Seminar this week was given by Dr. Ronald Walcott from the University of Georgia (UGA), Athens. He got his BS and MS degree from Iowa State University, and his PhD from UGA. While searching the internet for references related to this post, I found this interview with Dr. Walcott. Dr. Walcott studies seed-borne plant pathogens.
Picture creditBacterial fruit blotch (BFB) has become a significant pathogen over the years, in particular on watermelon. The first symptoms normally appear on the cotyledons, afterwards symptoms can sometimes be seen on the true leaves too. Under field conditions, it is really hard to distinguish these symptoms, because they are rather nondescript. The main problem occurs later in the season, when the fruits show irregularly shaped blotches, the fruits crack, and the insides of the fruit ooze out. Contrary to a NY Times report in May 1994, watermelons are not known to "explode." Still, these are not watermelons you want to buy or eat.
The disease is caused by the bacterial pathogen Acidovorax avenae subsp. citrulli (Aac), formerly considered to belong to the genus Pseudomonas. The disease cycle starts with infected seed, the most important source of primary inoculum. Since watermelons are typically seeded in flats, with many seedlings close together, maintained under high humidity, and watered by overhead irrigation, the pathogen can spread very easily from one seedling to the next, and a single infected seedling can infect the entire tray. The infection of the fruit actually occurs very early on, after the flower opens. The symptoms don't show up until much later. The infected fruit cracks open, seeds come out, can germinate in the soil (volunteer seedlings), and become a source of secondary inoculum.
BFB was first reported in Georgia in 1965, 4 years later it was observed at a research farm in Leesburg, Fl. In 1978 a strain was described that caused seedling blight, and did not show a hypersensitive response (HR) on tobacco or tomato. In 1987 there was an outbreak in the Mariana Islands, and in 1989 a strain was recovered from commercial plantings of watermelons in Florida and Indiana. Contrary to the 1978 strain, this strain caused seedling blight and fruit rot, and elicited an HR on tobacco and tomato. Since 1992, many US states have reported BFB, and there has been a significant amount of yield loss. In addition, growers have filed lawsuits against seed companies, the seed companies have in return restricted watermelon seed sales. Seeds now come with a disclaimer; the growers needs to accept the risk of BFB, and agree not to file any lawsuits.
In 1995, management guidelines were established in Georgia to control the pathogen, and these seemed to limit the problem initially, but then in 1999 and 2000 there were substantial outbreaks. Either the guidelines didn't work, or there was something else going on. Because of the increased movement of seeds, BFB currently occurs worldwide.
In 1999 there were also outbreaks on different crops. BFB was no longer restricted to watermelon, but was observed on canteloupe, melon, and pumpkin (oh no! What does that mean for Halloween?). There were often no obvious symptoms, other than a few small spots on the rind. However, below those spots, the rind doesn't develop, and the fruit goes bad. Some other hosts that the pathogen has been found on include cucumber, honeydew, hami melon, squash, bitter and bottle gourd. Seed transmission has been confirmed for several of these.
Dr. Walcott's lab investigated the genetic diversity of Aac. Using several different techniques, he discovered that at least two groups can be distinguished. Group I strains show less genetic variation than group II strains. Groups I strains have similar, moderate severity on a number of hosts, while group II strains is much more severe on watermelon, while being moderately aggressive on other hosts. The genome of a group II strain has recently been sequences, and annotation of the genome is currently in progress. Dr. Walcott is investigating the possibility of sequencing a group I strain too, so that differences at the genomic level can be correlated with differences in virulence.
Currently, the production of watermelon seed is not really conducive for Aac spread. The seeds are produced under cool, dry conditions, the seed production fields are visually inspected, and the seeds are tested for presence of Aac. But Aac continues to be a problem. Dr. Walcott therefore studied the mechanisms of seed infection. He figured there were 3 possibilities:
1. The bacteria penetrate through the ovary wall. This is unlikely, symptoms would be apparent.
2. The bacteria infect the plant systemically via the vascular system. However, there is no evidence of systemic infection.
3. The bacteria penetrate through the flower parts. Hmmm. This is promising.
Dr. Walcott considered that the bacteria may land on the stigma, move through the style, and end up in the ovary, and thought it the most likely possibility.
He took symptomless fruit, harvested the seed, and found that Aac can associate with seeds, without any symptoms on the fruit. He developed transgenic Aac bacteria expressing green fluorescent protein (GFP), so that he could track the bacteria easily. And indeed, he found the bacteria present in seed tissue, and he could track the bacteria following the path described above. He also noted that this type of infection is not unique to Aac, there are other pathogens that can do this. Using the GFP-tagged bacteria he also found out that the bacteria take about a week to travel from the stigma to the ovary via the pistil pathway. Once the bacteria reached the ovary, however, replication of the bacterium stopped. This explains the lack of symptoms.
Dr. Walcott discovered that bacterial motility was not important for colonization of the seeds, but that pollination was necessary. He also investigated the role of pollinating insects, and found in one experiment that bees did seem capable of spreading the infection, but these results need to be verified with additional experiments. The problem with this theory in practice is, however, that in commercial seed production fields, most pollination does not occur by bees, but by hand, so the bees may not be sufficient to explain the outbreaks seen.
Towards the end of seminar, Dr. Walcott discussed some of the experiments he has done to investigate the possibility of biological control. Although he found a good level of control with at least one biological control agent, this is not good enough for watermelon seed production with a zero-tolerance of Aac.
Further reading
Fessehaie, A., and Walcott, R.R. (2005) Biological control to protect watermelon blossoms and seeds from infection by Acidovorax avenae subsp. citrulli. Phytopathology 95:413-419.
Gitaitis, R.D. and Walcott, R.R. (2007) The epidemiology and management of seedborne bacterial diseases. Ann. Rev. Phytopathology 45: 371-397.
Lessl, J. T., Fessehaie, A. and Walcott, R. R.. 2007. Colonization of female watermelon blossoms by Acidovorax avenae subsp. citrulli and the relationship between blossom inoculum dosage and seed infestation. J. Phytopathology 155:114-121.
Walcott, R.R. (2005) Bacterial fruit blotch of cucurbits. The Plant Health Instructor. DOI:1094/PHI-I-2005-1025-02
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