Root rot caused by Poria weirii Murr. occurred when healthy roots of Douglas fir came into contact with inoculum in infected roots of the previous stand. Mycelium grew ectotrophically on the bark of the Douglas fir roots, frequently well in advance of growth in the wood, and penetrated to living tissues directly through sound as well as injured bark. Spread of the disease to adjacent trees took place where healthy and diseased roots were in contact, the mycelium apparently spreading to only a very limited extent through natural soil. It was shown that mycelium could invade roots of trees felled for at least 12 months and Douglas fir heartwood that had been buried in soil for at least 12 months. Viable Poria mycelium was isolated from infected roots as small as 2 cm in diameter 11 years after the trees had been cut. While Douglas fir and western hemlock appeared to be quite susceptible to infection, western red cedar, red alder, and bigleaf maple showed considerable resistance.

Reynolds, G. J., Windeis, C. E., MacRae, I. V., and Laguette, S. 2012. Remote sensing for assessing Rhizoctonia crown and root rot severity in sugar beet. Plant Dis. 96:497-505.Rhizoctonia crown and root rot (RCRR), caused by Rhizoctonia solani AG-2-2, is an increasingly important disease of sugar beet in Minnesota and North Dakota. Disease ratings are based on subjective, visual estimates of root rot severity (O-to-7 scale, where 0 = healthy and 7 = 1009Í-rotted, foliage dead). Remote sensing was evaluated as an alternative method to assess RCRR. Field plots of sugar beet were inoculated with /?. solani AG 2-2 IIIB at different inoculum densities at the 10-leaf stage in 2008 and 2009. Data were collected for (i) hyperspectral reflectance from the sugar beet canopy and (ii) visual ratings of RCRR in 2008 at 2, 4, 6, and 8 weeks after inoculation (WAI) and in 2009 at 2, 3, 5, and 9 WAi. Green, red, and near-infrared reflectance and several calculated narrowband and wideband vegetation indices (Vis) were correlated with visual RCRR ratings, and all resulted in strong nonlinear regressions. Values of Vis were constant until at least 26 to 507f of the root surface was rotted (RCRR = 4, wilting of tbliage starting to develop) and then decreased significantly as RCRR ratings increased and plants began dying. RCRR also was detected using airborne, color-infrared imagery at 0.25-and 1-m resolution. Rctnotc sensing can detect RCRR but not before initial appearance of foliar symptoms.The soilbome fungus Rhizoctonia soiani Kühn AG-2-2 inttaspeciftc groups IIIB and IV cause Rhizoctonia crown and root rot (RCRR) of sugar beet (Beta vutgaris L.) ( 11,73,74). Since the early 1990s, these pathogens have become widespread in sugar beetgrowing regions of Minnesota and North Dakota because of wet weather (40), planting of susceptible sugar beet cultivars (Al Cattanach, personal communication), and increased production of soybean, edible bean, and corn (69), which are alternate hosts of R. solani 20,32,73,74). Production of these susceptible rotation crops in the sugar beet cropping systetn allows R. solani inoculutn to build up in soil and contribute to disease outbreaks, Managetnent of RCRR is achieved through rotations of three or more years with non-host plants (57,58,75), early planting (10), and application of fungicides (22,27,28,67,72), Symptoms of RCRR include a dark-brown to gray rot that typically begins near the crown and spreads over the root surface, eventually causing cracking and sunken lesions (75). Petioles are black and rotted at the point of attachment to the crown. Sometimes, infections occur on the root tip or laterally on the root surface (75). Aboveground, foliage may show sudden and severe wilting and then chlorosis: severely infected plants eventually die. Disease severity typically is assessed by a visual rating scale based on the atnount of rot on the tap root (45). This rating system, however, is destructive and requires removal of roots from soil. Furthennore, visual disease assessments are subjective i...

Pitch canker, caused by Fusarium circinatum, is a disease affecting Monterey pine (Pinus radiata) and many other pine species throughout the world. The impact of pitch canker on Pinus radiata may be limited by systemic acquired resistance (SAR), a phenomenon that elevates resistance to a pathogen after initial challenge by that pathogen or another microorganism. Allocation of resources to defense, as a consequence of SAR, is presumed to reduce resources available to support growth and reproduction, but specific fitness consequences associated with SAR in P. radiata have not been measured. To quantify impacts of SAR on growth rate, a 2ˆ2 factorial experiment was established in which trees were either primed for SAR or unprimed, with half the trees in each of those two groups being inoculated with the pitch canker pathogen and the other half not inoculated. Priming for SAR was accomplished by inoculating one branch with F. circinatum and removing inoculated branches prior to subsequent challenge inoculations (= disease treatments). Disease treatments included three inoculations that were removed for measurement of lesion length, and three additional inoculations that remained on the tree as a representation of persistent disease. Control trees were mock inoculated with water. Main effects of priming and disease did not result in significant effects on growth rate. Based on hyperspectral canopy reflectance data, diseased trees were associated with higher difference vegetation index values and biomass. The absence of a negative impact on growth rate associated with SAR suggests that induction of resistance may have utility as a tool for management of pitch canker in plantations.

Summary Fusarium circinatum is widely regarded as a necrotrophic pathogen of pines that infects shoot tissue through mechanical or insect‐mediated wounds, causing girdling lesions that result in death of infected branches. However, in the study reported here, F. circinatum colonized 100% of seedling stems and 70% of mature tree branches that were not wounded. Hyphae were observed beneath the epidermis of non‐wounded shoot tissue within 14 days following inoculation. In both seedlings and branches, most infections of non‐wounded tissue did not induce symptoms for the duration of the trial (seven to eight weeks). In surveys of native Pinus radiata stands in California, F. circinatum was recovered from 7.5% to 100% of healthy‐looking seedlings (2–3 years old) across three of the four stands surveyed. These results suggest that wounding is not a requirement for shoot infection under all circumstances and that F. circinatum can grow within shoot tissue without causing symptoms.