Pathogenesis

The first step in the infection is phagocytosis of the bacteria by M cells associated with intestinal mucosal-associated lymphoid tissue (MALT) in the large intestine. These cells transport the bacteria beneath the epithelium, where they are discharged by exocytosis. The shigellas attach to specific receptors located at or near the bases of the epithelial cells and induce the process of endocytosis, which takes the bacteria into the epithelial cells enclosed in a phagosome. Intracellularly, they break out of the phagosome, multiply at a high rate in the cytoplasm, and kill the cells. Even though Shigella sp. are non-motile, they are moved efficiently from cell to cell by a process first described in 1995. A chromosomal gene of the bacterium codes for a protein that causes the host cell's actin filaments to form a progressively lengthening tail attached to one end of the bacterium (figure 24.14). Actin tails push the bacteria from one cell to another. The final result of the infectious process is sloughed areas of epithelium surrounding lymphoid tissues. The denuded areas are intensely inflamed, pus covered, and bleeding, the source of blood and pus in the diarrheal stool. ■ actin, p. 74 ■ MALT, p. 397

Some strains of Shigella dysenteriae, a species rarely encountered in the United States, produce a potent toxin known as the Shiga toxin. It is a chromosomally coded A-B toxin structurally similar to cholera toxin but otherwise unrelated. The toxin does not cause ADP ribosylation. Instead, the A subunit reacts with

Chapter 24 Alimentary System Infections

Epithelial M cell cell

Chapter 24 Alimentary System Infections

Epithelial M cell cell

Macrophage Shigella

Cell nucleus

(1) Shigellas are taken up by M cells and transported beneath the epithelium. Macrophages take up shigellas, die and release the bacteria.

Macrophage Shigella

Cell nucleus

(4) Shigellas multiply in the cytoplasm, and the infection extends to the next cell.

(5) Infected cells die and slough off. Intense response of acute inflammatory cells (neutrophils), bleeding and abscess formation.

Figure 24.14 Pathogenesis of Shigellosis The bacteria do not invade the intestinal epithelium directly, but are transported to the area underneath the epithelial cells by M cells.They then invade the epithelial cells from their inferior and lateral borders.The photomicrograph shows the actin tails (green) that form on intracellular shigellas (orange) and rapidly push these non-motile bacteria from cell to cell.

(1) Shigellas are taken up by M cells and transported beneath the epithelium. Macrophages take up shigellas, die and release the bacteria.

(2) The bacteria enter the inferior and lateral aspects of the epithelial cells by inducing endocytosis. The endosomes are quickly lysed, leaving the shigellas free in the cytoplasm.

(3) Actin filaments quickly form a tail, pushing the shigellas into the next cell.

(4) Shigellas multiply in the cytoplasm, and the infection extends to the next cell.

(5) Infected cells die and slough off. Intense response of acute inflammatory cells (neutrophils), bleeding and abscess formation.

Figure 24.14 Pathogenesis of Shigellosis The bacteria do not invade the intestinal epithelium directly, but are transported to the area underneath the epithelial cells by M cells.They then invade the epithelial cells from their inferior and lateral borders.The photomicrograph shows the actin tails (green) that form on intracellular shigellas (orange) and rapidly push these non-motile bacteria from cell to cell.

the host cell ribosome, thereby halting protein synthesis. The importance of this toxin is that it has a strong association with the hemolytic uremic syndrome, an often fatal condition that can follow Shigella dysenteriae dysentery. In this syndrome, red blood cells break up in the tiny blood vessels of the body, resulting in anemia and kidney failure, sometimes accompanied by paralysis or other signs of nervous system injury. Shiga toxin is also produced by strains of Escherichia coli that cause the hemolytic uremic syndrome.

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