First Report of Ear Soft Rot of Corn (Zea mays) Caused by Burkholderia gladioli in the United States.

During the summer of 2005, an uncharacterized disease was observed on sweet corn 'Mirai 301BC' commercially grown in Sunflower County, Mississippi. Initial symptoms developing at the base of the ear on interior husk leaves were brown, water-soaked, irregular lesions. These gradually enlarged up to 10 cm in diameter. Market value was significantly affected when the corn ears had visible symptoms of this disease. Bacterial cell streaming was observed at a magnification of ×675 from the diseased husk. A bacterium was consistently isolated from lesions on nutrient broth yeast (NBY) agar. Colonies on NBY were yellowish white, slightly convex, shiny, and circular with entire margins. Isolates MS102 and MS103, which were chosen for further characterization, were gram negative, lacked arginine dihydrolase, did not produce fluorescent pigment on Pseudomonas F medium, accumulated poly-β-hydroxybutyrate, and grew aerobically. The isolates were able to utilize l-arabinose, d-mannitol, N-acetylglucosamine, capric acid, malic acid, adipic acid, and phenylacetic acid, but not d-maltose. These characteristics are the same as those described previously for Burkholderia gladioli (3). Analysis of fatty acid methyl ester profiles (Sherlock version TSBA 4.10; Microbial Identification System, Newark, DE) characterized the isolates as B. gladioli (similarity indices: 0.23 to 0.38) and revealed that they have C_16:0 3OH, the most characteristic fatty acid for the genus Burkholderia. Confirmation was made by PCR amplification of the nearly complete16S rRNA gene (1,471 bp; GenBank Accession No. EU053154) using universal primers (forward: 5'-AGAGTTTGATCCTGGCTCAG and reverse: 5'-GGCTACCTTGTTACGACTTC). DNA sequence analysis demonstrated that the 16S rRNA gene of the bacterium shared highest identities (99.4 to 99.6%) with that of B. gladioli strains 321gr-6, 223gr-1, and S10 (4). A PCR product (approximately 300 bp) characteristic of B. gladioli also was obtained from both isolates using species-specific primers GLA-f and GLA-r (2). To confirm pathogenicity, cell suspensions (10⁸ CFU/ml in phosphate buffer) of isolates MS102 and MS103 were injected into interior husk leaves of field-grown sweet corn with a 20-gauge needle and syringe (2 ml per ear). Control corn ear husks were injected with phosphate buffer. After 3 days, ear rot symptoms were observed on all plants inoculated with the isolates but not those injected with phosphate buffer. Cell suspension of isolates dropped on nonwounded husks also incited the same symptoms as those inoculated with the syringe. Koch's postulates were fulfilled with reisolation from the inoculated tissues. The identity of the reisolated pathogen was proved by sequencing the 16S rRNA gene. This disease was previously reported in Brazil (1). To our knowledge, this is the first report of B. gladioli causing a disease of corn in the United States. Although the impact of this disease was not observed from 2005 to 2006 because of dry weather and rotation to other crops in the affected field, there is a potential that the bacterium could become established in corn-producing areas as a member of the corn ear rot complex if environmental conditions are favorable. Reference: (1) I. M. G. Almeida et al. Arq. Inst. Biol. Sao Paulo 66:141, 1999. (2) N. Furuya et al. J. Gen. Plant Pathol. 68:220, 2002. (3) M. Gillis et al. Int. J. Syst. Bacteriol. 45:274, 1995. (4) R. Nandakumar et al. Phytopathology (Abstr.) 95(suppl.):S73, 2005.