Listeria monocytogenes
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Listeria monocytogenes is a Gram-positive bacterium, in the division Firmicutes, named for Joseph Lister. Motile via flagella, L. monocytogenes can move within eukaryotic cells by explosive polymerization of actin filaments (known as comet tails or actin rockets). The name monocitogenes derives from the strong monocytic activity this organism produces in rabbits, which however does not happen in humans. Despite the name, more that half the patients present with increased levels of neutrophils in CSF.[1] Studies suggest that up to 10% of human gastrointestinal tracts may be colonized by L. monocytogenes.
Taxonomy
Bacteria; Firmicutes; Bacilli; Bacillales; Listeriaceae; Listeria; Listeria monocytogenes
Biology
Listeria monocytogenes is a Gram-positive, facultative anaerobe, nonsporulating bacillus with polar flagellae. It is a catalase-positive organism and exhibits motility, more specifically tumbling motility. Listeria produces acid but not gas in a variety of carbohydrates.[2] It has the ability to grow at temperatures as low as 0°C, which allow it to survive in a diverse array of environments such as soil, water, food products, and host cells.
Listeria uses the cellular machinery to move inside the host cell. It induces directed polymerization of actin by the ActA transmembrane protein, thus pushing the bacterial cell inside the host cell.
Infectious Cycle
The primary site of infection is the intestinal epithelium where the bacteria invade non-phagocytic cells via the "zipper" mechanism:
- 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 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.
L. monocytogenes can also invade phagocytic cells (e.g. macrophages) but only requires internalins for invasion of non-phagocytic cells.
- Following internalisation, the bacterium must escape from the vacuole/phagosome before fusion with a lysosome can occur. Two main virulence factors allow the bacterium to escape:
- Listeriolysin O (LLO - encoded by hly)
- Phospholipase C B (plcB).
- Secretion of LLO and PlcB disrupts the vacuolar membrane and allows the bacterium to escape into the cytoplasm where it may proliferate.
- Once in the cytoplasm, L. monocytogenes exploits host's actin for the second time:
- ActA proteins associated with the old bacterial cell pole, are capable of binding the Arp2/3 complex and thus induce actin nucleation at a specific area of the bacterial cell surface (being a bacilli, L. monocytogenes septates in the middle of the cell and thus has "new pole" and another "old pole").
- Actin polymerization then propels the bacterium unidirectionally into the host cell membrane. The protrusion which is formed, may then be internalised by a neighbouring cell, forming a double-membrane vacuole from which the bacterium must escape using LLO and PlcB.
Structure
Tropism
Natural Reservoir
- L. monocytogenes has been associated with such foods as raw milk, pasteurized fluid milk[3], cheeses (particularly soft-ripened varieties), ice cream, raw vegetables, fermented raw-meat sausages, raw and cooked poultry, raw meats (of all types), and raw and smoked fish.
- Its ability to grow at temperatures as low as 0°C permits multiplication in refrigerated foods. In refrigeration temperature such as 4°C the amount of ferric iron promotes the growth of L. monocytogenes.[4]
References
- ↑ Mandell, Gerald L.; Bennett, John E. (John Eugene); Dolin, Raphael. (2010). Mandell, Douglas, and Bennett's principles and practice of infectious disease. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0-443-06839-9.
- ↑ Chapter 13. Non-Spore-Forming Gram-Positive Bacilli: Corynebacterium, Propionibacterium, Listeria, Erysipelothrix, Actinomycetes, & Related Pathogens ,Jawetz, Melnick, & Adelberg's Medical Microbiology, 24th Edition ,The McGraw-Hill Companies
- ↑ Fleming, D. W., S. L. Cochi, K. L. MacDonald, J. Brondum, P. S. Hayes, B. D. Plikaytis, M. B. Holmes, A. Audurier, C. V. Broome, and A. L. Reingold. 1985. Pasteurized milk as a vehicle of infection in an outbreak of listeriosis. N. Engl. J. Med. 312:404-407.
- ↑ Dykes, G. A., Dworaczek (Kubo), M. 2002. Influence of interactions between temperature, ferric ammonium citrate and glycine betaine on the growth of Listeria monocytogenes in a defined medium. Lett Appl Microbiol. 35(6):538-42.