Davidson, J. A., Krysinska-Kaczmarek, M., Wilmshurst, C. J., McKay, A., Herdina, and Scott, E. S. 2011. Distribution and survival of ascochyta blight pathogens in field-pea-cropping soils of Australia. Plant Dis. 95:1217-1223.Phoma koolunga, Didymeila pinodes, and P. medicaginis var. pinodella were detected in DNA extracted from soil following field pea crops across four states in the southeastern and western regions of Australia. P. koolunga was commonly detected in soil from South Australia but rarely in other states whereas D. pinodes plus P. medicaginis var. pinodeila were widespread in all regions tested. The quantity of DNA of these pathogens detected in soils prior to growing field pea was positively correlated with ascochyta blight lesions on field pea subsequently grown in infested soil in a pot bioassay and also on field pea in naturally infected field trials. The quantity of DNA of the soilborne pathogens was greatest following a field pea crop and gradually decreased in the following 3 years. The DNA tests were used to quantify the DNA of the pathogens in field pea plants sampled from naturally infected field trials in South Australia over two seasons. The combined results of DNA tests and pathogen isolation from the plants indicated that P. koolunga and D. pinodes were equally responsible for the ascochyta blight symptoms in the diseased trials, while P. medicaginis var. pinodeila had a minor role in the disease complex.

No abstract

Ascochyta blight of field pea, caused by Didymella pinodes, Phoma medicaginis var. pinodella, Phoma koolunga and Didymella pisi, is controlled through manipulating sowing dates to avoid ascospores of D. pinodes, and by field selection and foliar fungicides. This study investigated the relationship between number of ascospores of D. pinodes at sowing and disease intensity at crop maturity. Field pea stubble infested with ascochyta blight from one site was exposed to ambient conditions at two sites, repeated in 2 years. Three batches of stubble with varying degrees of infection were exposed at one site, repeated in 3 years. Every 2 weeks, stubble samples were retrieved, wetted and placed in a wind tunnel and up to 2500 ascospores g À1 h À1 were released. Secondary inoculum, monitored using seedling field peas as trap plants in canopies arising from three sowing dates and external to field pea canopies, was greatest in early sown crops. A model was developed to calculate the effective number of ascospores using predictions from G1 BLACKSPOT MANAGER (Salam et al., 2011b; Australasian Plant Pathology, 40, 621-31), distance from infested stubble (Salam et al., 2011a; Australasian Plant Pathology, 40, 640-7) and winter rainfall. Maximum disease intensity was predicted based on the calculated number of effective ascospores, soilborne inoculum and spring rainfall over two seasons. Predictions were validated in the third season with data from field trials and commercial crops. A threshold amount of ascospores of D. pinodes, 294 g À1 stubble h À1 , was identified, above which disease did not increase. Below this threshold there was a linear relationship between ascospore number and maximum disease intensity.

We report the incidence of anthracnose caused by Colletotrichum trifolii on Cullen australasicum, a native Australian legume. Natural infection was observed on plants grown in a genetic resources characterisation experiment at Waite Research Precinct, Adelaide. The affected plants showed wilting of the branches and light brown lesions on the leaves. The characteristic symptom was a bluish black discolouration on the infected leaves and stems. In some plants, the infection spread from the leaves and stems across the entire plant leading to the death of the plant. Fig. 1. Wilting of stems observed on Cullen australasicum plants at the

Rain events in South Australia during the lentil harvest of 2010/2011 raised concerns as to whether grain had been infected with field moulds and associated mycotoxins. Grain samples from commercial crops were tested for the mycotoxins Deoxynivalenol (DON 0 Vomitoxin), Fumonisin B1 and B2 and zearalenone, which are produced by Fusarium spp. Sampling was biased towards more severely affected grain to increase the probability of detection of moulds and toxins, including worst case samples of discarded waste grain (screenings) from cleaning plants. No mycotoxins were detected although Fusarium spp. were detected in all but three of the samples. No Alternaria or Aspergillus spp. were detected. Fusarium spp. were detected at a higher level in grain harvested after a significant rain event in December 2010 compared to grain harvested prior to this event. Percentage of stained seed was higher in plants sampled in machinery wheel tracks compared to those from the remainder of the paddock. The fungal pathogen Ascochyta lentis was also detected on the grain but percentage infection was not affected by harvest date. No Botrytis spp. were detected on the samples. The pilot study identified that the lentil grain in these samples from the 2010/2011 harvest in South Australia was free of mycotoxins and posed no risk to humans or livestock.