Listeriosis: Difference between revisions

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===Epidemiology===
===Epidemiology===
===Virulence factors===
===Virulence factors===
1. Adhesion to the surface of mammalian cells.  Close interaction between host cells and <i>L. monocytogenes</i> makes invasion possible.  Numerous surface adhesion factors allow the pathogen to connect to host cells. <br>
1. Adhesion to the surface of mammalian cells.  Close interaction between host cells and <i> L. monocytogenes </i> makes invasion possible.  Numerous surface adhesion factors allow the pathogen to connect to host cells. <br>
     -
     -Lap adhesion protein uses an alcohol acetaldehyde dehydrogenase interaction with the host cell receptor, Hsp60, to adhere to intestinal cells. This Lap protein is required for full virulence. 
    -Ami protein associates to the bacterial surface via its C-terminal cell wall-anchoring (CWA) domain.  The CWA allow adhesion to host epithelial cells.
    -The gene segment <i> dltA </i> integrates D-alanine-polyphosphoribitol into lipoteichoic acids (LTAs)which contributes to cell adhesion.


==Clinical features==
==Clinical features==

Revision as of 09:23, 14 July 2013

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Etiology/Bacteriology

Taxonomy

Domain: Bacteria
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Listeriaceae
Genus: Listeria
Species: monocytogenes

Description

Listeria are gram positive facultative anaerobes observed to be bacilli in short chains. If a direct sample is observed under the microscope, Listeria can resemble cocci shapes and can be mistaken for streptococci. All species produce flagella at room temperature but do not express it at 37 degrees Celsius. These non-spore forming, catalase positive bacteria are found in soil, sewage, stream water and animal carriers.

Pathogenesis

Transmission

Infectious dose, incubation, and colonization

Epidemiology

Virulence factors

1. Adhesion to the surface of mammalian cells. Close interaction between host cells and L. monocytogenes makes invasion possible. Numerous surface adhesion factors allow the pathogen to connect to host cells.

    -Lap adhesion protein uses an alcohol acetaldehyde dehydrogenase interaction with the host cell receptor, Hsp60, to adhere to intestinal cells. This Lap protein is required for full virulence.  
    -Ami protein associates to the bacterial surface via its C-terminal cell wall-anchoring (CWA) domain.  The CWA allow adhesion to host epithelial cells. 
    -The gene segment  dltA  integrates D-alanine-polyphosphoribitol into lipoteichoic acids (LTAs)which contributes to cell adhesion.

Clinical features

Diagnosis

Treatment

Prevention

Host Immune Response

References

1. Conway, Tyrrell. “Genus conway”. “Microbe Wiki” 2013. Volume 1. p. 1-2.
2. http://www.cdc.gov/listeria/
3. D Cabanes, et al. "The Arsenal Of Virulence Factors Deployed By Listeria Monocytogenes To Promote Its Cell Infection Cycle." Virulence 2.5 (n.d.): 379-394. Science Citation Index. Web. 14 July 2013.
4. Burkholder KM, Kim KP, Mishra KK, Medina S, Hahm BK, Kim H, et al. Expression of LAP, a SecA2-dependent secretory protein, is induced under anaerobic environment. Microbes Infect 2009; 11:859- 67; PMID:19454322; http://dx.doi.org/10.1016/j. micinf.2009.05.006.


Created by Danielle Vinnedge, Naomi Quillin, Jennifer Gallup, students of Tyrrell Conway at the University of Oklahoma.