dysentery

Dysentery refers to inflammatory diarrhea involving invasion of the intestinal mucosa (typically colon), leading to blood, pus, and mucus in stool, often accompanied by fever, abdominal pain, and tenesmus (painful urge to defecate). This distinguishes it from watery, secretory diarrhea (e.g., from Vibrio cholerae or ETEC) which involves toxin-mediated fluid secretion without mucosal invasion.

Key pathogens: - Shigella (S. dysenteriae, S. flexneri): invades M cells of Peyer's patches, spreads cell-to-cell via actin polymerization; produces Shiga toxin which inhibits 60S ribosomal subunit, causing bloody diarrhea and potential HUS (though HUS more classic with EHEC O157:H7). - Entamoeba histolytica: protozoan causing amoebic dysentery; flask-shaped ulcers in colon, can lead to liver abscess (anchovy paste exudate) via hematogenous spread through portal circulation. - Campylobacter jejuni: comma-shaped, oxidase-positive organism from contaminated poultry/unpasteurized milk; associated with Guillain-Barré syndrome and reactive arthritis. - Enteroinvasive E. coli (EIEC): mimics Shigella pathogenesis and clinical presentation, plasmid-mediated invasion. - Salmonella (non-typhoidal): can also cause invasive diarrhea, especially in immunocompromised or sickle cell patients (risk for osteomyelitis).

Pathophysiology: These organisms invade and destroy colonic epithelial cells, causing mucosal ulceration, inflammation, and microabscesses, resulting in the characteristic bloody, mucoid stool. Fecal leukocytes are typically present on microscopy (distinguishing invasive from non-invasive diarrhea).

Clinical work-up: Stool studies showing fecal WBCs/RBCs, stool culture, and in suspected amoebic cases, stool O&P or serology. Treatment is pathogen-specific; antibiotics are avoided in EHEC (Shiga-toxin producing, non-invasive) due to increased HUS risk from toxin release, but may be used for Shigella, Campylobacter, and amoebic dysentery (metronidazole + luminal agent).

High-yield board point: Differentiate dysentery (invasive, bloody, fecal leukocytes present) from toxin-mediated secretory diarrhea (watery, no fecal leukocytes, e.g., cholera, ETEC, S. aureus food poisoning).