The evolution of multi drug resistant strain shigella sonnei from its ancestor E. Coli and predecessor S. Flexneri and its spread to Vietnam

Introduction
Shigella is a genus of Gram-negative, facultative anaerobic, nonspore-forming, nonmotile, rod-shaped bacteria. The genus is named after Kiyoshi Shiga, who first discovered it in 1897. The causative agent of human shigellosis, Shigella causes disease in primates, and is the only naturally found in humans and apes. Shigella is one of the leading bacterial causes of diarrhea worldwide and it is suggested that Shigella causes about 90 million cases of severe dysentery, with at least 100,000 of these resulting in death each year. Shigella originates from a human-adapted E. coli that has gained the ability to invade the human gut mucosa, spreading through fecal-oral transmission via contaminated food or water.
Depending on age and condition of the host, fewer than 100 bacterial cells can be enough to cause an infection. The infection results in the destruction of the epithelial cells of the intestinal mucosa. Some strains produce the enterotoxin shiga toxin, which is similar to the verotoxin of E. coli. The species invades the host through the cells in the gut epithelia of the small intestine. Shigella uses a type-III secretion system, which acts as a biological syringe to translocate toxic effector proteins to the target human cell. The effector proteins can alter the metabolism of the target cell, making it easier for intracellular motility of Shigella bacteria inside the host cell.
Unlike many other pathogenic bacteria, S. sonnei does not use flagella for its chemotoxicity and tissue invasion. Without flagella, S. sonnei can often escape the human immune system that usually mediates the innate and adaptive immunity by detecting the conserved domain on many bacteria that use flagellin for motility. Although S.