S. Kenaley, and
G. Hudler, Department of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853;
T. Harrington, Department of Plant Pathology, Iowa State University, Ames 50011; and
C. Logue, Cornell University, Cooperative Extension, Schenectady, NY 12308
Ceratocystis fagacearum (T.W. Bretz) J. Hunt is considered to be the most destructive vascular pathogen of oaks (Fagaceae: Quercus spp.) in the eastern, north-central, and south-central United States. (1,2,4). All red oak species (subgenus Quercus: section Lobatae) are highly susceptible to C. fagacearum, and infected trees typically die within 3 months of first symptom expression. However, members of the white oak group (subgenus Quercus: section Quercus) are moderately to highly resistant to C. fagacearum and rarely die from oak wilt (1,3). In early August of 2008, we received branch samples taken from wilting red oaks (Q. rubra L.) growing in a residential neighborhood in Scotia, NY (Schenectady County). The endoconidial state of the oak wilt fungus, Thielaviopsis quercina (B.W. Henry) A.E. Paulin, T.C. Harr. & McNew, was consistently isolated from the xylem in the branches. The cultures were identified based on hyphal and conidial morphology on acidified potato dextrose agar (aPDA) as well as sequences of the internal transcribed spacer (ITS) (GenBank Accession No. FJ347031) and large subunit (LSU) (GenBank Accession No. FJ347030) regions of nuclear ribosomal DNA (rDNA). The nucleotide identities for the ITS and LSU sequences were a precise match, 99 and 100%, to rDNA sequences (GenBank Accession Nos. AF043598 and AF222483, respectively) of other isolates of C. fagacearum. According to the homeowners at the site, 12 red oaks have died during the last 3 years, and each tree died within one growing season after oak wilt-like symptoms were noted. In a brief survey of nearby properties in late August of 2008, we found 12 additional trees that were either expressing crown symptoms of oak wilt (e.g., premature leaf casting, bronzing of leaf margins, and water-soaked leaves) or were standing dead and within close proximity (5 to 10 m) to symptomatic trees. Branch samples from four of the symptomatic trees revealed limited (spotted) or no vascular discoloration; however, C. fagacearum was isolated from each suspect tree on aPDA. Remnants of gray mycelial mats and associated pressure cushions were observed beneath the bark of one standing dead oak. The sweet fruit-like odor characteristic of the oak wilt fungus was immediately evident once the bark overlying the mats was removed. Prior to this discovery, the Susquehanna River in north-central Pennsylvania was considered to be the northeastern limit for oak wilt occurrence in the United States (2,4). To our knowledge, this is the first report of the fungus from New York and expands the known range of C. fagacearum to the northeast by at least 300 km, supporting the hypothesis that the range of this fungus continues to expand via animal vectors and/or human activities (2). An isolate of C. fagacearum from New York has been deposited at the Centraalbureau voor Schimmelcultures (CBS 123913).
References: (1) D. N. Appel. Ann. Rev. Phytopathol. 33:103, 1995. (2) J. Juzwik et al. Ann. Rev. Phytopathol. 46:13, 2008. (3) W. L. MacDonald et al. European oaks-susceptible to oak wilt? Page 131 in: Shade Tree Wilt Diseases. C. L. Ash, ed. The American Phytopathological Society, St. Paul, MN, 2001. (4) USDA Forest Service. Oak Wilt Distribution. Northeast Area, State and Private Forestry, St. Paul, MN. Online publication, 2005.