ABSTRACT
Angular leaf spot of cucurbits is generally considered to be caused by Pseudomonas syringae pv. lachrymans. It has a worldwide distribution and has been observed to emerge sporadically under humid and wet conditions. Reports of multiple P. syringae pathovars associated with the disease and lack of molecular analysis has left the true diversity of populations in the United States unclear. In this study, we collected 27 P. syringae strains causing foliar lesions and blighting on watermelon, cantaloupe, and squash in Florida, Georgia, and California over several years. Strains were fluorescent on King's medium B agar and displayed the typical phenotypic and biochemical characteristics of P. syringae. P. syringae pv. lachrymans is a member of genomospecies 2. However, the genetic profiles obtained through both MLSA (gyrB, rpoD, gapA, and gltA) and BOX-PCR (BOXA1R) identified 26 of the P. syringae strains to be distributed among three clades within genomospecies 1, and phylogenetically distinct from genomospecies 2 member P. syringae pv. lachrymans. A novel MLSA haplotype of the pathogen common to all states and cucurbit hosts was identified. Considerable genetic diversity among P. syringae strains infecting cucurbits is associated with the same disease, and reflects the larger ecological diversity of P. syringae populations from genomospecies 1.
ABSTRACT
A previously undescribed disease appeared on commercially grown fennel (Foeniculum vulgare) in Salinas (Monterey County), CA in March 2010. Initial symptoms consisted of small, dark brown-to-black lesions on leaves and stems. As disease progressed, lesions expanded in a linear fashion and eventually spread down the stems and into the bulbs. Once the disease reached the fennel bulbs, the plants were unmarketable. Eighteen, gram-negative, blue-fluorescing bacterial isolates were obtained on sucrose peptone agar from individual plants of two outbreaks from different fields in Salinas. The isolates were dome shaped on sucrose-amended media and produced necrotic lesions when injected into tobacco. Isolates were oxidase negative and did not rot potatoes or hydrolyze arginine. These reactions corresponded to Lelliot's group 1, which includes Pseudomonas syringae (2). The fennel isolates were identical to recently characterized isolates of P. syringae pv. apii from parsley grown in coastal California (1) and similar to the pathotype strain of P. syringae pv. apii according to DNA fragment banding patterns of amplicons generated from repetitive extragenic palindromic sequence (rep)-PCR using the BOXA1R primer. The isolates were distinct from the pathotype strain P. syringae pv. coriandricola. Like P. syringae pv. apii, the fennel isolates did not nucleate ice but did hydrolyze gelatine. Six isolates were tested for pathogenicity in each of two independent experiments with a total of six replications per isolate. Healthy, potted fennel plant stems of a proprietary cultivar were pierced once with insect display pins that had been dipped into bacterial colonies grown for 48 h on nutrient agar. Control stems were inoculated with sterile pins. Plants were incubated for 48 h at 100% relative humidity and then held in a greenhouse. After 4 to 6 days, inoculated fennel plants developed symptoms similar to those originally observed in the field. Bacteria isolated from surface-disinfested symptomatic tissue were fluorescent and identical to strains used to inoculate plants as evaluated by rep-PCR, thus fulfilling Koch's postulates. Control plants remained symptomless. To our knowledge, this is the first report of this pathogen causing a disease on fennel; the disease has been named bacterial streak. The disease occurred in three fields in 2010 and incidence was <1% in each case. Similar symptoms were also observed on fennel in the 2011 season in at least two fields. Previously, the host range of P. syringae pv. apii was reported to be restricted to celery. This research expands the natural host range of P. syringae pv. apii; thus, care should be taken in choosing Apiaceae crops for plantings subsequent to the occurrence of this pathogen. References: (1) C. T. Bull et al. Phytopathology 101:847, 2011. (2) R. A. Lelliott. J. Appl. Bacteriol. 29:470, 1966.
