Listeriosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]; Yazan Daaboul, M.D.


Listeria is commonly transmitted via contaminated food or via vertical transmission from mother to fetus. Following transmission, Listeria encodes thermoregulated virulence factor in the human host, invades the intestinal epithelium, and multiplies intracellularly within phagocytic phagolysosomes. It is able to escape lysosomal destruction by secreting phospholipases and listeriolysin O, a hemolysin that is responsible for lysis the vacuole's membrane. Listeria then migrates between cells by forming protrusions called filopods or "rockets" using polymerized actin and Gelsolin, an actin-binding protein. Microscopically, tissue infected with Listeria monocytogenes often demonstrates microscopic features of inflammation, exudate formation, and neutrophilia. In prolonged infections, macrophages may be abundantly present in tissue specimens, and granuloma formation may occur.


  • In adults, Listeria is usually found in soil, water, vegetation and fecal material. It is commonly transmitted via contaminated food.
  • Uncooked meats and vegetables (including refrigerated foods)
  • Unpasteurized (raw) milk and cheeses, as well as other foods made from unpasteurized milk
  • Cooked or processed foods, including certain soft cheeses, processed (or ready-to-eat) meats, and smoked seafood



Invasion of the Intestinal Epithelium

  • Uptake is stimulated by the binding of listerial internalins (Inl) to host cell adhesion factors such as E-cadherin or Met.
  • This binding activates certain Rho-GTPases which subsequently bind and stabilize the Wiskott-Aldrich syndrome protein (WASp).
  • WASp can then bind the Arp2/3 complex and serve as an actin nucleation point.
  • Subsequent actin polymerization extends the cell membrane around the bacterium, eventually engulfing it.
  • The net effect of internalin binding is to exploit the junction forming-apparatus of the host into internalizing the bacterium.

Intracellular Activity Within Phagocytes

Motility and Cell-to-Cell Invasion

Microscopic Pathology


  1. "Risk assessment of Listeria monocytogenes in ready-to-eat foods" (PDF).
  2. Tinley, L.G.; et al. (1989). "Actin Filaments and the Growth, Movement, and Spread of the Intracellular Bacterial Parasite, Listeria monocytogenes". The Journal of Cell Biology. 109: 1597–1608. Unknown parameter |quotes= ignored (help)
  3. "Listeria". 16 August 2006. doi:. Check |doi= value (help). Retrieved 2007-03-07.
  4. Southwick FS, Purich DL (1996). "Intracellular pathogenesis of listeriosis". N. Engl. J. Med. 334 (12): 770–6. doi:10.1056/NEJM199603213341206. PMID 8592552.
  5. Laine, R.O.; et al. (1998). "Gelsolin, a Protein That Caps the Barbed Ends and Severs Actin Filaments, Enhances the Actin-Based Motility of Listeria monocytogenes in Host Cells". Infection and Immunity. 66(8): 3775–3782. Unknown parameter |quotes= ignored (help)
  6. Galbraith, C.G.; et al. (2007). "Polymerizing Actin Fibers Position Integrins Primed to Probe for Adhesion Sites". Science. 315: 992–995. Unknown parameter |quotes= ignored (help)
  7. Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.
  8. Kumar, Vinay (2014). Robbins and Cotran pathologic basis of disease. Philadelphia, PA: Elsevier/Saunders. ISBN 1455726133.

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