Difference between revisions of "Listeria monocytogenes"

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A Microbial Biorealm page on the genus Listeria monocytogenes


Higher order taxa

Bacteria; Firmicutes; Bacilli; Bacillales; Listeriaceae; Listeria; L.monocytogenes


NCBI: Taxonomy

Listeria monocytogenes

Description and significance

Listeria monocytogenes are a Gram-positive rod-shaped bacterium that form single short chains (1), and can be resistant to the effects of freezing, drying, and heat (2) surprisingly well for a non spore forming bacterium. Listeria are mainly found in the soil, though Listeria monocytogenes, a pathogen, may specifically be found in raw foods, such as unpasteurized fluid milk (5), raw vegetables, raw and cooked poultry (4). It has the ability to grow at low temperatures; thus, allowing it to grow in refrigerated foods. Listeria monocytogenes was thought to be exclusively associated as infections in animals, but recently, this pathogenic species has also been isolated, in its dormant form, in the intestinal tract of small percentage of the human population (3). Because Listeria monocytogenes is an agent of listeriosis, a serious disease where the overt form has a severe mortality greater than 25 percent (3), sequencing of the bacterium’s genome is of significant importance. Sequencing the genome of this organism allows for the measurement and study of traits such as new aspects regarding virulence and evolution using comparative genomics and DNA arrays (6). 16S rRNA cataloging studies have also been conducted to demonstrate Listeria monocytogenes’ close relationship to different stains of listeriae, based on genome size, GC-content and other various characteristics (7), which also helped place the bacterium within the bacterial phylogeny constructed by Woese (3).

Genome structure

The genome of Listeria monocytogenes strain EGD-e is just one of several stains of the bacterium that have been sequenced. Strain EGC-e is 2,944,528 base pairs long with 2853 open reading frames and a GC content of 39% (NCBI). Other strains sequenced include Listeria monocytogenes str.4b F2365, which is 2,905,310 base pairs long with a GC content of 38% (NCBI). Currently the genomes of Listeria monocytogenes str. 1/2a F6854, and Listeria monocytogenes str. 4b H7858 are being sequenced (8). Listeria monocytogenes has a single circular chromosome. The ability of Listeria to inhabit a wide range of environments is attributed to the presence of 331 genes encoding different transport proteins, comprising 11.6% of the total gene compliment of L. monocytogenes. Listeria also has an extensive regulatory range occupying much of the total genome (8).

Cell structure and metabolism

Listeria monocytogenes do not form spores or branch and are motile via peritrichous flagella at room temperature (20º-25º), but surprisingly cannot synthesize flagella at body temperature (37º) (13). Because Listeria monocytogenes are intracellular pathogens, virulence is associated with the ability of bacteria to move into host cells by polymerization of host cell actin at one end of the bacterium, which helps them propel through cytoplasm. Flagellar motility is used more for spread of the bacteria outside the host environment (9, 13).


Listeria monocytogenes has been found widely distributed throughout the environment, especially in the soil and fecal matter. Studies have shown that infected animals may contribute to Listeria monocytogenes ’s dispersal into the environment through animal fecal matter and feedstuff (10). Listeria monocytogenes, as an intracellular pathogen, has been associated with severe food borne infections in humans and animals, though rarely through raw animal-derived food products (11). Listeria monocytogenes have also been shown to survive in different habitats with extreme conditions including high salt concentrations, high pH, and high temperature (3). Listeria monocytogenes can also form biofilms, which enables them as a community to attach to solid surfaces where they proliferate and become extremely difficult to remove (20).


Most Listeria monocytogenes are pathogenic to both animals and humans to some degree; however, the bacterium has been reported to be carried in the intestinal tract of a small percentage of the human population without apparent symptoms (3). As with many different pathogens, the virulence of this bacterium varies depending on the particular strain and with the susceptibility of the victim. Listeria monocytogenes has been associated with ingested raw and contaminated foods, such as raw and pasteurized dairy products (5), raw vegetables, raw meats and smoked fish (3). Because of its ability to grow at low temperatures, Listeria monocytogenes can be found growing in refrigerated foods as well (3). Listeria monocytogenes causes the disease listeriosis in humans, with common manifestations in septicemia (12), meningitis (13), encephalitis (13), corneal ulcer (14), pneumonia (15), and cervical infections in pregnant women, which may have resulted in spontaneous abortion or stillbirth (13). Patient symptoms include influenza- like symptoms, and gastrointestinal symptoms of vomiting and diarrhea (3). When Listeria monocytogenes invades the gastrointestinal epithelium and then enters the host’s monocytes, macrophages, or polymorphonuclear leukocytes, it becomes blood-borne and multiplies, both intracellularly and extracellularly. Intracellularly, it has access to the brain and transplacental migration to the fetus in pregnant women (16). In animals infected with Listeria monocytogenes, such as mice, the bacteria first appear in macrophages and then spread to hepatocytes in the liver (17). The bacteria stimulate a response that includes the production of gamma interferons, macrophage activating factors and a cytotoxic T cell response (17). The pathogenesis of Listeria monocytogenes thrives on its ability to survive and multiply in phagocytic host cells. Virulence is thus associated with the ability of the bacterium to move within the cytoplasm of the host cells by polymerization of host cell actin (9). Secreting the enzyme invasion allows Listeria monocytogenes to penetrate host cells of the epithelial lining. The immune system can usually eliminate the infection before it spreads by using T lymphocytes specifically for Listeria antigens (17). However, systemic disease may develop with a compromised immune system. Another virulence factor is the bacterium’s ability to bind to epithelial cells by means of adherence to D-galactose receptors on the host cell (16).

