Dr. E. Fidelma Boyd

Assistant Professor

Contact

Boyd

Office: 328 Wolf Hall
Lab: 341 Wolf Hall

Mailing address:
Department of Biological Sciences
Wolf Hall
University of Delaware
Newark, DE 19716

Phone: (302) 831-1088
Fax: (302) 831-2281
E-mail: fboyd@udel.edu

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Education

B.S., Ph.D.: National University of Ireland - Galway, Ireland
Postdoctoral: The Pennsylvania State University
Postdoctoral: Harvard University
Postdoctoral: Tufts University School of Medicine

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Research Interests

Vibrio cholerae, the causative agent of the dreaded diarrheal disease cholera

Cholera is still a major scourge for developing countries. This severe diarrheal disease is caused by the gram-negative bacterium Vibrio cholerae, which is a natural inhabitant of brackish and estuarine waters. Two virulence factors are indispensable, cholera Toxin (CT) and the Toxin Corregulated Pilus (TCP), and are encoded on integrative elements the CTXphi phage and the TCP island or Vibrio Pathogenicity Island-1 (VPI-1) respectively. My group identified a second pathogenicity island named VPI-2, which is present among O1 serogroup isolates (Jermyn and Boyd, 2002, 2005). VPI-2 contains genes putatively involved in sialic acid transport (dctPQM) and degradation of sialic acid (nanA, nanEK, nagA). Adjacent this nan-nag region is the gene that encode for a neuraminidase (nanH) (Jermyn and Boyd, 2002, 2005). NanH removes two sialic acid residues from the trisialogangliosides found in the intestinal mucin, converting them into GM1 gangliosides, which are the receptors of CT. We hypothesize that carriage of the VPI-2 region by V. cholerae O1 isolates gives them a fitness advantage and loss of the region from O139 isolates has resulted in their disappearance as a major cause of cholera.

Vibrio pathogenicity island-2 role in V. cholerae survival and fitness. One of our research goals is to determine the functional role of VPI-2 in vitro and in vivo. The genes required for sialic acid degradation are predominantly present in bacteria that are pathogens or commensals of humans (Almagro-Moreno and Boyd, BMC Evol. Biol. 2009 in revision). The release of free sialic acid by neuraminidase allows V. cholerae to uptake and catabolize sialic acid as a carbon and energy source giving them a competitive advantage (Almagro-Moreno and Boyd, unpublished data). We are also examining attachment of V. cholerae using atomic force microscopy.

Pathogenicity island evolution,: VPI-2 excision dynamics. Surprisingly little is known of pathogenicity island evolution and the mechanisms of acquisition or mobility within Vibrio cholerae. We determined the role of the VPI-2 encoded integrase in the excision process by constructing a knockout mutant (Murphy and Boyd, 2008). No excision product was found indicating that a functional cognate VPI-2 integrase is required (Murphy and Boyd, 2008). A second research goal is to determine pathogenicity islands stability and mobility, by examining VPI-2 excision dynamics and the role of island-encoded and host-encoded factors.

The Phage, The Pilus and allelic variation: Bacteriophage-Host interaction in Vibrio cholerae. CTXphi interacts with the bacterial host receptor TCP (a type IV pilus) and co-receptor TolA. Although the pIIICTX locus, proposed to mimic the E. coli pIII mediator of Ff phage infection, is well conserved among V. cholerae strains, the tcpA locus, which encodes the major pilin protein of TCP, has significant sequence divergence (Boyd and Waldor, 2002). We are examining the specificity of the pIIICTX-TcpA and the pIIICTX-TcpA/TolA interactions (Reen and Boyd, unpublished data).

Our results to date suggest that the divergence at the tcpA locus is not reflected in the pilin- pIIICTX interaction. The varied transduction efficiencies observed in wild-type strains were not observed in the isogenic mutants, which were found to be similar. In the Yeast two-hybrid system screen, the co-receptor TolA was shown to be unable to bind pIIICTX in the absence of TcpA, confirming the requirement for conformational change (Reen and Boyd, unpublished data).

Vibrio parahaemolyticus an emerging human pathogen

V. parahaemolyticus is a moderate halophile that is presence in all coastal water around the world. In the past decade, the geographic distribution of V. parahaemolyticus has been extended into more northerly climes, in particular the Pacific Northwest. This is most likely due to global warming and therefore the occurrence and prevalence of the organism is likely to continue to expand. V. parahaemolyticus is an enteric pathogen that causes gastroenteritis after the consumption of contaminated seafood, such as shellfish. In recent years a novel variant has emerged that has resulted in increased hospitalizations.

