Factors Affecting the Development of Wood Rot on Lemon Trees Infected with Antrodia sinuosa, Coniophora eremophila, and a Nodulisporium sp.

Brown heartwood rot, which often is found in branches within lemon groves in southwestern Arizona, is caused by two basidiomycete fungi, Antrodia sinuosa and Coniophora eremophila. Another fungus, a species of Nodulisporium, has been recovered from small, dying lemon tree branches with an internal white wood rot. Studies were conducted from 1999 through 2002 to compare the extent of wood decay caused by these fungi (i) on lemon tree branches at different times of the year, (ii) on different types of citrus, (iii) on some desert woody perennial plants, and (iv) on lemon tree branches treated with selected fungicides. The mean length of wood decay columns recorded in lemon tree branches inoculated with A. sinuosa, C. eremophila, and the Nodulisporium sp. during the time periods of November to January, February to April, May to July, and August to October was 2.9, 4.7, 13.3, and 15.2 cm, respectively. There was a significant linear correlation between the length of wood decay columns and air temperature for all three pathogens. The mean length of wood decay columns for all time periods in branches inoculated with A. sinuosa, C. eremophila, and the Nodulisporium sp. was 11.8, 5.8, and 9.6 cm, respectively. In two trials, wood decay columns were significantly greater on Lisbon lemon tree branches inoculated with A. sinuosa compared with those on Marsh grapefruit and Valencia orange trees inoculated with the same pathogen. Wood decay in the presence of the Nodulisporium sp. was greater on branches of lemon compared with grapefruit trees in two trials and on lemon compared with orange trees in one of two trials. With the exception of C. eremophila on creosote bush, each of the three wood rot pathogens caused some wood decay in branches of velvet mesquite, salt cedar, Mexican palo verde, and creosote bush, four common desert perennials found in southwestern Arizona. Compared with nontreated but inoculated lemon trees, the length of wood decay columns in branches inoculated with A. sinuosa, C. eremophila, and the Nodulisporium sp. in the presence of propiconazole was reduced by 79, 94, and 92%, respectively, and, in the presence of azoxystrobin, was suppressed by 71, 80, and 89%, respectively. Current management guidelines focus on minimizing branch fractures and other nonpruning wounds in conjunction with early detection and removal of infected branches before the onset of the increased wood decay development period extending from May to October.

Labyrinthula terrestris sp. nov., a new pathogen of turf grass.

A species of Labyrinthula that causes 'rapid blight' and death of turfgrass has been isolated and studied. We name this new species Labyrinthula terrestris and briefly summarize morphological characteristics and growth patterns of this pathogen of turfgrass.

First Report of a Labyrinthula sp. Causing Rapid Blight Disease of Rough Bluegrass and Perennial Ryegrass.

A Labyrinthula sp. was isolated from symptomatic rough bluegrass (Poa trivialis L.) and perennial ryegrass (Lolium perenne L.) from a golf course in Arizona. Initial symptoms were a water-soaked appearance and rapid collapse of small patches of turf foliage. The affected turf died, and patches coalesced to form large dead areas after several weeks. The symptoms were those of the disease recently termed "rapid blight" for which the causal agent has not been identified (1). Rapid blight was first observed in southern California in 1995 and has become increasingly problematic in 10 other states on several cool-season turfgrasses (1). In Arizona, it is associated with high salinity irrigation water. In microscopic examinations of symptomatic P. trivialis and L. perenne leaf tissue from November 2002 to February 2003, fusiform or spindle-shaped vegetative cells (4 to 5 × 15 to 20 µm) were observed in leaf cells. These cells are consistently associated with rapid blight (1) and are typical in size and shape of those described for Labyrinthula spp. (3,4). The fusiform cells were cultured in 1% horse serum water agar medium made with irrigation water (electrical conductivity [EC] = 3.5 to 4.0 dS/m) from a golf course in central Arizona with rapid blight. The cells readily formed colonies on this medium and exhibited gliding motility along a network of hyaline slime filaments as previously described for the genus Labyrinthula (3,4). Koch's postulates were fulfilled by inoculating P. trivialis and L. perenne seedlings with Labyrinthula sp. isolated from naturally infested P. trivialis in two experiments. The grasses were started from seed and grown as a lawn in containers in the laboratory. Both experiments were repeated once. In the first experiment, infested autoclaved leaf pieces of P. trivialis were used as inoculum. Inoculated leaf pieces were placed within each of several bundles of 4 to 6 leaves and held loosely in place with a 0.5-cm wide ring of tygon tubing. Seedlings were irrigated with sterilized irrigation water from the golf course (EC = 4.0 dS/m). In the second experiment, agar discs from Labyrinthula sp. colonies on 1% horse serum agar were used as inoculum by placing the agar discs in contact with leaves. Seedlings were irrigated with sterile tap water adjusted to 4.0 dS/m using synthetic sea salt (Instant Ocean, Aquarium Systems, Inc., Mentor, OH) Leaf tissue of all inoculated seedlings became water soaked within 3 to 7 days and collapsed within 10 days in both experiments. Fusiform cells were observed in inoculated leaf tissue cells, and the Labyrinthula sp. was reisolated from 100% of selected symptomatic seedlings. Control seedlings treated with noninfested leaf pieces or sterile agar pieces did not develop symptoms, and no fusiform cells were isolated from the leaf tissue. Labyrinthula spp. are usually associated with marine systems (3). Labyrinthula zosterae D. Porter & Muehlst. has been identified as the causal agent in a marine grass wasting disease (2), but to our knowledge, no Labyrinthula spp. have been described as pathogens of terrestrial plants. References: (1) S. B. Martin et al. Phytopathology (Abstr.) 92:(suppl)S52, 2002. (2) L. K. Muehlstein et al. Mycologia 83:180, 1991. (3) K. S. Porkorny. J. Protozool. 14:697, 1967. (4) D. Porter. Handbook of Protoctista. Jones and Bartlett, Boston, MA, 1990.

