Shigella dysentriae

Shigella dysenteriae Shigella is included in the family Enterobacteriacae, gram negative rod-shaped, not moving, not encapsulated, and more acid resistant than other enteropathogens. Shigella can invade colonic epithelial cell surface, rarely penetrates through the mucosa, so that no blood was found padabiakan hyperpyrexia and although there are symptoms of toxemia. After the invasion of colonic enterocytes, there was a change of surface microvilli which led to the formation of vesicles on the mucous membranes. Furthermore, can destroy intracellular phagocytic vacuole, into the cytoplasm to multiply and invade the adjacent cell. The ability to invade epithelial cells is associated with the presence of a large plasmid that is able to recognize the outer membrane protein as antigen invasions plasmid. Epithelial cells will die and mucosal inflammation. From the inflamed part is shigella produces exotoxin which is based on how the toxin is classified into neurotoxic, enterotoksik, and cytotoxic. This formed toxin that causes various symptoms of shigellosis, such as fever, malaise, and muscle pain. Shigella dysenteriae type 1 produces a potent sitotoksin protein known as Shiga toxin consists of two sub-unit structure, namely a) The functional subunit In the cytoplasm of functional sub-unit will catalyze and hydrolyze RNA of the 28S ribosomal subunit 60S, thus causing inhibition of protein synthesis that is permanent, resulting in cell death. b) Sub-binding unit Part-binding subunit is a glycolipid that functions to bind specific cellular receptors. This binding is followed by activation of receptor endocytosis mediator daritoksin generated.
Shiga toxin can cause hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. These events are often associated with cross-reaction caused by serotypes of E. coli infection that can also produce a toxin similar to Shiga toxin. Mechanisms of pathogenicity of these effects may involve an endothelial cell toxin binding (binding endothelial cell toxin), which can cause microangiopathic hemolysis and glomerular lesions.
 The mechanism of Dysentery Dysentriae Shigella entry into the human body through the gastrointestinal tract via oral. Because the bacteria that are genetically equipped to survive the low pH, Shigella ready to pass gastrin.Shigella acid transmitted through "food, fingers, feces, and flies" from one person to lain.Kebanyakan shigella infection cases occurred in children younger than than 10 years. Shigella invade humans by a series of processes patologi.Shigella invade mucosal epithelial cells (eg, M cells), by inducing phagocytosis. Shigella then out of the phagocytic vacuole, multiply and spread within the cytoplasm of epithelial cells, and spread within the cytoplasm of epithelial cells, and spread to a nearby cell. Shigella is difagosit by macrophages will stimulate apoptosis, but before apoptosis occurs, Shigella bacteria can get out of the phagocytic vacuole and attack cells that are nearby. Shigella invade apitel basolateral surface layer of the colon and stimulate the formation of IL-8.IL-8 is a chemokine that induces migration Polimorphonuclear Neutrophils (PMNs) from the bottom layer of epithelial cells into the intestinal lumen. PMNs damage the tight-junction when crossing mukosa.Kerusakan gives way to Shigella invasion and exacerbate inflammation. Shigella invasion mukosa.Mikroabses cause ulcerations in the intestinal wall and cause necrosis of the terminal ileum mucous membrane, superficial ulceration, bleeding, and pseudomembrane formation in the ulcerated area. Pseudomembrane composed of fibrin, leukocytes, cell debris, necrotic mucous membranes, and bacteria. The substance is what causes the stool mixed with blood and mucus (mucoid). Further, when the process subsided, Network granulsi filling and form scar tissue ulceration. The body's immune response to Shigella infection is as follows. Shigella infection followed by type-specific antibody response. IgA antibodies in the intestine may be important in limiting infection. These antibodies can be stimulated by the provision that has been attenuated strain of living through such oral vaccine trial. Serum antibodies against shigella somatic antigen is IgM. A series of antibody titer determination able to demonstrate specific antibodies. Colonic mucosal invasion of bacteria activate the transcription factor NF-κByang involved in the regulation of cytokine synthesis. Cytokine production occurs in Shigella.Sel infection cells produce IL-1, IL-6, interferon γ and β form a growth factor that is directly related to the inflammatory reaction. Inflammatory reaction lasts longer in children than men dewasa.Perbedaan showed an immune response in children less to deal with pathogens.