|Temple, T. - OREGON STATE UNIVERSITY|
|Stockwell, V. - OREGON STATE UNIVERSITY|
|Johnson, K. - OREGON STATE UNIVERSITY|
Submitted to: Acta Horticulturae
Publication Type: Proceedings
Publication Acceptance Date: December 1, 2007
Publication Date: N/A
Interpretive Summary: Fire blight, caused by the bacterium Erwinia amylovora, is an economically important disease of pear and apple and a barrier to the export of these fruits from US. Extensive research with apple led to a WTO conclusion that the likelihood of exported fruit serving as a pathway for dissemination of the fire blight pathogen is negligible. In contrast to apple, the consideration of pear fruit as a dissemination vehicle for E. amylovora has received little research attention. Therefore, inoculation experiments and a survey were conducted to evaluate the potential for E. amylovora being associated with mature symptomless winter pear fruit. In the orchard, E. amylovora on the surfaces of inoculated fruit declined dramatically and was undetected by 56 days. Assays revealed no evidence of migration of the pathogen from diseased tree branches into symptomless pear fruit. At harvest, E. amylovora could not be detected on the surface of 5599 of 5600 fruit from commercial orchards in the Pacific Northwest. One fruit yielded approximately 30 cells of the pathogen; however, mature fruit artificially contaminated with E. amylovora and later wounded required a dose of greater than 10,000 cells at a wound site to allow for persistence of the pathogen during cold storage. The risk of transmitting fire blight by way of pear fruit was shown to be extremely low and no greater than that for apple. The information will likely be valuable to quarantine officials and trade negotiators.
Technical Abstract: Over a four year period, we evaluated the potential for co-occurrence of E. amylovora with mature symptomless winter pear fruit by inoculation experiments and by survey of commercial orchards. Immature pear and apple fruit were inoculated in orchards with E. amylovora strain 153N as resuspended, lyophilized cells or ooze from diseased tissues. Regardless of inoculum type, populations of Ea153N on fruit declined by an order of magnitude every 3-4 days during the first two weeks after inoculation; at 56 days after inoculation, Ea153N was not detected except on 1 of 450 fruit with 4 CFU. After inoculation of flowers, calyx end survival of Ea153N on pear and apple fruit declined from high populations at petal fall to a few cells at harvest, with no detection of the pathogen after a 7-week cold storage. The potential for migration of Ea153N into symptomless pear fruit from blighted branches was evaluated by enrichment assay and nested PCR of internal fruit core tissues; these assays failed to detect the pathogen in healthy fruit from diseased trees. In harvest surveys, E. amylovora could not be detected on 5599 of 5600 fruit of d’Anjou pear sampled from orchards located in major production areas of the Pacific Northwest; one fruit yielded 32 CFU of the pathogen. In postharvest experiments, mature fruit contaminated with Ea153N and subsequently wounded required a dose of >10,000 cells at the wound site to allow for persistence of the pathogen through a 7-week cold storage. We conclude that epiphytic E. amylovora has similar survival characteristics on both pear and apple fruit, that it is not endophytic within mature symptomless pear fruit, its presence is exceptionally rare on commercially-produced fruit, and that epiphytic survival of E. amylovora through a postharvest chilling period is unlikely given the unrealistically high population size required for persistence.