Comparative genomic analysis of V. parahaemolyticus. We identified seven regions that were acquired by the new O3:K6 pandemic clone, which may play a role in the emergence and pathogenesis of these strains. We named these regions Vibrio parahaemolyticus island-1 (VPaI-1) to VPaI-7 (Hurley et al., 2006). Molecular analysis of a worldwide collection of isolates of V. parahaemolyticus demonstrated that the VPaI-1, VPaI-4, VPaI-5 and VPaI-6 regions are present exclusively in new O3:K6 and related strains recovered after 1995. A four-way genomic BLAST analysis of V. parahaemolyticus RIMD2210633 genome sequence verses the four published Vibrio species genomes, identified 24 regions of greater than 10 kb that are unique to RIMD2210633 (Boyd et al., 2008). Our data suggest that the new highly virulent O3:K6 clone arose from an O3:K6 isolate that acquired at least seven novel regions (Boyd et al., 2008).

Osmotic tolerance and acid tolerance in Vibrio parahaemolyticus. Salinity is an absolute requirement for growth and proliferation and V. parahaemolyticus can grow in up to 10% NaCl; however our knowledge of the mechanisms of osmotolerance in V. parahaemolyticus is limited. We have identified in the genome of V. parahaemolyticus a unique clustering of genes that show homology to osmotolerance systems, double the number present in other double the number of systems present in other Vibrio (Boyd et al., 2008; Naughton and Boyd, unpublished data). Our hypothesis is that this unique clustering and number of operons enhances V. parahaemolyticus ability to grow in fluctuating saline environments. Comparative physiological analysis determined that in all cases V. parahaemolyticus had a growth advantage (Naughton and Boyd, unpublished data). More recent data shows that growth in low salinity also protects at low pH, which is being investigated further (Whitaker and Boyd, unpublished data).

Vibrio vulnificus a highly invasive pathogen of both fish and humans

Vibrio vulnificus is a ubiquitous aquatic organism found throughout the world. As well as comprising part of the normal micro flora of coastal waters, V. vulnificus is a highly invasive pathogen of both fish and humans. V. vulnificus causes significant economic losses in the eel aquaculture and occurs in high numbers in oysters and other molluscs. This is highly problematic due to the popularity of raw oyster consumption since V. vulnificus infections in humans have a mortality rates greater than 50% in susceptible individuals. Our overall hypothesis is that V. vulnificus population structure consists of at least three major clades containing unique regions required for survival within its varied niches. We are using molecular genetics and genomics approaches to determine the key elements that allow the organisms to survive in molluscs, fish and humans.

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Teaching

• BISC 667 - Molecular Mechanisms of Pathogens

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Research Group

• Seth Blumerman, Ph.D. - Postdoctoral Fellow (Ph.D., University of Massachusetts Amherst).
• AnaLuisa Santos Ferreira de Vasoncelos Cohen, M.S. - Ph.D. Graduate Student (M.S., University of Reading, United Kingdom). Evolution and Emergence of the human pathogen Vibrio vulnificus.
• Salvador Almagro Moreno, M.S. - Ph.D. Graduate Student (M.S., National University of Ireland - Cork, Ireland). Sialic acid metabolism in Vibrio cholerae.
• Lynn Naughton, B.S. - Ph.D. Graduate Student (B.S., National University of Ireland - Cork, Ireland). Vibrio parahaemolyticus osmoregulation.
• William Brian Whitaker, B.S. - Ph.D. Graduate Student (B.S., Delaware Valley College). Vibrio parahaemolyticus acid tolerance response.
• Michael Napolitano - Undergraduate Student.
• Coral Wille - Undergraduate Student.

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Selected Publications

McCarthy, N., F.J. Reen, J.F. Buckley, J.G. Frye, E.F. Boyd and D. Gilroy. 2009. Sensitive and rapid molecular detection assays for Salmonella enterica serovar Typhimurium and Heidelberg. J Food Protection. In revision.

Moreno-Almagro, S. and E.F. Boyd. 2009. Insights into the evolution of sialic acid catabolism in Bacteria. BMC Evol Biol. In revision.

Naughton, L.M. and E.F. Boyd. 2009. Osmoadaptation among Vibrio species: unique genomic features and physiological response in V. parahaemolyticus. Appl Environ Microbiol. In revision.

Boyd, E.F., S. Amagro-Moreno, and M.A. Parent. 2009. Genomic islands are a distinct class of ancient integrative elements in bacterial evolution. Trends Microbiol. In press.

Moynihan, J.A., J.P. Morrissey, E. Coppoosle, W. Stiekema, F. O'Gara, and E.F. Boyd. 2009. Pseudomonas fluorescens the plant-associated biocontrol agent: Phylogeny and Phloroglucinol production. Appl Env Microbiol. In press.

Woods DF, Reen FJ, Gilroy D, Buckley J, Frye JG, Boyd EF. 2008. Rapid multiplex PCR and real-time TaqMan PCR assays for detection of Salmonella enterica and the highly virulent serovars Choleraesuis and Paratyphi C. J Clin Microbiol. 46(12):4018-2.

Boyd, E.F., A.L. Cohen, L.M. Naughton, T.T. Binnewies, D.W. Ussery, O.C. Stine, and M.A. Parent. 2008. Molecular analysis of the emergence of pandemic Vibrio parahaemolyticus. BMC Microbiol 8:110.

