Enterococcus malodoratus is a species of the genus Enterococcus and a gram positive bacteria capable of opportunistic pathogenic response. These microbes have a thick polypeptide layer.[1] Enterococcus can be found in the gastrointestinal tracts of humans and other mammals. In a study on the enterococcal flora of swine, E. malodoratus was found in the intestines and feces. It was not identified within the tonsils of swine, nor within cats, calves, dogs, horse, or poultry.[2] The name "malodoratus" translates to "ill smelling".[1]
| Enterococcus malodoratus | |
|---|---|
Scientific classification 
| |
| Domain: | Bacteria |
| Phylum: | Bacillota |
| Class: | Bacilli |
| Order: | Lactobacillales |
| Family: | Enterococcaceae |
| Genus: | Enterococcus |
| Species: | E. malodoratus
|
| Binomial name | |
| Enterococcus malodoratus Collins et al. 1984
| |
Physiology
editEnterococcus malodoratus is a nonmotile, facultatively anaerobic microbe, as well as a chemoorganotroph with fermentative metabolism.[1][3] The cells are coccoid in structure, found mostly in pairs or short streptococcus chains. Unlike many other Enterococcus species, E. malodoratus does not usually grow at 45 degrees Celsius, nor does it survive heating at 60 degrees Celsius for 30 minutes. It is nonpigmented. E. malodoratus does not produce methylcarbinol [1] or hydrolyze arginine.[4] In carbohydrate and raffinose broths, E. malodoratus forms acid.[4] It does not form endospores thus separating it from bacilli and clostridia species.[3]
Pathology
editThe genus Enterococcus is "capable of inducing platelet aggregation and tissue factor-dependent fibrin production, which may be relevant to the pathogenesis of enterococcal endocarditis".[5] The microbe is frequently the cause of hospital-acquired nosocomial infections, bloodstream infections, and urinary tract infections in its host. Though a normal part of the biota of the intestinal tract of humans and other mammals, Enterococci can also survive for lengths of time with adhesion to environmental surfaces; thus contributing to transmission and possible contagion between hosts.[6] The genus has also been proven to survive desiccation.[3] In general, the inhospitable, acidic, and competitive environment of the gastrointestinal tract limits the spread of enterococci. However, it is often during the early stages of a medical intervention that the enterococci can successfully move and colonize beyond the neutral area near the colon.[3]
Diagnosis/identification
editDNA methods have been used by researchers to correctly identify specific species within the genus Enterococcus. Using the chaperonin 60 gene (Cpn60), specific species of DNA sequencing can be distinguished in the ~600-bp region. It is imperative to correctly distinguish between Enterococcus species, as some species have been found to be resistant to some drug therapies. In fact, the genus Enterococcus has become important in the study of super infections and pathogenic resistance to antibiotics. E. malodoratus, specifically, has not yet been found to have developed that resistance.[7]
Historical
editUntil 1984, all Enterococcus species were considered part of the genus Streptococcus. It was during the 1980s that studies on fatty acid composition, nucleic acid hybridization, and comparative oligonucleotide cataloguing of 16S rRNA showed the significant differences between enterococci and streptococci.[8] The differences were enough to establish Enterococcus as a genus of its own. Each species within the enterococci category was reclassified, including E. malodoratus – originally known as S. faecalis subsp. malodoratus.[1]
References
edit- ^ a b c d e Collins, M. D.; Jones, D.; Farrow, J. A. E.; Kilpper-Balz, R.; Schleifer, K. H. (1984). "Enterococcus avium nom. rev., comb. nov.; E. casseliflavus nom. rev., comb. nov.; E. durans nom. rev., comb. nov.; E. gallinarum comb. nov.; and E. malodoratus sp. nov". International Journal of Systematic Bacteriology. 34 (2): 220–223. doi:10.1099/00207713-34-2-220. ISSN 0020-7713.
- ^ Gilmore, Michael (2002). Enterococci: Pathogenesis, Molecular Biology, and Antibiotic Resistance. Washington, D.C.: ASM Press. pp. 57–58. ISBN 1-55581-234-1.
- ^ a b c d Holt, John (1994). Bergey's Manual of Determinative Bacteriology. Baltimore: Williams & Wilkins. pp. 528–539. ISBN 0-683-00603-7.
- ^ a b Lebreton, Francois; Willems, Rob (2 Feb 2014). "Enterococcus Diversity, Origins in Nature, and Gut Colonization". National Center for Biotechnology Information. PMID 24649513. Retrieved 1 July 2014.
- ^ Johnson, Alan (1994). "The pathogenicity of enterococci". Journal of Antimicrobial Chemotherapy. 33 (6): 1083–1089. doi:10.1093/jac/33.6.1083. PMID 7928803.
- ^ Fraser, Susan (30 June 2014). "Enterococcal Infections". Medscape. Retrieved 1 July 2014.
- ^ Goh, Swee Han; Facklam, Richard (November 2000). "Identification of Enterococcus Species and Phenotypically Similar Lactococcus and Vagococcus Species by Reverse Checkerboard Hybridization to Chaperonin 60 Gene Sequences". Journal of Clinical Microbiology. 38 (11): 3953–9. doi:10.1128/JCM.38.11.3953-3959.2000. PMC 87524. PMID 11060051.
- ^ Sood, Sema; Malhotra, Meenakshi (2008), "Enterococcal infections and antimicrobial resistance" (PDF), The Indian Journal of Medical Research, 128 (2), New Delhi, India: Department of Microbiology, All India Institute of Medical Sciences: 111–121, PMID 19001673, retrieved 1 July 2014
Further reading
edit- Goh SH, Facklam RR, Chang M, et al. (November 2000). "Identification of Enterococcus species and phenotypically similar Lactococcus and Vagococcus species by reverse checkerboard hybridization to chaperonin 60 gene sequences". Journal of Clinical Microbiology. 38 (11): 3953–9. doi:10.1128/JCM.38.11.3953-3959.2000. PMC 87524. PMID 11060051.
- Holzapfel, W. H.; Wood, Brian J. B. (1995). The Genera of lactic acid bacteria. London: Blackie Academic & Professional. ISBN 0-7514-0215-X.
