Studies on the diseases of wheat in New Zealand caused by Septoria and Tilletia spp.
The literature on the pathogens Septoria tritici and Septoria nodorum, and the wheat diseases they cause has been reviewed, including methods of disease assessment and some aspects of fungicide application and mode of action. Both S. tritici and S. nodorum have ascogenous states, and these are a Mycosphaerella sp. and Leptosphaeria nodorum respectively. Perithecia of both were found in old leaf tissue in wheat stubble soon after harvest. Perithecia began to mature by the end of February, and wind-borne ascospores were trapped from March to June, 1974. Those of L. nodorum were trapped two weeks before any Mycosphaerella ascospores were found. The release of both ascospore types appeared to be in response to moisture. Viable ascospores of both types could still be detected in June. Ascospores of these two species would be capable of initiating infection in autumn-sown wheat crops some distance from other inoculum sources (i.e. pycnidia), and hence would be important in the epidemiology of the Septoria diseases of wheat. A field survey of wheat crops in Canterbury during 1973 failed to detect S. nodorum. Symptoms caused by this fungus were first seen on the basal leaves of volunteer wheat plants in spring of 1974, as discrete brown necrotic lesions, bordered by a ring of chlorotic tissue. The lesion did not coalesce, as do those caused by S. tritici. At no stage did pycnidia develop on leaves in the field, but when leaves with lesions were floated on a benzimidazole solution and placed under near ultra-violet (NUV) light for a 12 hour photoperiod, pycnidia developed four days later. Laboratory tests showed that a temperature of l8-24°C, light, 95-100% R.H. and senescing tissue were important factors governing the appearance of pycnidia of S. nodorum in leaf tissue. S. nodorum was isolated from these pycnidia, and inoculation experiments showed that the cultures of this fungus were pathogenic to wheat. Cultures which developed from ascospores of L. nodorum were found to be S. nodoxum and also shown to be pathogenic to wheat. Colonies of S. nodorum grew on malt, but better on oatmeal and potato-dextrose agar. Sporulation occurred after 20-30 days incubation at 20-22°C under a light regime of 12 hours NUV/12 hours darkness, and was greatest in those colonies grown on oatmeal agar. S. nodorum was not observed on the glumes of wheat. An examination of twenty-five Canterbury lines of wheat seed failed to reveal the presence of S. nodorum. S. txitici was common in wheat crops in Canterbury during 1973 and 1974. Symptoms first appeared on young leaves as discrete chlorotic lesions, which eventually coalesced into large necrotic lesions, containing black pycnidia, often with a broad chlorotic marginal zone. These lesions often covered the entire leaf area. By heading (G.S. 10), S. tritici infection could be found on all leaves of the wheat plant, but was not observed on the glumes. A 'black' and a 'white' cultural race of S. tritici was isolated from separate lesions on wheat plants from the field. These races, inoculated to wheat, produced identical symptoms and signs in the host plant, but in culture were distinct and did not produce any variants. Both could be isolated from lesions on leaves throughout the growing season of the plant, but at no stage in time were both races isolated from the same lesion. Pycnidia of S. tritici containing pycnidiospores, were also found to be present within old leaves of wheat stubble from February to June. Pycnidiospores from these pycnidia were still viable in May, but by June, their viability had markedly decreased. Aotea wheat plants in a replicated field trial became naturally infected by S. tritici. When sprayed with benomyl or mancozeb at ear emergence, a significant increase in 1000 grain weight was produced. This increase appeared to be due to a reduction of infection and delaying of senescence of the flag leaf. However, yield was not significantly increased, although there was 14% more grain produced from treated plots. Benomyl and thiophanate-methyl applied at tillering did not increase yield, although S. tritici was controlled for up to six weeks. Field assessments of six wheat varieties showed that Hilgendorf and Kopara showed some tolerance to S. tritici, Arawa and Karamu were moderately susceptible, and Aotea and Gamenya were highly susceptible. When inoculated with S. tritiei in the laboratory, these varieties reacted similarly. Varietal reaction to S. nodorum in the laboratory was similar to the S. tritici results. The literature on stinking smut, or bunt, (Tilletia caries, and Tilletia foetida) of wheat in New Zealand was reviewed, including data on incidence, control measures, and the assessment of fungicidal activity on seed by bioassay methods. Grain samples of eight wheat varieties from each of the 1970 to 1973 harvests were tested by means of a 'Washings test' for the presence of Tilletia teliospores. The main variety in New Zealand, Aotea, contained significantly more teliospores per sample than any other variety. Further Aotea samples were tested to indicate the incidence of bunt in the 1973 crop. A total of 244 Aotea wheat samples from the wheat growing counties of New Zealand were tested for Tilletia teliospores, with the number of samples tested per county being proportional to the area of wheat grown. Of these, 2 samples from the North Island, 6 from North Canterbury, 4 from Mid-Canterbury, 6 from South Canterbury and 4 from Southland were infected; the 22 infected samples being 9% of the total number tested. All teliospores detected were those of Tilletia caries, and all were present as trace amounts. A visual examination of 21 treated wheat seed samples from five grain merchants in Canterbury showed that the coverage of seed with fungicide, applied as a slurry, was very variable. This was confirmed by bioassay tests on nine samples which showed that nearly 30% of the seeds tested were receiving less than half the recommended rate of fungicide coverage, and approximately 6% of these seeds were receiving no fungicide at all. This appeared to be a fault of the slurry treating machine used, rather than that of the operators. Three samples of wheat seed, slurry treated by another type of machine, were found to be less variable in coverage.... [Show full abstract]