Using Predictions Based on Geostatistics to Monitor Trends in Aspergillus flavus Strain Composition.

ABSTRACT Aspergillus flavus is a soil-inhabiting fungus that frequently produces aflatoxins, potent carcinogens, in cottonseed and other seed crops. A. flavus S strain isolates, characterized on the basis of sclerotial morphology, are highly toxigenic. Spatial and temporal characteristics of the percentage of the A. flavus isolates that are S strain (S strain incidence) were used to predict patterns across areas of more than 30 km(2). Spatial autocorrelation in S strain incidence in Yuma County, AZ, was shown to extend beyond field boundaries to adjacent fields. Variograms revealed both short-range (2 to 6 km) and long-range (20 to 30 km) spatial structure in S strain incidence. S strain incidence at 36 locations sampled in July 1997 was predicted with a high correlation between expected and observed values (R = 0.85, P = 0.0001) by kriging data from July 1995 and July 1996. S strain incidence at locations sampled in October 1997 and March 1998 was markedly less than predicted by kriging data from the same months in prior years. Temporal analysis of four locations repeatedly sampled from April 1995 through July 1998 also indicated a major reduction in S strain incidence in the Texas Hill area after July 1997. Surface maps generated by kriging point data indicated a similarity in the spatial pattern of S strain incidence among all sampling dates despite temporal changes in the overall S strain incidence. Geostatistics provided useful descriptions of variability in S strain incidence over space and time.

Short-term weight loss and exercise training effects on glucose-induced thermogenesis in obese adolescent males during hypocaloric feeding.

Our purpose was to examine the effect of short-term weight loss and exercise training on the thermic effect of a glucose load in lean and obese adolescents. Nine obese (age 14.3 +/- 0.3 years, mean +/- s.e.m.) boys were examined during the first (Ob-pre) and sixth (Ob-post) week of caloric restriction (1300-1500 kcal/day, 5441-6279 kJ/day) and aerobic exercise conditioning (walk/jog/swim/calisthenics), and compared to age-matched lean controls (Con). A 100-g oral glucose tolerance test (OGTT) was administered while simultaneously measuring energy expenditure by indirect calorimetry every 30 min for 3 h. Posttest results revealed a decrease in body weight and body fatness in obese boys, but not to the level of that in lean controls (P less than 0.01). The thermic effect of glucose, calculated as the area under the response curve for three hours in excess of resting metabolic rate, was similar in Ob-pre and Con (0.77 +/- 0.14 vs. 0.57 +/- 0.28 kcal/kg lbm/3h), but decreased in Ob-post (0.29 +/- 0.08 kcal/kg lbm/3h, P less than 0.01). The area under the response curve for glucose was elevated in Ob-pre (328.1 +/- 12.2 mg/dl/3h) compared to Con (270.4 +/- 21.4 mg/dl/3h). The insulin response was similar in Ob-pre and Con (120.4 +/- 11.3 vs 125.6 +/- 12.4 mU/ml/3h), but decreased in Ob-post (89.6 +/- 15.1 mU/ml/3h, P less than 0.05). Thus, the improvement in peripheral insulin sensitivity with short-term exercise and weight loss was unaccompanied by favorable alterations in carbohydrate-induced thermogenesis in obese adolescents.