scholarly journals Verbenone reduces landing of the redbay ambrosia beetle, vector of the laurel wilt pathogen, on live standing redbay trees

2019 ◽  
Vol 22 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Xavier Martini ◽  
Lanette Sobel ◽  
Derrick Conover ◽  
Agenor Mafra‐Neto ◽  
Jason Smith
Plant Disease ◽  
2008 ◽  
Vol 92 (6) ◽  
pp. 976-976 ◽  
Author(s):  
A. E. Mayfield ◽  
J. A. Smith ◽  
M. Hughes ◽  
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.


EDIS ◽  
2008 ◽  
Vol 2008 (2) ◽  
Author(s):  
Jonathan H. Crane ◽  
Jorge E. Peña ◽  
J. L. Osborne

HS1136, a 7-page illustrated factsheet by Jonathan H. Crane, Jorge Peña, and J.L. Osborne, describes this insect-fungal pest attacking woody plants in the laurel family, including avocado. Includes descriptions, origin, detection and spread of the pest, plant hosts in the U.S., a map of counties with the beetle, plant host symptoms and damage, management strategies & restrictions, agencies working on the issue, research and extension efforts, and references. Published by the UF Department of Horticultural Sciences, February 2008. Revised December 2008.


2019 ◽  
Vol 113 (2) ◽  
pp. 980-987
Author(s):  
Paul E Kendra ◽  
Wayne S Montgomery ◽  
Teresa I Narvaez ◽  
Daniel Carrillo

Abstract Laurel wilt and Fusarium dieback are vascular diseases caused by fungal symbionts of invasive ambrosia beetles (Coleoptera: Curculionidae: Scolytinae). Both diseases threaten avocado trees in Florida. Redbay ambrosia beetle, Xyleborus glabratus, is the primary vector of the laurel wilt pathogen, Raffaelea lauricola, but in recent years this symbiont has been transferred laterally to at least nine other species of ambrosia beetle, which now comprise a community of secondary vectors. Dieback disease, caused by Fusarium spp. fungi, is spread by shot hole borers in the Euwallacea fornicatus species complex. In this study, we conducted field tests in Florida avocado groves to compare efficacy of four trap designs for detection of Scolytinae. Treatments included an 8-funnel Lindgren trap, black 3-vane flight interception trap, green 3-vane interception trap, white sticky panel trap, and an unbaited sticky panel (control). In two tests targeting E. nr. fornicatus and X. glabratus, traps were baited with a two-component lure (α-copaene and quercivorol). In a test targeting other species, traps were baited with a low-release ethanol lure. For E. nr. fornicatus, sticky panels and black interception traps captured significantly more beetles than Lindgren traps; captures with green traps were intermediate. With ethanol-baited traps, 20 species of bark/ambrosia beetle were detected. Trap efficacy varied by species, but in general, sticky traps captured the highest number of beetles. Results indicate that sticky panel traps are more effective for monitoring ambrosia beetles than Lindgren funnel traps, the current standard, and may provide an economical alternative for pest detection in avocado groves.


Plant Disease ◽  
2011 ◽  
Vol 95 (11) ◽  
pp. 1479-1479 ◽  
Author(s):  
J. J. Riggins ◽  
S. W. Fraedrich ◽  
T. C. Harrington

Laurel wilt is caused by the fungus Raffaelea lauricola T.C. Harrin., Aghayeva & Fraedrich and is lethal to redbay (Persea borbonia (L.) Spreng.), sassafras (Sassafras albidum (Nutt.) Nees), and other species in the Lauraceae (1). The fungus is carried by the redbay ambrosia beetle (Xyleborus glabratus Eichh.), which is native to Asia. After being discovered in Georgia in 2002 (1), X. glabratus and R. lauricola have spread rapidly, causing extensive redbay mortality in South Carolina, Georgia, Florida, and Mississippi (1,4). The disease has also been confirmed on sassafras in Florida, South Carolina (1), and Georgia. Questions remain as to whether laurel wilt will continue to spread on sassafras, which often occurs as scattered trees in the eastern United States. In June 2010, a homeowner reported that a sassafras tree north of Van Cleave, MS (30.668°N, 88.686°W) had begun wilting in late May. This landscape tree had three 10-m high stems (~20 cm in diameter at breast height). Dark staining in the xylem was observed around the entire circumference of all three stems and nearly all leaves were bronze colored and wilted. No ambrosia beetle tunnels were observed in the stems. No other symptomatic Lauraceae were encountered in the wooded area within 300 m. The nearest known location with laurel wilt on redbay was ~15 km away (4). A Lindgren funnel trap baited with manuka oil (2) was placed at the site in June and monitored biweekly until November, but no X. glabratus adults were captured. Chips from discolored xylem of the sassafras were surface sterilized, plated on cycloheximide-streptomycin malt agar, and R. lauricola was readily isolated (1). Identity of the fungus (isolate C2792 in collection of T. Harrington) was confirmed by using partial sequences of the 28S rDNA (3). The sassafras sequence was identical to that of all known sequences of R. lauricola in the United States, including GenBank No. EU123076 (the holotype isolate from redbay). To confirm pathogenicity, isolate C2792 was grown on malt extract agar and three redbay (average: 141 cm high and 12 mm in diameter at soil interface) and three sassafras (average: 170 cm high and 17 mm in diameter at soil interface) potted plants were wound inoculated with 0.2 ml of a spore suspension (4.9 × 106 conidia/ml) (1). Three control plants of each species were inoculated with sterile deionized water. After 8 weeks in a growth chamber at 26°C, all inoculated redbay and sassafras plants exhibited xylem discoloration above and below the inoculation point, two of the redbay and two of the sassafras had died, and the other plant of each species exhibited partial wilt (the main terminal or one or more branches). All control plants were asymptomatic. R. lauricola was reisolated from all inoculated symptomatic plants but not from controls. To our knowledge, this is the first report of laurel wilt on sassafras in Mississippi. Both redbay (4) and sassafras appear to be highly susceptible to the disease as it moves westward. Sassafras is less attractive than redbay to X. glabratus and it was thought that this might contribute to slowing the spread of laurel wilt once outside the range of redbay (2). Nonetheless, our observations confirm that sassafras can be infected where laurel wilt on redbay is not in the immediate vicinity. References: (1) S. W. Fraedrich et al. Plant Dis. 92:215, 2008. (2) J. L. Hanula et al. J. Econ. Entomol. 101:1276, 2008. (3) T. C. Harrington et al. Mycotaxon 111:337, 2010. (4) J. J. Riggins et al. Plant Dis. 94:634, 2010.


