Shigella Pathogenic Factors: Understanding the Mechanisms Behind Dysentery

Shigella, a genus of Gram-negative bacteria responsible for bacillary dysentery, employs a variety of pathogenic mechanisms to invade and damage the human intestinal tract. These mechanisms include invasiveness, endotoxins, and exotoxins, each playing a crucial role in the progression of the disease.

Invasiveness: Penetrating the Intestinal Barrier

One of the primary virulence factors of Shigella is its ability to invade host cells. The bacteria possess pili (fimbriae) that enable them to adhere to the epithelial cells lining the terminal ileum and colon. Through a process facilitated by invasin proteins, Shigella can penetrate these cells and replicate within the mucosal lamina propria, leading to localized infection and inflammation.

Endotoxins: Triggering Systemic and Local Damage

All Shigella species produce potent endotoxins, which are components of the bacterial cell wall. These endotoxins increase the permeability of the intestinal lining, allowing for greater toxin absorption and triggering systemic symptoms such as fever, altered mental status, and in severe cases, toxic shock.

In addition to systemic effects, endotoxins directly damage the intestinal mucosa, causing inflammation and ulceration. This damage results in the hallmark symptom of shigellosis: bloody, mucoid diarrhea. Moreover, endotoxins interfere with the enteric nervous system, leading to intestinal dysfunction, irregular motility, and spasms—particularly in the rectal sphincter—which manifest as abdominal pain and tenesmus.

Exotoxins: The Role of Shiga Toxin

Characteristics and Activity

Some strains of Shigella, particularly Shigella dysenteriae type 1 and certain type 2 strains, produce a potent exotoxin known as Shiga toxin. This toxin is heat-labile and can be inactivated at temperatures of 75–80°C over one hour.

Biological Effects

Shiga toxin exhibits three key biological activities: neurotoxicity, cytotoxicity, and enterotoxicity. Neurotoxicity can lead to neurological complications, cytotoxicity damages host cells and contributes to tissue destruction, and enterotoxicity disrupts normal intestinal function, exacerbating diarrhea and fluid loss.