The Shigella

Natural habitat is limited to intestinal tracts of humans and other primates

4 species of Shigella:

nonmotile: no flagella

1. Pathogenesis & Pathology

• limited to the gastrointestinal tracts infections
• Highly communicable (infective dose: 103 organisms)
• Invasion of the mucosal epithelial cells by induced phagocytosis ≫ lyse the phagocytic vacuole and escape from the phagocytic vacuole ≫ multiplication and spread within the epithelial cell cytoplasm ≫ propelled through the cytoplasm to adjacent cells, cell to cell passage ≫ release interleukin-1b by survived infected cell ≫ attraction of WBC ≫ Microabscesses in the wall of the large intestine and terminal ileum ≫ necrosis of the mucous membrane, superficial ulceration, bleeding

2. Toxins

A. Endotoxin : all Shigellae release LPS upon autolysis, irritate the bowel wall.

B. Shigella dysenteriae Exotoxin (Shiga toxin)

• S dysenteriae produce heat-labile exotoxin
• Like the toxin produced by EHEC
• Primary manifestation of toxin activity is the intestinal epithelium
• in a small subset of patients, mediate HUS

3. Clinical Findings

• Gastroenterites (shigellosis)
• Most common form is an initial watery diarrhea progressing within 1 to 2 days to abdominal cramps and tenesmus (with or without bloody stools)
• Asymptomatic carrier develops in a small number of patients (reservoir for future infections)
• A severe form of disease is caused by S. dysenteriae

4. Treatment, Prevention, & Control

• Antibiotic therapy shortens the course of symptomatic disease and fecal shedding
• Transmitted by food, fingers, feces, and flies from person to person
• Most cases are under 10 yrs of age
• Appropriate infection control measure should be instituted to prevent spread of the organism

Category: Microbiology Notes