Shigella spp. are non-spore forming, facultatively anaerobic, gramnegative rods that are transmitted fecal-orally and a major causative agent of dysentery in humans and non-human primates. 1,2 Shigella remains an important pathogen worldwide and is a major cause of morbidity among humans, particularly in children under the age of 5. 2 In the United States alone, it accounts for an estimated 450 000 infections per year. 2 Based on biochemical and serological properties, Shigella can be separated into four serotypes, which include sonnei, boydii, dysenteriae, and flexneri. All four serotypes are important causes of morbidity and mortality in humans particularly in low-resource areas. 2 Captive non-human primates may acquire shigellosis due to their close contact with humans or from conspecifics in endemically infected colonies, with S. flexneri being the most frequent serotype isolated. [1][2][3] The symptoms of shigellosis range from acute life threatening disease to subclinical carrier states. 1,4 Acute cases often present as severe dysentery with bloody mucoid diarrhea, anorexia, weight loss, and secondary dehydration resulting in rapid decline and potentially death. 1,4 The development of disease relies on invasion of bacteria into the colonic epithelial cells resulting in mucosal inflammation, hemorrhage, and necrosis. 5 While subclinical carriers appear clinically healthy, they remain an important source of infection to conspecifics and laboratory animal workers. 1 Animals may also develop non-enteric forms of the disease including reactive arthritis,