Marc A. Hughes

Dr. Marc A. Hughes

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Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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7 April 2017 in Biological Invasions
Verified
Journal Article
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MHMarc A. Hughes
Marc A. Hughes
JRJohn Riggins
John Riggins
FKF. H. Koch
F. H. Koch
ACA. I. Cognato
A. I. Cognato
CAC. Anderson
C. Anderson
JSJ. A. Smith
J. A. Smith

1 June 2008 in Plant Disease
Verified
Journal Article
Open access
AMA. E. Mayfield
A. E. Mayfield
JSJ. A. Smith
J. A. Smith
MHMarc A. Hughes
Marc A. Hughes
TDT. J. Dreaden
T. J. Dreaden
Laurel wilt is a vascular disease of redbay (Persea borbonia (L.) Spreng.) and other plants in the family Lauraceae in the southeastern United States. It is caused by a fungus (Raffaelea sp.) that is vectored by a non-native insect of Asian origin, the redbay ambrosia beetle (Xyleborus glabratus Eichhoff) (1). Since the initial detection of the redbay ambrosia beetle near Savannah, GA in 2002, laurel wilt has caused widespread mortality of redbay in Georgia, South Carolina, and Florida (1). In September 2007, an avocado (Persea americana Mill.) tree planted approximately 10 years earlier in a residential neighborhood in Jacksonville, FL was discovered to be infected with laurel wilt. The crown was in various stages of decline, including upper branches that were dead and leafless, those with wilted and drooping foliage, and those with healthy foliage. Removal of bark from wilted branch sections revealed black-to-brown streaks of discoloration in the sapwood and a few ambrosia beetle holes from which the discoloration extended into the adjacent wood. A Raffaelea sp. was isolated from discolored wood samples by surface sterilizing wood chips by submersion in a 5% sodium hypochlorite solution for 30 s and plating them on cycloheximide streptomycin malt agar (2). Small subunit (18S) sequences from the rDNA were amplified by PCR and sequenced with primers NS1 and NS4 (3). BLASTn searches revealed homology to Raffaelea sp. C2203 (GenBank Accession No. EU123076, 100% similarity, e-value of 0.0, and a total score of 1,886), which is known to be the causal agent of laurel wilt (1). The small-subunit rDNA sequence for this isolate has been deposited into GenBank and has been assigned accession No. EU257806. Pathogenicity of the laurel wilt pathogen on Persea spp. in growth chamber trials has been previously demonstrated (1). Laurel wilt is of concern to the commercial avocado industry and is a potential threat to the Lauraceae elsewhere in the Americas. References: (1) S. W. Fraedrich et al. Plant Dis. 92:215, 2008. (2) T. C. Harrington. Mycologia 73:1123, 1981. (3) T. J. White et al. Page 315 in: PCR Protocols, a Guide to Methods and Applications. M. A. Innis et al., eds. Academic Press, San Diego, CA, 1990.

21 November 2011 in Plant Pathology
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Journal Article
Open access
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RPRandy Ploetz
Randy Ploetz
JPJ. M. Pérez‐Martínez
J. M. Pérez‐Martínez
JSJ. A. Smith
J. A. Smith
MHMarc A. Hughes
Marc A. Hughes
TDT. J. Dreaden
T. J. Dreaden
YFY. Fu
Y. Fu
Laurel wilt, caused by Raffaelea lauricola , threatens native and non‐native species in the Lauraceae in the south‐eastern USA. Avocado, Persea americana , is the most important agricultural suscept of laurel wilt. Grafted plants (clonal scions on seedling rootstocks) of 24 cultivars were screened against the disease in the field from 2008 to 2010. Disease was induced with either mycelial plugs or conidial suspensions of R. lauricola . There were significant differences in the severity of disease that developed on different cultivars, and West Indian cultivars were most susceptible ( P  < 0·05). Simmonds, a West Indian cultivar that comprises 35% of the commercial production in Florida, was consistently susceptible and was used as a standard genotype in different studies. Disease severity increased significantly on cv. Simmonds as plant size (stem diameter) increased ( P  < 0·0042). In greenhouse studies, internal (sapwood) and external disease severities on cv. Simmonds were correlated ( P  < 0·0001), and a threshold was evident, in that external symptoms developed only after moderately severe symptoms had developed internally. Latent infection was uncommon; R. lauricola was usually isolated on a semiselective medium or detected via qPCR only from discoloured xylem of inoculated cv. Simmonds. As basipetal movement of the pathogen was common, its movement among trees via root grafts is probable. Greater understanding is needed of the movement of R. lauricola in naturally and artificially infected trees, and whether sufficient tolerance exists in avocado to assist in the management of this important new disease.