Application to Biotechnology

Listeria monocytogenes does not produce any known useful compounds or enzymes

Current Research

Research continues to be conducted on the characterization and function of Listeria monocytogenes (1,9,19, 20) to better understand its pathological activity and its continued effect on food products and household environments (2,16,18, 21). These characterizations include studies that examine enzymes that the bacterium uses (1), that further investigate the mechanism of motility and infection (9), that study different growth factors via heat-killed organisms (19), and explore relationships within biofilm communities (20). The genomes of several Listeria monocytogenes strains are in the process of being sequenced and with this information available, a more complete understanding of the natural history of this pathogen will be obtained. This understanding will further facilitate rational and effective control strategies to reduce human and animal listeriosis cases (10, 21).


1. Theivagt, A.E., Friesen, J.A. (2006). “Purification and characterization of Listeria monocytogenes HMG-CoA reductase” FASEB Journal 20 (4, Part 1): A472 MAR 6 2006.

2. Sallami, Lamjed; Marcotte, Michele; Naim, Fadia; Ouattara, Blaise; Leblanc, Claude; Saucier, Linda (2006). “Heat inactivation of Listeria monocytogenes and Salmonella enterica serovar Typhi in a typical bologna matrix during an industrial cooking-cooling cycle” Journal of Food Protection 69 (12): 3025-3030 DEC 2006.

3. Rouquette, C., Berche, P. (1996). The pathogenesis of infection by Listeria monocytogenes. 12(2): 245-258.

4. Dykes, Gary A. (2003). “Influence of the adaptation of Listeria monocytogenes populations to structured or homogeneous habitats on subsequent growth on chilled processed meat.” International Journal of Food Microbiology 85 (3) : 301-306 25 August, 2003.

5. Fleming, D.W., S.L. Cochi, K.L. McDonald, 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.

6. Doumith M, Cazalet C, Simoes N, Frangeul L, Jacquet C, Kunst F, Martin P, Cossart P, Glaser P, Buchrieser C. (2004) “New aspects regarding evolution and virulence of Listeria monocytogenes revealed by comparative genomics and DNA arrays.” Infect Immun. 2004 Feb;72(2):1072-83.

7. Feresu SB, Jones D. (1988). “Taxonomic studies on Brochothrix, Erysipelothrix, Listeria and atypical lactobacilli” J Gen Microbiol. 1988 May;134(5):1165-83.

8. Hain, T. (2006). Whole-genome sequence of Listeria welshimeri reveals common steps in genome reduction with Listeria innocua as compared to Listeria monocytogenes. Journal of bacteriology, 188(21), 7405-7415.

9. O'Neil, H. (2006). Listeria monocytogenes flagella are used for motility, not as adhesins, to increase host cell invasion. Infection and immunity, 74(12), 6675-6681.

10. Nightingale, K.K., et al. (2004). Ecology and Transmission of Listeria monocytogenes Infecting Ruminants and in the Farm Environment. American Society for Microbiology, 2004 Aug: 4458-4467.\

11. Mead, P.S., L. Slutsker, V. Dietz, L.F. McCraig, J.S. Bresee, C. Shapiro, P.M. Griffin, and R.V. Tauxe. (1999) Food-related illness and death in the United States. Emerg. Infect. Dis. 5:607-625.

12. Gray, M.L., and A.H. Killinger. (1966). Listeria monocytogenes and listeric infection. Bacteriol. Rev. 30:309-382.

13. Dussurget, O., Pizarro-Cerda, J., Cossart, P. (2004). Molecular determinants of Listeria monocytogenes virulence. Annuak Review of Microbiology 58: 587-610.

14. Holland, S., E. Alfonso, H. Gelender, D. Heidemann, A. Mendelsohn, S. Ullman, and D. Miller. (1987). Corneal ulcer due to Listeria monocytogenes. Cornea 6:144-146.

15. Whitelock-Jones, L., J. Carswell, and K.C. Rassmussen. (1989). Listera pneumonia. A case report. South African Medical Jounal 75:188-189.

16. Kazmierczak, M.J., Wiedmann, M., Boor, K.J. (2005). Alternative Sigma Factors and Their Roles in Bacterial Virulence 69(4): 527-543.

17. Mansfield, B.E., Freitag, N.E. (2003). Listeria monocytogenes pathogenesis: Exploration of alternative hosts. Abstracts of the General Meeting of the American Society for Microbiology 103: B-186.

18. Wagner, M.; Auer, B.; Trittremmel, C., et al. (2007) Survey on the Listeria contamination of ready-to-eat food products and household environments in Vienna, Austria. Zoonoses Public Health 54 (1): 16-22.

19. Sato, F., Imaizumi, T., Sashinami, H., et al. (2007). Upregulation of vascular endothelial growth factor by heat-killed Listeria monocytogenes in macrophages. Biochemical and Biophysical Research Communications 354 (2): 608-612.

20. Harvey, J., Keenan, K. P., Gilmour, A. (2007). Assessing biofilm formation by Listeria monocytogenes strains. Food Microbiology (London) 24 (4): 380-392.

21. Aarnisalo, K., Lunden, J., Korkeala, H., et al. (2007). Susceptibility of Listeria monocytogenes strains to disinfectants and chlorinated alkaline cleaners at cold temperatures. LWT - Food Science and Technology 40 (6): 1041-1048.

Edited by Jenny Hung student of Rachel Larsen and Kit Pogliano