Front Microbiol. 2015 Jan 15;5:803. doi: 10.3389/fmicb.2014.00803. eCollection 2014.
Comparative genomic analysis of clinical and environmental Vibrio vulnificus isolates revealed biotype 3 evolutionary relationships.
Frontiers in microbiology
Yael Koton, Michal Gordon, Vered Chalifa-Caspi, Naiel Bisharat
Affiliations
Affiliations
- Department of Medicine D, Emek Medical Center Afula, Israel ; Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology Haifa, Israel.
- Bioinformatics Core Facility, National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev Beer-Sheva, Israel.
PMID: 25642229
PMCID: PMC4295529 DOI: 10.3389/fmicb.2014.00803
Abstract
In 1996 a common-source outbreak of severe soft tissue and bloodstream infections erupted among Israeli fish farmers and fish consumers due to changes in fish marketing policies. The causative pathogen was a new strain of Vibrio vulnificus, named biotype 3, which displayed a unique biochemical and genotypic profile. Initial observations suggested that the pathogen erupted as a result of genetic recombination between two distinct populations. We applied a whole genome shotgun sequencing approach using several V. vulnificus strains from Israel in order to study the pan genome of V. vulnificus and determine the phylogenetic relationship of biotype 3 with existing populations. The core genome of V. vulnificus based on 16 draft and complete genomes consisted of 3068 genes, representing between 59 and 78% of the whole genome of 16 strains. The accessory genome varied in size from 781 to 2044 kbp. Phylogenetic analysis based on whole, core, and accessory genomes displayed similar clustering patterns with two main clusters, clinical (C) and environmental (E), all biotype 3 strains formed a distinct group within the E cluster. Annotation of accessory genomic regions found in biotype 3 strains and absent from the core genome yielded 1732 genes, of which the vast majority encoded hypothetical proteins, phage-related proteins, and mobile element proteins. A total of 1916 proteins (including 713 hypothetical proteins) were present in all human pathogenic strains (both biotype 3 and non-biotype 3) and absent from the environmental strains. Clustering analysis of the non-hypothetical proteins revealed 148 protein clusters shared by all human pathogenic strains; these included transcriptional regulators, arylsulfatases, methyl-accepting chemotaxis proteins, acetyltransferases, GGDEF family proteins, transposases, type IV secretory system (T4SS) proteins, and integrases. Our study showed that V. vulnificus biotype 3 evolved from environmental populations and formed a genetically distinct group within the E-cluster. The unique epidemiological circumstances facilitated disease outbreak and brought this genotype to the attention of the scientific community.
Keywords: Vibrio vulnificus; accessory genome; aquaculture; core genome; evolution; microbial genome; whole genome shotgun sequences
References
- Lancet. 1996 Dec 7;348(9041):1585-6 - PubMed
- Infection. 1998 Nov-Dec;26(6):399-401 - PubMed
- Front Microbiol. 2013 Dec 18;4:393 - PubMed
- Lancet. 1999 Oct 23;354(9188):1421-4 - PubMed
- Mol Biol Evol. 2014 May;31(5):1077-88 - PubMed
- Emerg Infect Dis. 2008 Dec;14(12):1875-82 - PubMed
- Bioinformatics. 2012 Dec 1;28(23):3150-2 - PubMed
- Nucleic Acids Res. 1999 Jun 1;27(11):2369-76 - PubMed
- Eur J Clin Microbiol Infect Dis. 1996 Mar;15(3):227-32 - PubMed
- Proc Natl Acad Sci U S A. 1993 May 15;90(10):4384-8 - PubMed
- South Med J. 2004 Feb;97(2):118-9 - PubMed
- Pediatr Infect Dis J. 2003 Jul;22(7):666-8 - PubMed
- FEMS Microbiol Ecol. 2008 May;64(2):209-18 - PubMed
- Emerg Infect Dis. 2009 Aug;15(8):1282-5 - PubMed
- J Infect Dis. 1984 Apr;149(4):558-61 - PubMed
- J Clin Microbiol. 2003 Jan;41(1):442-6 - PubMed
- Appl Environ Microbiol. 2008 Jan;74(1):80-5 - PubMed
- Bioinformatics. 2006 Jul 1;22(13):1658-9 - PubMed
- Emerg Infect Dis. 2005 Jan;11(1):30-5 - PubMed
- Microbiology. 2007 Mar;153(Pt 3):847-56 - PubMed
- BMC Genomics. 2014 Aug 29;15:737 - PubMed
- Microbiol Immunol. 2005;49(4):381-9 - PubMed
- APMIS. 1994 Nov;102(11):874-6 - PubMed
- An Med Interna. 1998 Sep;15(9):485-6 - PubMed
- Nucleic Acids Res. 2001 Jan 1;29(1):22-8 - PubMed
- Isr Med Assoc J. 2002 Aug;4(8):631-3 - PubMed
- Foodborne Pathog Dis. 2007 Fall;4(3):327-37 - PubMed
- PLoS One. 2013 Dec 30;8(12):e83357 - PubMed
- Ann Intern Med. 1988 Aug 15;109(4):318-23 - PubMed
- Euro Surveill. 2006 Aug 17;11(8):E060817.1 - PubMed
- BMC Genomics. 2008 Feb 08;9:75 - PubMed
- Clin Infect Dis. 1992 Aug;15(2):271-6 - PubMed
- Appl Environ Microbiol. 2013 Jun;79(12):3570-81 - PubMed
- J Microbiol Immunol Infect. 2003 Jun;36(2):81-8 - PubMed
- BMC Genomics. 2010 Sep 24;11:512 - PubMed
- Appl Environ Microbiol. 1982 Sep;44(3):640-6 - PubMed
- BMC Bioinformatics. 2010 Sep 15;11:461 - PubMed
- J Clin Microbiol. 2004 Sep;42(9):4137-40 - PubMed
- PLoS One. 2012;7(5):e37553 - PubMed
- Genome Biol. 2009;10(3):R25 - PubMed
- Infect Genet Evol. 2007 Dec;7(6):685-93 - PubMed
- Genome Announc. 2013 Apr 18;1(2):e0013613 - PubMed
- J Emerg Med. 1998 Jan-Feb;16(1):61-6 - PubMed
- Eur J Clin Microbiol Infect Dis. 2002 Jul;21(7):537-8 - PubMed
- Bioinformatics. 2000 Oct;16(10):944-5 - PubMed
- Bioinformatics. 2013 Apr 15;29(8):1072-5 - PubMed
- Int J Syst Bacteriol. 1994 Apr;44(2):330-7 - PubMed
- Bioinformatics. 2009 Jul 15;25(14):1754-60 - PubMed
- J Infect Chemother. 2010 Aug;16(4):272-9 - PubMed
- Genome Announc. 2014 Mar 20;2(2):null - PubMed
- Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W181-4 - PubMed
- Scand J Infect Dis. 1995;27(1):81-2 - PubMed
- Clin Infect Dis. 2002 Mar 1;34(5):714-5 - PubMed
- Appl Environ Microbiol. 2003 Jun;69(6):3203-12 - PubMed
- J Am Acad Dermatol. 1991 Mar;24(3):397-403 - PubMed
- Syst Biol. 2010 May;59(3):307-21 - PubMed
- Appl Environ Microbiol. 2010 Jul;76(14):4890-5 - PubMed
- Genome Announc. 2014 Nov 26;2(6):null - PubMed
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