Sheikh, M.A., J.A. Potter, K.A. Johnson, R.B. Sim, E.F. Boyd, and G.L. Taylor. 2008. Crystal structure of VC1805, a conserved hypothetical protein from a Vibrio cholerae pathogenicity island, reveals homology to human p32. Proteins: Structure, Function, and Bioinformatics 71(3):1563-1571.

Boyd, E.F. 2008. Bacteriophages in Vibrio cholerae genetics and evolution. In Vibrio cholerae: Genomics and Molecular Biology. Ed. G.B. Nair and S. Faruque. Humana Press.

Murphy, R.A. and E.F. Boyd. 2008. Three pathogenicity islands of Vibrio cholerae excise from the chromosome and form circular intermediates. J. Bacteriology 190(2):636-647.

Cohen, A.L., J.D. Oliver, A. DePaola, E. Feil, and E.F. Boyd. 2007. Molecular phylogeny of Vibrio vulnificus based on multilocus sequence analysis and a 33 kb genomic island correlates with pathogenic potential. Applied Environmental Microbiology 73:5553-5565.

Murphy, B.P., R. O'Mahony, J.F. Buckley, P. Shine, E.F. Boyd, D. Gilroy, S. Fanning. 2007. Investigation of a global collection of nontyphoidal Salmonella of various serotypes cultured between 1953 and 2004 for the presence of class 1 integrons. FEMS Microbiol Lett. 266(2):170-176.

Reen, F.J., S.A. Moreno, D. Ussery, and E.F. Boyd. 2006. The Genomic code: Inferring Vibrionaceae niche specialization. Nat. Rev. Microbiol. 4(9):697-704.

Hurley, C.C., A.M. Quirke, F.J. Reen, and E.F. Boyd. 2006. Four genomic islands that mark pandemic Vibrio parahaemolyticus isolates. BMC Genomics. 7:104

Quirke, A.M., F.J. Reen, M.J. Claessen, and E.F. Boyd. 2006. Genomic island identification in Vibrio vulnificus reveals significant genome plasticity in the important human pathogen. Bioinformatics. 22:905-910.

Jermyn, W.S., Y.A. O'Shea, A.M. Quirke, and E.F. Boyd. 2006. Genomics and the emergence of pathogenic Vibrio cholerae. In "Bacterial Genomes and Infectious Diseases". Ed. Chan VL, Sherman PM, Bourke B. Humana Press.

Reen, F.J. and E.F. Boyd. 2005. Adaptation of Vibrio species to the environment and host. In "Understanding Pathogen Behaviour". Ed. M. Griffiths and F. Dodds, Woodhead Publishing.

Reen, F.J. and E.F. Boyd. 2005. Molecular typing of epidemic and nonepidemic Vibrio cholerae isolates and differentiation of V. cholerae and V. mimicus isolates by PCR-single-strand conformation polymorphism analysis. J. Appl. Microbiol. 98:544-555.

Reen, F.J., E.F. Boyd, S. Porwollik, B. Murphy, D. Gilroy, S. Fanning, and M. McClelland. 2005. Genomic comparisons of recent Salmonella enterica isolates in milk filters from Ireland using a Salmonella microarray. Appl. Environ. Microbiol. 71:3:00.

Jermyn, W.S. and E.F. Boyd. 2005. Molecular evolution of the Vibrio Pathogenicity Island-2 (VPI-2): Mosaic structure among Vibrio cholerae and Vibrio mimicus natural isolates. Microbiol. 151:311-322.

Boyd, E.F. 2004. Bacteriophages and bacterial virulence. In "Bacteriophages: Molecular Biology and Applications". Eds. E. Kutter and A. Sulakvelidze. CRC Press.

Finnan, S., J. Morrissey, F. O'Gara, and E.F. Boyd. 2004. Genomic diversity of Pseudomonas aeruginosa isolates from cystic fibrosis patients in Ireland. J. Clin. Microbiol. 42:5783-5792.

O'Shea, Y., S. Finnan, F.J. Reen, J. Morrissey, F. O'Gara, and E.F. Boyd. 2004. The Vibrio seventh pandemic island-II is a 26.9 kb genomic island present in V. cholerae El Tor and O139 serogroup isolates that shows homology to a 43.5 Kb island in V. vulnificus. Microbiol. 150:4053-4063.

Porwollik, S., E.F. Boyd, C. Choy, P. Cheng, L. Florea, E. Proctor, and M. McClelland. 2004. Characterization of Salmonella enterica subspecies I genovars using microarrays. J. Bacteriol. 186:5884-5894.

O'Shea, Y.A., F.J. Reen, AM. Quirke, and E.F. Boyd. 2004. Evolutionary genetic relationships among Vibrio cholerae natural isolates based on multilocus comparative sequence analysis and multilocus virulence gene profiles. J. Clin. Microbiol. 42:4657-4671.

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