1 January 2015 in Plant Health Progress
Verified
Journal Article
Open access
MHMarc A. Hughes
Marc A. Hughes
JSJ. A. Smith
J. A. Smith
RPR. C. Ploetz
R. C. Ploetz
PKP. E. Kendra
P. E. Kendra
AMA. E. Mayfield
A. E. Mayfield
TPT. Pernas
T. Pernas
This recovery plan is one of several disease-specific documents produced as part of the National Plant Disease Recovery System (NPDRS) called for in Homeland Security Presidential Directive Number 9 (HSPD-9). The purpose of the NPDRS is to insure that the tools, infrastructure, communication networks, and capacity required to mitigate the impact of high-consequence plant disease outbreaks are such that a reasonable level of crop production is maintained. Each disease-specific plan is intended to provide a brief primer on the disease, assess the status of critical recovery components, and identify disease management research, extension, and education needs. These documents are not intended to be stand-alone documents that address all of the many and varied aspects of plant disease outbreak and all of the decisions that must be made and actions taken to achieve effective response and recovery. They are, however, documents that will help USDA guide further efforts directed toward plant disease recovery. Accepted for publication 13 October 2015. Published 17 November 2015.

18 February 2017 in Forests
Verified
Journal Article
Open access
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RPRandy Ploetz
Randy Ploetz
PKPaul E Kendra
Paul E Kendra
RCRobin Choudhury
Robin Choudhury
JRJeffrey A Rollins
Jeffrey A Rollins
Alina Sandra PuigAlina Sandra Puig
Alina Sandra Puig
TDTyler Dreaden
Tyler Dreaden
Laurel wilt kills members of the Lauraceae plant family in the southeastern United States. It is caused by Raffaelea lauricola T.C. Harr., Fraedrich and Aghayeva, a nutritional fungal symbiont of an invasive Asian ambrosia beetle, Xyleborus glabratus Eichhoff, which was detected in Port Wentworth, Georgia, in 2002. The beetle is the primary vector of R. lauricola in forests along the southeastern coastal plain of the United States, but other ambrosia beetle species that obtained the pathogen after the initial introduction may play a role in the avocado (Persea americana Miller) pathosystem. Susceptible taxa are naïve (new-encounter) hosts that originated outside Asia. In the southeastern United States, over 300 million trees of redbay (P. borbonia (L.) Spreng.) have been lost, and other North American endemics, non-Asian ornamentals and avocado—an important crop that originated in MesoAmerica—are also affected. However, there are no reports of laurel wilt on the significant number of lauraceous endemics that occur in the Asian homeland of R. lauricola and X. glabratus; coevolved resistance to the disease in the region has been hypothesized. The rapid spread of laurel wilt in the United States is due to an efficient vector, X. glabratus, and the movement of wood infested with the insect and pathogen. These factors, the absence of fully resistant genotypes, and the paucity of effective control measures severely constrain the disease’s management in forest ecosystems and avocado production areas.

1 September 2008 in Florida Entomologist
Verified
Journal Article
Open access
AMA. E. Mayfield
A. E. Mayfield
JPJ. E. Peña
J. E. Peña
JCJ. H. Crane
J. H. Crane
JSJ. A. Smith
J. A. Smith
CBC. L. Branch
C. L. Branch
MHMarc A. Hughes
Marc A. Hughes