB toxin, inhibits protein synthesis via ribosomal RNA cleavage). SAME family as STEC’s Shiga-like toxin. → uniquely severe disease + HUS association.

Clinical: incubation 1-3d. Watery diarrhea+fever → dysenteric phase (frequent small-volume blood/mucus stool + severe cramping + TENESMUS). Complications: toxic megacolon, perforation, HUS (S. dysenteriae type 1 specific: microangiopathic hemolytic anemia+thrombocytopenia+AKI), occasional seizures (children).

Amoebic Dysentery

Organism: E. histolytica. Ingestion of quadrinucleate cysts → excyst small intestine → trophozoites colonize colon. Disease ONLY if trophozoites INVADE (most = asymptomatic cyst-passer/carrier). Invasion needs virulence factors (Gal/GalNAc lectin adherence, cysteine proteases) + host factors (not fully understood). FLASK-SHAPED ULCERS (narrow at surface, wide in submucosa) via DIRECT CYTOLYSIS — different mechanism from Shigella’s invasion-inflammation cascade.

Clinical: more GRADUAL onset, LESS systemic toxicity/fever than shigellosis (imperfect but real bedside clue). Stool: “ANCHOVY SAUCE” (blood+mucus, less watery) vs bacillary’s more watery-bloody — unreliable distinction alone, need lab confirmation. Key complication: AMOEBIC LIVER ABSCESS (own topic) — trophozoites enter portal vein from invaded ulcer.

Comparison Table

Laboratory Diagnosis

Stool microscopy: fecal leukocytes+RBC (bacterial/invasive process, general). MOTILE TROPHOZOITES WITH INGESTED RBC (erythrophagocytosis) on FRESH WARM wet mount = classic amoebiasis finding. Shigella NOT directly visualized on wet mount, needs culture.

Stool culture (MacConkey, XLD, Hektoen): Shigella = non-lactose-fermenting, NON-MOTILE (unusual for Enterobacteriaceae — useful distinguisher). Serogrouping by slide agglutination.

Stool antigen (ELISA, E. histolytica-specific) + PCR: distinguishes pathogenic E. histolytica from morphologically IDENTICAL non-pathogenic E. dispar (microscopy CANNOT distinguish these) — increasingly preferred for amoebiasis.

Treatment

Shigellosis: fluids + antibiotics (azithromycin, ciprofloxacin, ceftriaxone per resistance) — antibiotics GENUINELY shorten illness + reduce transmission (unlike most bacterial diarrheas where supportive care suffices) — reflects low dose/high transmissibility.

Amoebic dysentery: TWO-DRUG sequence —

1. Metronidazole/tinidazole (tissue-active, kills invasive trophozoites)
2. THEN luminal agent (paromomycin or diloxanide furoate, clears residual cysts tissue drug doesn’t reach) Skipping step 2 → asymptomatic but still cyst-shedding = public health transmission risk.

Dysentery as a Syndrome

Dysentery — bloody, mucoid, painful diarrhoea with tenesmus — is a syndrome, not a diagnosis, and the two dominant causes, bacillary dysentery (shigellosis) and amoebic dysentery, differ enough in mechanism, stool appearance, and treatment that distinguishing them matters directly for management, even though both present with the same core symptom triad.

Bacillary Dysentery (Shigellosis)

The Organism

Shigella is a non-motile, Gram-negative rod of the Enterobacteriaceae, genetically extremely close to E. coli (close enough that some taxonomists consider them the same species by strict genomic criteria, though clinical practice retains the separate genus) — four species/serogroups exist: S. dysenteriae (serogroup A, the most virulent, producing the most severe disease and epidemic potential), S. flexneri (serogroup B, the commonest cause in developing countries), S. boydii (serogroup C), and S. sonnei (serogroup D, the commonest cause in industrialized countries, generally causing milder disease).

Pathogenesis

Shigella’s defining pathogenic feature is a remarkably low infective dose — as few as 10–100 organisms can establish infection, dramatically lower than Salmonella’s 10³–10⁶ or cholera’s 10⁸–10¹⁰, since Shigella is genuinely acid-resistant and survives gastric transit far better than most enteric pathogens; this low infective dose is exactly why shigellosis spreads so efficiently by direct person-to-person contact and fomites, not just contaminated food/water. Once past the stomach, Shigella invades colonic epithelial cells directly (via M cells, then spreading cell-to-cell using actin-based motility, without ever needing to cross into the bloodstream) — a genuinely invasive disease mechanism, in sharp contrast to cholera’s purely toxin-mediated, non-invasive pathology. This invasion triggers intense colonic mucosal inflammation, ulceration, and micro-abscess formation, which is what actually produces the blood and mucus in the stool — a direct tissue-destruction picture rather than cholera’s purely secretory one.

