Listeriosis, food poisoning, treatment, progression, disease, genes, Pluchea quitoc
Listeriosis, a disease caused by Listeria monocytogenes- a facultative, intracellular bacterium, spreads through contaminated food. It affects epithelial cells and macrophages and has a mortality rate of about 30%. The bacterium can cross the blood brain barrier, causing meningitis, and the placental barrier, causing abortion. Some mechanisms for entry into cells include the InlA- E-cadherin adhesion and InlB-Met pathway. hly, one of the many genes activated during infection, leads to the production of Listeriolysin O (LLO). LLO and two distinct phospholipases are indispensable to the spread of Listeria. Phosphatidylinositol-specific phospholipase C (PI-PLC) activates a host protein kinase C (PKC), which facilitates the escape of the bacterium from the primary vacuole, along with LLO. Once inside the cell’s cytoplasm, Listeria replicates. At this point, both the original bacterium and the daughter cells use Act A protein to exploit the cell’s machinery to polymerize actin. Actin-based motility propels the Listeria throughout the cell and facilitates its intercellular spread. Current curative methods include ampicillin, gentamicin, and chloramphenicol, reserved for life threatening infections. Treatment via plant extracts of Pluchea quitoc is in the experimental stage. This review focuses on tracking the progression of the L. monocytogenes bacterium from its entry to spread.
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