Drippy blight is an emergent disease of red oaks, caused by the interaction between a kermes scale insect (Allokermes galliformis) and a bacterium (Lonsdalea quercina subsp. quercina). Multi-locus sequence analysis was used to confirm the bacterial pathogen’s identity and its relationship to other phylogenetically related Enterobacteriaceae species. Further, Koch’s postulates were performed on sapling red oaks. Prior to the discovery of drippy blight disease in Colorado, in the United States, the bacterium was reported on oak trees in California but was limited to acorn infections. The scale insect, A. galliformis, was previously known to occur on pin oak in the eastern United States but was not previously associated with either this bacterium or the production of significant branch dieback associated with drippy blight. In addition to a description of this new disease, this research documents a host range expansion of L. quercina subsp. quercina to northern red oak (Quercus rubra), Shumard oak (Q. shumardii), and pin oak (Q. palustris) and extends the reported host range of A. galliformis to include northern red and Shumard oaks.
The focus of investigation in this study was to consider the potential of arthropods in the dissemination of the bacterium involved in drippy blight disease, Lonsdalea quercina. Arthropod specimens were collected and tested for the presence of the bacterium with molecular markers. The bacterium L. quercina was confirmed on 12 different insect samples from three orders (Coleoptera, Hemiptera, and Hymenoptera) and eight families (Buprestidae, Coccinellidae, Dermestidae, Coreidae, Pentatomidae and/or Miridae, Apidae, Formicidae, and Vespidae). Approximately half of the insects found to carry the bacterium were in the order Hymenoptera. Estimates of the insects that are contaminated with the bacterium, and likely carry it between trees, is conservative because the documented insects represent only a subset of the insect orders that were observed feeding on the bacterium or present on diseased trees yet were not able to be tested. The insects contaminated with L. quercina exhibited diverse life histories, where some had a facultative relationship with the bacterium and others sought it out as a food source. These findings demonstrate that a diverse set of insects naturally occur on diseased trees and may disseminate L. quercina.
Thousand cankers disease (TCD) is caused by the walnut twig beetle (Pityophthorus juglandis) vectoring the fungal canker pathogen Geosmithia morbida, which can result in severe dieback and eventual death to species of walnut (Juglans spp.) and wingnut (Pterocarya spp.). This disease is most devastating to the highly valued species J. nigra (black walnut). This species is primarily grown and harvested for timber production in the Central Hardwood Region of the United States, which comprises part of its native range. Management options for TCD are limited; therefore, finding resistant genotypes is needed. Initial studies on black walnut susceptibility to G. morbida documented some genetic variation and suggested potential resistance. Furthermore, G. morbida is thought to be native to the United States, which may have allowed for co-evolution. To capture the representative genetic diversity and screen for resistance to G. morbida, J. nigra families were collected from across the native range. These wild trees, in conjunction with seedlings developed in a black walnut timber improvement program, were planted in a common garden in Fort Collins, Colorado and repeatedly inoculated with G. morbida over the course of four years and three growing seasons. Improved seedlings exhibited larger cankered areas than wild J. nigra of the same provenance. Cankers induced by G. morbida in wild germplasm were smaller on J. nigra collected from the western and central portions of the native range compared to those collected from the eastern portion. Although trees from the western and central part of the range still incurred cankers, our findings indicate that variation in genetic resistance to G. morbida is present in black walnut. This study was performed with G. morbida independent of the walnut twig beetle, but our results suggest the limited G. morbida resistance observed in J. nigra will prevent the full compromise of black walnut to TCD. Results from this study should be taken into consideration in future black walnut breeding programs.
The walnut twig beetle (Pityophthorus juglandis Blackman) vectors Geosmithia morbida, the causal agent of thousand cankers disease in Juglans, and is particularly damaging to Juglans nigra L. (black walnut). Native hosts of P. juglandis are distributed in the southwestern United States where winter temperatures tend to be higher than those found within the native range of black walnut. To better understand temperature effects on survival of P. juglandis, we initiated studies to determine: 1) seasonal variations in cold tolerance, as measured by the supercooling point (SCP), and 2) upper and lower lethal temperatures (LT). In the lower LT study, Xyleborinus saxeseni (Ratzeberg) was tested for comparison. Insects were either exposed to increasing or decreasing temperatures and then checked for survival. Upper and lower LTs were estimated using a logistic model. For the SCP study, data were grouped into seasons. Seasonal mean SCPs were highest in summer (-15.4°C) and lowest in fall (-18.1°C). The upper lethal limit estimations required to kill 99% of the population (LT99) for adults and larvae were 52.7 and 48.1°C, respectively, and lower limit LT99 estimations for adults and larvae were -18.1 and -18.7°C, respectively. The lower median LT (LT50) of X. saxeseni was -24.7°C. These studies, as well as beetle survival in infested Colorado trees where temperatures reached -29°C in February 2011, suggest P. juglandis could survive the winter in much of the native range of black walnut, but may be limited in trees where temperatures regularly exceed the lower LT.
Geosmithia morbida is well documented as the causal agent of thousand cankers disease of black walnut trees. However, it is not well understood how G. morbida strains differ in virulence and how their interactions with co-occurring pathogens contribute to disease severity. In this study, we systematically investigated virulence of genetically distinct G. morbida strains. Overall, we found varying degrees of virulence, although differences were not related to genetic groupings. Furthermore, the pathogen Fusarium solani is also commonly isolated from thousand canker-diseased trees. The degree of disease contribution from F. solani is unknown, along with interactions it may have with G. morbida. This research shows that coinoculation with these pathogens does not yield a synergistic response.
Fungal endophytic communities in needles of field-grown Pinus flexilis previously inferred to carry major gene resistance (R) to white pine blister rust (WPBR) or to lack it (S) were surveyed to identify unique microbes that may be recruited by WPBR-resistant genotypes. Resistant and susceptible trees were sampled in each of 11 P. flexilis populations for a total of 50 trees sampled. Through next-generation sequencing, this study showed a diverse needle mycobiota in P. flexilis, of which many remain unknown, regardless of the presence or absence of the WPBR resistance gene, Cr4. Ascomycota dominated the mycobiota (88.9%) followed by Basidiomycota (4.4%) and Chytridiomycota (0.03%), and the remaining 6.7% were unclassified. Shared ( n = 105) and unique ( n = 48 in R and n = 49 in S) fungal taxa, including differentially abundant operational taxonomic units, were identified that could provide insights into core mycobiota and host genotype-specific fungal groups. Marginal variation of the fungal diversity and structure was observed between host genotypes, which indicates that neither Cr4 nor the physiological differences associated with the presence or absence of the gene affects mycobiota recruitment. Instead, other parameters, including host size (diameter at breast height) and site elevation, significantly influenced the variability of the composition and structure of the fungal endophytic community. Further investigations are needed to understand the relationship of unique or differentially abundant taxa with one genotype or the other, and to determine the role of the needle mycobiota in WPBR disease development in natural stands of P. flexilis.
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