Mycologia ◽  
2011 ◽  
Vol 103 (5) ◽  
pp. 1028-1036 ◽  
Author(s):  
Thomas C. Harrington ◽  
Hye Young Yun ◽  
Sheng-Shan Lu ◽  
Hideaki Goto ◽  
Dilzara N. Aghayeva ◽  
...  

Plant Disease ◽  
2011 ◽  
Vol 95 (12) ◽  
pp. 1588-1588 ◽  
Author(s):  
M. Hughes ◽  
J. A. Smith ◽  
A. E. Mayfield ◽  
M. C. Minno ◽  
K. Shin

Laurel wilt is a fungal vascular disease of redbay (Persea borbonia (L.) Spreng) and other plants in the family Lauraceae in the southeastern United States (1). The disease is caused by Raffaelea lauricola T. C. Harr., Fraedrich & Aghayeva, which is vectored by the exotic redbay ambrosia beetle (Xyleborus glabratus Eichhoff) (2). Pondspice (Litsea aestivalis (L.) Fern.) is an obligate wetland shrub listed as endangered in Florida and Maryland and threatened in Georgia (4). On 29 August 2008, 369 of 430 (85%) pondspice trees observed at St. Marks Pond in St. John's County, Florida were dead and/or dying (4). Stem samples were collected from plants with wilted and reddened foliage, entrance holes with boring dust characteristic of ambrosia beetle attack, and dark discoloration in the outer sapwood. Discolored stem sections were surface disinfested for 30 s in a 5% sodium hypochlorite solution and then plated onto cycloheximide streptomycin malt extract agar (1). Smooth, cream-buff, submerge hyphae with uneven margins resembling R. lauricola (2) was observed growing from all sapwood pieces. DNA was extracted from a single isolate (PL 392) and the 18s small subunit rDNA was PCR amplified and sequenced with primers NS1 and NS4 (3), resulting in a 1,026-bp amplicon. A BLASTn search showed identical homology to R. lauricola strain PL 159 (GenBank Accession No. EU257806). The 18s small subunit rDNA sequence was deposited into GenBank (FJ514097). In May 2011, a spore suspension was made by flooding a single-spore culture plate of isolate PL 392 with 2 ml of sterile water, collecting the spores by pipette, and quantification by hemacyometer to 1.5 × 106 spores/ml. Pathogenicity tests were conducted on 1 to 1.5 m tall pondspice plants. Six saplings were wounded by a 3/32-inch drill bit, with four receiving 50 μl of the spore suspension and two serving as water-inoculated controls. All plants were kept in a greenhouse under ambient temperature. Within 21 days, all fungal-inoculated saplings displayed complete canopy wilt, typical of laurel wilt. R. lauricola was later recovered from all four infected plants, completing Koch's postulates. To determine if the vector can reproduce in pondspice, infected stem sections were placed in a plastic rearing box indoors at room temperature, and both callow and mature adult female X. glabratus emerged in October and November 2008. Although laurel wilt has been previously observed on pondspice in South Carolina and Georgia (1), this is the first confirmation of the disease on pondspice in Florida and the first confirmation of the vector from stem material of this host. References: (1) S. W. Fraedrich et al. Plant Dis. 92:215, 2008. (2) T. C. Harrington et al. Mycotaxon 104:399, 2008. (3) M. A. Innis et al. PCR Protocols, A Guide to Methods and Applications. Academic Press. San Diego, CA, 1990. (4) J. A. Surdick and A. M. Jenkins. Pondspice (Litsea aestivalis) Population Status and Response to Laurel Wilt Disease in Northeast Florida. Florida Natural Areas Inventory, Tallahassee, FL, 2009.


2017 ◽  
Vol 141 (8) ◽  
pp. 653-664 ◽  
Author(s):  
M. A. Hughes ◽  
X. Martini ◽  
E. Kuhns ◽  
J. Colee ◽  
A. Mafra-Neto ◽  
...  

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