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Shigella is a genus of Gram-negative, non-spore-forming, nonmotile, facultatively anaerobic, rod-shaped bacteria within the family Enterobacteriaceae[1][2][4]. It consists of four species (S. dysenteriae, S. flexneri, S. boydii, S. sonnei) and is the causative agent of shigellosis (bacillary dysentery), a severe diarrheal disease in humans[1][5]. Shigella invades the epithelial lining of the colon, causing cell death, inflammation, and sometimes toxin-mediated complications such as hemolytic-uremic syndrome (via Shiga toxin in S. dysenteriae)[1][2]. It is a leading cause of bacterial diarrhea worldwide and is only naturally found in primates, with transmission primarily via the fecal-oral route or contaminated food/water[1][3][5]. Antibiotic resistance is an increasing problem, and laboratory work with Shigella requires strict biosafety precautions due to its low infectious dose and transmission risk[2][3]. Shigella is best viewed as an infectious bacterial genus, not as a discrete molecular or pharmacological drug target. For drug discovery or biomarker querying, defined molecular entities (e.g., Shiga toxin, type III secretion system) should be used rather than the entire genus.
Inhibition of bacterial DNA gyrase (fluoroquinolones), Inhibition of protein synthesis (chloramphenicol), Inhibition of cell wall synthesis (beta-lactams such as ampicillin, cephalosporins), Inhibition of folate pathway (trimethoprim-sulfamethoxazole), Inhibition of macrolide protein synthesis (azithromycin)
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