Comparing the Feeding Damage of the Invasive Brown Marmorated Stink Bug to a Native Stink Bug and Leaffooted Bug on California Pistachios

California currently produces about a quarter of the world’s pistachios. Pistachio nuts are susceptible to feeding by stink bugs and leaffooted bugs; therefore, the invasive presence of the highly polyphagous brown marmorated stink bug, Halyomorpha halys (Stål) (Hemiptera: Pentatomidae), is a concern to California pistachio growers. We aimed to assess the potential of H. halys to cause yield loss and nut damage to pistachios, which had not yet been assessed in the field. Over two years, terminal branch ends with pistachio clusters were enclosed in organdy cages from spring to fall and exposed to either H. halys, the native stink bug Chinavia hilaris Say (Hemiptera: Pentatomidae), or leaffooted bug Leptoglossus zonatus (Dallas) (Hemiptera: Coreidae), for 4–7-day feeding periods at different times of the season. We found that H. halys adults cause more epicarp lesions (external damage) when recorded at harvest time than the native species. They did not, however, cause more kernel necrosis (internal damage) than the two native species tested, which is a more relevant damage criterion for commercial production. There were no differences among insect species for any other recorded damage criteria. We conclude that H. halys could cause similar damage as the native species but note that H. halys population densities in California are still low and future damage levels will be dependent on this pest’s population density.

Assessing Feeding Damage from Two Leaffooted Bugs, Leptoglossus clypealis Heidemann and Leptoglossus zonatus (Dallas) (Hemiptera: Coreidae), on Four Almond Varieties

Leaffooted bugs (Leptoglossus spp; Hemiptera: Coreidae) are phytophagous insects native to the Western Hemisphere. In California, Leptoglossus clypealis and Leptoglossus zonatus are occasional pests on almonds. Early season feeding by L. clypealis and L. zonatus leads to almond drop, while late season feeding results in strikes on kernels, kernel necrosis, and shriveled kernels. A field cage study was conducted to assess feeding damage associated with L. clypealis and L. zonatus on four almond varieties, Nonpareil, Fritz, Monterey, and Carmel. The objectives were to determine whether leaffooted bugs caused significant almond drop, to pinpoint when the almond was vulnerable, and to determine the final damage at harvest. Branches with ~20 almonds were caged and used to compare almond drop and final damage in four treatments: (1) control branches, (2) mechanically punctured almonds, (3) adult Leptoglossus clypealis, and (4) adult Leptoglossus zonatus. Replicates were set up for eight weeks during two seasons. Early season feeding resulted in higher almond drop than late season, and L. zonatus resulted in greater drop than L. clypealis. The almond hull width of the four varieties in the study did not influence susceptibility to feeding damage. The final damage assessment at harvest found significant levels of kernel strikes, kernel necrosis, and shriveled almonds in bug feeding cages, with higher levels attributed to L. zonatus than L. clypealis. Further research is warranted to develop an Integrated Pest Management program with reduced risk controls for L. zonatus.

Kernel Necrosis of ‘Pawnee’ Pecan: Expanded Distribution and Relation to Yield, Tree Size, and Canopy Location

Pecan [Carya illinoinensis (Wangenh.) K. Koch.] kernel necrosis is a malady characterized by development of a dark necrotic area at the basal end of the kernel. This problem is particularly severe on ‘Pawnee’ at some locations during certain years. Currently, the cause of kernel necrosis is not known. Initially, this problem appeared confined to certain cultivars in a north Texas orchard in the Red River Basin and ‘Oklahoma’ in a central Oklahoma orchard adjacent to the Deep Fork River. After El Paso, TX, producer reports of an unknown problem on ‘Pawnee’, mature nuts from orchards near El Paso, north Texas, and southern, central and northeastern Oklahoma were evaluated for kernel necrosis. Kernel necrosis was abundant on ‘Pawnee’ nuts from El Paso and southern Oklahoma, moderate at the north Texas site, and at low levels in one northeastern Oklahoma orchard. None was found in two ‘Pawnee’ orchards, one in central Oklahoma and the other in northeastern Oklahoma. In another study, yield was monitored on hedge-pruned ‘Pawnee’ pecan trees over a 5-year period to determine the relationship with kernel necrosis. The incidence of kernel necrosis was greater when yield was less. A third study sampled nuts from the lower and upper one-third of canopies from randomly selected trees varying in trunk size. Kernel necrosis frequency was similar in the upper canopy among different trunk sizes, but the incidence in the lower tree canopy decreased as trunk size increased.

The Occurrence of Pecan Kernel Necrosis

Pecan [Carya illinoinensis (Wangenh.) C. Koch] kernels (cotyledon) of ‘Pawnee’ displayed a consistent malady not described previously that was designated as “kernel necrosis.” The most severe form of the problem was blackened, necrotic tissue engulfing the basal one-half to one-third of the kernel. The mildest form was darkened tissue in the dorsal grove at the basal end of the kernel. The problem was first observable during the gel stage of kernel development. No symptoms of kernel necrosis were visible on the shuck (involucre). Kernel necrosis was more prominent on ‘Pawnee’, ‘Choctaw’, and ‘Oklahoma’ than other cultivars observed. At maturity, nuts with kernel necrosis had a larger volume than nuts with normal kernels. There were few differences in elemental concentrations of normal kernels from a severely affected orchard and an orchard with little kernel necrosis, and none of the differences appeared to be associated with this disorder. ‘Pawnee’ kernels with necrosis had more phosphorus, zinc, and manganese than normal kernels. Basal segments of necrotic kernels had more boron and acetic acid-extractable and water-soluble calcium than distal segments or normal kernels. Higher elemental concentrations in basal segments of necrotic kernels did not appear sufficient to cause tissue damage. Soil from the orchard with severe kernel necrosis had unusually high concentrations of nitrate, expressed as nitrogen (NO3-N), in the soil profile. Groundwater used for irrigation was contaminated with 34 mg·L−1 NO3-N. An experiment on ‘Pawnee’ evaluated three nitrogen (N) rates, 0, 0.8 g·cm2 cross-sectional trunk area applied in March, and 1.6 g + 1.6 g + 1.2 g·cm2 cross-sectional trunk area N applied during the second week in March, first week in June, and first week in September, respectively, on the incidence of kernel necrosis, leaf N concentration, soil NO3 concentration, yield, nut quality, and growth over 5 years. Leaf N was affected by treatment only once during the study. Nitrates accumulated in the soil, increasing 24% in 3 years when no supplemental N was applied, except in the contaminated irrigation water. Kernel necrosis was either unaffected by N treatment or during 1 year, kernel necrosis was highest without supplemental N application. Tree yield, kernel quality, and growth were unaffected by N treatment. Yield fluctuations among years were apparent demonstrating that an abundant N supply did not prevent alternate bearing. Kernel necrosis was a severe problem in one orchard and was identified in several orchards at low frequencies. The cause of kernel necrosis remains unknown.