A Microbial Biorealm page on the genus Listeria ivanovii
Higher order taxa
Bacteria; Firmicutes; Bacilli; Bacillales; Listeriaceae
Description and significance
L. ivanovii is a non-spore forming, gram-positive, rod shaped bacteria. L. ivanovii is pathogenic, mainly infecting small ruminants and cattle, causing septicemic disease. Human cases of disease caused by L. ivanovii are extremely rare.1
L. ivanovii contain one circular chromosome of 2,928,879 base pairs with an average G+C content of 37.1%. L. ivanovii contains six complete rRNA operons, 2,782 protein coding-genes, and 67 tRNA genes. The L. ivanovii genome contains 86 pseudogenes, of which 37 are truncated and 53 are interrupted by frameshift mutations.1
Cell and Colony Structure
L. ivanovii are short (0.4-0.5 x 0.5-2 µm), motile rods. L. ivanovii colonies are 0.5-1.5mm in diameter and appear a greyish blue color.6 When grown close to Rhodococcus equi on blood agar, L. ivanovii gives rise to a shovel-shaped patch of synergic haemolysis. This is used to differentiate L. ivanovii from Listeria monocytogenes. L. monocytogenes, which is the only other pathogenic species of Listeria, is weakly haemolytic and does not produce a shovel-shape when grown next to R. equi.3
L. ivanovii is a facultative anaerobe that makes ATP by aerobic respiration when oxygen is present, but is also capable of switching to fermentation. L. ivanovii are catalase positive and have the ability to ferment various carbohydrates, such as: glucose, lactose, trehalose, and glycerol.6
L. ivanovii is thought to inhabit the surface layer of soil rich in decaying plant matter. L. ivanovii infect vertebrate host via the oral route on contaminated food.4 Listeria sp. are capable of growth under diverse growth conditions, such as high salt concentrations (10% NaCl), pH 4.5 to 9, and temperatures of 0º-45ºC.2
Upon becoming ingested by a ruminent, L. ivanovii develop a characteristic intracellular life cycle that includes six virulence factors. These steps include: early escape from the phagocytic vacuole, multiplication in the host cell cytoplasm, directional intracytosolic motility by induction of actin polymerization at one pole of the bacterial cell, protrusion of centrifugally moving bacteria within the cytoplasmic evaginations, and phagocytosis of the pseudopod-like structures by neighboring cells, in which the cycle reinitiates.1 Successful infection of L. ivanovii within a host can lead to septicemic disease with enteritis, neonatal sepsis and abortion.5
1 Vazquez-Boland, J., et al. 2001. Pathogenicity islands and virulence evolution in Listeria. Microbes and Infection, 3(7), 571-584.
2 Chakraborty, T., et al. 2000. Genome organization and the evolution of the virulence gene locus in Listeria species. Int. Journal of Medical Microbiology, 290, 167-174.
3 Gonzalez-Zorn, B. et al. 1999. The smcL gene of Listeria ivanovii encodes a shingomyelinase C that mediates bacterial escape from the phagocytic vacuole. Molecular Microbiology, 33(3), 510-523.
4 Buchrieser, C., et al. 2011. Complete Genome Sequence of the Animal Pathogen Listeria ivanovii, Which Provides Insights into Host Specificities and Evolution of the Genus Listeria.” Journal of Bacteriology, 193(23), 6787-6788.
5 Engelbrecht, F., et al. 1998. A novel PrfA-regulated chromosomal locus, which is specific for Listeria ivanovii, encodes two small, secreted internalins and contributes to virulence in mice. Molecular Microbiology, 30(2), 405-417.
6 Div. of Bacteriology Uppsala, Sweden. (2010, March 9). Listeria ivanovii. Retrieved from Swedish VetBact website: http://www.vetbact.org/vetbact/?artid=168#
Edited by Erica Ferrelli, a student of Dr. Lisa R. Moore, University of Southern Maine, Department of Biological Sciences, http://www.usm.maine.edu/bio