S. dysenteriae type 1 additionally produces Shiga toxin, an AB toxin that inhibits host protein synthesis by cleaving ribosomal RNA — this is the same toxin family (Shiga-like toxin) that Shiga-toxin-producing E. coli (STEC, covered under the next topic) produces, and is responsible for S. dysenteriae’s uniquely severe disease and its specific association with haemolytic uremic syndrome (HUS), a complication otherwise more classically linked to STEC.

Clinical Manifestations

After a short incubation (1–3 days), illness often begins with watery diarrhoea and fever before progressing to the classic dysenteric phase — frequent, small-volume, blood- and mucus-streaked stools with severe abdominal cramping and tenesmus (a painful, persistent urge to defecate despite an empty rectum, from the intense rectal inflammation). Complications include toxic megacolon, intestinal perforation, and — specifically with S. dysenteriae type 1 — HUS (microangiopathic haemolytic anaemia, thrombocytopenia, acute kidney injury) and, occasionally, seizures in children.

Amoebic Dysentery

The Organism and Mechanism

Entamoeba histolytica causes amoebic dysentery via ingestion of quadrinucleate cysts (the infective, environmentally resistant form), which excyst in the small intestine to release trophozoites that colonize the colon. Disease occurs only when trophozoites actually invade the colonic mucosa — most infected individuals remain asymptomatic cyst-passers/carriers rather than developing invasive disease, since invasion depends on both organism virulence factors (a galactose/N-acetylgalactosamine lectin mediating adherence, and cysteine proteases enabling tissue destruction) and host factors that are not yet fully understood. Invasive trophozoites produce characteristic flask-shaped ulcers — narrow at the mucosal surface, widening in the submucosa — through direct cytolysis of host cells, a genuinely different mechanism from Shigella’s cell invasion/inflammatory cascade.

Clinical Manifestations

Amoebic dysentery tends to have a more gradual onset than shigellosis, with less pronounced systemic toxicity/fever for a comparable degree of local bowel symptoms — a real, if imperfect, clinical clue distinguishing the two syndromes at the bedside before any stool result returns. Stool is classically described as containing blood mixed with mucus in a less watery, more “anchovy-sauce”-like consistency compared to bacillary dysentery’s more watery-bloody stool, though this distinction is genuinely unreliable enough that laboratory confirmation is needed rather than relied on alone. The dominant, most feared complication is extraintestinal spread to the liver as amoebic liver abscess (covered as its own topic, given how clinically distinct and important it is), reflecting trophozoites entering the portal venous circulation from an invaded colonic ulcer.

Comparing the Two at the Bedside

Laboratory Diagnosis

Stool microscopy is the first step for both, but looks for genuinely different things: numerous faecal leukocytes and RBCs support a bacterial/invasive process generally; motile trophozoites with ingested RBCs (erythrophagocytosis) on a fresh, warm wet mount is the classic, relatively specific finding for active invasive amoebiasis, while Shigella itself is not directly visualized on a wet mount and requires culture. Stool culture on selective media (MacConkey, XLD, or Hektoen enteric agar) with biochemical confirmation (non-lactose-fermenting, non-motile — a genuinely useful distinguishing feature from most other Enterobacteriaceae, since immotility is unusual in this family) identifies Shigella; serogrouping by slide agglutination follows. Stool antigen tests (ELISA for E. histolytica-specific antigen) and PCR (able to distinguish pathogenic E. histolytica from the morphologically identical but non-pathogenic E. dispar, a distinction plain microscopy cannot make) are increasingly the preferred methods for amoebiasis given microscopy’s real limitations in both sensitivity and species specificity.

Treatment

Shigellosis: fluid replacement plus antibiotics (azithromycin, ciprofloxacin, or ceftriaxone depending on local resistance — antibiotic treatment genuinely shortens illness duration and reduces transmission, unlike most other bacterial diarrhoeas where supportive care alone often suffices, reflecting shigellosis’s low infective dose and high transmissibility). Amoebic dysentery: metronidazole or tinidazole (a tissue-active amoebicide, killing invasive trophozoites) followed by a luminal agent (paromomycin or diloxanide furoate, clearing residual cysts from the bowel lumen that the tissue-active drug doesn’t reliably reach) — this two-drug sequence matters because treating with a tissue agent alone can leave the patient asymptomatic but still shedding cysts, a genuine public-health transmission risk if the luminal step is skipped.

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